From (Neurocritical Care 2012;16:343)

The Risks of Blood Transfusion in Patients with Subarachnoid Hemorrhage: Response to Dr. Paul E. Marik

Peter Le Roux and Michael Diringer

To the Editor,

We read Dr. Marik’s letter with interest. He makes some valuable comments and is correct when he states: more research is needed. We respectfully disagree, however, with his conclusion that the consensus conference recommendations about anemia and transfusion in subarachnoid hemorrhage (SAH) are not supported by the literature. We believe that a more critical appraisal of a wider body of literature is entirely consistent with them. In addition, we feel that his letter emphasizes many potential risks (not all of which apply to SAH patients) but ignores the potential benefit of transfusion in this population.
Dr. Marik makes the following points to support his conclusion that transfusion use should be restricted: (1) transfusion has immunosuppressive and pro-inflammatory properties; (2) improved oxygen delivery does not necessarily lead to increased offloading; (3) aged blood may have adverse effects and nitric oxide depletion could potentially exacerbate vasospasm; and (4) studies associate transfusion with worse outcome.
1.
There is little doubt that transfusion of aged non-leuko-reduced blood has immunosuppressive and pro-inflammatory consequences. Still, the link between these properties and mortality and functional outcome is not well defined. Furthermore, these risks appear to be attenuated with leuko-reduction and reduced storage time. Finally, the potential benefit that transfusion may have in patients with cerebral ischemia and prevention of stroke may far exceed the increased risk of infection.
2.
Dr. Marik suggests that even if transfusion improves oxygen delivery it will not improve offloading to tissue. He cites two clinical studies of septic patients that demonstrate that increased oxygen delivery did not translate into increased global oxygen uptake, even in patients with an oxygen debt. There are a number of reasons to question the relevance of those studies to the issue at hand. In the first, patients had sepsis and multi-organ failure, a very different pathologic state than SAH. In addition, measurements were only made over that first few hours after transfusion, too soon for the blood to have had time to rejuvenate (see below). Finally, the measurements were global; organ specific responses could easily have been diluted. The second paper cited investigated the effects of dobutamine on oxygen offloading and not transfusion.
The work by Dhar et al. [1] is cited to argue that transfusion does not improve oxygen offloading in SAH, since the CMRO2 did not change. However, as was discussed in that paper, CMRO2 would not increase unless there was ongoing active ischemia. The timing of the transfusion was such that patients primarily had regions of oligemia; in those regions transfusion lowered abnormally high oxygen extraction fraction (OEF), indicating improved flow-metabolism coupling and reduced risk of ischemia.
3.
Red blood cells (RBC) deteriorate during storage losing 2,3-DPG and nitric oxide (NO). The clinical consequences are incompletely understood. Over several hours after transfusion the cells undergo a rejuvenation process with restoration of normal levels of these factors [2]. In addition, pre-transfusion use of rejuvenation solutions improves post-transfusion RBC function [3]. Thus, while, as Dr. Marik has shown in sepsis [4], transfused blood may initially be ineffective, over several hours this may not be the case. In SAH where onset of ischemia is delayed, maintaining higher hemoglobin (Hgb) levels with transfusion before the onset of ischemia will allow time for rejuvenation. Thus the concerns that lack of stored NO may exacerbate vasospasm are theoretical at best and ignore that NO is rapidly restored as the RBCs are rejuvenated [2]. Dr. Marik cites one paper that found an association between transfusion and angiographic vasospasm [5]. However, in this study, patient outcome was not associated with transfusion during a patients’ ICU course. Furthermore, the study was retrospective in nature and so it is conceivable that the association exists simply because the patients were transfused to treat delayed cerebral ischemia (DCI).
4.
Dr. Marik argues that the literature indicates that transfusion is associated with worse outcome in SAH patients. Four cohort studies are cited that suggest an association between transfusion and worse outcome after SAH. Yet the work of Broessner et al. [6] who observed that transfusion of RBCs was not associated with ICU mortality or unfavorable long-term outcome in SAH patients was not cited. Due to the retrospective nature of the cited studies each has a potentially fatal flaw; none of the analyses took into account timing, i.e., did transfusion precede the onset of DCI or was it administered as part of the management of DCI? Hence the cause of the poor outcome may be the DCI not the transfusion. We have attempted to address this problem using a propensity score to correct for likelihood of receiving a transfusion and found that transfusion may not have an adverse effect on patients with DCI. Instead any potential deleterious effects may only occur in those at low risk for ischemia.

Two randomized clinical trials (RCT) in transfusion are cited. The one performed in children does not apply to the SAH population. Even the TRICC trial does not since patients with SAH were not included. Furthermore, only 13% (838 of 6,451) of the screened patients were randomized and so, many patients with impaired cardiovascular or cerebrovascular reserve, who are less tolerant to anemia, may have been excluded from the trial [7]. In addition, the quality of transfused blood has changed since 1999 when the TRICC trial was published and this likely will alter outcomes. For example, findings in the Anemia and Blood Transfusion in Critically Ill Patients (ABC) study were consistent with TRICC [8]. However, in the Sepsis Occurrence in Acutely Ill Patients (SOAP) study that used the same methodology as ABC, but was performed several years later, transfusion was not associated with worse outcomes [9]. In the last several years leuko-depletion, which may be associated with fewer adverse transfusion effects, has been widely adopted, and, in general, transfusion has become safer.

Dr. Marik cited the American College of Surgeons National Surgical Quality Improvement Database to indicate that transfusion is harmful. By contrast, a more recent study of septic patients found no such relationship [9]. Still neither of these populations is comparable to SAH. It is important to point out that over the years we have repeatedly learned that generalization of study findings beyond the target population is an unwise and sometimes dangerous proposition.
We do not argue that transfusion is risk free; however, we believe many of those discussed in the letter do not necessarily apply to SAH patients. Yet, even assuming that risk does exist, use of transfusion needs to be considered not only in terms of risk but also in terms of potential benefit. There are several reasons to suggest that transfusion may be helpful to SAH patients at risk for DCI.
1.
Delay cerebral ischemia is the most common cause of preventable secondary injury in SAH. This occurs despite the use of several high-risk interventions including hypervolemia, induced hypertension and angioplasty. Transfusion could provide a lower risk more effective treatment for DCI.
2.
Experimental evidence links anemia with reduced brain tissue oxygen (PbtO2) and increased neuron injury after acute brain injury [10–12]. In the normal brain, compensatory vasodilation occurs with Hgb <10 g/dL [13], so brain hypoxia usually is manifest only at lower Hgb levels (e.g., <6–7 g/dL). However, when cerebrovascular reserve is impaired, e.g., in patients with SAH, tissue hypoxia and cell injury may develop at a higher Hgb. Using cerebral microdialysis in poor-grade SAH patients, Hgb ? 9 g/dL was identified as an independent factor associated with cerebral tissue injury [14]. In a similar study, Kurtz et al. [15] who excluded patients who required an FiO2 >60% linked Hgb <10 g/dL with cellular energy dysfunction.
3.
A recent paper compared the impact of three different interventions to treat DCI in SAH patients. The ability of fluid boluses, induced hypertension and transfusion to improve oxygen delivery to oligemic brain regions was measured using PET [16]. Transfusion of 1 unit of blood was far more effective that either of the other two routinely utilized interventions.
4.
Several observational studies suggest anemia in SAH is associated with worse outcome [17–19], and therefore avoidance of low Hgb may be warranted. The optimal Hgb threshold for RBCT in SAH patients remains unclear although a recent clinical study suggests that an Hgb > 11 g/dL is associated with less cerebral infarction and improved outcome after SAH [17].
Herein in this dilemma for the physician: over-transfuse or under-transfuse. To make this decision requires an understanding of patient physiology. In the ICU, clinicians routinely adjust treatment dose and care based on multiple factors. It is difficult to simulate this in a clinical trial [20]. Randomization to two relatively fixed treatment protocols may not be interpretable in a way that easily informs practitioners and can disrupt the potentially important relationship between level of disease and dose of therapy in a very specific manner, or practice misalignment [21]. This was apparent in the TRICC trial where patients with ischemic heart disease had a significantly different response and in an opposite direction to the two fixed RBCT thresholds than patients without ischemic heart disease [21], i.e., transfusion was “good” in those with reduced cardiovascular reserve. Consistent with this, physicians working in U.S. and Canadian academic neurocritical care units who regularly care for SAH patients transfuse SAH patients based on their perceived cerebrovascular reserve. In particular clinicians are less willing to accept a restrictive transfusion threshold in the setting of DCI: in these patients 30% say they target Hgb >11 g/dl [22]. This practice is entirely consistent with the most recent Guidelines for Transfusion [23] recommendations of the American Society of Anesthesiologists Task Force, [24] and the Canadian Guidelines [25] that suggest transfusion requirements may need to be titrated to parameters of illness severity rather than arbitrarily defined Hgb levels.
5.
To prevent infarction associated with vasospasm requires improved oxygen delivery. When blood is transfused, oxygenation in the brain improves [26–28]. However, it does not increase in about 20–25% of patients. This may be associated with the age of blood, patient sex, starting point of Hgb or PbtO2.
Our original comments and recommendations stand:
1.
It remains unclear whether RBCTs are simply a marker of disease severity or an independent cause of worse outcome.
2.
The results of the TRICC trial and subsequent observational studies of transfusion in general critical care do not and should not apply to SAH patients.
3.
For now, clinicians will need to base transfusion decisions for SAH patients in the context of conflicting information and so should focus on an individualized assessment of anemia tolerance, consider blood conservation strategies, and understand the potential risks and benefits of blood transfusion. This sentiment is echoed in recent published recommendations which state: “Decisions regarding blood transfusion in patients with SAH must be assessed individually because optimal transfusion triggers are not known…” [23].

The risks of transfusion are well understood. However there also are patients who benefit from transfusion. The important question is who will benefit from a transfusion. Perhaps how we transfuse is wrong, i.e. to a Hgb threshold. Perhaps some other endpoint of resuscitation is needed? Here we agree with Dr. Marik: more research and research specific to the SAH population is needed.

References
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Posted by: “Dr.Mohamed El Tahan”

on Anesthideas

 
However, did your surgeon prepare the bypass
machine with extra reservoir !. In reality, as your description this is
ATA III post traumatic aortic dissection and massive bleeding is normal.

First, i would to clarify this missed point which raised by Dr. Bilal and you, this may be related to my unclear initial post. We are talking here about “Traumatic Aortic Transection” which named as “Dissection” or less accurately “Rupture” without presence of any aneurysmal dilatation or dissecting aneurysm. This usually results from the blunt chest trauma after deceleration injuries of the isthmus of the aorta because of its tight attachment to the ligamentum arteriosus which is the obliterated ductus arteriosus. This isthmus injury may extend in both caudal direction to the descending aorta and cranial direction to involve the left subclavian artery and rarely the carotid artery. [Kyobu Geka. 1991 Oct;44(11):965-8., Eur J Vasc Endovasc Surg. 2006 Jan;31(1):18-27.]

Second, we could not apply neither the Debakey classification of aortic dissections nor the Crawford classification of thoracoabdominal
aortic aneurysms (TAA) to this type of injury. So, simply the present case was not at all TAA class III (aneurysms involve the lower portion of the descending thoracic aorta and most of
the abdominal aorta). Svensson et al., class 5 would be the best description of the present injury. (class 1: classic aortic dissection, class 2: intramural hematoma /hemorrhage, class 3: subtle-discrete aortic dissection, class 4: plaque rupture and ulceration, and class5: traumatic and iatrogenic aortic dissection). [Circulation 1999; 99:1331-1336]

We had 23 cases since 2007 in my current referral center with intraoperative death of one case (before exploration) and 3 deaths after surgery because of other trauma related morbidities such as sepsis, ARDS and ventilation-associated penumonia. More than 50% of these case were presented with late aortic transection in similar to Kallistratos et al. [Am J Emerg Med. 2011 Sep 9]. I have involved in the intra-operative of 13 cases of them. All of them were approached through left throacotomy with one lung ventilation (my routine) or two lumg ventilation (by some colleagues) and surgery varied from simple repair, synthetic grafting and/or repair of the subclavian and carotid arteries. We did not use any of the distal aortic perfusion techniques such as passive or active shunts (between the proximal and distal aorta), left heart bypass (left atrium-femoral artery), and partial of full cardiopulmonary bypass (femoro-femoral). In all cases,
cardiopulmonary bypass was present in the OR but not primed. The aortic cross clamp time was less than 30 min in 21 cases and was 40 min in 2 cases including the present case. Two cases developed postoperative short term renal impairment. No case had either early or late paraplegia.

In Egypt, at my original tertiary Mansoura Emergency Hospital in the Middle of Nile Delta we have about 9-14 cases annually. I have only an old statistics for the estimated annual incidence of aortic transection of 7500 to 8000 cases in the United States in 1989 [Ann Thorac Surg 1989; 48: 1–2.].

As Joe mentioned before, there is no doubt that thoracic endovascular aortic repair (TEVAR) has lower Major respiratory complications and shorter hospital stays than with the traditional direct thoracic aortic repair (DTAR). Unfortunately, we do not have expert surgeon or interventionist to do them. [Arch Surg. 2012 Mar;147(3):243-9, Eur J Vasc Endovasc Surg. 2006 Jan;31(1):18-27.]

I would not allow the surgeon to open the chest before he done a double circulation canulation taking the right subclavian artery as upper
circulation which will allow you to keep the brain with the upper body
perfused and then the right femoral artery canulation will assume the
kidney and lower body circulation. Femoral vein canulation for veinous
circulation. When every the bypass is ready and connected I would allow
the thoracotomy. I let the patient cool down till 34 C, give a full dose heparin to the patient and let him start.

First; Augoustides JG, Pantin EJ and Cheung AT in their chapter no. 21 “Thoracic Aorta” in the Kaplan’s Cardiac Anesthesia Textbook, 2010, Pages 638-38, clarified that Standard CPB can be used for the repair of
aneurysms limited to the aortic root and ascending aorta that do not
extend into the aortic arch. Aneurysms that involve the aortic arch
require CPB with temporary interruption of cerebral perfusion (DHCA).
Aortic aneurysms of the descending thoracic aorta require lateral
thoracotomy for surgical access. Aneurysmal resection requires cross-clamping with or without distal aortic perfusion.

Second; the use of simple cross clamping without distal perfusion techniques or the need for partial or full heparinization is recommended for the aortic transection in expert centers with expected clamping time less than 30 min. [Kyobu Geka. 1991 Oct;44(11):965-8., J Cardiothorac Vasc Anesth 2001;  15(6): 761-763, Ann Thorac Surg 1985; 39:37.]. Moreover, Augoustides JG, Pantin EJ and Cheung AT wrote “despite its physiologic consequences, this technique remains popular because it is simple andhas proven clinical outcomes”.

Third; Estrera et al. concluded in their retrospective review that the use of the combined adjuncts of CSF drainage and distal aortic perfusion has all but eliminated the incidence of immediate postoperative neurologic deficit in nonemergent patients withaneurysms of the descending thoracic aorta. These results showed be interpreted with cautious in the view of its retrospective and non-randomized methodologydesign. [Ann Thorac Surg 2001;72:481– 6]

Fourth, there is very nice description by Norris EJ in his interesting chapter of “Anesthesia for Vascular Surgery” in the Miller’s Anesthesia Textbook, 2009, as follows;

- Descending thoracic and thoracoabdominal aortic surgery can be performed without
extracorporeal support (i.e., left heart bypass or cardiopulmonary bypass).
Large series of the “clamp-and-sew†technique have been published with
relatively favorable outcomes, but these cases are from institutions with the greatest clinical experience and the shortest cross-clamp times. Advocates of
this technique favor its surgical simplicity.

-Other than the location and extent of the aneurysm, the duration of
cross-clamping on the aorta is the single most important determinant of
paraplegia and renal failure with the clamp-and-sew technique. Clamp times ofless than 20 to 30 minutes are associated with almost no paraplegia. [J Vasc Surg 1986; 3:389-404., J Thorac Cardiovasc Surg 1981; 81:669-674.] When clamp times are between 30 and 60 minutes (the
vulnerable interval), the incidence of paraplegia increases from approximately
10% to 90% as time progresses.

My last patient ATA III have received 29 RBC, 18 FFP 32 PLT. I usually put continuous tranxenamic acid.
I totally agree that blood loss during TAA repair can be profound which necessitates the use of antifibrinolytic, intraoperative cell salvage, autologus blood transfusion and other blood conservative strategies. This will be correct with the use of phlebotomy to collect the patient’s blood on the reservoir of the bypass or with the use of full bypass rather than the other distal aortic perfusion techniques. I am a fan of tranexamic acid after withdrawal of approtonin. Unfortunately, it was out of stock during the doing of the present case. There was only 500 mg remaining!!

I miss if you insert a CSF catheter drainage (this would help for the postoperative managment )

Omar, you raised an important issue of long debate in the literature as i
will show now. But, i agree with you if it was Crowfiel TAA class III,
there is no doubt this would necessitate lumbar drainage to CSF pressure
of 10 mm Hg rather than 15 mm Hg, pressure transducer zero-referenced to the
midline of the brain and to use any of the above distal
aortic perfusion techniques as needed. [Augoustides JG, Pantin EJ and Cheung AT, Anesth Analg 2010;111:46 –58]

The answer of your question is “No i did not use it for that emergent surgery, especially in the view of short duration of cross clamp”. You can find below similar evidences. I reserve its use of TAA class III and IV rather than transections.

As you know the concept behind the use of CSF drainage it to augment the spinal cord perfusion pressure (SCPP) during aortic cross clamp for thoracic aortic surgery as SCPP = MAP – CSF pressure. There is a long debate about the target CSF drainage pressure and level of transducer. This was nearly solved to be 10 mm Hg rather than 15 mm Hg. [Anesth Analg 2010;111:46 –58]

Again, Norris EJ in the Miller’s Anesthesia Textbook, 2009 mentioned that:

- paraplegia is a devastating complication of aortic surgery. The incidence of
paraplegia is reported to be 0.5% to 1.5% for coarctation repair, 0% to 10% for
thoracic aneurysm repair, 10% to 20% for thoracoabdominal repair, and as high as
40% for extensive dissecting TAA repair.

-Any of the various methods of distal bypass are likely to be beneficial when the
anticipated cross-clamp time islonger than 30 minutes, but they are probably not beneficial when cross-clamp time is less than 20 minutes.

-Although CSF drainage is widely used during TAA repair, the technique is not
without risks. Potential complications include headache, meningitis, chronic CSF
leakage, spinal or epidural hematoma, and subdural hematoma. [Anesth Analg 2010;111:46 –58, J Cardiothorac Vasc Anesth 1995; 9(6): 734-747, J Cardiothorac Vasc Anesth 2005; 19(3): 392-399] A recent retrospective review of 230 patients who underwent TAA repair with CSF
drainage at the Johns Hopkins Hospital reported eight subdural hematomas (3.5%). [J Vasc Surg 2002; 36:47-50.]

-Hypothermia is probably the most reliable method of neuroprotection from
ischemic injury. By reducing oxygen requirements by approximately 5% for each
degree centigrade, a twofold prolongation of tolerated cross-clamp time is
achieved by cooling even to mild hypothermia (34°C). [Also, Augoustides JG, Pantin EJ and Cheung AT wrote the same]

I used passive hypothermia to 34 C during the present case.

Estrera et al considered the following cases as exclusion from the use of CSF drainage; the cases with rupture, acute trauma, infection, or prior paraplegia. [Ann Thorac Surg. 2009 Jul;88(1):9-15; discussion 15.].

In the present case, i had an emergent traumatic aortic transection with expected short calmping time, so i found CSF drainage would be not cost-effective.

The Checklist Project

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In a nationally representative sample, higher patient satisfaction was associated with less emergency department use but with greater inpatient use, higher overall health care and prescription drug expenditures, and increased mortality. ( doi:10.1001/archinternmed.2011.1662)

Resuscitative thoracotomy in the ED can be considered futile care when (a) prehospital CPR exceeds 10 minutes after blunt trauma without a response, (b) prehospital CPR exceeds 15 minutes after penetrating trauma without a response, and (c) asystole is the presenting rhythm and there is no pericardial tamponade.

Article

In April 2001, the ACS-COT Subcommittee on Outcomes gave their final recommendations regarding EDT.24,26(See Table 2.) As expected there was insufficient evidence to support a Level I recommendation for this practice guideline. Their Level II recommendations are as follows:

The above Level II recommendations also are applicable to the pediatric trauma population.

What is the true survival rate of this procedure? Of studies reporting EDT, 7035 procedures were performed with a survival rate of 7.83%. These procedures were stratified by the mechanism of injury. The survival rate for EDT based on penetrating trauma was 11.16%. The survival rate for EDT based on blunt trauma was 1.6%. The survival rate for EDT based on penetrating cardiac injury was 31.1%22,25,26,29Four series included pediatric trauma patients. The overall survival rate for 142 patients who required an EDT was 6.3%. When stratified by the mechanism of injury, the survival rate for penetrating trauma was 12.2% vs. 2.3% for blunt trauma. There was no reliable data reporting penetrating cardiac injuries in the pediatric population.How may survivors succumb to severe neurologic impairment? Of the series reporting neurologic outcomes, 4520 patients were subjected to EDT. There was a 5% overall survival rate. Of these survivors, 15% survived with severe neurologic impairment.What are the valuable physiologic predictors of favorable outcomes? Physiologic predictors of outcomes for EDT have been identified. In 1983, Cogbill and associates determined four statistically significant indicators that portend a dismal outcome. They are: 1) no signs of life at the scene; 2) no signs of life in the ED; 3) no cardiac activity at the time of EDT; and 4) persistent hypotension (SBP < 70 mmHg) despite aortic occlusion. Five years later, Branney and his group determined that the absence of vital signs in the face of blunt trauma also led to a poor outcome.22,25,26,29

Accepted IndicationsPenetrating thoracic injury- Traumatic arrest with previously witnessed cardiac activity (pre-hospital or in-hospital)- Unresponsive hypotension (BP < 70mmHg) Blunt thoracic injury- Unresponsive hypotension (BP < 70mmHg)- Rapid exsanguination from chest tube (>1500ml)Relative IndicationsPenetrating thoracic injury- Traumatic arrest without previously witnessed cardiac activityPenetrating non-thoracic injury- Traumatic arrest with previously witnessed cardiac activity (pre-hospital or in-hospital)Blunt thoracic injuries- Traumatic arrest with previously witnessed cardiac activity (pre-hospital or in-hospital)ContraindicationsBlunt injuries- Blunt thoracic injuries with no witnessed cardiac activity- Multiple blunt trauma- Severe head injury

Azygos vein on R

Can cut ligaments on bottom of hilium and then clamp it.

Ladd AP, Gomez GA, Jacobsen LE, et al., Emergency room thoracotomy: updated guidelines for a level I trauma center. Am Surgeon2002;68:421–4.

This group from the Indiana University School of Medicine developed and published a protocol for Emergency Room Thoracotomy (ERT) in 1995, after reviewing their own experience with 160 patients undergoing ERT. The present study was undertaken to evaluate this protocol, reviewing the records of all patients undergoing ERT over the next 5 years. Of the 79 patients, 65 had suffered gunshot wounds and 14 stab wounds. The authors’ protocol divided patients into 4 physiologic classes. Class I patients had no signs of life: full arrest, absent reflexes, and no ECG activity. Class II were agonal: and electrical activity on ECG but no pulse. Class III were in profound shock, with BP < 60 torr, and Class IV were in mild shock, BP > 60 but < 90 torr. The authors found that there were no survivors among patients who were Class I or II at the scene, or Class I on ED arrival, and they therefore recommend that ERT not be performed henceforth for these groups.

I put into the right atrium whatever catheter is available and has a connector to be allowed to have a connection to venous fluids being administered

Then I place a right angled clamp, curved Glover vascular clamp, Satinsky clamp, or whatever I have across the atral appendage even occluding the catheter for a secord or two.   I then ask for a large silk suture – 0 or 00 will do and I just tie it secure around the atrium, but not occluding the catheter.   Works every time.   Hemostatic.   I use this same technique when I need to crash onto the pump in the OR with the atrial catheter connected to the pump.    I can place a purse string later if necessary.    If there are lots of people around, I will tie the knot on the silk suture, and then NOT cut the suture, but wrap it Roman sandle style around the catheter, so as to secure it so that none of the many people in the room or during transport can inadvertently pull it out.    I then leave the silk ends long and un cut in case I need to use the loos ends for something else , but it someone cuts then at the second knot on the catheter, then I dont say anything, and just get moving with the resuscitation or move to the OR.  (Mattox)

3-0 prolene with large curved MH needle to repair cardiac injuries. consider teflon pledgets

can use 6 mm staples place 5 mm apart

can staple around foley 3 staples on either side then deflate

never put finger in, only on

put 14 F foley in 3 cm and fill balloon with saline, pull back 1 cm if no output

vent all air out before clamping

pull on it only enough to slow bleeding to an ooze

Four Uses of ED Thoracotomy

1 Relief of Tamponade

2 Hemorrhage from Intrathoracic Source

3 Cross Clamping of Pulmoanry Hilum after suspected air embolism

4 Cross Clamping of Aorta as last ditch adjunct to CPR

Asystole is contraindication, but what of PEA (J AM Coll Surg 2004;199:211)

Blunt trauma=5 minutes of CPR, bilat chest tubes. If no signs of life call code; if signs then open chest

Factors suggesting discontinuation of resuscitation during thoracotomy

Systolic blood pressure remains <70 mmHg after 15 min despite fluid volume resuscitation Self-sustaining rhythm is not achieved within 15 min of start of thoracotomy Need for aortic cross-clamping in an attempt to restore myocardial and cerebral perfusion Absence of a pericardial effusion without cardiac activity on opening of the chest Emergence of signs of secondary devastating injuries with an independently poor outcome

:

D. Lockey, K. Crewdsen and G.E. Davies, Traumatic cardiac arrest: who are the survivors?, Ann Emerg Med 48 (3) (2006), pp. 240–244.

Recent article on thoracotomy for abd exsanguin, 16% of the group survived neuro intact (J Trauma 2008;64:1)

Rhee PM, Acosta J, Cridgeman A, et al. Survival after emergency department thoracotomy: review of published data from the past 25 years. J Am Coll Surg 2000;190:288-98.

Following anterolateral thoracotomy, opening and evacuation of the pericardial cavity,2,3the wound is controlled by digital compression or with the use of clamps if the laceration is atrial. The laceration may then be closed with a standard skin stapler using wide (6 mm) staples. The staples are placed at a 3–5 mm intervals with additional ones placed only if required to achieve haemostasis. Following stapling, the laceration may be safely oversewn using a 4/1 polypropylene suture in the operating theatre.

May be worth doing to increase organs for donation as well (J Am Coll Surg 2010;211:450)

Western Trauma published multi-center trial (J Trauma 2011;70(2):334)

States blunt trauma may not be an exclusion and even field cpr of 9 min for blunt and 15 min for penetrating. Asystole on arrival had neuro intact survivors.

• EDTs should be performed rarely in patients sustaining cardiopulmonary arrest secondary to blunt trauma due to the unacceptably low survival rate and poor neurologic outcomes;22
• EDT should be limited to those that arrive with vital signs at the trauma center and experience a witnessed cardiopulmonary arrest;16
• EDT is best applied to patients sustaining penetrating cardiac injuries who arrive at trauma centers after a short scene and transport time with witnessed signs of life;12,13
• EDT should be performed in patients sustaining penetrating non-cardiac thoracic injuries.12,13,15,16,22,23 They did acknowledge the difficulty in ascertaining whether the thoracic injury was cardiac or non-cardiac and promoted the use of EDT to establish the diagnosis; and
• EDT should be performed in patients sustaining exsanguinating abdominal vascular injuries although these patients experience a low survival rate.

When is ED Thoractomy Futile?

Resuscitative thoracotomy in the ED is a resource-intense procedure
that is quite stressful and demands accurate evidence-based guidelines
for its cost effective application; there has been an ongoing search to
define when this heroic resuscitative effort is futile.

The Western Trauma Association recently published a multi-center
study to identify injury patterns and physiologic profiles at ED arrival
that are compatible with survival. During the 6 year study period, 56
patients survived to hospital discharge. Specifically, the purpose of
the study was to define the limits of resuscitative ED thoracotomy to
enable the development of rational guidelines to withhold or terminate
resuscitative efforts.

Contrary to some recommendations, the study found that with the
exception of an overtly devastating head injury, blunt trauma does not
preclude meaningful survival after ED thoracotomy. In addition, the
study documented survival of 7 patients with asystole found at the time
of thoracotomy.

The study concluded that resuscitative thoracotomy in the ED can be
considered futile care when (a) prehospital CPR exceeds 10 minutes after
blunt trauma without a response, (b) prehospital CPR exceeds 15
minutes after penetrating trauma without a response, and (c) asystole
is the presenting rhythm and there is no pericardial tamponade.

Clinical Pearl Suggested by Dr. Michael Winters, Univ of Maryland, Dept. of EM

Reference: Moore EE, et al. Defining the
limits of resuscitative emergency department thoracotomy: a
contemporary Western Trauma Association perspective J Trauma 2011;70:334-9.

NAEMSP/ACS-COT Guidelines for Withholding or Termination of Resuscitation in Prehospital Traumatic
Cardiopulmonary Arrest

1. Resuscitation efforts may be withheld in any blunt trauma patient who, based on out-of-hospital personnel’s thorough primary
   patient assessment, is found apneic, pulseless, and without organized ECG activity upon the arrival of EMS at the scene.
2. Victims of penetrating trauma found apneic and pulseless by EMS, based on their patient assessment, should be rapidly assessed for
   the presence of other signs of life, such as pupillary reflexes, spontaneous movement, or organized ECG activity. If any of
   these signs are present, the patient should have resuscitation performed and be transported to the nearest emergency
   department or trauma center. If these signs of life are absent, resuscitation efforts may be withheld.
3. Resuscitation efforts should be withheld in victims of penetrating or blunt trauma with injuries obviously incompatible with life, such
   as decapitation or hemicorporectomy.
4. Resuscitation efforts should be withheld in victims of penetrating or blunt trauma with evidence of a significance time lapse since
   pulselessness, including dependent lividity, rigor mortis, and decomposition.
5. Cardiopulmonary arrest patients in whom the mechanism of injury does not correlate with clinical condition, suggesting a
   nontraumatic cause of the arrest, should have standard resuscitation initiated.
6. Termination of resuscitation efforts should be considered in trauma patients with EMS-witnessed cardiopulmonary arrest and 15 min
   of unsuccessful resuscitation and CPR.
7. Traumatic cardiopulmonary arrest patients with a transport time to an emergency department or trauma center of more than 15 min
   after the arrest is identified may be considered nonsalvageable, and termination of resuscitation should be considered.
8. Guidelines and protocols for TCPA patients who should be transported must be individualized for each EMS system. Consideration should be given to factors such as the average transport time within the system, the scope of practice of the various EMS providers within the system, and the definitive care capabilities (i.e., trauma centers) within the system. Airway management and IV line placement should be accomplished during transport when possible.
9. Special consideration must be given to victims of drowning and lightning strike and in situations where significant hypothermia
   may alter the prognosis.
10. EMS providers should be thoroughly familiar with the guidelines and protocols affecting the decision to withhold or terminate
    resuscitative efforts.
11. All termination protocols should be developed and implemented under the guidance of the system EMS medical director. On-line medical control may be necessary to determine the appropriateness of termination of resuscitation.
12. Policies and protocols for termination of resuscitation efforts must include notification of the appropriate law enforcement agencies
    and notification of the medical examiner or coroner for final disposition of the body.
13. Families of the deceased should have access to resources, including clergy, social workers, and other counseling personnel, as
    needed. EMS providers should have access to resources for debriefing and counseling as needed.
14. Adherence to policies and protocols governing termination of resuscitation should be monitored through a quality review
    system.

validated in this study ((J Trauma. 2011;71: 997–1002)

Internal Defibrillation

20 J for the first shock, 40 J subsequent

Partial Pericardotomy

this report (Ann Emerg Med 2012;59(4):265) advocates leaving pericardium intact and just suctioning blood until surg involves. of course, the 3 L blood loss that ensued could be avoided by just opening the hole

Alkalemia

hypokalemia (and sensitization to dig related arrhythmias)

reduction of ionized calcium leading to neurologic symptoms

Stimulates anaerobic metabolism

Metabolic Alkalosis

Plasma bicarb>45

seek to lower it to

• Nasogastric Suction/Vomiting
• Diuretics-from increased loss of urinary electrolytes and water. Cl loss balanced by reabsorbtion of bicarb, H+ moves into cells to allow eflux of K. Mg loss promotes loss of K
• Hyperaldosteronism
• Volume depletion: contraction alkalosis. Stimulation of renin-angiotensin to waste H+
• Organic Ion administration-Lactate, acetate, and citrate. (need 8 units of blood to affect pH.)
• Posthypercapnia-if chronic

Contraction alkalosis because relatively more bicarb in a smaller space (sketchy concept)

Patients need NaCl and Potassium Chloride

Can give hydrochloric acid

need 0.1 to 0.2 N solution (100 to 200 mmol per liter)

0.5 * kg * desired reduction in bicarb=mmol of acid needed

Volume in L of 0.1 M=desired mEQ/100 mEq/L

Using 0.2 desired mEq/200 mEq/L

Infuse at 0.2 mEq/kg/hour

Cl responsive if urine Cl is

Vomiting, gastric drainage, diuretics, lactate, acetate

Cl Resistant if Cl>20 mEq (Mineralcorticoid excess or K depletion)

excess mineralcorticoid (cushings, hyperaldo, ACTH tumors, licorice, renal art stenosis, steroids,)

severe k deficiency

mag deficiency

associated with high mortality (South Med J 1987;80(6):729)

3 Causes from a Renal Perspective

from Joel Topf

1. Conditions with chloride depletion with secondary collecting duct hydrogen stimulation
2. Conditions with primary stimulation of the collecting duct hydrogen secretion
3. Increased Alakli Intake with renal failure

Respiratory alkalosis:

Acute

a.HCO3- drops 1 to 3.5 mEq/L for every 10 mm Hg drop in P CO2 .

Limit of compensation: bicarbonate is rarely below 18 mEq/L.

Chronic (renal compensation starts within 6 hours and is usually at a steady state by 1.5 to 2 days)

a.HCO3- drops 2 to 5 mEq/L for every 10 mm Hg drop in P CO2 .

Limit of compensation: bicarbonate is rarely below 12 to 14 mEq/L.

Pseudorespiratory Alkalosis

severely reduced pulmonary perfusion with normal alveolar ventilation (i.e. you’re bagging a shocked patient)

less CO2 is delivered and more CO2 is extracted (b/c of poor systemic perfusion and poor relative pulmonary perfusion respectively)

So get arterial eucapnia or even hypocapnia with a severely acidotic and hypercapnic venous and tissue state

Malpractice

LAWSUITS: PART 1 AN ATTORNEY’S PERSPECTIVE From High Risk Emergency Medicine, sponsored by the Center for Emergency Medicine Education William H. Ginsburg, JD, Principal Member, Cotkin, Collins and Ginsburg, Los Angeles and Santa Ana, California, and Las Vegas, Nevada Introduction:

poor charting causes most lawsuits; physicians use deductive reasoning (ie, premise followed by conclusion); attorneys use inductive reasoning (start with conclusion and work backward to find premise on which conclusion can be justified); both valid methods of reasoning, although physicians must deal with “hot” facts and have little time, whereas attorneys have “cold” facts and have much time to find premise Basis of claims:

“if it isn’t in the chart, it wasn’t done”; “if you didn’t put it in the chart, you didn’t consider it”; “if it’s written down in the chart incorrectly, then you didn’t understand it”; “if you didn’t give all of the best medications or cocktail of medications, then you didn’t know what you were doing” Image of physicians:

American public no longer places physicians on pedestal; physicians make too much money, charge too much, and often do not know what they are doing Medical defenses:

medical perfection not required; “doctor who gets an untoward result is not necessarily negligent if his or her care otherwise was within the standard of care applicable to the community and the circumstances”; physicians must base decisions on judgment, which does not always yield good clinical result; mistakes and medical errors are not necessarily negligence; “where there is more than one recognized method of diagnosis or treatment and no one of them is used exclusively and uniformly by all practitioners of good standing, a physician is not negligent if in exercising his or her best judgment he or she selects one of the approved methods which later turns out to be a wrong selection or one not favored by certain other practitioners” Jurors’ attitudes:

impression jurors form of defendant physician extremely important; failure to diagnose or (in retrospect) effectively treat a condition does not constitute malpractice; jurors willing to listen to reasoning behind physician’s thought process; willing to listen to expert witnesses and physician; by end of case, speaker wants jurors to walk away wanting defendant to be their emergency physician if they ever need one; jurors unwilling to resolve doubts in favor of physician when physician fails to obtain complete history and conduct adequate physical examination Charting:

speaker does not like template charting unless blanks available for physician to fill in that demonstrate physician knows patient thoroughly and he or she considered and ruled out most serious conditions first; physicians should read notes from previous care givers (eg, paramedics, nurses) and initial their comments, indicating physician read them (unless this is done, “nobody believes that you read the paramedic run, nobody believes that you read the nurses’ notes”) Trial law: “trial law is not a game but it is theater, and consequently, I’ll never tell you what to say, but I’ll tell you how to say what you want to say properly”; “a good director doesn’t change the script; a good director changes the intonation, the presentation, and the method of the words that remain steady and true to the authorbut they’re presented in such a way that they make the impression that we want them to make” Consultations:

“when in doubt, obtain a consultation”; physician should think about and predetermine threshold, ie, situations in which he or she would call in consultant Patient expectations: jurors are also patients; jurors react angrily and define standard of care without regard to expert witnesses if they think that plaintiff was not treated as jurors would want to be treated in plaintiff’s circumstance; patients want to know truth about what is going on (do not want to be left alone with no explanation); do not care about other patients physician has to treat; want regular contact by physician; do not want to see loved one suffer; want responsive and attentive consulting and nursing staff; want to be treated as if they are important; want clear and complete explanations; involve patient’s family when possible and practical (avoid giving impression health care staff does not care; chart process of involving family); want continuity of care Consultants:

in court they claim, “if only I had been called,” “if only he or she had told me,” “if only I had known” Do not delay important diagnostic tests: still practicing defensive medicine because no limit to amount for which physicians can be sued or to circumstances that give rise to medical malpractice litigation Suggest and chart adjunct examinations: under law of negotiable instruments, last physician to see patient before serious condition discovered is liable for missing diagnosis; if woman who presents with ganglion on wrist says she has not been to doctor in 10 yr, and emergency physician does not recommend she see physician for complete physical examination (including gynecologic examination) and chart it, physician can be liable if serious condition discovered subsequently; if follow-up appointment necessary, physician or staff should help patient make appointment and document that this was done Medical records:

good charting no substitute for good judgment and patient rapport, but key to avoiding lawsuits; chart should show reasoning process that led to differential diagnosis and that physician considered all serious diagnoses first; give patient clear, readable, understandable follow-up instructions in appropriate language; speaker favors voice-activated dictation systems for charts; medical records have 3 purposes—1) remind original health care professionals what they have done, 2) alert other health care professionals to what has already been done, 3) serve as evidence in litigation Elements of good medical records:

are they legible? do they say what needs to be said? are they so convincing that they are difficult to attack? do not include comments that indict others; if, for example, consultant uncooperative, do not resort to name calling but chart how many times consultant was called, what was communicated, and “everything that you did, so that later on he can’t say, ‘he never told me about the child’s temperature’”; impossible to win case when physician cannot read his or her own writing; never alter chart improperly (use single line through deleted material and make reference point; at bottom of chart place reference symbol with change and reason for change); copy of any document physician produces for patient should go into chart (eg, prescriptions); unusual events should be charted and explained (eg, patient falling off gurney); because of epidemic of addiction, do not prescribe opioids without first checking to make sure real need present Language to avoid:

do not inadvertently use condescending language in charts and consultation reports; “the parents seemed responsible” innocent entry, but parents were ethnic Hispanic, physician was white, and jury was primarily Hispanic (took great offense); instead write, “procedure explained and parents agreed”; “she was a difficult woman” (female jurors take great offense; instead, “she was a difficult person” or “she was unruly and hard to manage, angry, and upset”); do not use phrases like “he was acting as though he was gay,” “typically Hispanic,” “typically Jewish,” “she was obviously faking” (instead, “symptoms appeared to be psychosomatic”); may need to be persuasive to get patient to agree to tests and/or further observation (be persuasive and chart your efforts); famous plaintiff’s argument—“sloppy in charting is sloppy in practice” Questions and Answers Sending patient through gatekeeper of HMO or to county hospital if patient indigent: no problem if patient not in critical condition; emergency physician can be liable until patient under care of another physician; be diligent in protecting patient; case of psychotic man who was treated, then told to go to county hospital for further treatment; patient never went to county hospital and stabbed woman to death in carjacking incident; plaintiff argued physician liable because physician should have physically taken patient to facility or made sure responsible person was taking care of him; in emergency situations, do what is right for patient and deal with insurance later; may be liable for delay in care Are small minority of physicians causing majority of lawsuits?

so-called malpractice crisis not caused by indemnity payouts but by cost of running system (mostly fees for attorneys and expert witnesses); physicians who are repeatedly sued usually dropped by insurance company Dealing with hospitalist who disagrees with physician’s recommendation:

physician’s duty to protect patient; if he or she believes hospitalist wrong, clearly chart reasons and communications with hospitalist, or petition chair of department with another physician

LAWSUITS: PART 2 MEDICOLEGAL CASE STUDIES—B. Joshua Rubin, MD, President and Chief Executive Officer, EMSource, Roseville, California; William H. Ginsburg, JD, Principal Member, Cotkin, Collins and Ginsburg, Los Angeles and Santa Ana, California, and Las Vegas Issues of consent Separate consent form for lumbar puncture (LP): LP not particularly dangerous or complicated procedure; other than fact that employer or group may require it, form not necessary because if emergency exists, consent implied; if procedure performed on child, may only accomplish making parents nervous by asking for additional consent; true informed consent comes from physician/patient relationship and communication, not from signature; in addition to signed informed consent form, Ginsburg would like to see statement in chart saying procedure was discussed with patient or patient’s parents, that risks and alternatives explained, and that party agreed to procedure (“worth 10 informed consent forms”) 8-yr-old with facial laceration that brought in by neighbors: parents gone for weekend and cannot be reached; no consent needed; do what is best for patient Adolescent girl with vaginal bleeding: says she is pregnant, wants to be treated, but does not want family notified; adolescent patients need physician’s protection and confidentiality, plus law requires it; every state has “emancipated minor” law; legislative intent is to protect children so they can access needed medical care for certain conditions (eg, contraception, sexually transmitted diseases [STDs], pregnancy); physician could be liable for adverse events resulting from notifying parents Telephone advice: give selective first aid advice in cases involving, eg, arterial wound, chemical in eye, ingestion of toxin; use telephone log to track calls and to document type of advice given, eg, primary first aid advice, medical advice; if patient had been seen before phone call, put him or her in touch with physician who provided care Issues related to duty to third parties Medications that impair: man 26 yr of age complaining of severe headache requests meperidine (Demerol) for typical migraine headache; receives injection and is discharged 30 min later; on way home, patient crashes into another automobile; everyone involved in crash sues physician and hospital http://www.audio-digest.org/pages/htmlos/06210.5.4446057220213861273/EM2118 (1 of 5)10/30/2004 10:33:14 PM View Written Summary: Emergency Medicine, 21:18 Discussion: physician has duty to report to Department of Motor Vehicles (DMV) any condition resulting in episodes of syncope; failure to report makes physician liable; discharging patient too quickly after administering narcotic or other medication that causes drowsiness makes physician liable if patient operates vehicle or machinery and injures self or third party; reasonable approach is to make sure patient comes to hospital with someone capable of taking him or her home; if not, make sure patient gets into taxicab, or that patient kept under observation long enough for effects of medication to wear off; whenever medication given, obtain informed consent and document in chart Duty to third party: physician has duty to notify police if patient discloses that he or she plans to hurt somebody; discharge instructions must instruct patients with seizure disorder, lapse of consciousness, narcotic therapy, eye patch, or similarly impairing condition not to drive; be aware of state laws; to avoid liability, notify DMV of patient’s impairment STDs: 22-yr-old man treated for presumed Chlamydia (culture negative); wife sues physician 2 yr later because she is infertile and alleges infertility secondary to infection; she claims no one told her she needed to be treated Approach: no report to Department of Public Health required in this case because culture negative; respect patient’s confidentiality but must tell him to inform sex partner(s); report positive cultures to Department of Public Health Difficult patients Patient with acute myocardial infarction (MI) leaving against medical advice: give patient medication but tell him or her medication no substitute for being admitted to hospital; let patient know he or she welcome to return at any time; most important to make sure patient competent, ie, has capacity to understand relevant information, consequences of various options, and communicate information about that choice (“oriented times 4” not enough); document that physician determined patient able to understand relevant information and could respond appropriately to questions; be persuasive and chart attempts to get patient to stay, including telling patient about possibility of death or serious injury and contacting consultants and/or family doctor Intoxicated man 50 yr of age with scalp laceration, slurred speech, and ataxia: patient announces tired of waiting and going to leave; attempts to convince him to stay unsuccessful; when physician explains patient may need to be restrained, he starts walking out; patient weighs 250 lb, 6 ft 4 in Discussion: call security guard or have police intervene; do not put self or staff in harm’s way; if patient competent, let patient leave Medical staff issues Consultant disagrees with emergency physician on patient’s need for admission: if by phone, ask consultant to come in and see patient; if consultant disagrees after evaluating patient and emergency physician feels strongly that consultant wrong, emergency physician has obligation to keep patient in emergency department (ED) Chain of command: new theory that has been applied to nurses and now being applied to physicians as well; emergency physician should consult colleague, head of department, chief of staff (move up chain of command) to protect patient; recommended that ED have bylaws that specify course of action in such situations (usually involves calling in third party to help make decision) Consultant coming in: man 25 yr of age with stab wound to abdomen, free air on x-ray, orthostatic vital signs; surgeon busy but calls in orders to have patient admitted to intensive care unit (ICU); emergency physician concerned patient should go directly to operating room (OR) but believes since all information has been given to surgeon, responsibility for patient has been transferred to surgeon Discussion: until patient seen and evaluated by another attending physician, emergency physician responsible for that patient, especially one going to wrong place in hospital

Standard of Care

In professional negligence cases, a defendant physician may be liable for actions where there was a duty to provide care, a care standard was breached, and as a result of that breach, damage or injury was done to another.8 Each of these elements must be present and proven by a preponderance of evidence for a finding of medical liability.8 In addition, simply demonstrating that a mistake or an adverse event occurred is not sufficient for a finding of negligence.9 Thus, the outcome of medical malpractice cases depends on the definition of the relevant professional care standard or practice custom of the medical community. Clearly, in our scenario there was a duty to provide care, but was a care standard breached? (Annals EM NOv 2004)

res ipsa loquitur, meaning “the thing speaks for itself.”8 In this situation, a plaintiff makes a claim on the basis of circumstantial evidence, inferring that the adverse outcome could not have occurred in the absence of negligence on the part of the defendant. Negligence in cases employing res ipsa is generally apparent to the layperson, such as in the performance of a procedure on the wrong body part, and therefore an expert witness to establish a standard is not usually required. Despite the foregoing exceptions, the expert witness remains the most common way in which the standard of care is defined in medical-legal proceedings.

Why do Doctors get Sued

No claims physicians spent longer, joked more (JAMA 1997;27(7):) Tone of voice most important factor. Higher dominance and lower concern/anxiety associated with suits. (Surgery 2002;132(1):5)

Analysis of relation between negligence and outcome of litigation in NY (NEJM 1996;335:26:1963)

Special Defenses to Malpractice Cases

Ulnar Nerve

From Mike Stone for Ulnar

Block at the level of the knee fossa; just before the branch to the tibial and peroneal

Reference: How Much Time Does it Take to Get a Pressure Ulcer? Integrated Evidence from Human, Animal, and In Vitro Studies. Ostomy Wound Management. 54(10):26-8, 30-5, 2008.

• “Screening reconciliation” for all ED patients should include routinely obtaining from each patient at each ED visit a list of the patient’s current medications (usually done by the triage nurse).
• “Focused reconciliation,” as directed by the emergency physician, based on medical relevance, should include seeking additional information about the patient’s medications (exact drug list, dosage/route, etc.) from the patient’s pharmacy, primary care physician, family, etc.
• “Full reconciliation” for admitted patients should be completed by the receiving inpatient unit and pharmacist.

(This information is current as of January 2007. The Joint Commission may change or amend its FAQs, and accuracy should be confirmed by visiting its National Patient Safety Goals Web site.)

When the patient is sick an authoritative/directive leadership style is more effective than empowering in a simulation study. (J Applied Psychology 2005;90(6):1288)

debriefing is probably garbage.

WHO put out psychological first aid which makes a lot more sense, to me at least.

EAST Guidelines for Pneumo/Hemothorax

(The Journal of TRAUMA 2011;70(2):510)

Diagnosis

1. Ultrasound can reliably be used to identify pneumothorax and pleural effusion (Level 2).

2. CT of the chest is indicated in patients with persistent opacity on chest radiograph after tube thoracostomy to determine whether significant undrained fluid exists (Level 2)

3. Primary VATS of stable penetrating thoracoabdominal wounds is safe and effective for the diagnosis and management of selected diaphragm and pulmonary injuries

(Level 2).Management of Massive Hemothorax1. Patient physiology should be the primary indications forsurgical intervention rather than absolute numbers of initial or persistent output (Level 2).2. 1500 mL via a chest tube in any 24-hour period regardless of mechanism should prompt consideration for surgicalexploration (Level II). Management of Hemothorax1. All hemothoraces, regardless of size, should be consideredfor drainage (Level 3).2. Attempt of initial drainage of hemothorax should be witha tube thoracostomy (Level 3).3. Persistent retained hemothorax, seen on plain films, afterplacement of a thoracostomy tube should be treated withearly VATS, not a second chest tube (Level 1). 4. VATS should be done in the first 3 days to 7 days ofhospitalization to decrease the risk of infection and conversionto thoracotomy (Level 2).5. Intrapleural thrombolytic may be used to improve drainageof subacute (6-day to 13-day duration) loculated orexudative collections, particularly patients where risks ofthoracotomy are significant (Level 3).Management of Occult Pneumothorax1. Occult pneumothorax, those not seen on chest radiograph, may be observed in a stable patient regardless of positivepressure ventilation (Level 3).

3. Scoring systems are not accurate in predicting whichpatients will need a tube thoracostomy for occult pneumothorax(Level 3).4. A persistent air leak on postinjury day 3 should prompt aVATS evaluation (Level 2)

patho of tension
more pathophys of tension

Tube Drainage Indications for Thoracotomy

20 cc per kilo initially or 5 cc/kg/hr or 25 cc/kg total to OR

1.5 liters initially or 350  (200) cc/hr or 2 1/2 liters total.

The presence of more than 1500 mL of blood in the initial chest tube drainage, drainage of more than 200 mL an hour for 2-4 hours, or ongoing transfusion requirements mandate surgical exploration with open thoracotomy

CT Chest is useful (J Am Surgeon 2001;67:660-664)

West Study on Retained Hemothorax

RH <=300 cc and pneumothorax as initial indication for trauma thoracostomy tube placement.

“The Box”

Notch and Clavicles (roof), Nipple line are lateral (sides), Costal Margins (bottom)

Echo initially and repeat in 6 hours.  C-XR initially and in 6 hours.  Can use helical CT to evaluate for pericardial fluid, just as good.

“The box:” definition of proximity to the heart for penetrating injuries. X = wounds that produced cardiac injuries (Nagy KK, J Trauma 1995)

Thoracoabdominal

Nipple Line to costal margins/below the scapula

Both cavities and worry about the diaphragm

DPL is good here, use low cut-off 5000 RBCs per cc

7% risk of occult diaphragmatic injury (J Trauma 2003;55(4):646)

J Trauma. 1997 Oct;43(4):624-6.Penetrating left thoracoabdominal trauma: the incidence and clinical presentation of diaphragm injuries. OBJECTIVE: The objective of this study was to (1) determine the incidence of diaphragmatic injuries in penetrating left thoracoabdominal trauma and (2) evaluate the role of laparoscopy in detecting clinically occult diaphragmatic injuries. PATIENTS AND METHODS: One hundred nineteen consecutive patients with penetrating injuries to the left thoracoabdominal region presenting to Los Angeles County-University of Southern California Medical Center were prospectively evaluated during an 8-month period. Either celiotomy (with hemodynamic instability or peritonitis) or laparoscopy was performed. Results of the clinical examination and roentgenographic findings were recorded preoperatively. RESULTS: One hundred seven patients were fully evaluated. Fifty patients required emergent celiotomy. Fifty-seven patients underwent laparoscopy. The overall incidence of diaphragmatic injuries was 42% (59% for gunshot wounds, 32% for stab wounds). Among the 45 patients with diaphragmatic injuries, 31% had no abdominal tenderness, 40% had a normal chest roentgenogram, and 49% had an associated hemopneumothorax. Fifteen of the patients undergoing laparoscopy (26%) had occult diaphragm injuries. CONCLUSION: (1) The incidence of diaphragmatic injuries in association with penetrating left thoracoabdominal trauma is high. (2) The clinical and roentgenographic findings are unreliable at detecting occult diaphragmatic injuries. (3) Laparoscopy is a vital tool for detecting occult diaphragmatic injuries among patients who have no other indications for formal celiotomy.  

Rib Fx

X-Ray if ribs 1-2, 9-12, pathological fx, or elderly

1st or 2nd rib is fx along with another rib-get angio

Flail-3 ribs in two places

Traumatic Asphyxia

Pulmonary Contusion

Epidural analgesia probably reduces vent days and nosocomial pneumonia (J Surg 2004;136(2):426)

A Prospective Randomized Trial of Nebulized Morphine Compared with Patient-Controlled Analgesia Morphine in the Management of Acute Thoracic Pain [Original Articles] Fulda, Gerard J. MD, FACS, FCCM; Giberson, Frederick MD, FACS; Fagraeus, Lennart MD, PhD From the Departments of Surgical Intensive Care (F.G. and G.J.F.) and Anesthesia (L.F.), Christiana Care Health Services, Newark, Delaware. Submitted for publication October 26, 2004. Accepted for publication May 10, 2005. Presented at the 63rd Annual Meeting of the American Association of the Surgery of Trauma, September 29–October 2, 2004, Maui, Hawaii. Address for reprints: Gerard J. Fulda, MD, FACS, FCCM, Director, Surgical Intensive Care, Associate Director of Trauma, Christiana Care Health Services, Room 2325, 4755 Ogletown-Stanton Road, Newark, DE 19718; email: gfulda@christianacare.org. Abstract Background: Successfully managing pain for the trauma patient decreases morbidity, improves patient satisfaction, and is an essential component of critical care. Using patient-controlled analgesia (PCA) morphine to control pain may be complicated by concerns of respiratory depression, hemodynamic instability, addiction, urinary retention, and drug-induced ileus. Morphine is rapidly absorbed by mucosal surfaces in the respiratory tract, achieving systemic concentrations equal to 20% of equivalent intravenous doses. The purpose of this study was to evaluate the safety, efficacy, and utility of nebulized morphine in patients with posttraumatic thoracic pain. Methods: This double-blinded, prospective study randomized patients with severe posttraumatic thoracic pain into two groups. The experimental group (NMS) received nebulized morphine every 4 hours and normal saline by PCA. The control group (PCA) received nebulized saline every 4 hours and morphine by PCA. Dose adjustments were made based on patient response to treatments using a 10-point visual analog scale (VAS) for pain. Pulmonary function, pain relief (VAS), level of sedation (0–3), total drug administration, and systematic side effects were recorded. Results: Forty-four patients were randomized (22 per group). Seven hundred seventy observations were made. The mean 4-hour dose of morphine was 11.96 ± 3.4 mg for NMS and 6.22 ± 4.7 mg for PCA (p < 0.001). Patients with NMS had lower heart rates compared with PCA (79 ± 11 bpm versus 92 ± 12 bpm; p < 0.001) and were less sedated ( 0.33 ± 0.7 versus 0.56 ± 0.9; p = 0.03). The mean pain level (VAS) was 3.38 ± 1.8 for NMS and 3.84 ± 2.7 for PCA (p = 0.2). There was no difference between pain levels before and after dosing. There were no differences between groups with respect to arterial blood pressure, respiratory rate, vital capacity, mean forced expiratory volume in 1 second, spirometric volumes, or Sao 2. Conclusion: Nebulized morphine can be safely and effectively used to control posttraumatic thoracic pain. Pain can be successfully managed while vital capacity, mean forced expiratory volume in one second, and spirometric volumes are maintained. Compared with PCA morphine, nebulized morphine provides equivalent pain relief with less sedative effects. Treatment and Dosing All patients had, at baseline, pulmonary function assessments before study initiation. Pulmonary function assessments consisted of forced expiratory volume in 1 second (FEV 1), maximum spirometric capacity, vital capacity, pulse oximetry, arterial blood pressure, and heart rate. Each patient then received an intravenous loading dose of morphine sulfate 0.07 mg/kg (approximately 5 mg). This was to provide all patients with a baseline level of pain control. Patients then received a continuous intravenous infusion of study medication, either morphine 1 mg/h (PCA group) with no on-demand morphine or an equivalent amount of 0.9% saline solution via PCA (NMS group). Both groups also received a nebulized study drug of either 0.9% saline solution (PCA group) or morphine sulfate 8 mg/mL Normal Saline (NSS) (NMS group) every 4 hours around the clock (ATC). In summary, the PCA group received nebulized saline every 4 hours with PCA morphine, and the NMS Group received nebulized morphine every 4 hours with PCA saline. The rational for the initial doses and interval was based on published pharmacokinetic data. 4,5 This data suggest that inhaled morphine administered every 4 hours follows similar kinetics and elimination as a single intravenous injection. However, the dose of nebulized morphine needs to exceed twice the intravenous dose to provide similar bioavailability and half-life. Nebulized morphine was prepared and administered as follows. Morphine and placebo vials were prepared and blinded by the pharmacist. Standard injectable morphine sulfate with preservative was used (Abbott Labs, Chicago, IL). The patient’s nurse provided the correct dosage of study medication to the respiratory therapist. The nurse and therapist were responsible for ensuring that normal saline was added to the study medication to equal a 3 ml total volume. The solution was nebulized using a Respirguard II nebulizer system with the Acorn II nebulizer (Vital Signs, Inc., Totowa, NJ). This system produces an aerosol with a mass median aerodynamic diameter of 1.67 µm with an output of 0.34 mL/min at 8 L/min. The patient received the nebulizer treatment for 10 to 12 minutes. (J Trauma 2005;59(2)

OLD Folks do poorly with Rib Fractures

Bergeron E et al: Elderly trauma patients with rib fractures are at greater risk of death and pneumonia. J Trauma 54:478, 2003;

Small RCT shows NIV staves off intubation (CHEST January 2010 vol. 137 no. 1 74-80 )

Chest. 2010 Jan;137(1):74-80. Epub 2009 Sep 11.Noninvasive ventilation reduces intubation in chest trauma-related hypoxemia: a randomized clinical trial. Hernandez G, Fernandez R, Lopez-Reina P, Cuena R, Pedrosa A, Ortiz R, Hiradier P.Critical Care Medicine, Hospital Virgen de la Salud, Toledo, Mezquite n degrees 12, 6 degrees A, 28045, Madrid, Spain. ghernandezm@telefonica.netBACKGROUND: Guidelines for noninvasive mechanical ventilation (NIMV) recommend continuous positive airway pressure in patients with thoracic trauma who remain hypoxic despite regional anesthesia. This recommendation is rated only by level C evidence because randomized controlled trials in this specific population are lacking. Our aim was to determine whether NIMV reduces intubation in severe trauma-related hypoxemia. METHODS: This was a single-center randomized clinical trial in a nine-bed ICU of a level I trauma hospital. Inclusion criteria were patients with Pao(2)/Fio(2)<200 for >8 h while receiving oxygen by high-flow mask within the first 48 h after thoracic trauma. Patients were randomized to remain on high-flow oxygen mask or to receive NIMV. The interface was selected based on the associated injuries. Thoracic anesthesia was universally supplied unless contraindicated. The primary end point was intubation; secondary end points included length of hospital stay and survival. Statistical analysis was based on multivariate analysis. RESULTS: After 25 patients were enrolled in each group, the trial was prematurely stopped for efficacy because the intubation rate was much higher in controls than in NIMV patients (10 [40%] vs 3 [12%], P = .02). Multivariate analysis adjusted for age, gender, chronic heart failure, and Acute Physiology and Chronic Health Evaluation II at admission revealed NIMV as the only variable independently related to intubation (odds ratio, 0.12; 95% CI, 0.02-0.61; P = .01). Length of hospital stay was shorter in NIMV patients (14 vs 21 days P = .001), but no differences were observed in survival or other secondary end points. CONCLUSION: NIMV reduced intubation compared with oxygen therapy in severe thoracic trauma-related hypoxemia.PMID: 19749006 [PubMed - indexed for MEDLINE]

Pneumothorax

32-40 French

Thoracotomy-20 cc/kg of initial blood, >7cc/kg/hr, decompensation, increased hemothorax

If you get supine AP x-ray, look for deep sulcus sign

1.25% of percent of Pneumo spontaneously absorbed each day, more c 100% O2

Can get a delayed Pneumo up to 4 days post line placement

Normally film 6 hours after initial chest x-ray in trauma, but article suggests 3 hours sufficient (JEM 20:3) and a second prospective trial (J Trauma 65(3):549)

Spontaneous Pneumothoraces

One shot of manual aspiration is supported and efficacious.  If it fails, don’t try again, move on to chest tube or Heimlich valve (Am J Resp Crit Care Med 165:1240, 2002)

Author, country, date Patient group Study type Outcomes Key results Study weaknesses

Garramone et al, 1991, USA 26 trauma patients aged 14–65 with occult pneumothorax (OPTX) on abdominal CT. Classified as <5×80 mm or > = 5×80 mm Retrospective chart review Complications of OPTX, respiratory or haemodynamic compromise No patient had haemodynamic or respiratory complications. Retrospective Small numbers Of 18 with small OPTX: 2 had chest drains for increasing subcutaneous emphysema, 1 for increasing PTX. Of 13 patients with larger OPTX 4 had prophylactic chest drains, 3 for increasing subcutaneous emphysema 2 for increasing effusion Collins et al, 1992, USA 23 patients aged 18–82 with occult pneumothorax Retrospective chart review Length of hospital stay (mean) 13.4 days vs 8.8 days Small study Retrospective Length if ICU stay 6.3 days vs 3.3 days Not randomised Immediate chest tube (n = 12) vs observation (n = 11) Complications 1 pt in immediate chest tube group: had laceration of intercostal artery. 2 observed pts had eventual chest tubes for enlarging pneumothorax or haemothorax Enderson et al 1993 USA 40 adult trauma patients PRCT Length of hospital stay 12.9 vs 17.6 days Small study Randomized to immediate chest tube (n = 19) or observation (n = 21) Length of ICU stay 2.8 vs 3.2 days Complications Immediate chest tube: 1 pneumonia, 8 atelectasis. Observation group 3 tension pneumothorax, 5 progression pneumothorax, 1 pneumonia, 1 empyema, 3 atelectasis Wolfman et al 1998 , USA 44 pts aged 17 months –70 yrs with occult pneumothorax, classified according to size into miniscule, anterior or anterolateral. Chest tube inserted dependent on size and at trauma surgeons discretion Prospective non-randomized Complications 15/16 with miniscule observed, 2 had delayed chest drain for pneumothorax progression. 12/20 anterior observed 1 developed tension pneumothorax. 8 with anterolateral had immediate chest drain, no complications Small numbers Both adults and children Brasel et al 1999 , USA 39 adult patients with occult pneumothorax randomised to chest tube (n = 18) or observation (n = 21) PRCT Respiratory distress 1 pt with chest tube was intubated for stridor. 3 observed pts had resp distress with pneumothorax progression Only 39 of 86 eligible pts recruited Holmes et al2000 , USA 11 children <16yrs with occult pneumothorax presenting to level 1 trauma centre. 1 had chest tube, 10 observed Prospective observational cohort study Complications No haemodynamic or respiratory complications Small numbers paediatric population
J Trauma. 1993 Nov;35(5):726-9; discussion 729-30.Links Tube thoracostomy for occult pneumothorax: a prospective randomized study of its use. Enderson BL, Abdalla R, Frame SB, Casey MT, Gould H, Maull KI. Department of Surgery, University of Tennessee Graduate School of Medicine, Knoxville. Occult pneumothorax is defined as a pneumothorax that is detected by abdominal computed tomographic (CT) scanning, but not routine supine screening chest roentgenograms. Forty trauma patients with occult pneumothorax were prospectively randomized to management with tube thoracostomy (n = 19) or observation (n = 21) without regard to the possible need for positive pressure ventilation, to test the hypothesis that tube thoracostomy is unnecessary in this entity. Eight of the 21 patients observed had progression of their pneumothoraces on positive pressure ventilation, with three developing tension pneumothorax. None of the patients with tube thoracostomy suffered major complications as a result of the procedure. Hospital and ICU lengths of stay were not increased by tube thoracostomy. Patients with occult pneumothorax who require positive pressure ventilation should undergo tube thoracostomy.

Prospective multicenter of occult pneumo (J Trauma 2011;70:1019)

Only 14% failed obs approach on mech vent

no patient developed tension or decompensation

Hemothorax

Can Respir J. 2008 Jul-Aug;15(5):255-8.Links

Residual hemothorax after chest tube placement correlates with increased risk of empyema following traumatic injury.

Karmy-Jones R, Holevar M, Sullivan RJ, Fleisig A, Jurkovich GJ.

Department of Surgery, Harborview Medical Center, Seattle, Washington 98664, USA. rkarmyjo@swmedicalcenter.com

BACKGROUND: Empyema complicates tube thoracostomy following trauma in up to 10% of cases. Studies of potential risk factors of empyema have included use of antibiotics, site of injury and technique of chest tube placement. Residual fluid has also been cited as a risk factor for empyema, although the imaging technique to identify this varies. OBJECTIVE: To determine whether residual hemothorax detected by chest x-ray (CXR) after one or more initial chest tubes predicts an increased risk of empyema. METHODS: A study of patients admitted to two level I trauma centres between January 7, 2004, and December 31, 2004, was conducted. All patients who received a chest tube in the emergency department, did not undergo thoracotomy within 24 h, and survived more than two days were followed. Empyema was defined as a pleural effusion with positive cultures, and a ratio of pleural fluid lactate dehydrogenase to serum lactate dehydrogenase greater than 0.6 in the setting of elevated leukocyte count and fever. Factors analyzed included the presence of retained hemothorax on CXR after the most recent tube placement in the emergency room, age, mechanism of injury and injury severity score. RESULTS: A total of 102 patients met the criteria. Nine patients (9%) developed empyema: seven of 21 patients (33%) with residual hemothorax developed empyema versus two of 81 patients (2%) without residual hemothorax developed empyema (P=0.001). Injury severity score was significantly higher in those who developed empyema (31.4+/-26) versus those who did not (22.6+/-13; P=0.03). CONCLUSIONS: The presence of residual hemothorax detected by CXR after tube thoracostomy should prompt further efforts, including thoracoscopy, to drain it. With increasing injury severity, there may be increased benefit in terms of reducing empyema with this approach.

Small hemothoraces can probably be left undrained (< 1.5 cm), if there is a coincident pneumo, then probably put it in (Am J of Surgery 2006;192:722)

Cardiovascular Trauma

Myocardial Concussion

Brief dysrhythmia, hypotension or LOC c no lasting effects, no autopsy evidence

Myocardial Contusion

Most commonly from mva

Autopsy evidence

Can cause vasospasm or thromboembolism

Pericardial effusion +- friction rub, S3 gallop, rales, elevated CVP

2 mechanisms of injury:  transient reduction in bloodflow and transient dysrhythmias

70% of pts have tachycardia

EKG is the screening exam, if negative, do not have to admit

Common ekg abnormalities are PVCs, 1st degree av block, RBBB (Right ventricle is closest to anterior chest wall)

It is possible to have problems 12-72 hours after injury

If available, gated radionucleotide angiography is excellent test

Thalium also good

Monitor for 12 hours then can send home, b/c no life threatening problems seen after this time

If decreased cardiac output, can use dobutamine or IABP

Send 1 Troponin and get EKG:  both normal, young patient, send home (Journal of Trauma 50:237 2001) 100% sensitivity

Another study used 0 and 8 hour trops (J Trauma 2003;54:45-51.)

Abnormal Admit to Tele Bed

If the patient is unstable, get an echo

troponin specific but insensitive for myo injury in trauma (Anesthesiology 2004;101:1262)

Excellent Blunt Cardiac Injury Review (Crit Care Clin 2004;20:57)

Acute Pericardial Tamponade

2% of penetrating chest trauma

CVP increases to greater than 15

Becks triad-distant heart sounds, JVD, hypotension.  Also see pulsus paradoxus

EKG-electric alternans-alternates amplitude every other beat from decreased oscillation of heart, much more common in chronic effusion.

Chronic=water bottle heart on X-ray

Myocardial Rupture

Possible complication of CPR

Computed tomography screens stable patients at risk for penetrating cardiac injury

KK Nagy, SH Gilkey, RR Roberts, JJ Fildes and J Barrett Department of Trauma, Cook County Hospital, Chicago, IL, USA. kknagy@aol.com

OBJECTIVE: To determine the accuracy of CT of the chest in diagnosing thepresence of cardiac injury in stable patients with penetrating chestinjuries. METHODS: A retrospective chart review of a convenience sample ofstable patients with penetrating thoracic wounds evaluated for hemopericardium using chest CT at an urban level I trauma center. RESULTS:60 stable patients with penetrating wounds in proximity to the heartunderwent CT. Three patients had radiographic evidence of pericardialfluid, and 1 had an equivocal study. These 4 patients underwent subxiphoidpericardial window exploration: 2 had only clear fluid present, the other 2had hemopericardium. The latter patients had a total of 3 cardiac and 1diaphragmatic injuries, which were repaired at subsequent sternotomy. Noneof the 56 patients who had negative CTs had further clinical evidence ofcardiac injury. The sensitivity, specificity, and accuracy of CT in thissetting for hemopericardium are 100% (95% CI 18-100%), 96.6% (95% CI88-100%), and 96.7% (95% CI 89- 100%), respectively. CONCLUSION: Chest CTmay be a useful test for diagnosing the presence of hemopericardium in thesetting of penetrating thoracic injury. With the caveat that the patientmust be removed from a closely monitored environment, the authors the useof CT in stable patients with penetrating chest wounds whenever echocardiography is unavailable.

Go to source: Computed tomography screens stable patients at risk for penetrating cardiac injury — Nagy et al. 3 (11): 1024 — Academic Emergency Medicine

Intubation of Tamponade

(Resus 2008 Ho AM Timing of tracheal intubation in traumatic cardiac tampondade)

Esophageal and Diaphragmatic Trauma

Barium is the only acceptable contrast for esophageal perf (Acta radiologica 2000;41:482)

Esophageal Perforation (Boerhaave’s)

Esophagus has no serosa, so perf = direct access to mediastinum

DX by pain, possibly pleuritic

Hamman’s crunch from air surrounding heart

Pleural effusion

C-XR:  mediastinal air, L pleural effusion, pneumothorax, increased mediastinum

Get Esophogram 1st gastro then barium

Rx:  Broad spectrum ABX, NGT

In a message dated 7/19/2006 3:20:07 P.M. Central Standard Time,docrickfry@aol.com writes: And I  have just as valid anecdotes–at least two of our tubed patients—NOT trickled but given full esophageal contrast swallows with barium–injuries found, and in our institution in 21 years one never yet missed with it–so–what does that prove–as …… The issue here might be with the medium used.  BARIUM is the only  acceptable medium to use in esophagograms to look for leaks.  I have never  understood, nor can I find any scientific reason or support for, the urban  legend that one should use gastrographin for an esophagogram.    Gastrographin is DANGEROUS, in that if aspirated, can cause chemical  pneumonitis.   It also has a significant false negative  rate.    Virtually every trauma and thoracic surgery textbook  chapter that I can find recommends BARIUM.   Thoracic and trauma surgeons who present at national meetings recommend BARIUM, and ridicule gastrographin.      SO……………………………     the contrarian views  on this link server might be due to the fact that those reporting false negative results with esophagograms were using the wrong media. k mattox

andre consider yourself fortunate to have never had a significant aspiration of gastrografin i have practiced radiology for 35 years and have never had a fatal complication of intravascular contrast administration. i have had, very early in my career before I knew better, two deaths caused by aspiration of gastrografin. The use of barium is reliable and barium is inert in the neck and mediastinum. Could not the inflammation that you describe have been caused by the leakage from the perforation rather than the barium? HOWEVER, barium comes in all sizes and flavors. Barium paste would be unlikely to be reliable. Too thick to exit many of the perforation sites. Same goes for thick barium suspension. A moderately dilute “full strength” barium (30-40%) is likely to be the best option for finding holes. a CAVEAT i have mentioned here before bears repeating. If there are penetrations near the EG junction or if you are doing a esophagogram in a patient who might have a concomitant intraperitoneal perforation, start with gastrografin since barium does sometimes cause a severe peritonitis. sal

Penetrating Esophageal Injuries

From: McSwain, Norman E Jr. <nmcswai@tulane.edu> Date: May 29, 2008 3:33 PM Subject: RE: Delayed oesophageal injury To: “Trauma &amp; Critical Care mailing list” <trauma-list@trauma.org>I would have closed the injury, pulled muscle over the areas of repair and WOULD NOT have place any drains. Drains create fistulae. Muscle provides sealing coverage.  NPO x 48 hours of antibiotics. IV fluids. Esophageal swallow to access the repair in 48-72 hours. This is assuming a standard sized stab wound < 2 cm on each side and no vascular injury I would not have created a spit fistula nor a jejunostomy I would have treated a GSW the same way unless massive tissue destruction

Diaphragmatic Injuries

L much weaker than right in blunt trauma b/c liver protects right.  Most likely sight of injury posterio-lateral portion of L diaphragm

Diaphragm can extend to L2/L3 posteriorly

15 year review of all patients with blunt diaphragm injury [n=13]: Results:  77% left, 23% right  30% missed during the initial evaluation Delay 1 one – 10 years (Patselas TN. Am Surg 2002; 68:633-9.)

Penetrating

Laparoscopy study in 110 patients with left-chest penetrating trauma and no indications for laparotomy: Diaphragm injury in 24% 21% of these had a normal CXR 31% of these had hemo/pneumothorax (Murray JA. J Am Coll Surg 1998; 187:626-30.) (Gibb’s Lecture)

Miscellaneous

Valve Rupture

Most commonly aortic

Cervicothoracic Seatbelt Sign

Not necessarily indicative of underlying injury.  Most of those with injury will have some other physical sign (J Trauma 52:618 2002) (Am Surg 68:441, 2002)

Pulmonary Contusion

may have no signs on initial x-ray

opacities appear at 6 hours and usually resolve by 72 hours.

Review Article

Emergent Pneumonectomy

Am Surg. 1996 Nov;62(11):967-72. Survival after trauma pneumonectomy: the pathophysiologic balance of shock resuscitation with right heart failure. Baumgartner F, Omari B, Lee J, Bleiweis M, Snyder R, Robertson J, Sheppard B, Milliken J. Division of Cardiothoracic Surgery, Harbor-UCLA Medical Center, Torrance, California, USA. Emergency pneumonectomy for trauma has a high mortality. Although exsanguination is a major factor leading to death, mortality remains high even after adequate resuscitation and is thought to be related to pulmonary edema and right heart failure. We present a series of nine patients who underwent pneumonectomy at Harbor-UCLA from penetrating (7) and blunt (2) trauma. Two patients survived; three initially survived the surgery but died postoperatively of hypoxemia and right heart failure; four died intraoperatively (2 from right heart failure and 2 from exsanguination). One survivor required open cardiac massage for asystole. Careful attention to prevent volume overloading before and during trauma pneumonectomy and maintaining a negative fluid balance postoperatively may contribute to survival in these patients.

Always Consider Bronchial Injuries if Mediastinal Damage (Ann Thorac Surg 2004;78:2157)

Penetrating Esophageal Injuries

Rare. Article on factors affecting outcome (Br J Surg 2004;91:1513)

Lung Wounds

can do tractotomy for gunshot wound to the lung use a GIA 80 stapler across the tract to open it up nicely

Bronchopleural Fistula

Can use endobronchial blockers to isolate (J Trauma 2006;61:755)

Endobronchial Bleeding

it’s a big deal. Albumin in the blood destroys surfactant

Lung Sequestration Syndrome

oversew area of dead lung

Penetrating Cardiac Trauma

Injury 2005;36(6):745-750 Haemopericardium in stable patients after penetrating injury: Is subxiphoid pericardial window and drainage enough?–Small study (14 patients) of conservative management of pericardial blood

Study of blind subxiphoid pericardiotomy (J Trauma 2006;61:582)

Do we need a chest xray

absence of palpation tenderness and hypoxia identified most of pathology (Ann Emerg Med 2006;47(5):415)

Macklin Effect

Macklin effect: a peripheral alveolus ruptures and the air tracks centrally along the interstitium into the mediastinum and soft tissues (NEJM, May 17, 2007, pg. 2083).

Intercostal Bleeding can be ameloriated with a foley (Injury 42 (2011) 958–959)

Tracheal Injuries

intrathoracic tracheal injuries will need 4th ICS posterolateral thoracotomy

fix posterior wall through an incision in the anterior wall

segmental blood supply at 4 o’clock and 8 o’clock

You can use lung windows on CT C-Spine to diagnose pneumothorax (Injury (2012) 43:51–54)

Severe Traumatic Brain Injury

Severe injury=GCS<8

Suspect elevated ICP if:

GCS<8 or

GCS ≤ 10 and:

Hematoma volume > 30 ml (A,B,C,/2)

Midline Shift > 1 cm

Pineal shift > 5 mm

Compression of the Lateral Ventricles

CT Interpretation

New BTF Recs

B. Level II

Blood pressure should be monitored and hypotension (systolic blood pressure 90 mm Hg) avoided.

C. Level III

Oxygenation should be monitored and hypoxia (PaO

2 60 mm Hg or O2 saturation 90%) avoided.

B. Level II

Mannitol is effective for control of raised intracranial pressure (ICP) at doses of 0.25 gm/kg to 1 g/kg body weight. Arterial hypotension (systolic blood pressure 90 mm Hg) should be avoided.

C. Level III

Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes.

C. Level III

Pooled data indicate that prophylactic hypothermia isnot significantly associated with decreased mortality when compared with normothermic controls. However, preliminary findings suggest that a greater decrease in mortality risk is observed when target temperatures are maintained for more than 48 h. Prophylactic hypothermia is associated with significantly higher Glasgow Outcome Scale (GOS) scores when compared to scores for normothermic controls.

B. Level II

Periprocedural antibiotics for intubation should be administered to reduce the incidence of pneumonia. However,

it does not change length of stay or mortality. Early tracheostomy should be performed to reduce mechanical ventilation days. However, it does not alter mortality or the rate of nosocomial pneumonia.

C. Level III

Routine ventricular catheter exchange or prophylactic antibiotic use for ventricular catheter placement is not

recommended to reduce infection. Early extubation in qualified patients can be done without increased risk of pneumonia.

C. Level III

Graduated compression stockings or intermittent pneumatic compression (IPC) stockings are recommended,

unless lower extremity injuries prevent their use. Use should be continued until patients are ambulatory. Low molecular weight heparin (LMWH) or low dose unfractionated heparin should be used in combination with mechanical prophylaxis. However, there is an increased risk for expansion of intracranial hemorrhage.

B. Level II

Intracranial pressure (ICP) should be monitored in all salvageable patients with a severe traumatic brain injury (TBI; Glasgow Coma Scale [GCS] score of 3–8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals

hematomas, contusions, swelling, herniation, or compressed basal cisterns.

C. Level III

ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission:

age over 40 years,

unilateral or bilateral motor posturing, or

systolic blood pressure (BP) 90 mm Hg.

B. Level II

Treatment should be initiated with intracranial pressure (ICP) thresholds above 20 mm Hg.

C. Level III

A combination of ICP values, and clinical and brain CT findings, should be used to determine the need for treatment.

B. Level II

Aggressive attempts to maintain cerebral perfusion pressure (CPP) above 70 mm Hg with fluids and pressors should be avoided because of the risk of adult respiratory distress syndrome (ARDS).

C. Level III

CPP of <50 mm Hg should be avoided.

C. Level III

Jugular venous saturation (50%) or brain tissue oxygen tension (15 mm Hg) are treatment thresholds. Jugular venous saturation or brain tissue oxygen monitoring measure cerebral oxygenation.

B. Level II

Prophylactic administration of barbiturates to induce burst suppression EEG is not recommended.

High-dose barbiturate administration is recommended to control elevated ICP refractory to maximum standard medical and surgical treatment. Hemodynamic stability is essential before and during barbiturate therapy.

Propofol is recommended for the control of ICP, but not for improvement in mortality or 6 month outcome. High-dose propofol can produce significant morbidity.

B. Level II

Patients should be fed to attain full caloric replacement by day 7 post-injury.

B. Level II

Prophylactic use of phenytoin or valproate is not recommended for preventing late posttraumatic seizures (PTS).

Anticonvulsants are indicated to decrease the incidence of early PTS (within 7 days of injury). However, early PTS is not associated with worse outcomes.

B. Level II

Prophylactic hyperventilation (PaCO2 of 25 mm Hg or less) is not recommended.

C. Level III

Hyperventilation is recommended as a temporizing measure for the reduction of elevated intracranial pressure (ICP).

Hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often

critically reduced.

If hyperventilation is used, jugular venous oxygen saturation (SjO

2) or brain tissue oxygen tension (PbrO2) measurements are recommended to monitor oxygen delivery.

A. Level I

The use of steroids is not recommended for improving outcome or reducing intracranial pressure (ICP). In patients with moderate or severe traumatic brain injury (TBI), high-dose methylprednisolone is associated with increased mortality and is contraindicated.

Guidelines

Guidelines for Management of TBI (Brain Trauma Taskforce, braintrauma.org)

Not following these guidelines led to poorer outcome (Acta Neurochir 1999;141(11):1203-8)

ED Goals

systolic blood pressure (SBP) > 90 at all times and preferably a SBP = 120 mmHg, MAP > 85 mm Hg, ICP < 20 mm Hg, CPP > 60 mmHG, O2 saturation > 90%, and PaO2 > 60 mm Hg

Any episode of hypotension or hypoxia dramatically increases head injury mortaility (Archives of Surg 2001:136;1118-1123)

A single episode of hypotension (BP <90 mmHg) or hypoxia (PaO2 <60 mmHg) during the initial resuscitation was associated with a 150% increase in morbidity and mortality–Chestnut RM. J Trauma 1993; 34:216-222.

New study shows that hypotensive increases the mortality dramatically, but not more than non-head injured trauma patients (J Trauma 2005;59:830-835)

Injuries

Coup Contracoup

brain hits opposite wall first. Air bubble in soda bottle (Neurocritical Care 2004;1:384)

Diffuse Axonal Injury

Widespread structural failure of axons

Who Needs Surgery?

Prognosis

Crash Prognosis Calculator

motor component of GCS is most important as well as the ability to obey simple one-step commands

Early Prognostic Indicators: Patient Age >60 (but the older you are, the worse you do) Motor of GCS Pupillary Size/Reactivity in one study, 10% of patients presumed to have no chance for recovery had only moderate to no neuro disabilities at 12 months. Get article J trauam 1996;41:99 If a bullet has penetrated the brainstem or basal ganglia, nobody survives

Somatosensory evoked potentials are best predictors (Inten Care Med 2005;31:765)

Predictive ability of the GCS score (J Neurosci Nursing 2007;39(2):68) Age, GCS, and pupillary reaction are the most predictive Motor Score is most important part of the gcs

ICP Monitoring

ICP Monitor, either ventriculostomy or bolt (parenchymal strain gauge) if abnormal CT or normal CT c 2 of 3:  SBP<90, Age>40, posturing

Cerebral Perfusion Pressure

CPP=MAP-ICP

Raising CPP Conceptually a decreased CPP causes vasodilation resulting in higher ICPS, allegedly raising CPP will break this cycle. Lund Therapy on the other hand: emphasizes reduction of microvascular pressures to minimize edema. Maintain normal or high colloid osmotic pressure, reduce systemic blood pressures, and vasoconstrict precapillary vasculature. Use CPP of 60 as per most current recs from BTF

Norepinephrine but not dopamine was able to increase CBF in patients with head injury (Crit Care Med 2004;32(4):1049)

the paper for optimization of fluid balance in head injury (Crit Care Med 2002;32(4):739) better outcome if ICP<25,MAP>70,CPP>60, and fluid balance toward positive >-594. latter was indepenendent of the other three.

two studies on blood flow and tissue oxygenation in brain using norepi (Perfusion/O2=Inten Care Med 2004;30(5):791) (CPP–Crit Care Med 2004;32(4):1049)  and ( Intensive Care Med. 2004 Jan;30(1):45-50.Pharmacokinetics and pharmacodynamics of dopamine and norepinephrine in critically ill head-injured patients.)

Review of Vasopressors for Neurologic Injuries (Neurocrit Care 2009;11:112)

CPP and Hypoxia (Crit Care 2005;9:R670)

risk of hypoxia high at CPP<60. If >70, then it is much less

Herniation

Article 1

Article 2

Elevated ICP

Review (Crit Care Med 2005;33(6):1392)

Figure. Addenbrooke’s Neurosciences Critical Care Unit Intracranial Pressure (ICP) Management AlgorithmCVP, central venous pressure; ICP, intracranial pressure, Sjo2, jugular oxygen saturation; NCCU, neurosciences critical care unit; CPP, cerebral perfusion pressure; Pto 2 , tissue oximetry; LPR, lactate/pyruvate ratio; SOL, space-occupying lesion; CSF, cerebrospinal fluid; Rx, treatment; PAC, pulmonary artery catheter; Spo2 , arterial oxyhemoglobin saturation; Temp, temperature; iv, intravenously; NG, nasogastrically; EVD, external ventricular drainage; EEG, electroencephalogram; THAM, Tris(hydroxymethyl)-aminomethane; re-CT, repeat computed tomography. From: Nortje: Crit Care Med, Volume 36(1).January 2008.273-281

ICP>20

When managing CPP one needs to use the blood pressure seen by the brain, not the heart. This is a matter of physics, not opinion (or as Marisa Tomei says in My Cousin Vinny, it’s a fact). While it is of course possible to measure the height of the column of blood above the heart, convert it to mmHg, and subtract it from the MAP measured at the heart, I think it is vastly more efficient and accurate to zero the transducer at the ear and tape it next to the patient’s head, so that it rises and falls with the patient. On this point your mileage can not vary. (Bleck)

keep head 30 to 45 degrees

Treat any fever aggressively

Eucapnia

Ensure CO2 35-40

Review of hyperventilation (Chest 2005;127(5):1812)

hypervent more than 24 hours is almost certainly not helpful and most likely deleterious

Hyperventilation stops working after 12-24 hours and brain resets at new CO2 (Chest 2005;127(5):1812)

Rx ICP or Augment CPP???

Use ICP oriented therapy if slope of MAP/ICP regression line is at least 0.13=pressure-passive patients. If the slope is < 0.13, then raise blood pressure/CO to control ICP (J Neurosurg 2005;102:311)

Osmotic Therapy

A recent review demonstrated that perhaps we should consider hypertonic, not mannitol the gold standard for ICP measurement (Crit Care 2012;16:113)

Mannitol

comatose trauma patients while waiting for OR should get 1.2-1.4 G/kg of mannitol (wide open) followed by 14 cc/kg of NS wide open, though HTS is probably better. (Cochrane 2005 Mannitol for acute traumatic brain injury)

Ultra-early high-dose (1.4 G/kg) mannitol administration (given rapidly) in the emergency room is the first known treatment strategy significantly to reverse recent clinical signs of impending brain death, and also to contribute directly to improved long-term clinical outcomes for these patients who have previously been considered unsalvageable. (J Neurosurg. 2004 Mar;100(3):376-83)

for ICP elevations, use 0.25-1.0 G/kg. Bolus at rate not to exceed 0.1 g/kg/min replace urinary losses of fluid works by diluting blood and decreasing viscosity effects are rheologic (a science dealing with the deformation and flow of matter). Also may increase cardiac output. Can increase CBF even when there is no effect on ICP increased blood flow causes reactive vasoconstriction which decreases ICP

But the osmotic diuresis can lead to hypotension and accumulation of mannitol in CNS can lead to a rebound effect

Maximal effects are seen at 20-60 minutes, lasts 6 hours administer over 10-15 minutes to avoid hypotension most effective in lowering ICP when CPP is below 70 hypotension is a contraindication to mannitol use

Up to Osm of 320-330

normal osmole gap is more indicative that it is safe to give the next dose of mannitol than serum osmalality (Crit Care Med 2004 32, p.986)

plasma volume expander duration of 90 minutes to ~6 hours

also may be free radical scavenger and may inhibit apoptosis

Mass General Mannitol Protocol

Meta-Anal of Hypertonic vs. Mannitol shows hypertonic is better (Crit Care Med 2011;39:554)

Hypertonic saline

3% 250 cc bolus over 10-15 minutes (~4 cc/kg)

Can get hyperchloremic acidosis (add amp of bicarb to bag). Keep Na<160 and Osm<330 (Some would say 360 for hypertonic saline)

7.5% in dextran is half NaCl and half NaAcetate (~2 cc/kg)

23.4% (4-molar saline (4000 mEq Na+/litre)) It is impossible to give a lot of it by mistake (like you could perhaps with 500 ml bags of 1.8% or 3% saline) since it comes in 20  or 30 ml ampoules (can be given 30 cc at a time) Use 20-40 ml of it as a slow IV push (2 minutes) to lower worrisome ICP (40 mmHg), and often run small volumes of it (2-5 ml/hr) by continuous (syringe in “Gemini” pump) infusion to maintain a hyperosmolar state during enteral nutrition. Some patients need a little furosemide every now and then to prevent progressive ECF expansion with this therapy, others (probably under the influence of the CPP-driven MAP of 90-100 or so) just diurese both salt and water and do not develop ECF expansion despite large (600+ mmol/day) intakes of sodium.

ideal dose of 23.4% is prob. 0.5ml/kg can repeat up until 2 ml/kg (most people just give one 30 ml amp per dose)

Give over 10 minutes into a central line

Stephan Mayer’s Protocol

In one protocol, 3% half acetate and half chloride was effective for TBI (Crit Care Med 1998;26(3):440)

Head to Head Mannitol and Hypertonic (Crit Care 2005;9:R530-40) Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients – a randomized clinical trial

9. Vialet R, Albanese J, Thomachot L, et al: Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL/kg 7.5% saline is more effective than 2 mL/kg 20% mannitol. Crit Care Med 2003; 31:1683–1687

12. Francony G, Fauvage B, Falcon D, et al: Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure. Crit Care Med 2008; 36:795–800

13. Battison C, Andrews PJ, Graham C, et al: Randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury. Crit Care Med 2005; 33:196–202, discussion 257–198

14. Berger S, Schurer L, Hartl R, et al: 7.2% NaCl/10% dextran 60 versus 20% mannitol for treatment of intracranial hypertension. Acta Neurochir Suppl (Wien) 1994; 60:494–498

15. Freshman SP, Battistella FD, Matteucci M, et al: Hypertonic saline (7.5%) versus mannitol: A comparison for treatment of acute head injuries. J Trauma 1993; 35:344–348

16. Harutjunyan L, Holz C, Rieger A, et al: Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients: A randomized clinical trial [ISRCTN62699180]. Crit Care 2005; 9:R530–R540

17. Mirski AM, Denchev ID, Schnitzer SM, et al: Comparison between hypertonic saline and mannitol in the reduction of elevated intracranial pressure in a rodent model of acute cerebral injury. J Neurosurg Anesthesiol 2000; 12:334–344

18. Zornow MH, Oh YS, Scheller MS: A comparison of the cerebral and haemodynamic effects of mannitol and hypertonic saline in an animal model of brain injury. Acta Neurochir Suppl (Wien) 1990; 51:324–325

onset 15-30 minutes, lasts 1-3 hours

permeability of BBB to sodium is low, so sets up osmotic gradient. The reflection coefficient of HTS is higher than mannitol. Increases MAP and CO. Restores neuronal membrane potential and modulates inflammatory response by reducing adhesion of leukocytes.

Review article (Anesth Analg 2006;102:1836)

when calculating osmal for brain effects, include glucose, but not the BUN

Excellent Editorial (Crit Care Med 2006;34(12):3037)

Study vs. placebo in SAH with ICP (Crit Care Med 2006;34(12):2912)

2cc/kg over 30 min of 7.5% in 6% hydroxyethyl starch 200/0.5 solution

Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain.(Crit Care Med. 1998 Mar;26(3):440-6.)

Use of 3% vs. mannitol for brain relaxation in cranis; same effectiveness, less diuresis with 3% (Anesth 2007;107:697)

Hypertonic sodium lactate (inten care med 2009;35:471) more effective than mannitol in rct

two articles show the saftey of 3% and 7.5% administered peripherally (J Trauma 36(3):323) and (JAMA. 2010;304(13):1455-1464)

Hypertonic vs. Mannitol Comparison–Hypertonic is better

Sodium Bicarb as Omostic Therapy

Neurocrit Care 2010;13:24

85 ml of 8.4% sodium bicarb infused over 30 minutes

effective without hyperchloremic acidosis

RCT comparing the two: 100 ml of 5% vs. 85 ml of NaBicarb 8.4% (Neurocrit Care 2011;15:42)

ICP Monitoring Waves

Normal

P2 Elevations

Rounding/Monotonous

Lundberg A,B, & C waves

Normal

P1=percussion wave, pulsation of choroid plexus, sharp consistent in amplitude

P2=tidal wave, rebound after arterial percussion. Variance in amplitude

P3=dichrotic wave, immediately follows the notch after P2 (which corresponds to the dichrotic notch arterially)

P2 predominance occurs prior to all discernability disappearing

P2:P1 > 0.8 has been thought to be associate with disproportionate increase in ICP, especially when the ICP is > 10

this study shows not necessarily true after a waveform analysis (Am J of Crit Care 2008;17:54

CSF Drainage

IVC if not already placed

Barb Coma

has side effects of hypotension and cv depression 10 mg/kg loading dose over 30 minutes then 5 mg/kg/h over next 3 hours. pts become anergic and poikilothermic so signs of infection such as fever, wbc, and tachycardia may all be suppressed

Causes hypokalemia (Intensive Care Med. 2002 Sep;28(9):1357-60.)

The reason hypokalemia occurs in barbiturate intoxication (or barbiturate-induced coma) is the same as it is for hypokalemia in moderate hypothermia; barbiturates poison the Na++/K+ pump resulting in translocation of sodium and chloride, and transiently, K+, in response to the Gibbs-Donan effect.

Use thiopental (5-10 mg/kg then 3-5 mg/kg/hr) or pentobarbital (10 mg/kg over 30 minutes then 5 mg/kg every hour x 3 doses then 1-2 mg/kg/hr) as they have shorter duration of action

Decompressive Craniectomy

if ICP is persistently above 35 during the first 24 hours after decompression has a 100% mortality it should extend to the floor of the middle fossa cranioplasty should be performed within 1 to 3 months to prevent the “syndrome of the trephined”

In adults with severe diffuse traumatic brain injury and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and the length of stay in the ICU but was associated with more unfavorable outcomes. ((10.1056/NEJMoa1102077) N Engl J Med 2011)

Decompressive Laparotomy

ICP and IAP are correlated (Inten Care Med 2005;31:1577)

THAM may lower ICP as well

GHB may be better than barbs

Repeat CTs

scans obtained within 3-6 hours of injury may not indicate final lesion size a scheduled scan 12-24 hours post-injury in severe tbi seems warranted ICP monitors do not require proph abx other than one dose 30 minutes prior to placement pts need 1 week of dilantin ICP treatment treat normal patients at 20, treat s/p crani pts at 15

Intracranial Volume Targeted (“Lund Concept”)

Ways it’s been described:

Antihypertensive and intracranial volume-targeted therapy

Physiological volume regulation of the intracranial compartments

Central premise:

Impaired autoregulation and blood brain barrier occur in the injured brain

This makes MAP and cerebral capillary hydrostatic pressure driving force behind cerebral edema, and therefore ICP

Furthermore, supporting the CPP with pressors can promote more cerebral edema

Therefore, a good CO with normotension and mild vasoconstriction of precapillary cerebral vessels decreases ICP

The volume-targeted “Lund Strategy” has several components

Reduction of stress response and cerebral energy metabolism (low dose pentothal, sedation)

Reduction of capillary hydrostatic pressure with systemic antihypertensives (metoprolol and clonidine)

Reduction of capillary hydrostatic pressure with precapillary vasoconstrictors (low-dose pentathol & ergotamine)

Maintenance of colloid osmotic pressure and control of fluid balance

Reduction of cerebral blood volume

What it looks like

Euvolemia to Hypervolemia

Normotension using beta-blockers (metoprolol) and alpha-agonists (clonidine)

Low dose pentothal and dihydroergotamine

CPP typically near traditional limits, but lower CPP tolerated in preference of antihypertensive therapy

ICP effectively kept <20 most of the time

Outcomes

Efficacy of the protocol has been evaluated in experimental and clinical studies

Surrogate physiological/biochemical improvements (lactate/pyruvate ratio in the penumbra zone by microdialysis)

Non-randomized/non-controlled studies suggest significant mortality benefit

Subjective clinical experiences favorable

full description and review (Inten Care Med 2006;32:1475)

Licox and PbtO2

should be pvO2 > 20

Immediate Surgery

Midline shift>5mm or mass effect

Large or enlarging hematoma

Depressed skull fracture

Posterior fossa mass lesion

Open wound

LICOX

Review Article (Neurocritical Care 2004;1:392)

Hyperventilation adversely affects PbtO2 (Br J Neurosurg 2003;17(4):340-346)

needs 60-90 minutes run in time to equilibrate

Better Review(Curr Opin Crit Care 2002;8:115-120

Hyperoxia causes cerebral vasoconstriction (Curr Opin Crit Care 2004;10:105

In dogs, better neuro outcome when 21% O2 used in brain injury than 100% (Stroke 1998;29:1679)

Review article summarizing some weak human studies showing that cerebral blood flow decreases with hyperoxia (>133 mmHg) (Br J Anaeth 2003;90:774)

Increased fiO2 changed PbO2 but also jug venous saturation (Anesth Analg 2003;97:851)

Study of waht PbO2 is actually measuring: CBF and difference between Art and venous blood, since it is just a clark electrode, it would make sense that this value rises when you turn up the fiO2 but this does not translate into better O2 delivery (Crit Care Med 2008;36:1917)

Licox waveform tracks CPP regardless of autoregulation (Anesth Analg 2010;110:165)

Cerebral Blood Flow

transcranial dopplers PET Xenon CT Scanning If TCD has been calibrated to a quantitative measure of CBF, it can relaibly track changes in CBF can pick up low flow in the initial 24 horus and vasospasm several days post-injury

Vents in Heads

hyperventilation works by adjustment of CSF pH in order to cause vasoconstriction. Carbonic anhydrase activity in the choroid plexus will adjust to this new pH and eliminate the vasconstriction. Within 4 to 6 hours, there is either a normalization of arteriolar vessel caliber or actually a hyperemia resulting in elevated ICPs. Keep CO2 at 35

Hypocapnia is actually a really bad idea (crit care med 2010;38:1348)

Transfusion in Head Injury

keep crit between 30-35 to maximize oxygen delivery but minimize decreased blood flow due to viscosity

Seizure prophylaxis

for 1st week.  Dilantin may cause drug fever.

Dilantin

Keep on for the first week

Free dilantin should be 1-2

Nutrition

feed glutamine containing immune diet for 5-10 days if GCS<8

Temperature

Must manage aggressively any increased temp

use cooling blanket. Wrap hands and feet to prevent shivering. 24 C was just as effective as 7 C and was assoc with less shivering (Crit Care Med 2005;33(7):1672)

Anticoagulation

Lovenox

Hold for 72 hours post-injury, post change in status, or post procedure

Herniation

Uncal-uncus of temporal lobe forced against tentorium cerebelli.  CN III compressed, ipsilateral dilated pupil

Central Transtentorial-from above

Cerebellotonsilar-tonsils through foramen magnum, bilat pinpoint

Upwards transtentorial-pontine compression, Bilat pinpoint

Pulmonary and Cardiac Sequelae

usually seen in Subarachnoid Hemorrhage (Inten Care Med 2002;28:1012)

Electric Disturbances

due to stimulation of posterior hypothalamus

problems are tachyarrhythmias and signs of ischemia

t-wave abnormalities are usually benign

ventricular hypokinesis is more rare but can be fatal

Neurogenic Pulmonary Edema

believed to be due to catecholamine hypersecretion

Article of Systemic Complications after Head Inj (Anaesthesia 2007;62:474)

any severe tbi (not just aSAH) can cause sympathetic surge which can cause direct injury of the myocardium

Neurogenic pulmonary edema can occur up to 14 days after the original TBI. catecholamine storm is implicated.

intense pulmonary vasoconstriction; increased intravascular hydrostatic pressure; and transudation of plasma fluid into extravascular space

these cause direct endothelial injuries

EAST Guidelines

O:In patients without ICP monitors the indications for mannitol are signs of transtentorial herniation or progressive neurological deterioration. Avoid hypovolemia with fluid replacement. Serum osmolality should be < 320 mOsm to prevent renal failure. Boluses may be more effective than continuous infusion. The use of barbiturates in the control of intracranial hypertension Guidelines G: High-dose barbiturates may be tried in hemodynamically stable salvageable patients with intracranial hypertension refractory to therapy (both medical and surgical). G: Replace 140% of resting metabolism caloric expenditure in non-paralyzed patients (100% in paralyzed patients) using enteral or parenteral formulas with at least 15% protein by the 7th day. O: Most preferable option is jejunal feeding by gastrojejunostomy. S: Prophylactic use of anticonvulsants is not recommended for late post-traumatic seizures. O: Anticonvulsants may be used to stop early post-traumatic seizures in patients at high risk for seizures following head injury. Note that phenytoin and carbemazapine have been shown to be effective stopping early post-traumatic seizures but no outcome benefit has been demonstrated.

Factor VII

Reduced mortality and hematoma size if given within four hours of intracerebral hemorrhage placebo RCT ARR 11% 30 day mortality(NEJM 2005;352:777-85)

Sodium Abnormalities

Hyponatremia either CSW or SIADH key differentiation is hypovolemia. treatment oral salt- 3-4 g po/ng tid hypertonic saline 25 to 75 cc/hr of 3% fludrocortisone 0.1 to 0.3 mg/day is typical dose. has side effects of hypokalemia, htn, and possibly chf Urea oral 30 g bid or tid for one day or iv 80 g as 30% solution over 6 hours (40 g in 150 cc NS as a IV drip, infused over 8 hours) SIADH can also be treated with Lasix Demeclocycline abx which induced reversible DI. 300 mg 2-4 times per day. May take 3-4 days in order to see effects. Hypernatremia is DI polyuria over over 200 cc/hr for greater than three hours with a urine SG <1.005 with a rising sodium Treatment DDAVP .5 to 2 mcg sc or iv q 8-12 or vasopressin 1-3 units per hour

Cerebral Salt Wasting

Consider Diabetes Insipidus

vasopressin drip

Brain Trauma can be the source of hypotension (J Trauma 2003;55:1065)

Our approach is to measure the urine osmolality and make the fluid coming in at least as hypertonic as the urine coming out (no, this is not the man in white at the start of Catch-22).  If the patient is getting tube feeding, then you can add salt to the feeds as an alternative to hypertonic saline.  Normal saline is not going to raise the serum osmolality, but the latter won’t fall as fast if you give normal saline than if you give 5% dextrose.  The patient may get better before the osmolality falls significantly, so you may get by with normal saline not because it is the correct thing to do but because the hypothalamus was able to cause free water excretion. Tom Bleck

csw most often from lesions to the hypothalamus or forebrain

loss of weight is suggestive as pt is fluid depleted

- low pulmonary capillary wedge presure (PCWP < 8 mm Hg) or low central venous pressure (CVP < 6 mm Hg) if invasive measurement of volume status available

- urine Na+ markedly elevated (variable in SIADH) & urine volume increased in CSW

- high BUN and Hematocrit supports CSW (prerenal azotemia and hemoconcentration)

- elevated serum K+ not usually seen in SIADH and implies CSW

- serum uric acid often increased in volume depletion (CSW) while low in SIADH

- may add oral salt or hypertonic saline to ensure positive sodium balance

- amount of sodium required to correct deficit obtained by multiplying deficit in serum sodium by total body water (50-60% of ideal body weight) and correcting at no more than 1 mmol/L per hour (risk of precipitating central pontine myelinolysis with rapid correction)

- may prevent further salt loss with volume expansion by using mineralocorticoid fludrocortisone which enhances sodium reabsorption by acting directly on tubule (but can cause hypokalemia, fluid overload and hypertension)

- very effective in preventing hyponatremia from SAH (ARR of 25%, NNT 4) and reduced need for dobutamine to augment cerebral perfusion

Fluids

in post hoc analysis of SAFE, albumin was assoc. with higher mortality (NEJM 2007;357:874)

Adrenal Insufficiency

prospective study shows it’s there more than we think (Crit Care Med 2005;33:2358)

ISOLATED BRAIN INJURY AS A CAUSE OF HYPOTENSION IN THE BLUNT TRAUMA PATIENT Mahoney, E.J., et al, J Trauma 55(6):1065, December 2003

THE RELATIONSHIP OF INTRAOCULAR PRESSURE TO INTRACRANIAL PRESSURE Ann Emerg Med 43(5):585, May 2004 METHODS: In this prospective study, from Ohio State University, the correlation between IOP and ICP was evaluated in 27 ICU patients without known glaucoma who were undergoing invasive monitoring of ICP due to a variety of conditions that included intracranial hemorrhage, ischemic stroke, trauma, tumor or shunt malfunction. A total of 76 measurements of IOP with a handheld Tono-Pen XL applanation tonometer were performed simultaneously with invasive ICP measurement. RESULTS: At a cut-off of 20 mmHg as an indicator of pressure elevation, the sensitivity and specificity of IOP measurement for elevated ICP were each 100%. All patients with elevated ICP had increased IOP, and all with normal IOP had normal ICP. Although there was a high overall correlation between IOP and ICP (r=0.83), differences between the two parameters were increased with increasing pressure levels and the potential difference between the two techniques at higher ICP ranges could be as great as 40cm H2O. CONCLUSIONS: Results from this pilot study require verification, but suggest that noninvasive measurement of IOP might prove to be a useful indicator of elevated ICP. 19 references (hiestand-1@medctr.osu.edu)

Signs of Herniation

Unilateral or bilateral unreactive, dilated pupil Extensor posturing (decerebrate) A sharp decline in GCS

decerebrate posturing=brainstem dysfunction

decorticate posturing=brainstem functioning

Reversal of Antiocogaulation and Antiplatelet Drugs

Cochrane Database Syst Rev. 2005 Oct 19;(4):CD001049. Related Articles, Links Mannitol for acute traumatic brain injury. Wakai A, Roberts I, Schierhout G. St Vincent’s Hospital, Department of Emergency Medicine, Dublin 4, Ireland. wakai@indigo.ie BACKGROUND: Mannitol is sometimes effective in reversing acute brain swelling, but its effectiveness in the ongoing management of severe head injury remains unclear. There is evidence that, in prolonged dosage, mannitol may pass from the blood into the brain, where it might cause increased intracranial pressure. OBJECTIVES: To assess the effects of different mannitol therapy regimens, of mannitol compared to other intracranial pressure (ICP) lowering agents, and to quantify the effectiveness of mannitol administration given at other stages following acute traumatic brain injury. SEARCH STRATEGY: The review drew on the search strategy for the Injuries Group as a whole. We checked reference lists of trials and review articles, and contacted authors of trials. The searches were last updated in April 2005. SELECTION CRITERIA: Randomised trials of mannitol, in patients with acute traumatic brain injury of any severity. The comparison group could be placebo-controlled, no drug, different dose, or different drug. We excluded cross-over trials, and trials where the intervention was started more than eight weeks after injury. DATA COLLECTION AND ANALYSIS: The reviewers independently rated quality of allocation concealment and extracted the data. Relative risks (RR) and 95% confidence intervals (CI) were calculated for each trial on an intention to treat basis. MAIN RESULTS: In the acute management of comatose patients with severe head injury, the administration of high-dose mannitol resulted in reduced mortality (RR= 0.56; 95% CI 0.39 to 0.79) and reduced death and severe disability (RR= 0.58; 95% CI 0.47 to 0.72) when compared with conventional-dose mannitol. One trial compared ICP-directed therapy to ‘standard care’ (RR for death= 0.83; 95% CI 0.47 to 1.46). One trial compared mannitol to pentobarbital (RR for death= 0.85; 95% CI 0.52 to 1.38). One trial compared mannitol to hypertonic saline (RR for death= 1.25; 95% CI 0.47 to 3.33). One trial tested the effectiveness of pre-hospital administration of mannitol against placebo (RR for death= 1.75; 95% CI 0.48 to 6.38). AUTHORS’ CONCLUSIONS: High-dose mannitol may be preferable to conventional-dose mannitol in the acute management of comatose patients with severe head injury. Mannitol therapy for raised ICP may have a beneficial effect on mortality when compared to pentobarbital treatment, but may have a detrimental effect on mortality when compared to hypertonic saline. ICP-directed treatment shows a small beneficial effect compared to treatment directed by neurological signs and physiological indicators. There are insufficient data on the effectiveness of pre-hospital administration of mannitol.

Vialet 2003 compared mannitol to hypertonic saline. Eligible patients were those with severe head injury (GCS8) who required intravenous infusions of an osmotic agent to treat episodes of intracranial hypertension resistant to standard therapy (cerebrospinal uid drainage, volume expansion and/or inotropic support, hyperventilation). The mannitol group received 20% mannitol solution. The hypertonic saline group received 7.5% hypertonic saline. The infused volume was the same for both solutions:

2 ml/kg body weight in 20 minutes. The aim was to decrease ICP

to .25 mm Hg or to increase CPP to .70 mm Hg. In case the

rst infusion failed, the patient received a second infusion within

ten minutes after the end of the rst infusion. Treatment failure

was de ned as the inability to decrease ICP to .35 mm Hg or to

increase CPP to .70mmHg with two consecutive infusions of the

selected osmotic solution. In that case, the protocol was stopped,

and patients were followed up for mortality or 90-day neurologic

status. Because 20% mannitol can crystallize at ambient temperature,

injections could not be performed in a blinded manner.

Twenty patients were randomised, ten to each group. Outcome

was assessed at 90 days using the Glasgow Outcome Scale administered

by a practitioner who was blind to acute patient care.

One trial compared mannitol to hypertonic saline (Vialet 2003).

This trial was randomised and single blind. Only patients with

head injury and persistent coma who required osmotherapy to treat

episodes of intracranial hypertension resistant to standard therapy

were included. For mannitol compared to hypertonic saline in

the treatment of refractory intracranial hypertension episodes in

comatose patients with severe head injury, the RR for death was

1.25 (95% CI 0.47 to 3.33).

Brain oedema peaks at 3–5 days after hemispheric strokes. Patients with brainstem or cerebellar strokes might develop substantial oedema in the first couple of days. Few patients develop enough oedema to warrant medical intervention.193 Patients requiring intervention usually have large multilobar infarctions.194, 195, 196 and 197 Cerebellar infarctions with oedema can obstruct flow of cerebrospinal fluid, leading to acute hydrocephalus and increased intracranial pressure.192

Hypertonic Saline Reduced Intracranial Pressure From Brain Trauma

Article content is available to ACEP members only; if you are an ACEP member, but do not have a Web account, please take a moment to create one now.

By Sherry Boschert (Elsevier Global Medical News – 05/04/2006)

SAN FRANCISCO (EGMN)-Osmotic therapy using hypertonic saline reduced intracranial hypertension in 24 patients with traumatic brain injury while improving cerebral perfusion pressure and brain tissue oxygen levels, Dr. Archie Defillo reported.

The treatments caused no complications in these patients. Judging from the findings of this small series of patients, hypertonic saline appears to be a safe alternative to mannitol for osmotic therapy to control intracranial pressure after traumatic head injury, Dr. Defillo said at the annual meeting of the American Association of Neurological Surgeons.

With his associates, Dr. Defillo reviewed records on head trauma patients with intracranial pressure greater than 20 mm Hg for longer than 20 minutes in the absence of response to nociceptive stimuli, and who had not received other osmotic agents after traumatic brain injury. The 24 patients were infused with 30 ml of 23.4% sodium chloride solution over a 15-minute period. Patients with low hemoglobin levels received blood transfusion to maintain a constant oxygen delivery.

The hypertonic saline decreased intracranial pressure absolute values by a mean of 35% from baseline, consisting of a 10 mm Hg decrease in the first hour and an 8 mm Hg decrease sustained in hours 2-6, said Dr. Defillo of Hennepin County Medical Center, Minneapolis.

“Six millimeters of mercury can be the difference between profound ischemia and normal brain tissue oxygen values,” he noted.

Cerebral perfusion pressures and brain tissue oxygen levels improved over the course of osmotic therapy. Cerebral perfusion pressures increased by a mean 14% (8 mm Hg/hr). Brain tissue oxygen levels showed a steady, linear increase ranging from 3% after the first hour of hypertonic saline to 25% by 6 hours after infusion.

Mean arterial pressures remained stable, with the only significant change being a 4 mm Hg decrease 6 hours after infusion.

The greatest benefit from hypertonic saline osmotic therapy was seen in patients with higher intracranial pressure or lower cerebral perfusion pressure.

Hypertonic saline does not cause the rebound effect that can be seen with mannitol, Dr. Defillo noted. Repeat doses of hypertonic saline were not associated with fluid depletion, hypovolemia, or hypertension.

The next research step should be a prospective trial comparing hypertonic saline with mannitol for osmotic therapy in head trauma patients, commentators suggested.

Traumatic brain injury can lead to increased intracranial pressure due to brain edema, blood clots, subdural hematomas, or other intracerebral hemorrhages. The mainstay of nonsurgical management is osmotic therapy.

Copyright 2006 Elsevier Global Medical News. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.

Hypertonic Saline a Viable Treatment for Controlling Intracranial Pressure in Patients with Traumatic Brain Injury Contact:  Betsy van Die

(847) 378-0517 or bvd@aans.org

EMBARGOED FOR RELEASE ON APRIL 24

SAN FRANCISCO (April 24, 2006) – Controlling intracranial pressure (ICP) is an essential component of effectively treating patients with traumatic brain injury (TBI). TBI patients may develop increased ICP as a result of edema (brain swelling), blood clots, subdural hematomas, or other intracerebral hemorrhages. Because the brain is surrounded by the rigid skull, high ICP can cause compression or squeezing of the softer brain tissue, preventing enough blood from getting to the brain tissue. The result can be damage to brain cells. Even a short period of increased ICP can cause permanent damage. Raised ICP, along with hypotension and hypoxia, can increase the mortality rate in TBI patients by 70 percent. TBI survivors are often left with significant cognitive, behavioral, and speech disabilities, and some patients develop long-term medical complications, such as seizures.

Osmotic therapy is the cornerstone of nonsurgical management of ICP. There are theoretical reasons why hypertonic saline (HTS) may be a more effective and safe osmotic agent than mannitol. Neurosurgeons at Hennepin County Medical Center (HCMC) in Minneapolis recently assessed the effectiveness of HTS as a single osmotic intervention for controlling ICP and its effect on cerebral perfusion pressure (CPP) and brain tissue oxygen (PtO2).

The results of this study, Hypertonic Saline (HTS) and its Effect on Intracranial Pressure (ICP) and Brain Tissue Oxygen (PtO2), will be presented by Archie Defillo, MD, 4:15 to 4:30 p.m. on Monday, April 24, 2006, during the 74th Annual Meeting of the American Association of Neurological Surgeons in San Francisco. Co-authors are Gaylan L. Rockswold, MD, PhD, Jon Jancik, PharmD, and Sarah B. Rockswold, MD.

HTS produces massive movement of water out of edematous swollen cells and into the blood vessels. This movement of water out of the brain can reduce swelling and improve cerebral blood flow. This specific action of HTS is due to its reflection coefficient of 1. The high numbers of particles in the solution pull water from a low-pressure compartment to a higher-pressure one. Compared with another osmotic diuretic such as mannitol, in which the reflection coefficient is 0.9 (allowing some leakage outside the blood vessels), HTS will not leak outside the capillaries in the presence of an intact blood-brain barrier.

An analysis of 24 consecutive TBI patients (21 males and 3 females, ages 17-64, mean age: 37.5) admitted to the surgical intensive care unit (SICU) at HCMC was conducted. The use of other medications to control ICP was an exclusion criteria to prevent inaccurate results. Blood pressure (BP), mean arterial pressure (MAP), central venous pressure (CVP), heart rate, temperature, intake and output were monitored hourly. Serum sodium, osmolality, and arterial blood gases were checked every six hours. Hemoglobin levels, blood urea nitrogen (BUN), serum potassium, chloride, magnesium and phosphate levels were checked daily.

The goal of the therapy was to maintain an ICP of less than 20 mmHg, a CPP between 55 and 70 mmHg, and PtO2 of 20mmHg or higher. When ICP increased to more than 20 mmHg, 30 milliliters of a 23.4-percent solution of HTS was administered as a single dose or repeated doses to control ICP levels. Hemoglobin levels less than 10 gr/dl were corrected via blood transfusion to maintain a constant oxygen delivery (VDO2).

The following results were noted:

• Mean absolute value for ICP showed a 35 percent decrease compared to baseline. In the three different subgroups, the significant decrease occurred within the first hour after HTS infusion, with the following decreases noted: 26-percent in group 1, 51 percent in group 2, and 44 percent in group 3.
• CPP mean absolute value increased by 14 percent. CPP values were recorded in three subgroups: 40-54mmHg in group 1, 55-69mmHg in group 2, and 70 mmHg and higher in group 3. There was a mean increase of 40 percent in group 1, 12 percent in group 2, and 3 percent in group 3. In all groups, there was a sustained response for four hours after the initial infusion.
• PtO2 values were recorded in three different subgroups: 10-19 in group 1, 20-29 in group 2, and 31 mmHg and higher in group 3. None of the means were statistically different in the three subgroups; there was a steady linear increment ranging from 2.9 percent after the first hour to 25 percent by six hours after infusion.

“There were no complications as a result of this treatment, so in conclusion, HTS is a viable option for decreasing ICP and improving CPP and PtO2 in TBI patients,” said Dr. Defillo. “Studying a larger patient pool would provide an even better assessment of the effectiveness of HTS as a treatment option for TBI,” concluded Dr. Defillo.

Founded in 1931 as the Harvey Cushing Society, the American Association of Neurological Surgeons (AANS) is a scientific and educational association with more than 6,800 members worldwide. The AANS is dedicated to advancing the specialty of neurological surgery in order to provide the highest quality of neurosurgical care to the public. All active members of the AANS are certified by the American Board of Neurological Surgery, the Royal College of Physicians and Surgeons (Neurosurgery) of Canada or the Mexican Council of Neurological Surgery, AC. Neurological surgery is the medical specialty concerned with the prevention, diagnosis, treatment and rehabilitation of disorders that affect the entire nervous system, including the spinal column, spinal cord, brain and peripheral nerves.

Arterial carbon dioxide partial pressure (PaCO2) Because cerebral blood flow and PaCO2 are linearly related withinphysiologically relevant ranges, hyperventilation had becomean entrenched practice in cerebral resuscitation. Reductionin PaCO2 was presumed to augment cerebral perfusion pressurefavourably by reducing the cross-sectional diameter of the arterialcirculation and thus cerebral blood volume. This would offsetincreases in intracranial pressure. Although the logic behindthis practice can be appreciated, in fact, it is contradictedby direct examination of cerebral well being. The most salientevidence is derived from TBI investigations. These studies supporta different concept, that being worsening of perfusion by hyperventilation-inducedvasoconstriction in ischaemic tissue. Indeed, the volume ofischaemic tissue, elegantly assessed with positron emissiontomography in TBI patients, was markedly increased when moderatehypocapnia was induced.20 This is consistent with the only prospectivetrial of hyperventilation on TBI outcome, which observed a decreased number of patients with good or moderate disability outcomeswhen chronic hyperventilation was employed.45 It remains unevaluatedwhether acute hyperventilation improves outcome from pendingtranstentorial herniation or when rapid surgical decompressionof a haematoma (e.g. epidural) is anticipated. Within the contextof focal ischaemic stroke, clinical trials have found no benefitfrom induced hypocapnia,17 62 although hyperventilation is sometimesemployed in cases of refractory brain oedema. Use of hyperventilationduring cardiopulmonary resuscitation may serve to increase mean intrathoracic pressure thereby decreasing perfusion pressureand is not advocated.5 Consequently, there are few data to supportuse of hyperventilation in the context of cerebral resuscitation.

20 Coles JP, Fryer TD, Coleman MR, et al. Hyperventilation following head injury: effect on ischemic burden and cerebral oxidative metabolism. Crit Care Med (2007) 35:568–78.[CrossRef][ISI][Medline] 21 Drummond JC, McKay LD, Cole DJ, Patel PM. The role of nitric oxide synthase inhibition in the adverse effects of etomidate in the setting of focal cerebral ischemia in rats. Anesth Analg (2005) 100:841–6.[Abstract/Free Full Text] 22 Elsersy H, Mixco J, Sheng H, Pearlstein RD, Warner DS. Selective gamma-aminobutyric acid type A receptor antagonism reverses isoflurane ischemic neuroprotection. Anesthesiology (2006) 105:81–90.[CrossRef][ISI][Medline] 23 Elsersy H, Sheng H, Lynch JR, Moldovan M, Pearlstein RD, Warner DS. Effects of isoflurane versus fentanyl-nitrous oxide anesthesia on long-term outcome from severe forebrain ischemia in the rat. Anesthesiology (2004) 100:1160–6.[CrossRef][ISI][Medline] 24 Fay T. Observations on generalized refrigeration in cases of severe cerebral trauma. 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Pupillary constriction is mediated via a parasympathetic pathway, which requires integrity of the third nerve and its nuclei in the brain, which lie close to areas involved in consciousness. Third nerve palsy initially causes mydriasis followed by loss of reactivity to light. Classically, ipsilateral third nerve palsy has been attributed to compression of the nerve on the free edge of the tentorium. It may also occur because of kinking of the nerve over the clivus or ‘buckling’ of the brainstem as a result of an increase in supra-tentorial pressure.80 In the presence of unilateral third nerve palsy, the consensual light reflex (opposite eye constricting in response to bright light) should still be present. Optic nerve injury (more common with frontal injuries) will impair both the direct and indirect responses and may lead to fixed or sluggish pupils, which may display spontaneous fluctuations (hippus).139 Bilaterally fixed pupils occur in around 20–30% of patients with severe head injury (GCS after resuscitation: 70–90% of these patients will have poor outcome (vegetative or dead) when compared with around 30% with bilaterally reactive pupils.57 64 66 Unreactive pupils are associated with the presence of hypotension, lower GCS, and closed basal cisterns on CT.4 14 163 The underlying pathology influences the prognostic value of unreactive pupils: patients with epidural haematoma fare better than those with subdural haematoma.115 116 123 129 Unilaterally unreactive pupils have an outcome intermediate between bilaterally reactive and unreactive pupils. Pupil asymmetry is associated with an operable mass lesion in around 30% of patients.18

Table 7 Marshall CT classification of TBI

Category Definition Diffuse injury I (no visible pathology) No visible intra-cranial pathology seen on CT scan Diffuse injury II Cisterns are present with midline shift < 5 mm and/or lesion densities present   No high- or mixed-density lesion > 25 ml, may include bone fragments and foreign bodies Diffuse injury III Cisterns compressed or absent with mid-line shift 0–5 mm No high- or mixed-density lesion > 25 ml Diffuse injury IV Mid-line shift > 5 mm No high- or mixed-density lesion > 25 ml Evacuated mass lesion Any lesion surgically evacuated Non-evacuated mass lesion High- or mixed-density lesion > 25 ml, not surgically evacuated Go to source>> Table 8 Outcome related to Marshall CT classification. TCDB, Traumatic Coma Data Bank; EBIC, European Brain Injury Consortium. Outcome is defined using the Glasgow Outcome Scale

Category Outcome94

Go to source>>

Hypotension Numerous observational studies have confirmed the association between systemic hypotension occurring at any point after injury and poor outcome.16 The largest study,19 a prospective reviewof more than 700 patients from the American TCDB, found thata single episode of hypotension during the period from injurythrough resuscitation was associated with an approximate doublingof mortality and a parallel increase in morbidity in survivors.This association persists when age and the presence or absenceof hypoxia and extra-cranial injuries are taken into account.Similar associations have been found in other studies. A prospectiveAustralian study38 found that early (resuscitation) and late(definitive care) hypotension were separately and additivelyassociated with increased mortality. The duration and numberof episodes of hypotension are correlated with mortality.90 The findings in children are similar provided appropriate correctionof adequate arterial pressure is made for age.118 Retrospectivedata117 suggest that intra-operative hypotension is also important,with a three-fold increase in mortality in those patients experiencing intra-operative hypotension. The precise mechanism for the enhancedsusceptibility of the injured brain to hypotension is not clear,33 143 but up to 90% of head-injured patients have been found tohave evidence of ischaemic damage at autopsy.48

Hypoxia Most,19 68 93 but not all90 observational studies in TBI havefound an association between observed early hypoxia [SpO2 <90% or <7.9 kPa (60 mm Hg)] and poor outcome. The associationis not as strong as for hypotension, and may be less importantin children.118 Hypoxia may be a marker of the severity of brainor systemic injury, or it may be a secondary insult to the atrisk brain. It may also be a surrogate marker for marked hypercapnia,which would be expected to lower cerebral perfusion pressure.Animal work suggests that, in rats, the combination of hypoxiaand percussive trauma leads to a small increase in oedema formation when compared with the percussive trauma alone, presumably becauseof the increasing inability of injured cells to maintain ionichomeostasis.164

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Concerns Raised Over Head Injury Studies

Information from Industry

NEW YORK (Reuters Health) Feb 22 – Using high-dose mannitol to treat head injuries may not be a sound strategy as the three main studies supporting this practice may not have even taken place, according to a report in British Medical Journal for February 24.

Between 2001 and 2004, a research group led by Brazilian neurosurgeon Dr. Julio Cruz published three trials showing that high-dose mannitol is preferable to the conventional dose in treating head injury. In particular, a reduction in death and disability was noted at 6 months by using high- rather than standard-dose mannitol.

However, concerns over the data began to surface. In an editorial accompanying one of the studies, the validity and reliability of the findings were called into question, largely because the research was conducted “at only one institution.” A later investigation by the Cochrane Collaboration was unable to verify that any of the studies had actually occurred.

In the present report, appearing in the British Medical Journal for February 24, Dr. Ian Roberts, coordinating editor of the Cochrane Injuries Group, and colleagues describe the numerous unsuccessful efforts they took to verify the data from Cruz’s studies.

One major problem in confirming the data was that Dr. Cruz committed suicide in 2005. Another problem was that Dr. Roberts’ team could not determine where the patients included in the studies had come from. The Federal University of Sao Paulo, which was listed as Dr. Cruz’s affiliation on the papers, later told the investigators that it had never employed Dr. Cruz.

Dr. Roberts’ team contacted the living co-authors in an effort to retract the reports. These authors declined to seek retraction and supported Dr. Cruz, commenting that “he would never have been able to do something false.”

After considerable efforts to confirm the data, Dr. Roberts and colleagues conclude, “We are left with serious doubt about important studies but with no way of determining with confidence whether the results are fabricated or real. The main author is dead. There is no institution to investigate. The implications for patients are serious.”

BMJ 2007;334:392-394.

Hypotension and Head Inj

Neurogenic hypotension in patients with severe head injuries. OBJECTIVE: To examine the occurrence of hypotensive episodes in patients with severe traumatic brain injuries that are not of hypovolemic origin and to investigate possible neurogenic or iatrogenic causes of such episodes. METHODS: We reviewed Traumatic Coma Data Bank (TCDB) records of the 248 patients with early hypotension. We attempted to eliminate episodes related to hemorrhagic hypovolemia by excluding patients with (1) extracranial injuries of Abbreviated Injury Scale scores > 3 (n = 99, 40%); (2) postresuscitation hematocrit levels < 35% (n = 76, 30.6%); (3) hematocrit levels decreasing to < 35% during the first 24 hours after injury (n = 47, 19%); and (4) patients with conflicting data (n = 5, 2%). This left 21 patients (8.5%) without discernible extracranial causes for their hypotension. RESULTS: Of these 21 patients, 4 had no extracranial injuries and 4 had only a single injury with Abbreviated Injury Scale score = 1. Hypotensive episodes were not associated with terminal or unsalvageable status. Mortality was 43%. Of the multiple factors investigated, the only two that were strongly associated with these “unexplained” hypotensive episodes were the presence of a diffuse injury pattern on computed tomography (n = 15, 71%) and the early use of mannitol or furosemide (n = 16, 76%) (It was policy at TCDB centers that hypotensive patients not receive diuretics until they were resuscitated.) CONCLUSIONS: (1) Some episodes of severe traumatic brain injury-related hypotension may be of neurogenic origin. (2) The risk/benefit ratio of early diuretic use in patients with severe traumatic brain injuries may be too high to support liberal use. These data strongly support the need for a study involving prospective collection of data describing the early blood pressure courses in such patients. (J Trauma. 1998 Jun;44(6):958-63)

Isolated brain injury as a cause of hypotension in the blunt trauma patient. BACKGROUND: Emerging evidence suggests that, contrary to standard teaching, isolated brain injury may be associated with hypotension. This study sought to determine the frequency of isolated brain injury-induced hypotension in blunt trauma victims. METHODS: Hypotensive adult trauma patients were categorized according to the cause of hypotension: hemorrhagic (hemoglobin < 11.0), neurogenic, isolated brain, or other. Their clinical data and outcomes were compared. RESULTS: The cause of hypotension was hemorrhagic in 113 (49%), isolated brain injury in 30 (13%), neurogenic in 14 (6%), and other causes in 24 (10%). Fifty (22%) were indeterminate. Hemorrhagic, isolated brain, and neurogenic groups were similar in age, Injury Severity Score, and systolic blood pressure. The Glasgow Coma Scale score of the isolated brain group was lower than in the hemorrhagic group (4.4 vs. 8.4, p < 0.05). Mortality was higher in the isolated brain group compared with the hemorrhagic group (80% vs. 50%, p < 0.05) and in the subgroup of hemorrhagic patients with versus without associated brain injury (57% vs. 39%, p < 0.05). CONCLUSION: Isolated brain injuries account for 13% of hypotensive events after blunt trauma and are associated with an increased mortality compared with hemorrhage-induced hypotension. In hypotensive brain-injured patients, hemorrhagic sources should be excluded rapidly, and the focus should be on resuscitation. (J Trauma. 2003 Dec;55(6):1065-9)

Nonoperative Management of Epidural Hematomas and Subdural Hematomas: Is it Safe in Lesions Measuring One Centimeter or Less? (J Trauma Volume 63(2), August 2007, pp 370)Results: There were 122 lesions <=1 cm and 82 lesions >1 cm. In the first group, 115 were managed nonoperatively, with 111 good outcomes (minimal deficit with a Rancho Los Amigos score [RLAS] >=3), two poor outcomes (severely disabled with RLAS <3), and two deaths. Twenty-eight patients with lesions greater than 1 cm had concomitant cerebral edema (CE) with an 89% mortality rate. The mortality rate in this group without CE was 20%, demonstrating the presence of CE in this group may have adversely affected the mortality rate, regardless of intervention.

Conclusions: This data suggests that EDH or SDH <1 cm thick can be safely managed nonoperatively unless there is concomitant CE.

ICP Monitoring

ICP changes in a limited number of patterns after TBI 9:

1. Low (<20 mm Hg) and stable ICP: This pattern is seen after uncomplicated head injury or during the early hours after severe TBI, before brain swelling evolves. 2. High (>20 mm Hg) and stable ICP: This is the most common pattern seen after severe TBI. 3. ICP waves: These reflect reduced intracranial compliance and are discussed in detail below. 4. ICP changes related to changes in ABP: These occur in the presence of abolished cerebral autoregulatory responses when ICP changes directly with ABP. 5. Refractory intracranial hypertension: In the absence of aggressive treatment strategies this may progress to herniation and death. ICP WAVE FORM

In 1965, Nils Lundberg et al. characterized ICP slow waves.51 “A” waves or “plateau” waves are steep increases in ICP from baseline to peaks of 50-80 mm Hg that persist for 5-20 min. These waves are always pathologic and may be associated with early signs of brain herniation, such as bradycardia and hypertension. They occur in patients with intact autoregulation and reduced intracranial compliance and represent reflex, phasic vasodilatation in response to reduced cerebral perfusion.52,53 The development of plateau waves leads to a vicious cycle, with reductions in CPP predisposing to the development of more plateau waves, further reductions in CPP and irreversible cerebral ischemia. “B” waves are rhythmic oscillations occurring at 0.5-2 waves/min with peak ICP increasing to around 20-30 mm Hg above baseline. They are related to changes in vascular tone, probably due to vasomotor instability when CPP is at the lower limit of pressure autoregulation. “C” waves are oscillations occurring with a frequency of 4-8/min and are of much smaller amplitude than B waves, peaking at 20 mm Hg. They occur synchronously with ABP, reflect changes in systemic vasomotor tone, and are of no pathologic significance.

Analysis of the ICP wave form in the time domain reveals three fundamental components: pulse wave form, respiratory wave form, and slow waves. The pulse wave form has several harmonic components, the fundamental of which has a frequency equal to the heart rate. The amplitude of this component (AMP) is used for the evaluation of various ICP-derived indices (see below). The respiratory wave form is related to the frequency of the respiratory cycle and occurs at 8-20 waves/min. Slow waves are generally less precisely defined than those described by Lundberg et al. and encompass all waves within the frequency limits of 0.05-0.0055 Hz (20 s to 3 min).

Several studies have shown that low power of slow waves may predict poor outcome after TBI.54 There is also a strong correlation between slow waves and fluctuations in the electroencephalogram,55 supporting the presence of a primary neuropacemaker in the brainstem responsible for fluctuations in CBF and generation of slow waves. Maintenance of ICP slow waves after TBI might therefore represent preservation of this pacemaker activity and of brainstem function.

CVR

The ICP response to slow spontaneous changes in ABP depends on the pressure-reactivity of cerebral vessels. This is a key component of pressure autoregulation and disturbed pressure reactivity implies disturbed pressure autoregulation. A pressure reactivity index (PRx) can be derived from continuous monitoring and analysis of slow waves in ABP and ICP.9,56 PRx is the linear correlation coefficient between ABP and ICP and its value ranges from -1 to +1. When the cerebrovascular bed is normally reactive, an increase in ABP leads to cerebral vasoconstriction within 5-15 s and a secondary reduction in CBV and ICP. Opposite effects occur when ABP is reduced. When CVR is impaired, changes in ABP are passively transmitted to CBV and ICP. PRx is determined by calculating the correlation coefficient of consecutive time-averaged data points of ICP and ABP recorded over a 4-min period.56 A negative value for PRx, when ABP is inversely correlated with ICP, indicates a normal CVR, and a positive value a nonreactive cerebral circulation. PRx correlates with standard measures of cerebral autoregulation based on transcranial Doppler ultrasonography 56 and abnormal values are predictive of poor outcome after TBI.20 PRx can be monitored continuously and has been used to define individual CPP targets after TBI.57

PRESSURE VOLUME COMPENSATORY RESERVE

The relation between ICP and changes in intracerebral volume can be used to define an index of compensatory reserve (RAP). RAP is the relationship (R) between the AMP (A) and the mean ICP over 1-3 min (P).58 Values of this index also range from -1 to +1. In the first, flat, part of the ICP-volume curve there is lack of synchronization between AMP and ICP, representing good compensatory reserve. Here the RAP is zero and the ICP wave form amplitude is low. On the steep part of the curve, when compensatory reserves begin to fail, AMP varies directly with ICP and RAP is +1. ICP wave form amplitude now begins to increase as mean ICP increases, at first slowly and then more rapidly as compensatory reserves are exhausted. Finally, on the terminal part of the curve, RAP is <0. Now there is terminal derangement of the cerebral vasculature and a decrease in pulse pressure transmission from the arterial bed to the intracranial compartment resulting in low or absent ICP wave form amplitude. RAP can therefore be used to indicate a patient’s position on the pressure-volume curve and may be used to predict the response to treatment and the risk of clinical deterioration or herniation.50 RAP <0.5 in association with ICP >20 mm Hg is predictive of poor outcome after TBI.58

More recently, the Spiegelberg brain compliance monitor has been used to provide similar information. This method relies on the measurement of the ICP response to a known small increase in volume by inflating and deflating the air pouch at the end of the Spielberg ICP catheter. Although the device is still a research tool, it offers the possibility of early warning of critical decompensation and risk of herniation 59 but its correlation with outcome has not been demonstrated.

(Anesth & Analg Volume 106(1), January 2008, pp 240-248)

Traumatic Subdural Hygromas review article (J Trauma 2008;64:705)

Penetrating Injuries

Penetrating Head Injury

Management of penetrating head injury is largely guided by principles learned during large-scale military conflicts. Although these injuries were historically regarded as nonsurvivable, current data suggest that good, functional improvement can occur if decompressive hemicraniectomy and limited debridement with excellent dural closure occur very soon after injury.[13] This recommendation is generally limited to high-velocity, military-grade weaponry. A notable exception to these observations includes penetrating injuries through the thalamus or brainstem (zona fatalis).[44] In these cases, surgical intervention will not change the imminent and likely mortality. As with severe closed TBI, the use of antibiotic prophylaxis, antiseizure medication for early postinjury seizures, CT scanning to assess the extent of injury, and ICP monitoring for those with GCS < 8 are recommended at the level of Option (Level III).[7-9,11] In addition to damaging areas of parenchymal tissue, it is important to rule out cerebrovascular injury or compromise. Recent studies suggest that both traumatic vasospasm (associated with poor outcomes and secondary injury) and traumatic aneurysms can occur in a high percentage of patients with penetrating injury.[2,45,46] That said, evaluation of the cerebral vasculature with either CT angiography or digital subtraction angiography should be strongly considered (Level III).[14]

Delayed Injuries / DASH

especially in coumadin folks

CT and observe if minor trauma s LOC or amnesia

if LOC, most likely need repeat CT and 24 hours observation

One man’s jury-rigged approach:

Minor head trauma (the definition of this in the anticoagulant literature seems to be different than most other head trauma lit, they actually define minor as NO LOC and NO AMNESIA, just a bop to the head)

• Most folks would still say scan these patients once and then observe for 6 hours. A few would say just observe, a very few would say admit for 24 hours. I watch them for 6 hours and then get the CT scan.

Head trauma with LOC, but GCS 15

• definitely scan, definitely observe at least 6 hours, most would say either rescan or admit for 24 hours

Head trauma with LOC, but GCS < 15

• scan, almost certainly admit for 24 hours, probably rescan prior to d/c

DASH (Neurosurgery 58:851-856, 2006)

Low Dose ASA led to secondary bleeding not seen on initial CT in patients with normal neuro exams (J Trauma 2009 67(3):521)

EMJ BET on the topic recommends further obs after initial CT

A study with the majority of patients without loc shows obs may be enough in this croup on warfarin and/or plavix (Journal of Trauma-Injury Infection & Critical Care December 2011 – Volume 71 – Issue 6 – pp 1600-1604)

Another crappy study showed delayed injuries (Ann Emerg Med 2012; Menditto et al.)

Secondary Intracranial Bleeding

Low Dose ASA led to secondary bleeding not seen on initial CT in patients with normal neuro exams (J Trauma 2009 67(3):521)

100 pts with age >65 with mild head trauma and GCS>15 on low dose ASA and already had neg head ct (almost all < 3 hrs from injury). Repeat head CTs were done at least 12 hours later. 4 pts had hemorrhage on repeat. 1 died, 1 had  crani with good outcome, 2 had good outcome.

Even patients with GCS of 15 need CT if they are on plavix, or anti-coagulant (J Trauma 2011;70:E1)

6.Jones K, Sharp C, Mangram AJ, Dunn EL. The effects of preinjury clopidogrel use on older trauma patients with head injuries. Am J Surg. 2006;192:743–745.

10.Ivascu FA, Howells GA, Junn FS, Bair HA, Bendick PJ, Janczyk RJ. Predictors of mortality in trauma patients with intracranial hemorrhage on preinjury aspirin or clopidogrel. J Trauma. 2008;65:785–788. Ovid Full Text Mount Sinai Serials Request Permissions Bibliographic Links [Context Link]

11.Mina AA, Knipfer JF, Park DY, Bair HA, Howells GA, Bendick PJ. Intracranial complications of preinjury anticoagulation in trauma patients with head injury. J Trauma. 2002;53:668–672. Ovid Full Text Mount Sinai Serials Request Permissions Bibliographic Links [Context Link]

12.Ohm C, Mina A, Howells G, Bair H, Bendick P. Effects of antiplatelet agents on outcomes for elderly patients with traumatic intracranial hemorrhage. J Trauma. 2005;58:518–522. Ovid Full Text Mount Sinai Serials Request Permissions Bibliographic Links [Context Link]

Reversal of Anti-Plt Drugs

plt transfusions associated with worse outcome in pts with GCS >12 and ICH (J Trauma. 2011;71: 358–363). Not a causation study.

Craniectomy

review article

Improves outcome, ICP, CPP (Injury. 2010 Jul;41(7):934-8. 2010 Mar 12.)

Decompressive craniectomy: surgical control of traumatic intracranial hypertension may improve outcome.

Eberle BM, Schnüriger B, Inaba K, Gruen JP, Demetriades D, Belzberg H.

Department of Surgery, Division of Acute Care Surgery (Trauma, Emergency Surgery and Surgical Critical Care), Los Angeles County and University of Southern California Medical Center, Los Angeles 90033-4525, United States.

Abstract

INTRODUCTION: The purpose of this study was to assess the role of decompressive craniectomy (DC) in patients with post-traumatic intractable intracranial hypertension (ICH) in the absence of an evacuable intracerebral haemorrhage.

METHODS: Retrospective study at LAC+USC Medical Centre including patients who underwent DC for post-traumatic malignant brain swelling or ICH without space occupying haemorrhage, during the period 01/2004 to 12/2008. The analysis included the effect of DC on intracranial pressure (ICP) and timing of DC on functional outcomes and survival.

RESULTS: Of 106 patients who underwent DC, 43 patients met inclusion criteria. Of those, 34 were operated within the first 24 h from admission. DC decreased the ICP significantly from 37.8+/-12.1 mmHg to 12.7+/-8.2 mmHg in survivors and from 52.8+/-13.0 to 32.0+/-17.3 mmHg in non-survivors. Overall 25.6% died (11 of 43), and 32.5% (14 of 43) remained in vegetative state or were severely disabled. Favourable outcome (Glasgow Outcome Scale 4 and 5) was observed in 41.9% (18 of 43). No tendency towards either increased or decreased incidence in favourable outcome was found relative to the time from admission to DC. Six of the 18 patients (33.3%) with favourable outcome were operated on within the first 6h.

CONCLUSIONS: DC lowers ICP and raises CPP to high normal levels in survivors compared to non-survivors. The timing of DC showed no clear trend, for either good neurological outcome or death. Overall, the survival rate of 74.4% is promising and 41.9% had favourable neurological outcome.

Hypothermia

35 seems to be as good as 33 in a before and after trial (J Trauma 66(1), January 2009, pp 166-173)

When the patient is sitting up, the effective BP is less than at the phlebostatic axis. Difference is 2 mm Hg per inch systolic BP (J Clin Anesth 2009;21:72)

Sympathetic Hyperactivity

review article also discusses beta blockers

Nimodipine for Traumatic SAH

doesn’t help in SR (Lancet Neurol 2006;5:1029) and Cochrane (Calcium Channel Blockers for Acute Traumatic Brain Injury)

Hypothermia

The Lancet Neurology, Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial

Findings

Enrolment occurred from December, 2005, to June, 2009, when the trial was terminated for futility. Follow-up was from June, 2006, to December, 2009. 232 patients were initially randomised a mean of 1·6 h (SD 0·5) after injury: 119 to hypothermia and 113 to normothermia. 97 patients (52 in the hypothermia group and 45 in the normothermia group) did not meet any of the second set of exclusion criteria. The mean time to 35°C for the 52 patients in the hypothermia group was 2·6 h (SD 1·2) and to 33°C was 4·4 h (1·5). Outcome was poor (severe disability, vegetative state, or death) in 31 of 52 patients in the hypothermia group and 25 of 56 in the normothermia group (relative risk [RR] 1·08, 95% CI 0·76—1·53; p=0·67). 12 patients in the hypothermia group died compared with eight in the normothermia group (RR 1·30, 95% CI 0·58—2·52; p=0·52).

Interpretation

This trial did not confirm the utility of hypothermia as a primary neuroprotective strategy in patients with severe traumatic brain injury.

Glucose

Probably shoot for 180 mg/dl.

Tight plasma control leads to hypoglycemia in the injuryed areas of th ebrain (Neurocrit Care 2010;12:317)

In an sICH population, hyperglycemia was associated with increased mortality when present in the ED, no idea if treating it makes a difference (Neurocrit Care 2010;13:67)

Feeding

transpyloric nutritition reduces incidence of overall and late pneumonia

and improves nutriitional efficacy (Inten Care Med 2010;36:1532)

Cranial Gunshot Wounds

retrospective review (J Trauma 2010;69:770)

Pts with GCS>8, normal pupils, and only single lobe involvment may benefit from resus

Bilobar or intraventric blood has dismal outcome

DVT Prophylaxis

seems early (0-72 hrs) proph is safe for stable bleeds (The Journal of Trauma: Injury, Infection, and Critical Care Issue: Volume 70(2), February 2011, pp 278-284)

    |      |      |   Podcast

Compliance with Trauma Guidelines reduces Mortality

including damage control, transfusion, and ventilatory management (Crit Care Med 2012;40:778)

use full body ct scout as lodox for bullet location

Falls from Height

LD90 for fall=7 stories

The median lethal dose (LD50) for falls is 4 stories, or 48 ft, and the lethal does for 90% (LD90) of test subjects is 7 stories, or 84 ft. Reference: Rosen P, ed. Emergency Medicine: Concepts and Clinical Practice. 4th ed. Mosby-Year Book, Inc; 1998:352.

Prognostic factors are height, impact surface, and the body part which first hits the ground (Crit Care Med 2005;33:1239)

Over 50% in autopsy study had cardiac trauma (in half of these, it was the cause of death), consider thoracotomy (J Trauma 2004;57:301)

ABCs in trauma room often stand for Accuse, Blame, and Criticize, Deny, Exaggerate

Anaesthetic ABCD:AvoidBlockCancelDefer

Consultant> A    appear> B    blame> C    criticize> D    disappear

power vacuum needs to be filled

Airway-Ask patient to take deep breath (Gives A,B, and LOC)

Breathing

Circulation Search For Bleeding

Disability (pupils/moves extremities)

Expose and then cover (Strip, Flip, Touch, and Smell)

Finger (rectal)/FAST Exam/Foley

Glucose/Girl (pregnancy test)

Hang Antibiotics

Inject (tetanus)

Primary Survey

Secondary Survey

Tertiary Exam The tertiary exam was first introduced in 1993 by Enderson et al to assist with the diagnosis of any injuries that were not identified during the primary and secondary survey. The tertiary survey involved repetition of the primary and secondary surveys, meticulous physical examination, repetition of the history of the trauma history, and review of all laboratory and radiographic studies. These authors’ use of this tertiary survey resulting in diagnosis of missed injuries in 36 of 399 patients (9%). The most common reason for injuries to be missed was altered level of consciousness. None of the missed injuries resulted in death, but one missed injury resulted in disability and seven required operative intervention. In a second large series, a tertiary trauma survey detected 56% of the injuries missed during the initial assessment within 24 hours of admission.

Military is switching to <C>ABC for catastrophic hemorrhage to urge immediate use of tourniquets, dressings, and hemostatic agents

BATLS

(Emerg Med J 2006;23:745)

Consider an A-line if they need blood or pressors for hypotension

Lab Tests

Lactate/Base Deficit probably more useful then serial crits

Venous base deficit correlated perfectly with arterial in trauma patients (J Trauma. 2011;71: 793–797)

Study of serial crits (Injury 2006;37:46)

Delta crit @ 4 hours had only 40% sensitivity, specificity of 95%. LR- 0.64 LR+ 7.1

One study shows 90% sensitivity??? for serious bleeds (J Trauma 2007;63:312) over 30 minutes

Airbags

Sodium azide is contained in airbags, shot c spark causing huge gas expansion and releasing talc, if airbag doesn’t properly deploy, then can get NaOH (sodium hydroxide,) which can give contact dermatitis

Pain Management

Use fentanyl 1-2 ug/kg instead of morphine

Consider SQ Ketamine .25 mg/kg then .1 mg/kg/hr.  Use 26 gauge cannula in the SubQ space on the anterior abd wall.  Avoid if possibility of head injury

(?)

Fluid Resuscitation

delayed fluid resuscitation in penetrating torso injuries resulted in shorter hospitalization and less complications (NEJM 331:17; 1105-1109 Oct 1994)

Shock

Blood:  external chest abd retroperitoneal pelvis long bone

Non-Blood:  pneumo tamponade myocardial contusion spinal shock

do not assume aortic injury is the cause of shock

“janitorial injuries”

Best article on traumatic aortic disruption Fabian J Trauma 1997 42:374

new strategy of delayed aortic repair with BP/HR monitoring and control

Brain injury article J Trauma 1993 34:216

Mannitol has to be given by bolus not continuous infusion to be beneficial

pelvis injuries

lateral compression horizontal fracture of the anterior ring look at the sacrum’s arcuate lines

vertical shear, tape the feet together

hemoperitoneum goes to the OR first, otherwise to angio suite

put pinky in sternal notch, index finger will be in the cricothyroid

Not true 80/70/60 pulse rule, but they will disappear in the predictable manner (Deakin et al BMJ Sept 2000)

do not need plain films after getting ct abd/pelvis, just reformat (J Trauma 55(4):665, October 2003)

Levels of Trauma Center Shitstorm

SNAFU FUBAR AMF YoYo

Farming-manure to vegetables

Scalea TM et al: Central venous blood oxygen saturation: an early, accurate measurement of volume during hemorrhage. J Trauma 28:725, 1988;

“Rookies talk tactics, experts discuss logistics”

Tactics/Strategy/Team

General Operative Management

for abd, prep knee to chin

for ext, prep entire ext and 1 unaffect lower ext

neck, prep entire chest

Lethal triad of hypothermia, coagulopathy, and acidosis

always choose the repair option which fails best

figure of eight, first bite to lift the tissue, 2nd bite to get the bleeder

(Peterson J Traum Volume 58(5).May 2005.1078-1 81)

Do not use bovine fibrin glue anymore, it may sensitize to ATIII

Relative Bradycardia

Bradycardia actually incredibly common and predicts bad outcome in some groups (J Trauma 2009;67:1051)

Bradycardia may be present very often in hypovolemic/hemorrhagic shock.  There is a biphasic response, the first and the one we commonly think of is catecholamine surge with resulting tachycardia and increased card output.  Later on, there is actually a cardiac vagal response resulting in bradycardia.  This may be present in up to 1/3 of hypovolemic patients (BMJ 2004;328:451-453 (21 February))

bradycardia is more common than tachycardia in acute blood loss (9.McGee S, Abernathy WB, Simel DL. Is this patient hypovolemic? JAMA 1999; 281:1022–1029)Bezold-Jarisch

Bradycardia may be present very often in hypovolemic/hemorrhagic shock.  There is a biphasic response, the first and the one we commonly think of is catecholamine surge with resulting tachycardia and increased card output.  Later on, there is actually a cardiac vagal response resulting in bradycardia.  This may be present in up to 1/3 of hypovolemic patients (BMJ 2004;328:451-453 (21 February))

ATLS HR/BP correlations with degree of shock are crap (Resus 2010;81:1142)

Additional articles about bradycardia during bleeding

J Accid Emerg Med 1995;12:1

J Am Coll Surg 2003;196:679

J Trauma 1998;45:534

not being tachycardic actually portends a worse outcome in the setting of shock (J Trauma. 2011;71: 789–792)

Automated BPs are Inaccurate

they overestimate the BP until SBP > 110

this may be the root of the phenomena of insanely high BPs when pt’s first arrive

J Trauma. 2003;55:860 –863.

CPR for Trauma

retrospective prehospital study. DNR if apneic and pulseless on arrival or asystolic or PEA with rate<40 (J AM Coll Surg 2004;198:227)

Another study shows prognosis in traumatic arrest is the same as medical (Crit Care Med 2007;35:2251)

Massive Transfusion Protocol

Rectal Exam

Reasons to Omit Digital Rectal Exam in Trauma Patients: No Fingers, No Rectum, No Useful Additional Information (J Trauma 2005;59(6):1314)

Level I has only limited air elimination abilities (J Clin Anesthesia 1997;9:233)

Study objective: Most injured patients taken by ambulance to hospital emergency departments do not require emergency surgery, yet most US trauma centers require a surgeon to be present on their arrival. If a clinical decision rule could be developed to accurately identify which injured patients require emergency operative intervention, then such “secondary triage” criteria could permit a trauma center to more efficiently use their surgeons’ time. Methods: We analyzed 7.5 years of data (8,289 consecutive trauma activations) in our prospectively maintained Level I trauma center registry. We used classification and regression tree analyses to generate clinical decision rules using standard out-of-hospital variables to identify emergency operative intervention (within 1 hour) by a general surgeon (for adults) or a pediatric surgeon (if _14 years). Results: Emergency operative intervention occurred in 3.0% of adults and 0.35% of children. For adults, summoning a surgeon for any one of 3 criteria (penetrating mechanism, systolic blood pressure _96 mm Hg, pulse rate _104 beats/min) could reduce surgeon calls by 51.2% while failing to identify emergency operative intervention in only 0.08% (rule sensitivity 97.2% and specificity 48.6%). For children, no rule at all (ie, never automatically summoning a surgeon) would fail to identify emergency operative intervention in only 0.35% of patients, and use of a single criterion (penetrating mechanism) would reduce surgeon calls by 96.2% while failing to identify emergency operative intervention in only 0.09% (rule sensitivity 75.0% and specificity 96.5%). Conclusion: We have derived simple decision rules for trauma centers that, if validated, could substantially reduce the need for routine surgeon presence on trauma patient arrival. These rules demonstrate low false-negative rates. [Ann Emerg Med. 2006;47:135-145.]

article discussing the evidence (Annals of EM 2006;47(5):405)

Damage Control

Scalea [19] has condensed the principles of damage control: only blood loss kills early; gastrointestinal injury causes problems later; everything takes longer than you think; an injury may be missed during hurried laparotomy in an unstable patient; hypothermia, acidosis, and coagulopathy lead to more of the same; the best setting for a critically ill patient is the intensive care unit.

Damage control Review article by Feliciano

Low iCal at arrival is associated with bad outcome (J Trauma Volume 61(4), October 2006, pp 774-779)

Cochrane Database Syst Rev. 2004;(3):CD004173. MAIN RESULTS: There is a limited literature relating to this topic but none of the studies identified met the inclusion criteria for this review. REVIEWERS’ CONCLUSIONS: There is no clear evidence that ATLS training (or similar) impacts on the outcome for victims of trauma, although there is some evidence that educational initiatives improve knowledge of what to do in emergency situations. Further, there is no evidence that trauma management systems incorporating ATLS training impact positively on outcome. Future research should concentrate on the evaluation of trauma systems incorporating ATLS, both within hospitals and at the health system level, by using rigorous research designs.

Resus from Severe Hemorrhage (Crit Care Med 1996;24(2):12S)

mention the Bickell Study (NEJM 1994;331:1105) delayed till operating room vs. immediate.

give fluids when inducing or pericode

Hypertonic Saline (Trauma Resus update Lancet 2004;363:1988)

HCT and Hb are the same

J Trauma, Volume 62(5).May 2007.1310-1312

HCT may be low or normal or sick patients (Journal of Trauma and Acute Care Surgery Volume 72(1), January 2012, p 54–60)

Helmets

Trauma & Motorcyclists (Injury 2007;38:1131)

Pull helmet edges in the lateral direction

What you can ligate

Nugget Approach to Bleeding

Journal of Emergency Medicine Volume 34, Issue 3, April 2008, Pages 319-320

how to properly apply direct pressure

Interventional Radiology in Trauma

INJURY Volume 39, Issue 11,  Pages 1229-1308 (November 2008)Interventional Radiology in Trauma Care Edited by S.J.A. Sclafani and I.D.S. Civil

Complications after Exploratory Laparotomy

in one study, very low (Journal of Trauma-Injury Infection & Critical Care: September 1996 – Volume 41 – Issue 3 – pp 509-513)

EM Traumatologists

Article in surgery literature

Indications for bullet removal

1. Just under the skin, and residing in a pressure area where the bullet is painful when the patient sits or lies down.
2. Visibly bulging beneath the skin and causing cosmetic distress.
3. In a joint space
4. In the globe of the eye.
5. In a vessel lumen causing ischaemia or with the risk of embolisation to the heart, lungs or peripheral vessles.
6. Impinging on a nerve or nerve root and causing pain.
7. Localised abscess formation (usually due to dirt or clothing fragments entrained by the bullet).
8. Required for forensic investigation and the patient and surgeon are in full agreement that the removal will not result in increased pain, suffering, complications or injury and both agree to the removal.
9. Documented elevated lead levels, usually in a child and occurring several months after injury (extremely rare)

Vasopressors

Vasopressors kill trauma patients, don’t do it (J Trauma 2008;64:9)

Balloon Pump

Balloon Pump to Stop Abd/Pelvis Bleeding

(J Trauma 2010;68(4):942)

Assar AN, Zarins CK. Endovascular proximal control of ruptured abdominal aortic aneurysms: the internal aortic clamp. J Cardiovasc Surg (Torino). 2009;50:381–385. Mount Sinai Serials Bibliographic Links [Context Link]  Gupta BK, Khaneja SC, Flores L, Eastlick L, Longmore W, Shaftan GW. The role of intra-aortic balloon occlusion in penetrating abdominal trauma. J Trauma. 1989;29:861–865. Ovid Full Text Mount Sinai Serials Request Permissions Bibliographic Links [Context Link]  Karkos CD, Bruce IA, Lambert ME. Use of the intra-aortic balloon pump to stop gastrointestinal bleeding. Ann Emerg Med. 2001;38:328–331. Ovid Full Text Mount Sinai Serials Bibliographic Links [Context Link] Harma M, Harma M, Kunt AS, Andac MH, Demir N. Balloon occlusion of the descending aorta in the treatment of severe post-partum haemorrhage. Aust N Z J Obstet Gynaecol. 2004;44:170–171. Mount Sinai Serials Bibliographic Links [Context Link] Rieger J, Linsenmaier U, Euler E, Rock C, Pfeifer KJ. [Temporary balloon occlusion as therapy of uncontrollable arterial hemorrhage in multiple trauma patients]. Rofo. 1999;170:80–83. Mount Sinai Serials Bibliographic Links [Context Link]

10 F sheath

20-mm berenstein balloon introduced to 50 cm

slowly inflate dwith saline until friction is felt against wall

eventually placed in infrarenal aorta

identify absent femoral pulses

5% Hypertonic as a Resus Fluid

Mikey likes it

Journal of Trauma: Injury, Infection, and Critical Care  68(5), May 2010, pp 1172-1177

or my 1.3%

1 amp of 44.6 bicarb in 500 ml of NSmakes 550 of total volume=Na 121.6Cl 77Bicarb 44.6to extend to 1 literNa 217Cl 138.6 BiCarb 801.3% Saline solution

Intestinal Allis Clamps

can be used to close organs

Prognosis

We are very poor at predicting prognosis in the trauma ICU ((J Trauma. 2010;68: 1279–1288)

Isolated Episodes of Hypotension

Even a single drop < 105 SBP associated with severe injuries (J Trauma. 2010 Jun;68(6):1289-94; discussion 1294-1295.)

Delay to IR

each hour of delay is associated with an almost ~50% increase in mortality in a J trauma retropsective study ( J Trauma 2010;68:1296)

Crash-2 Tranexamic Acid

Lancet 2010

1g tranexamic acid over 10 minutes followed by infusion of 1 g over 8 hours

within 8 hours of injury

sig hemorrhage or predicted sig. hemorrhage (SBP < 90 or HR > 110)

1.5% reduction in mortality (all-cause)

Planned reanalysis shows must be given within 3 hours to be effective (Lancet 2011;377:1096)

Review Article (J Trauma 2011;71:S9)

Stopping Vessel Bleeding

use dead head from three way stopcock held in forceps (J Trauma 2010;69(2):466)

EMS Scene Time

The authors state: “In this study, we were unable to support the contention that shorter out-of-hospital times… improve survival among injured adults with field-based physiologic abnormality… Our findings are consistent with those of previous studies that similarly have failed to demonstrate a relationship between out-of-hospital time and outcome using different patient populations, trauma and EMS systems, regions, data sources, and confounders“

Emergency Medical Services Intervals and Survival in Trauma: Assessment of the “Golden Hour” in a North American Prospective Cohort Ann Emerg Med. 2010 Mar;55(3):235-246

from resus.me

ATLS Shock Classification Doesn’t Work

An excellent discussion section in this paper states: ‘it is clear that the ATLS classification of shock that associates increasing blood loss with an increasing heart rate, is too simplistic. In addition, blunt injury, which forms the majority of trauma in the UK, is usually a combination of haemorrhage and tissue injury and the classification fails to consider the effect of tissue injury‘

Testing the validity of the ATLS classification of hypovolaemic shock Resuscitation. 2010 Sep;81(9):1142-7

from resus.me

Resuscitation Volume 82, Issue 5, May 2011, Pages 556-559

Vitals in the Elderly

normal vital signs are in no way reassuring in the elderly

get scared when the SBP < 100 and/or HR > 90

(j trauma 2010;813)

Crystalloid

>1500 ml  of crystalloid assoc with increased risk of death after multivariate (The Journal of Trauma: Injury, Infection, and Critical Care Issue: Volume 70(2), February 2011, pp 398-400)

Optimal emergency department SBP cutoff values for hypotension were 85 mm Hg for patients aged 18 to 35 years, 96 mm Hg for patients aged 36 to 64 years, and 117 mm Hg for elderly patients. (Arch Surg. 2011;146(7):865-869)

Steroids for Pneumonia

small rct from france shows reduced mortality for trauma patients given hydrocortisone for the outcome of HAP (JAMA. 2011;305(12):1201-1209)

Hypotensive Resuscitation

New RCT of OR management showed hypotensive resus is safe and may have mortality benefit (J Trauma 2011;70:652)

Blunt Traumatic Arrest

Can have tension pneumothorax with no clinical signs and then gain immediate ROSC (Emerg Med J-2009-Mistry-738-40)

Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA)

(J Trauma 2011;71(6):1869)

FIRST Trial – HES for Pentrating Trauma

Resuscitation with hydroxyethyl starch improves renal

Trauma)

Br J Anaesth. 2011 Nov;107(5):693-702

Helicopter vs. Ground Transport

(JAMA 2012;307(15):1602)

chopper use assoc. with increased survival in major trauma. This was a retrospective propensity score analysis.

“All things are poison and nothing is without poison.  Solely the dose determines that a thing is without poison.”

–Paracelsus

Tox Links

Vaults of Erowid

www.lycaeum.org

www.householdproducts.nlm.nih.gov

www.ansci.cornell.edu/plants

www.dartmouth.edu/~toxmetal

www.toxed.com

www.microdex.com/products/poisondex

www.clinicalpharmacology-ip.com

Mnemonics

Do not adsorb to charcoal

PHAILS

Pesticides;

Hydrocarbons;

Acids and alkali;

Iron;

Lithium; and

Solvents

Repeat Dose Charcoal

ABCD

Antimalarials (quinine) and aminophylline (theophylline);

Barbiturates (Phenobarbital) and beta-blockers (nadolol);

Carbamazepine

Dapsone

and Dilantin (Phenytoin)

Valproate

Theophylline

Toxins Accessible To Hemodialysis

Small Molecule, Low Protein Binding, Water Soluble

I STUMBLE

Isopropyl Alcohol

Salicylates

Theophylline (caffeine)

Uremia

Methanol

Barbiturates, beta-blockers (water soluble, such as atenolol)

Lithium

Ethylene glycol

Vital Sign/PE Mnemonic

s

Bradycardia (PACED)

Propranolol or other beta-blockers, poppies (opiates), propafenone, phenylpropanolamine

Anticholinesterase drugs

Clonidine, calcium-channel blockers

Ethanol or other alcohols

Digoxin

Tachycardia (FAST)

Free base or other forms of cocaine

Anticholinergics, antihistamines, amphetamines

Sympathomimetics (cocaine, amphetamines), solvent abuse

Theophylline

Hypothermia (COOLS)

Carbon monoxide

Opiates

Oral hypoglycemics, insulin

Liquor

Sedative-hypnotics

Hyperthermia (NASA)

Neuroleptic malignant syndrome, nicotine

Antihistamines

Salicylates, sympathomimetics

Anticholinergics, antidepressants

Hypotension (CRASH)

Clonidine, calcium-channel blockers

Reserpine or other antihypertensive agents

Antidepressants, aminophylline

Sedative-hypnotics

Heroin or other opiates

Hypertension (CT SCAN)

Cocaine

Thyroid supplements

Sympathomimetics

Caffeine

Anticholinergics, amphetamines

Nicotine

Rapid respiration (PANT)

PCP, paraquat, pneumonitis (chemical)

ASA and other salicylates

Non-cardiogenic pulmonary edema

Toxin-induced metabolic acidosis

Slow respiration (SLOW)

Sedative-hypnotics (including GHB)

Liquor

Opiates, sedative-hypnotics

Weed (marijuana)

Miosis (COPS)

Cholinergics, clonidine

Opiates, organophosphates

Phenothiazines, pilocarpine

Sedative-hypnotics

Mydriasis (AAAS)

Antihistamines

Antidepressants

Atropine and other anticholinergics

Sympathomimetics

Drugs Causing Pneumonitis Or Pulmonary Edema

(

MOPS

)

Meprobamate, methadone

Opiates, organophosphates

Phenobarbital, propoxyphene, phenothiazines

Salicylates, smoke inhalation (including cocaine smoke), solvents

Causes of high Osmal Gap

ME DIE

Methanol

Ethylene glycol

Diuretics (osmotic diuretics like mannitol)

Isopropyl alcohol

Ethanol

Also acetone

Drugs that cause Seizures

Aspirin

Tramadol (Ultram®, Ultracet™)

Tricyclic antidepressants

Bupropion (Wellbutrin®, Zyban®)

Diphenhydramine (Benadryl®)

Amphetamines/Cocaine

Venlafaxine (Effexor®)

Smells of Toxicology (River’s)

Nitrites, Isopropyl alcohol:  fruit like

Phenols:  disinfectant

Cyanide:  bitter almonds

Chloral Hydrate:  pear-like

Arsine, phosphorous, tellerium, organophosphates:  garlic

Turpentine:  violets

Hydrogen Sulfide:  rotten eggs

Camphor, naphthalene:  mothballs

Phosgene:  hay

Methylsalicylate:  wintergreen

Presentations

Brady+Vomiting=Digoxin

Also av or nodal block with atrial or ventricular irritability

Tachy+Vomiting=think theo

Extrapyramidal Toxidrome

TROD seen with zines, haldol, reglan

Tremor, torticollis, trismus

Rigidity

Opisthotonos, Oculogyric Crisis

Dysphonia, dysphagia

Activated Charcoal

AC only helps in tylenol overdose if given within 1 hour of ingestion (J Toxicol Clin Toxicol 2001;39(6):601)

Position Statement Am Acad Toxicol, no AC after 1 hour can be supported by evidence, only give in patients with intact or protected airway

A different opinion on charcoal

Malignant Hyperthermia

Rare inherited disorder: autosomal dominant with variable expression and incomplete penetrance

May occur up to 24 hours after the use of succinylcholine or inhaled anesthetics

From abnormal calcium channels

AMS, rigidity, hyperthermia, autonomic instability, acidosis

Active Cooling

Benzos

Dantrolene-1 mg/kg IV may repeat to dose of 10 mg/kg.  2 mg/kg PO QID for 2 days after.

Malignant HYperthermia Review

Date Rape Drugs

GHB and flunitrazepam

Barbs, benzos, ambien, carisoprodol, chloral hydrate, GHB, THC, Cocaine, methamphetamines, XTC, PCP and Ketamine, Scopolamine

Statins

Cholesterol membrane instability, muscle affected most

Rhabdomyolysis b/c of coenzyme Q inhibition in mitochondria.  Myopathy and hepatotoxicity

.

TB Meds

Isoniazid (INH)

>20 mg/kg needs evaluation

>79 mg/kg can lead to seizures

May be asymptomatic for up to 2 hours post ingestion

N/V, photophobia, hallucinations, dizziness, ataxia, slurred speech, lethargy progressing to grand mal seizures, coma, and death

Blocks GABA formation (active b6 catalyzes glutamate to GABA, INH makes you pee out B6 and decreases enzymatic formation of active B6), also inhibits conversion of lactate to pyruvate, so lactic acidosis

Benzos

Pyridoxine (B6) should be administered to match gram for gram dose of INH up to 5 grams.  If dose unknown, give 5 grams empirically

Effects diminish rapidly, so 6 hours observation, then D/C

Side effect is hepatitis:  10% have elevated enzymes, 10% of those get hepatitis, 10% of those die from it.

Can also cause niacin deficiency:  pellagra=diarrhea, dementia, dermatitis

Rifampin

Causes all fluids to turn red

Ethambutol

Optic Neuritis

Pyrazinamide

Hepatic dysfunction

Antimalarial Meds

Mefloquine

gives vivid dreams

Quinine

Cinchoism=n/v, hearing loss, tinnitus, HA.

Also blocks Na and K channels in heart causing QRS/QT prolongation, requiring Bicarb.  TDP as well.  Give MdAC.  Can get blindness from direct retinal toxicity.

Chloroquine

GI Symptoms, Hypokalemia, QRS/QT prolongation, severe hypotension.  Give 2 mg/kg diazepam over 30 min then 1-2 mg/kg/day.  EPI .25 ug/kg/min until systolic > 100.  Validated in France where this used to be a popular suicide med.

Dapsone

MetHb

Paraphenylenediamine (Para, PPD)

In hair dyes

Respiratory failure, myoglobinuria, vomiting, tongue swelling.  Causes cancer.

Hydrazine

can cause stat epilepticus, contained in jet fuel

Baclofen

Withdrawal

Fever, AMS, rebound spasticity, rhabdo, organ failure

Can be caused by catheter malfunction, empty reservoir, dead batteries

RX:  restart the pump, oral baclofen, benzos

Poisonings in Lab workers

CO, Cyanide, Azides, MetHb inducing chemicals

Fatal inhalations-CO, Hydrogen Sulfide, Asphyxiants, NOs, Smoke, Halogens

Blood Screening-Na Azide, cyanide, CO, sulfide

Sodium Azide (NaN3)

Highly toxic and highly explosive

Used in detonators and as preservative in lab reactions

In vapor form, colorless, pungent.

Sx arise suddenly and dissipate in a few hours

ABD cramps, chest pain, dysphoria, faintness, flushing, headache, incontinence, n/v, palpitations, weakness, agitation, diarrhea, hyperventilation, hypo or hypertension, leukocytosis, pallor, syncope, sweats, tachycardia, and vomiting.  Larger doses can give blindness, dilated pupils, NCPE, myocardial dysfunction, myocarditis, shock, seizures and coma.  Uncouples oxidative phosphorylation.

GI Decon and supportive care

Mitochondrial Toxins

propofol

b. cereus toxin

valproate

hiv meds

can see ketoacidosis, lactic acidosis, myopathy

Propofol Infusion Syndrome

Inten Care Med 2003;29:1417

cardiac depressant

infusion syndrome is associated with catecholamine and steroid tretament simultaneous with propofol

consider after >48 hours of infusion

catechols-increased CO causes increased clearance requiring higher doses

Causes cardiac failure and rhabdomyolysis

>5 mg/kg/hr is considered high dose and puts pts at risk

Nail Polish Removers

most contain acetonitrile which is converted to cyanide in vivo.

Dystonic Reactions

buccolingual-protruding or pulling sensation of tongue

Torticollic-neck or facial spasm

Oculogyric-roving or deviated gaze

Tortipelvic-abd rigidity and pain

Opisthotonic-spasm of entire body

Give 50 mg of benadryl IV

Strychnine

seizure while awake, lift back off bed

muscle spasms

Strychnine poisoning is an unusual but dramatic poisoning in which convulsions are the major threat to life. Convulsions are predominantly at the spinal level, and the key to recognition of this poisoning is observation of convulsive activity in the awake patient without a postictal phase. Successful treatment requires aggressive airway control and treatment of seizures with benzodiazepines or barbiturates. Neuromuscular blockade may be required. Gastrointestinal decontamination is usually indicated in recent acute ingestions but may precipitate convulsions. Recovery from strychnine poisoning is usually complete and rapid if treatment is aggressive. In the absence of trauma, compartment syndrome, rhabdomyolysis, or anoxic central nervous system injury, no neurologic or musculoskeletal sequelae are expected. Confirmation of strychnine poisoning is best obtained by submitting urine or gastric aspirate for analysis utilizing a qualitative test such as thin layer chromatography (TLC).

Malignant Hyperthermia

Dextromethorphan

DXM

skittles, red hots, triple cs

Reglan

Metoclopramide

Rate of Akasthisia is directly related to rate of infusion. Over 10 minute infusion sig. less side effects than 2 minute IV Bolus (EMJ 2005;22(9):621)

Toxin Induced Hyperthermia

Crit Care 2007; 11:236

Colchicine

review of toxicity

Methotrexate

Methotrexate (MTX) is a chemotherapeutic drug that is structurally similar to folic acid. MTX inhibits dihydrofolate

reductase, an enzyme that reduces folic acid to tetrahydrofolic acid. This inhibition interferes with DNA

synthesis and cell reproduction. MTX is used in the treatment of a variety of illnesses including cancer, rheumatoid

arthritis, systemic lupus erythematosus, and psoriasis. It is given intravenously, intramuscularly, orally

and intrathecally.

Methotrexate toxicity develops due to increased patient susceptibility during treatment, excessive parenteral

or intrathecal administration, therapeutic errors by patients (e.g. taking MTX orally daily instead of weekly),

self-administration to induce abortion, or intentional oral overdoses. Clinical manifestations of toxicity include

nausea, vomiting, diarrhea, mucositis, stomatitis, esophagitis, elevated hepatic enzymes, renal failure, rash,

myelosuppression (leukopenia, pancytopenia, thrombocytopenia), acute lung injury, tachycardia, hypotension,

and neurologic dysfunction (depression, headache, seizures, motor dysfunction, stroke-like symptoms, encephalopathy,

coma). Toxic effects may occur hours to days to weeks after MTX administration or overdose.

Treatment of MTX toxicity includes the administration of activated charcoal in the event of a recent, oral overdose.

Renal failure may be prevented by adequate hydration and urinary alkalinization with sodium bicarbonate.

There are three antidotes that have been used for MTX toxicity: leucovorin, thymidine and glucarpidase.

Leucovorin (folinic acid) is the reduced and active form of folic acid. It selectively “rescues” normal cells from

the toxic effects caused by MTX’s inhibition of the production of reduced folates. The recommended dosage in

most cases is 100 mg/m

2 intravenously every 3 to 6 hours until the plasma MTX level is less than 0.01

mcmol/L or for 3 days or longer if levels are not available. Thymidine rescues cells from the cytotoxic effects of

MTX. Its use is investigational and is only given along with other therapies. Glucarpidase (carboxypeptidase) is

an antidote that has been used recently for MTX toxicity in combination with leucovorin. It converts MTX to an

inactive form and rapidly lowers MTX blood levels. It is given as a single bolus of 50 units/kg intravenously

over 5 minutes. Leucovorin should be continued for 48 hours after glucarpidase administration. Hemodialysis

and hemoperfusion have been used to lower MTX levels. Intrathecal overdoses require special measures including

cerebrospinal fluid drainage and exchange, steroids, and antidotes. (Maryland ToxTidbits)

Dinitrophenol (DNP)

Fatal 2,4-dinitrophenol poisoning . . . coming to a hospital near you. Siegmueller C, Narasimhaish R. Emerg Med J 2010 May 29 [Epub ahead of print]

Abstract

Dinitrophenol (DNP) is an industrial chemical used in the manufacture of explosives, herbicides, dyes, and wood preservatives.  When ingested, DNP uncouples mitochondrial oxidative phosphorylation, interfering with the cells’ ability to store energy as ATP.  Instead, the energy is dissipated as  heat, causing severe hyperthermia that in case reports has proven very difficult if not impossible to control. In addition, the ATP depletion causes release of calcium from the sarcoplasmic reticulum in muscles.  The resulting uncontrolled muscular contraction produces even more heat. Patients with DNP toxicity often die of hyperthermia, multi-organ failure, and cardiovascular collapse. Presenting signs and symptoms of acute DNP toxicity include hyperthermia, diaphoresis, nausea and vomiting, and diarrhea.

In the 1930s, DNP was often used as a diet aid after a clinical pharmacologist found that — by increasing the metabolic weight — controlled doses of DNP could cause an average loss of 1.5 – 2.0 pounds per week.  One laboratory brought out a product called Formula 281, that contained DNP 1.5 grains.  The promotional brochure gushed: “Here, at last, is a reducing remedy that will bring you a figure men admire and women envy, without danger to your health or change in your regular mode of living.” Enthusiasm for these products waned when it became apparent that the gap between the “therapeutic” and toxic doses was extremely narrow, and customers taking even the recommended dose started to go blind from “dinitrophenol cataracts“.

Unfortunately, DNP is being sold again — over the internet — as a weight-loss product.  This fascinating case report from  London describes an adult male who suicidally ingested 14×200 mg DNP tablets purchased from a website.  On arrival at hospital 12 hours after ingestion, he had vomiting and diarrhea, diaphoresis, and dehydration.  His pulse was 150/min, BP 104/64, respiratory rate 28.min, and temperature 38.4°C.  The clinicians instituted  treatment recommended by the U.K. National Poison Information Service guidelines, including fluids, cooling, and sedation. However, the patient’s condition deteriorated and he developed respiratory failure and an asystolic cardiac arrest from which he could not be resuscitated.

The authors make the point that the U.K. NPIS guidelines recommend treating DNP toxicity with dantrolene if the patient’s temperature is greater than 39-40°C.  Although this is based — as far as I can determine — on just a single abstract, the pharmacology makes sense: dantrolene specifically inhibits calcium release from sarcoplasmic reticulum.  The authors argue that the NPIS threshold for administering dantrolene may be set too high, and that giving it earlier in significant DNP toxicity may be beneficial.

Drug Stuffers and Body Packers

Mules

The protocol from EMJ

Review of Blood Purification

From Adv in Chronic Kidney Dis

    |      |      |   Podcast

Cyclical changes in lung volume from standard mechanical ventilation causes lung injury, ideally, patients would be ventilated with full alveoli. The longer the inspiratory time, the better the oxygenation. If inspiratory time becomes greater than expiratory time, then CO2 will build up. In APRV, patients baseline is a high PEEP level. Intermittently, this level is released to a lower peep level to allow expiration. Bilevel Ventilation or BIPAP (not BiPAP™) are synonymous c APRV

Compliance of Tubing

The compliance of regular tubing is greater than the lungs of patients with high APRV settings/ARDS, so tubing will absorb some of the pressure, must change to non-compliant tubing

APRVarticle by Nader (Curr Opin Crit Care 2004;10:549)

Better Habashi article (Crit Care Med 2005;33(3S):S228)

  Address patient sedation

(tachypnea in PSV is often from inadequate sedation) Beware of tachypnea with small tidal volumes

Review article on the benefits of spont breathing in APRV (Crit Care 2005;10(1):102)

and another (Curr Opin Crit Care 2006;12:13)

Using APRV vent for HFV

achieves RR of 60 set Ti 0.6 seconds set Te 0.4 seconds set Pressure High 40-50 (adjust per MAP goal, watch for BP drop on initiation—if such occurs reduce and/or add preload if such a “gauntlet” does the trick) Rise Time 100% set Pressure Low 0

CONCLUSIONS: PEEPi varied significantly among ventilators. Inspiratory and expiratory work ofbreathing varied between ventilators when spontaneous breathing occurred during the ventilator’sinspiratory phase. (Anesth Analg 2011;113:529–33)

|      |      |   Podcast

(Adapted from the National Emergency Airway Course  http://www.theairwaysite.com and The Airway Cam Guide to Intubation)

RSI evidence review (Can J Anesth 2007;54(9):748)

AirwayCam Videos

Levitan Pocket Guide

http://vam.anest.ufl.edu/airwaydevice/videolibrary/index.html#airtraq

http://groups.msn.com/DrMAGBOULAIRWAYPAGE/homepage.msnw

www.airway911.com

Hemodynamic Compromise post-intubation

Universal Algorithms

  Universal    Main    Crash    Failed    Difficult

Scanned from Manual of Emergency Airway Management by Walls et al.

Three Emergent Indications for Intubation

Can’t Protect Airway

(Gag reflex is absent in up to 37% of population, so a poor predictor of airway protection (J Accid Emerg Med 16(6):444, 1999)

Lancet. 1995 Feb 25;345(8948):487-8,Clin Otolaryngol. 1993 Aug;18(4):303-7)

• Can they talk?
• Can they swallow and manage secretions?

Can’t Maintain Ventilation/Oxygenation

• SaO2 <90% on High Flow O2 or PaO2<60 on FiO2>40%
• PaCO2 >55 if baseline is normal, or >10 increase from baseline
• Respiratory Rate

Expected decline in Clinical Status

• Deterioration/Impending Compromise
• Transport
• Airway protection during procedures (ie. endoscopy)

Other Reasons include:

• Supply/Demand imbalance of perfusion. Patients with compromised perfusion (elevated lactate) do not need the metabolic load of tachypnea when 50% of the body’s oxygen may be used to perfuse the lungs
• Mechanical Obstruction, or need for Core
• Rewarming,
• Inadequate respiratory compensation for met acidosis CO2 should=(1.5 [HCO3-] + ± 2) (J Trauma 2004;57(5):993-997)

Study that drunks and tox folks can stay non-intubated even with low GCS. Only 73 pts.  (J Emerg Med 2009 Nov;37(4):451-5.)

Assess for Potential Difficult Airway

The difficult airway is something you can predict, the failed airway is something that happens to you.  Perform the difficult airway assessment on any patient who has any chance of needing intubation during their stay in the ED.

Difficult to Bag

Beard

Obesity

No Teeth

Elderly (>55)

Snores

Results: During a 24-month period, 22,660 attempts at MV were recorded. 313 cases (1.4%) of grade 3 MV, 37 cases (0.16%) of grade 4 MV, and 84 cases (0.37%) of grade 3 or 4 MV and difficult intubation were observed. Body mass index of 30 kg/m2 or greater, a beard, Mallampati classification III or IV, age of 57 yr or older, severely limited jaw protrusion, and snoring were identified as independent predictors for grade 3 MV. Snoring and thyromental distance of less than 6 cm were independent predictors for grade 4 MV. Limited or severely limited mandibular protrusion, abnormal neck anatomy, sleep apnea, snoring, and body mass index of 30 kg/m2 or greater were independent predictors of grade 3 or 4 MV and difficult intubation. Conclusions: The authors observed the incidence of grade 3 MV to be 1.4%, similar to studies with the same definition of difficult MV. Presence of a beard is the only easily modifiable independent risk factor for difficult MV. The mandibular protrusion test may be an essential element of the airway examination. (Anesthesiology 105(5), November 2006, pp 885-891)

Difficult to Intubate    (Validated Emerg Med J 2005; 22:99-102)

Look at head and neck

Evaluate 3-3-2

Mallampati

(Using Samsoon and Young mod, which added class IV, 1987)

Obstruction=hot potato voice, can’t handle secretions, and Stridor (if audible=90% obstruction)

Neck Mobility

S for saturation reserve (Ann Emerg Med June 2006)

Difficult Extraglottic Device

• Restricted Mouth Opening
• Obstruction: at or below the level of the larynx

• Disrupted or distorted airway. If the seat or seal of the device is disrupted

• Stiff lungs or cervical spine. Poor lung compliance or inability to extend neck may hamper seal

Difficult Cricothyrotomy

Surgery/Disrupted Airway

Hematoma

Obese/Access Problems (Can’t get to neck)

Radiation

Tumor

MA of difficult airway prediction (Anesthesiology 2005; 103:429–37) best values from combo of mallampati and thyromental distance, but still crappy.

Surveys indicate 10-25% of patients with trisomy 21 have AAI. Two thirds of these cases are due to laxity of transverse ligament, whereas one third are due to abnormal odontoid development. Although this association has been depicted on radiographs, the clinical incidence of serious cervical spine injury is not increased in this population compared with other populations. About 25% of patients with rheumatoid arthritis have atlantoaxial instability, which is thought to be due to chronic inflammation. Congenital skeletal dysplasias may cause resultant odontoid hypoplasia. Marfan syndrome may involve to ligamentous laxity, and acute inflammatory processes can affect the retropharyngeal, neck or pharyngeal spaces.

Rheumatoid Arthritis destroys ligaments causing increased movement of dens in spinal canal

A physical examination may reveal the characteristic stigmata of OSAS including a short thick neck, nasal obstruction, tonsillar hypertrophy, narrow oropharynx, retrognathia, and obesity. Although these clinical features are typical, they are not reliable predictors of the presence of severity of the disease.49 Physical examination and laboratory studies may also reveal the presence of unexplained right heart dysfunction or erythrocythemia, suggesting the severity of OSAS. (Laryngoscope 1989)

Obstructive Sleep Apnea Syndrome and Postoperative Complications.

Clinical Use of the STOP-BANG Questionnaire.

Arch Otolaryngol Head Neck Surg. 2010;136(10):1020-1024.

Additional info on prediction of difficult airway

Miscellaneous Statistics

The incidence of failed airways is 10x greater in term pregnant women, they should always be considered a difficult airway.

Intubation must displace the tongue somewhere, that somewhere is the submandibular space, if that space is occupied by infection/tumor or entirely absent=difficult airway

Failed Laryngoscopy (with 3 attempts) :  1 in 200-300 intubations

Can’t intubate/can’t ventilate (CICV):  1 in 10,000-20,000 intubations

PGY 1 or 2: 65% successful on 1st attempt of laryngoscopy PGY 3/4/Attending 85% successful on 1st attempt  of laryngoscopy

We performed as well as anesthesiologists in trauma intubations (Academic Emergency Medicine Volume 11, Number 1 66-70)(Ann Emerg Med. 2004;43:48-53)

Complications in 1000 trauma intubations for absolute and relative indications

J Trauma 2009;66(1):32)

The Seven Ps of Rapid Sequence Intubation

Equipment Preparation

All equipment at the bedside, including backup devices (should be present at every intubation) Have RSI and post-intubation meds already drawn up. An amp of phenylephrine is also a nice thing to have at the bedside in case the intubating agents cause vasodilatory hypotension.

Mnemonic for Equipment during routine intubation (Weingart)

Bag

Airway (oral airway)

Suction (preferably two)

Intubating equipment (tube, blades, etc.)

Capnometer

Lubricating the ET tube cuff may lower rates of aspiration (anesthesiology 2001;95:377)

Straight to cuff with 35 degree bend probably is best (ACADEMIC EMERGENCY MEDICINE2006;13:1255–1258)

Preoxygenation

Eliminate all the N2 in the FRC Some BVMs allow active breathing by the patient of 100% O2 while others will give only ~30%. Need duckbill one way valve and an exhalation port. Do not let the patient take a single room air breath from the beginning of this phase. Kids desaturate much more quickly than adults.  So they are not just little adults, they are little, fat adults 8 vital capacity breaths while wearing a non-rebreather mask is also an alternative.  These masks can be augmented to provide near 100% FiO2 by placing a valve over both vents, providing flow at 15 lpm, and tightly fitting the mask to the face (Resuscitation, April 2003, 57:1, 69 – 72)

When a patient is at <90% saturation, be scared, as this level is right at the nose dive point of the oxygen desaturation curve

Benumof’s seminal study on time to desaturation (pdf) and where he actually go the calculations (Br J Anaesth 1996;76:284)

Abandon the “hold your breath while intubating” method, it just leads to added stress and underestimates the amount of time you have to intubate

Maximum oxygen in lungs is 87% as 6.5% taken up by CO2 and 6.5% by water vapor.  While the fast track (8 vital capacity breaths) method will cause this 87% concentration, it will not fill the tissue and venous compartments.  Therefore the traditional method will in various studies allow up to 3 minutes of extra time (Benumoff Lecture)

The fast track method

NRB only provides 70-80% fiO2 at best

Much longer time to desat in the obese if you preoxygenate in sitting position (British Journal of Anaesthesia 2005 95(5):706-709)

better laryngeal exposure as well (Lee BJ, Kang JM, Kim DO (2007) Laryngeal exposure during laryngoscopyis better in the 25 degrees back-up position than in the supine position. Br J Anaesth 99:581–586)

Patients who can not preoxygenate well with mask should be placed on NIV (Am J Respir Crit Care Med 2006;174:171)

Can then use Vent to continue oxygenation until ready to intubate (JEM 2006;30(1):63)

Place on AC: IFR-30 LPM, FiO2-100%, RR-15, Vt-500 cc, PEEP-based on situation

attach a ETCO2 line to set-up

Two rcts showed better preox when it is preceded with maximal exhalation(Anesth Analg 2003;97:1533) and (Can J Anesth 2000;47:1144) functional recovery time of 8.5 min after 1 mg/kg of Sux (Anesthesiology 1997;87:979)

Airway press <15 cm H20 rarely causes insufflation >25 will often cause it (Br J Anaesth 1987;59:315 and Acta Anaesthesiol Scand 1961;5:107)

Can J Anaesth. 2007 Jun;54(6):448-52. Click here to read Links Efficacy of preoxygenation using tidal volume and deep breathing techniques with and without prior maximal exhalation. Nimmagadda U, Salem MR, Joseph NJ , Miko I. Department of Anesthesiology, Advocate Illinois Masonic Medical Center, 836 W. Wellington Avenue, Chicago, IL 60657, USA. PURPOSE: We evaluated the influence of prior maximal exhalation on preoxygenation in 15 adult volunteers using tidal volume breathing (TVB) for five minutes and deep breathing (DB) for two minutes with and without prior maximal exhalation. METHODS: Inspired and end-tidal oxygen, nitrogen and carbon dioxide were monitored continuously and recorded during room air breathing and at 30-sec intervals during 100% oxygen TVB or DB (rate of 8 breaths.min(-1)). RESULTS: Tidal volume breathing with prior maximal exhalation resulted in an end-tidal oxygen concentration (ETO(2)) slightly higher (P = 0.028) at 0.5 and 1.0 min as compared with TVB without prior maximal exhalation at the same time periods. Regardless of whether TVB was preceded by maximal exhalation or not, 2.5 min was required to reach a mean ETO(2) value of 90% or higher. With DB, there were no differences in ETO(2) values at any time period and 1.5 min was required to reach an ETO(2) of 90% or greater, with or without prior maximal exhalation. CONCLUSIONS: Maximal exhalation prior to TVB slightly steepens the initial rise in ETO(2) during the first minute, but confers no real benefit if maximal preoxygenation is the goal. Maximal exhalation prior to DB has no added value in enhancing preoxygenation.

Study of 3 minutes vs 4 deep breaths vs 8 deep breaths (Anesth 2003;99:841)

comparison of Self-inflating manual resuscitators (SIMRs, i.e. bvms)  for preox  If there is not a one-way exhalation valve, useless for preox(Anesthesiology 2000;93:693)

Preox for claustrophobic Pt (Anesthesiology 104(2))

Nasal Cannula (Fio2 increases 4% per lpm from 24-44%) Benumof’s Airway Management

Mask with reservoir bag (10 lpm = > 80 %) Benumof’s

Finger pulse oximeter lags in poor perfusion states (Can J Anesth 2004;51(5):432)

Can also use a SGA for preox and then take it out to intubate a la Darren Braude

Keep them in semi-fowlers

• Normal values of functional residual capacity in the sitting and supine positions. Intensive Care Med 8:173–177
• Pre-oxygenation in the obese patient: effects of position on tolerance to apnoea. Br J Anaesth 95:706–709
• Laryngeal exposure during laryngoscopy is better in the 25 degrees back-up position than in the supine position. Br J Anaesth 99:581–586

Apneic Oxygenation

a new article on the morbidly obese shows extension of time to desat if left on nasal cannula (J Clin Anesth 2010;22:164)

P

retreatment

Who needs pretreatment?

·        Tight Brain (Elevated ICP/Head Injury/CVA)

·        Tight Vessels (Aortic Dissection/AAA)

·        Tight Heart (ACS)

·        Tight Lungs (Asthma)

        Reflex responses to intubation

The larynx one of the most richly innervated areas in the body, this is a primitive airway protection scheme.

·        Bronchospasm can result from laryngoscopy and from intubation. Stimulation of the carina also causes Bronchospasm.

·         Laryngoscopy and intubation also cause increased ICP, both directly and by the catecholamine surge.  Succinylcholine increases ICP by causing more afferent traffic to brain, increasing metabolic activity.

·        Catecholamine surge from adrenal cortex during laryngoscopy and intubation.  Hypercapnia and hypoxia are causes of huge catecholamine surge.

        Non-Pharmacologic Methods to Blunt Reflex Response

·        Limit time of laryngoscopy

·        Atraumatic laryngoscopy

        Pretreatment Meds (LOAD)

Optimally, give premedications 3-5 minutes before RSI

·        Lidocaine

o       Use in tight brain to attenuate reflex increase in ICP from laryngoscopy/intubation

o       Use in tight lungs to blunt bronchospastic response

o       1.5 mg/kg Rapid IVP

While there is evidence that it blunts ICP rise and cough response, there is no good evidence that this has clinical results (Robinson N. Emerg Med Journal 2001; 18(6):453- 7.) Literature is pretty good on endotracheal suctioning.

·        Opiates

o       Use in tight brain/tight vessels/tight heart to blunt catecholamine surge

o       Fentanyl 3 ug/kg slow IVP

At this stage, Emergency Airway Course only recommends Lidocaine and Fentanyl: LOAD is dead

Intralingual succinylcholine injection provides a rapid onset of muscle relaxation in an emergency.Anaesthesia. 2001 Dec;56(12):1213.

Reglan

in GI bleeds/full stomachs

Esmolol

1-2 mg/kg ~ 3min beforehand

1. Feng CK, Chan KH, Liu KN, et al. A comparison of lidocaine, fentanyl, and esmolol for attenuation of cardiovascular response to laryngoscopy and tracheal intubation. Acta Anaesthesiol Sin. Jun 1996;34(2):61-7. [Medline].
2. Helfman SM, Gold MI, DeLisser EA, et al. Which drug prevents tachycardia and hypertension associated with tracheal intubation: lidocaine, fentanyl, or esmolol?. Anesth Analg. Apr 1991;72(4):482-6.

3 mcg/kg of remifentanyl can also be used

Old pretreatment regimens (atropine, defasiculating paralytics)

P

aralysis after Induction

·

RSI Review (Can J Anesth 2007;54(9):748)

Brutane (forcing non-paralyzed musculature) is the worst choice of medications

Induction/Sedative Agents

·        Etomidate or Versed .3 mg/kg

·        Ketamine or Propofol 1.5 mg/kg

·        Pentothal 3 mg/kg

Etomidate mycoclonus can be attenuated c small dose benzo

Use ½ dose of induction agents if vital signs are unstable or the patient is elderly. Consider using a dose of zero if the sympatholysis may result in decreased BP

In a analysis of NEAR data, thiopental, methohexital, and propofol appeared to facilitate RSI over etomidate and versed.  The postulated reason for this is that these agents allow a deeper plane of sedation making up for inadequate waiting time for paralysis.  (Acad EM 10:6, 2003)

Dose based on ideal body weight; estimate by Broca index: (height in cm-100 for men, -105 for women)

ketamine for head injury review (emerg med australia 2006;18(1):37-44) (also see sedative section)

best evidence from EMJ

editorial on the use of ketamine in intubation ( Chest. 2007 Dec;132(6):2054)

Ketamine may be the best choice for hemodynamically unstable

Ketamine is safe and may be the preferred sepsis agent (Etomidate versus ketamine for rapid sequence intubation in

acutely ill patients: a multicentre randomised controlled trial Lancet 2009)

Pharmacodynamics and kinetics of propofol in the shocked patient. Short message–give less, even if you resuscitate them, give less (Anesthes 2004;101:647) and (Anesth Analg 2006;103:1339-1340)

Sedation without Paralysis

Complications of emergency intubation with and without paralysis. (Am J Emerg Med. 1999 Mar;17(2):141-3)

Do not give sedatives without paralytics, as there is a good 6 minutes of IPIST (Interval of Progressively Increasing Sphincter Tone) between administration and full sedation

Can get MR free good intubating conditions with propofol 2.5 mg/kg, opioids, and 4% lidocaine spray of larynx (Acta Anaes Scand 1996;40(6):752)

Not as successful

Rapid sequence intubation for pediatric emergency airway management. Pediatr Emerg Care 18. (6): 417-423.2002; Airway management by US and Canadian emergency medicine residents: a multicenter analysis of more than 6,000 endotracheal intubation attempts. Ann Emerg Med 46. (4): 328-336.2005; Full TextA comparison of rapid sequence intubation and etomidate only intubation in the prehospital air medical setting. Prehosp Emerg Care 4. (1): 14-18.2000; Abstract The utilization of midazolam as a pharmacologic adjunct to endotracheal intubation by paramedics. Prehosp Emerg Care 4. 14-18.2000; Abstract

More Stuff on this

And even more stuff

Paralytics

Paralytics spare pupils (Shah.  Emergency Neurology, p.5)

and article in neuro lit

Depolarizing

Succinylcholine is the only one used in the US.

Sux dosing 1.5-2 mg/kg, always better to give more than less.

Action in 45 seconds, clinical duration 6-8 minutes

Typically causes a rise of 0.5 mEq/L of potassium

Dose based on actual not ideal body weight, gives better conditions in the fattys (Anesth Analg 2006;102(2):438)

When not to use Succinylcholine:

·        Any strokes with hemiparesis from 3 days to 6 months

·        Burns/trauma >24 hours old

·        NMJ Disease

·        Myopathies/Muscular Dystrophies

Theoretical Concerns

·        Intraocular pressure:  commonly used by anesthesiologists in this situation.  (Anesth Clin North Am 1996 14:125-150 and Anesthesiology 1985; 62: 637-640)

·        Preexisting Hyperkalemia (Renal failure is not a contraindication): In a retrospective study of all patients  with hyperkalemia (38 of 40,000) receiving sux, there were not adverse events (Anesth Analg 2002 Jul;95(1))

·        Known plasma cholinesterase deficiency: (only risk is prolonged duration of action)

Burns:  no real risk as long as less than 7 days from the burn or several months after (after healing, return of normal appetite, and return to normal weight)

Direct Muscle Damage:  no risk until 4-5 days after insult

Guillain-Barre:  do not use during and for months afterward

ICU:  If chronic muscle atrophy, may be better not to use for up to a year afterwards

Myopathies:  Contraindicated forever if inherited

(From correspondence from G. Gronert, MD)

Multiple Sclerosis: Review of Sux & neuromuscular disorders (Anesth 1984;61:173)

Not a great idea in patients with MS induced paresis (Curr Opin Anaes 2002;15:365)

Case Series of Numerous MS Patients who received Sux (Ann Chir Gynaecol. 1984;73(5):299-303)

1 case report in the literature of hyperkalemia in MS (JAMA 1970;213:1867)

Sux remains 90% effective at room temperature for 3 months, longer if not exposed to light (Rosen’s 2001)

Lasts for months at room temp (Emergency Medicine Journal 2007;24:168-169)

Sux can be injected intralingually if unable to obtain IV access (Intralingual/Intraoral in Adult Anaesthesia 56:12, 1213 Dec 2001)

Submental/Intralingual use of Nalaxone–23-gauge, 1.5-inch needle attached to a 3-mL syringe was inserted in the midline, midway between the mandible and the thyroid cartilage. It was directed 1 inch superior, and 2 mL of naloxone solution was injected. The SM area was then massaged for 30 seconds

Intralingual naloxone injection for narcotic-induced respiratory depression. Ann Emerg Med 1987;16:572-573. Mercurio JP: Emergency submental injection. JADA 1967;74:717-719.

Redden RJ, Miller M, Campbell RL: Submental administration of succinylcholine in children. Anesth Prog 1984;12:1087-1091.

If you wait 60 seconds, then induction agent is irrelevant (British Journal of Anaesthesia 2005 95(5):710-714)

A  second doseof suxamethonium in the presence of masseter spasm. This shouldnot have occurred for two reasons:

1. Masseter spasm is an early sign of malignant hyperpyrexia (MH),which has a mortality rate even with dantrolene of around 5%.Suxamethonium is a significant precipitant in susceptible individuals.
2. Repeated doses of suxamethonium change the paralysing effect of the drug from one that wears off within 3–5 minutes(“Phase I block”) to one resembling a non-depolarising neuromuscularblock (“Phase II block”) which lasts significantly longer. Ithas been long established that this type of block may beginat doses of 2 mg/kg.2

IM Sux-need 4mg/kg to get 2-3 minute induction time (Anaesthesia 2007;62:757)

Sux and Hyperkalemia

Anesthesiology 2006; 104:158–69 (massive review down to receptor level)

Ped Emerg Care 2000;16(6):441–can not blunt hyperkalemia with non-depols

Chest 1992;102(4):1259–can not blunt hyperkalemia with non-depols

Seminars in Anesthesiology 1985;4:65–same

Anesth 1975;43:89–article references by Anesth 2006

JAMA 1969;210:490

Anesthesiology. 1973 Jul;39(1):13-22.–The response of denervated skeletal muscle to succinylcholine, using canine muscles both normal and denervated

25. R.E. Tobey, P.M. Jacobsen, C.T. Kahle, R.J. Clubb and M.A. Dean, The serum potassium response to muscle relaxants in neural injury. Anesthesiology 37 (1972), pp. 332–337. View Record in Scopus | Cited By in Scopus (8) 26. A.A. Birch, G.D. Mitchell, G.A. Playford and C.A. Lang, Changes in serum potassium response to succinylcholine following trauma. JAMA 210 (1969), pp. 490–493. View Record in Scopus | Cited By in Scopus (10)

27. G.A. Gronert, Potassium response to succinylcholine. JAMA 211 (1970), p. 300.

Anaesth Intensive Care. 1990 Feb;18(1):92-101.Links Suxamethonium and hyperkalaemia. review including 0.7-1.2 rise in renal pts

Nondepolarizing

• Benzylsoquinolones-curare, atracurium.  These cause histamine release
• Aminosteroids
  • Vecuronium- Priming dose for vecuronium .01 mg/kg followed by .15 mg/kg will make it act quicker or use high dose vecuronium .3 mg/kg (Acta Anaes Scand 1993;37(5):465)
  • Pancuronium-Only if others not available
  • Rocuronium-ignore package dosing and use 1 mg/kg (46 min paralysis at this dose)
  • Gantacurium-new extremely short acting non-depolarizing???
  • cisatracurium 0.15 mg/kg intubating, 0.005 mg/kg pretreatment, Onset 5 minutes, duration 45 min

  d

• It seems ketamine is a better for rapid intubation situation that priming dose when using rocuronium and propofol (Can J Anesth 2010;57:113) They used 0.5 mg/kg

Sugammadex

is being tested; it binds to roc and completely reverses its effects

Phase II Study: Anesthesiology 2007;106:935-43

Ephedrine 70 ug/kg Placebo Esmolol 0.5 mg/kg CO 9.1 8 5.5 Onset of Roc 0.6 mg/kg in sec 52 87 114

(Acta Anaesthesiol Scand. 2003 Oct;47(9):1067-72.)

Aspiration is less likely with NMBA

1 mg/kg of Sux will give excellent intubating conditions 63-80% of time

Time until diaphragmatic movement were the same between 1 mg/kg and 0.5 mg/kg dose (Donati, François – Muscule Relaxation for Rapid Sequence Induction IARS 2006 Review Course Lectures)

Prefasic dose of Rocuronium is 0.03 mg/kg 3-5 min before intubation

You must increase dose of sux to 2mg/kg  if prefasic dose of non-depol is given

Corrugator Supercillii, which moves the eyebrow in response to facial nerve stim has response to NMBAs similar to vocal cords and diaphragm.

Article on intubating without paralysis (Br J Anaesth 2005;94(2):150)

lidocaine sprayed on cords

remifentanyl 2 mcg/kg

ROCURONIUM VERSUS SUCCINYLCHOLINE FOR RAPID SEQUENCE INDUCTION INTUBATION Background Rapid sequence induction (RSI) of anaesthesia is a method of quickly producing optimal conditions for intubation in the emergency situation. Classically, succinylcholine (also known as suxamethonium) is the muscle relaxant used because of its rapid onset and brief duration. Contraindications for its use include severe burns, major crush injuries, neurological disease involving acute wasting of major muscle and family history of malignant hyperthermia. Rocuronium is another rapid onset muscle relaxant with fewer contraindications than succinylcholine but its duration is significantly longer. The aim of this meta-analysis was to assess whether rocuronium is as effective as succinylcholine at producing ideal intubating conditions during RSI. Results Twenty six studies were identified that met the inclusion criteria. Succinylcholine produced a small but statistically significant increase in the number of excellent versus non-excellent intubation conditions (relative risk (RR) 0.87; 95% CI 0.81 to 0.94). There was no significant difference between the two agents when comparing excellent or good intubating conditions with poor conditions or failure to intubate. When propofol was used in place of thiopental, there was no difference in the numbers of excellent conditions produced by either rocuronium or succinlycholine. SOCRATES says Succinylcholine produces excellent intubation conditions more consistently than rocuronium and remains the first choice muscle relaxant for RSI. In cases where it is contraindicated, rocuronium is a valid alternative, especially if combined with propofol. Perry J, Lee J, Wells G. Rocuronium versus succinylcholine for rapid sequence induction intubation. In: The Cochrane Database of Systematic Reviews. 2005 Issue 4 CD 002788

Train of Four

Number of Twitches After Stimulation

Amplitude

Corresponding Level of Neuromuscular Blockade

4

all 4 equal

0% (no blockade)

4

declining

< 75%

3

declining

75-85%

2

declining

85-90%

1

single weak

91-99%

0

none

100%

4:1 50% same 70% occupied 2-3 twitches same 75-85% occupied 1 twitch weak >90% Post tetanic twitching >5 occurs just beofre rgaining 1 twitch of TOF

To Reverse, Need 1 twitch

Neostigmine 0.07 mg/kg, mix in same syringe with equal volume of glycopyrolate

Paralytics actually increase LES tone (Br J Anaesth 1984;56:37)

Sux without pretreatment causes quicker desatuaration than rocuronium or sux with pretreatment (Anaesthesia 2010;65:358)

and here again in obese patients (

Acta Anaesthesiologica Scandinavica

Volume 55, Issue 2, pages 203–208, February 2011

Perceptions of Paralysis

First article from Bronx VA

The experience of paralysis when awake is not so bad, but hypercarbia seems to suck (J Clin Anesth. 1993 Sep-Oct;5(5):369-74.)

2nd article used anesthesiologists as patients

Med Dosing in the Obese Patient

P

rotection and Positioning

Cricoid Pressure (Sellick’s) NOT RECOMMENDED

from 20-30 seconds after drugs until tube confirmation.  Have assistant apply with third finger and thumb.  Place their index finger on the thyroid cartilage, this will allow you to move it during laryngoscopy to retain BURP pressure. The proper amount of cricoid pressure can be learned by pushing on the bridge of your nose with middle finger and thumb until it hurts.

But perhaps, the proper amount is no amount at all. All studies are inconclusive. (Canad J Anesthesia 1997;44:414 in JB) and it often screws up tube placement (Airway·Cam Book)

  Position the patient

·        Leave patient sitting until last moment in CHF/Reactive Airway Disease

·        Do not bag unless sat starts to fall below 90.  If you bag with paralysis and properly performed cricoid pressure, 1-2 cc of air is insufflated per tidal volume ventilation.

·        Also consider bagging patients with increased ICP.

·        Never bag without an oral airway, just as you would not perform a rectal exam without a glove

P

lacement and Confirmation

Wait till defasiculations cease if using Succinylcholine; flick the mandible to see if pt sufficiently blocked and

Intubate

• see below

 Confirm Placement

ETCO2 Detector-yellow is mellow.  If tan, give 6 breaths.  If still tan probably in trachea, but consider direct laryngoscopy to confirm.  Purple with a Pulse, Pull the tube.  If purple without a pulse, confirm with direct laryngoscopy. If using wave-form CO2, then tracheal intubation should produce waveform. Vinegar in an animal model turned permanently turned indicator yellow (Journal of Emergency Medicine Volume 28, Issue 1 , January 2005, Pages 5-11)

The colour ranges for the Portex® device (Smiths Medical ASD, Keene, NH) are blue, green, green-yellow, and yellow, which correspond to levels of 0–1, 1–2, 2–5, and >5% CO2, respectively. Normally, end-tidal CO2 is > 4%.1,2

Primary assessment (Lung sounds) more for tube depth than confirming tracheal placement.

Self-Inflating Bulb-reliable even with uncuffed tubes (Acad Emerg Med April 2003, 10:4)

Can confirm depth by ballotment. Location of the Endotracheal Tube by Pilot Balloon-CuffCounter-Ballottement (Anesth Analg. 1995 Jul;81(1):135-8)

If confirming in a coded patient, first attempt to verify with DL-Displace tube posteriorly to be able to see it going through the cords (Benumoff 2nd ed)

Also can place a boughie down tube, if you hit a stop point, it is in the bronchi and tube is between the cords. But you need to know what you are doing to get to 100% (American Journal of Emergency Medicine (2005)23:754–758

Tube Cuff Pressure

We probably inflate too much (Academic Emergency Medicine Volume 11, Number 5 490-491)

Emergency Physicians Cannot Inflate or Estimate Endotracheal Tube Cuff Pressure Using Standard Techniques (Annals EM 44:4 Oct 2004) and (AJEM 2006;24:139)

15-25 mmHg is optimal

Cuff Pressure Journal Club

1. Knowlson GTG, Bassett HFM. The pressure exerted on the trachea by endotrachealinflatable cuffs. Br J Anaesth 1970;42:834e7.2. Seegobin R, van Hasselt GL. Endotracheal cuff pressure and tracheal mucosal bloodflow: endoscopic study of effects of four large volume cuffs. BMJ 1984;288:965e8. 3. Susuki N, Kooguchi K, Mizobe T, et al. Postoperative hoarseness and sore throatafter tracheal intubation (effect of low intracuff pressure of endotracheal tube andusefulness of cuff pressure indicator). Masui 1999;48:1091e5.4. Pelc P, Prigogine T, Bisschop P, et al. Tracheo-oesophageal fistula: A case report andreview of literature. Acta Otorhinolaryngol Belg 2001;55:273e8.5. Spittle N, McCluskey A. Tracheal stenosis after intubation. BMJ 2000;321:1000e2.6. Friis J, Turner A, Da Fonseca J. Overinflated tracheal tube cuff. Emerg Med J2009;26:182

(From Cliff on resus.me)

A study from China tested the hypothesis that an appropriate tracheal tube cuff (ETTc) pressure even in short procedures would reduce endotracheal intubation–related morbidity. They compared bronchoscopic appearance of tracheal mucosa, and patient symptoms of tracheal injury, in two groups of elective surgical patients anaesthetised and intubated between 120 and 180 minutes: a control group without measuring ETTc pressure, and a study group with ETTc pressure measured and adjusted to a range 15-25 mmHg. The endoscopist was blinded to the study group allocation.

The mean ETTc pressure measured after estimation by palpation of the pilot balloon of the study group was 43 +/- 23.3 mm Hg before adjustment (the highest was 210 mm Hg), and 20+/- 3.1 mm Hg after adjustment (p< 0.001). The incidence of postprocedural sore throat, hoarseness, and blood-streaked expectoration in the control group was significantly higher than in the study group. As the duration of endotracheal intubation increased, the incidence of sore throat and blood-streaked expectoration in the control group increased. The incidence of sore throat in the study group also increased with increasing duration of endotracheal intubation. Fiberoptic bronchoscopy showed that the tracheal mucosa was injured in varying degrees in both groups, but the injury was more severe in the control group than in the study group.

So..time to get a cuff manometer for your ED or helicopter? Perhaps you already have one. What do you think?

Correlations Between Controlled Endotracheal Tube Cuff Pressure and Postprocedural Complications: A Multicenter StudyAnesth Analg. 2010 Nov;111(5):1133-7

Pulse Ox

Distally placed pulse ox has a 60-90 second lag from true saturation

Postintubation Management

• Secure Tube

• Post Intubation Medications

Ativan 4-6 mg

Versed 0.1 mg/kg bolus, then 0.1 mg/kg/hr 2-5 mg/hr  (Drip 50 mg in 250 cc NS, Start at 10-25 cc/hr)

Propofol .5-1 mg/kg then 25-100 mcg/kg/min, start at 10 cc (100 mg)/hr which correlates with 1 mg/kg/hour

• C-XR, NGT, and ABG.
• If possible place pt at 45°

HOB 30°

Big Tubes

Secure ‘em

NGT

HME

ABG

Inline Suction

ETCO2

BVM c peep valve

Cuff Pressure

Avoid post-intubation paralytics

Vecuronium .1 mg/kg then .03 mg/kg  q25-45 min or 1-2 mcg/kg/min

use 2 electrodes over the ulna nerve, give train of four.  shoot for 2 twitches while holding the thumb in abduction

Acute quadriparetic myopathy syndrome (AQMS) can result in longstanding paresis if NMBAs are given in doses which are too high.

Abnormal Vital Signs Postintubation

Bradycardia

Assume hypoxia and therefore tube displacement until proven otherwise

Desaturation

Displaced tube

Obstruction-pass suction catheter through tube

Pneumothorax

Equipment failure-take off vent and bag patient

if all of the above have been evaluated, consider shunt physiology

Hypotension

• Pneumothorax
• Decreased Venous Return from PPV, disconnect from vent for 30-60 seconds and observe for increased BP and decreased pulse.  Consider reducing PEEP and decreasing Vt.  Auto-PEEP in obstructive airway disease.
• Induction Agents-diagnosis of exclusion, give fluid bolus
• Cardiogenic-fluid bolus

Skills of Airway Management

Using a BVM

Always use an oral airway

·        Take mask off of bag

·        Lay over nose and let fall on the face

·        Place thumb and first finger on mask with port against thumb web

·        Attach the bag

·        Use the other fingers to grasp along mandible, pulling face into mask

2 hand method:  place  both thumbs on mask, facing the patient’s feet.   Index fingers on mentum of chin.  Other fingers performing jaw thrust.

Use 2 nasal and oral airway if difficult to ventilate.

• comparison of 4 standard bags with high-flow oxygen • Duck-bill mask with one-way valve gives FiO2 >0.9, other bags ~0.3 • Laerdal Silicone Resuscitator®, Mallinckrodt Capno-Flo® > 0.9 • Sims-Intertech 1st Response®, Vital Signs Code Blue® < 0.4 • Know your bag well: they’re differentNimmagadda U et al. Efficacy of preoxygenation with tidal volume breathing: Comparison of breathing systems. Anesthesiology 2000 Sep 93 693 -698 (Ron Wall’s Lecture)

Esophageal sphincter is 20-25 cm H2O in normal healthy, less in sick or dead

Pressures < 16.5 cm H20 are unlikely to cause gastric insufflation (Br J Anaes 1987;59:315)

Once the LES is opened, much lower pressures will cause continued insufflation (Arch Dis Child 1983;58:373)

Better technique may be to use mask and ventilator (Journal of Emergency Medicine 2006;30(1):63)

Airway pressure  < 15 cmH20 rarely causes insufflation, but > 25 often will (Br J Anaesth 1987;59:315 and Acta Anaes Scand 1961;5:107)

Nasopharyngeal Airways

Short Female Size 6 (pin 1cm from flange)

Average Female/Short Male Size 6

Tall Female/AVerage Male Size 7

Tall Male Size 8

width does not matter, only length so that it is above cricoid but below tongue

(Emerg Med J 2005;22:394-396)

NRB = ~65-80% Ø BVM = > 90% • New Hi-Ox® Mask >80% @ 8L/min

New smart bag limits IFR (Intensive Care Medicine Volume 34, Number 2 / February, 2008)

Article on proper way to open the jaw and hold the mask

Facemask position ofr edentulous patients (see image above) Anesthesiology May 2010 – Volume 112 – Issue 5 – pp 1190-1193

Two hand mask grip is better than one hand (Anesthesiology 2010; 113:873–9)

Paralysis augments the ability to mak ventilate (Anaesthesia 2011;66:163)

Laryngoscopy and Intubation

The tongue is your enemy, the epiglottis is your friend.

A proposed model

for direct laryngoscopy and tracheal intubation (Anaesthesia 2008;63:156)

When passing the tube, first touch the hard palette with the tube’s bevel lying horizontally.  Guide the tube to the soft palette.  Approach the cords from the right so as not to obscure your view.  At the last second, rotate the tube counterclockwise 90° to allow narrowest area to go through the cords.

Macintosh must indirectly lift the epiglottis by use of the hyoepiglottic ligament.  If the macintosh blade is too short for the patient, you may be able to reach the valeculla, but have inadequate traction to lift the epiglottis.

Teach residents by telling them to life the head off of the bed with the blade rather than tilting the head back with the blade

Cognitive Tasks of Intubation

Task Task CompletionPosition Patient Ears to Notch Open Mouth Translation of Mandibles Place Blade 1″ of blade centered in mouth Find Epiglottis Sliver of epiglottis seen Press thyroid backwards Valeculla transforms from potential to actual space Seat blade tip epiglottis lifts Lift laryngoscope head lifts off bed Place Tube See tube anterior to notch

Increased head elevation/neck flexion results in much better view (Annals EM 2003;41(3):322)

Mike Murphy agrees with editorial in same issue (Ann Emerg Med 2003;41(3):338)

Ideal positioning causes the external auditory meatus to be on the same horizontal line as the sternal notch. If this is accomplished using the ramp method in this photo, obesity will not cause difficulty (Obesity Surgery 2004;14:1171)

Another review article showing same in pregnant, obese woman  (Can J Anaesth 1989;36(6):668)

RCT with crossover of extension vs. 7cm head elevation, trend towards better with ramp, sig. better in obese or poor head extenders (Anesth 2001;95:836)

Validation of the ears to sternal notch in anesthesia patients (Journal of Clinical Anesthesia (2012) 24, 104–108)

Laryngeal exposure was superior at 25° than supine (Br J Anaesth 2007;99:581)

Laryngoscopy with straight blade allowed better view, but intubating conditions were better with the curved blade. (Can J Anesth 2003, 50:5 p. 501-506)

For difficult laryngoscopy, can try the left-molar approach.  It may offer an improved laryngeal view.  It can also be used to augment fiberoptic intubation attempts.  (Anes 92:1, Jan 2000) and (Anaes 2002 57:1028-1044)

Consider having assistant grab the tongue with a 4×4 before the insertion of the blade.

BURP and mandibular advancement gave the best visualized view. Either one alone helped over none in inexperienced laryngoscopists (Anesthesiology 2004; 100:598–601)

Comparision of cricoid/burp/bimanual laryng. (Ann EMerg Med 2006;47(6):548): on cadaver models, only bimanual consistently improved view

Cormack-Lehane is scale for view of cords

Plastic Blades result in lower number of successful intubations (Anesthesiology 2006;104(1):60)

 How to actually placed the tube

Crash Airway

Nearly Dead, Newly Dead

Still may consider using Sux if any muscle tone at all

The Predicted Difficult Airway

If BVM and intubation are predicted to be successful, do double set-up RSI with failed airway equipment already set up and cric set open

Sigma configuration for tube (Anesthesiology 2007;106(5):1069)

Quick Look

Give intubating dose of propofol, perform laryngoscopy, give paralytics if a good view is obtained

Blind Nasotracheal Intubation

Consider awake BNTI in a predicted difficult airway

start with 32 french trumpet anesthetize through it to get post pharynx

Use the left nostril or if using the right turn tube 180°

Facilitated by neutral head position and ET tube cuff inflation to 15cc.  This study used trachlite without guidewire (Can J Anesth 50(5):511, May 2003)

depth is 26-28 cm at nares

aim towards contralateral nipple

Levitan’s Excellent Review Article

Retrograde Intubation

(Anesthesiology 2006;104(1):48)

Awake Intubation and Fiberoptic Intubation

Failed Airway

Can’t Intubate/Can’t Ventilate or three failed attempts

Best Attempt Definition:

1. Performed by a reasonably experienced laryngoscopist
2. No significant muscle tone
3. Use of optimal sniff position
4. Use of external laryngeal manipulation
5. One change in length of blade
6. One change in type of blade

Devices and Techniques for the Failed/Difficult Airway

Eschmann/Gum Rubber Bougie/Gum Elastic Bougie

Pass till 20 cm at the teeth, you will feel it sliding over tracheal rings.  Railroad the tube over the Eschmann while the laryngoscope is still in the mouth.

The laryngoscopist obtains the optimal laryngeal view. The bougie is then passed below the epiglottis and through the vocal cords. This should elicit a clicking feel at the distal end of the GEB due to the “hockey stick” angled distal end [5]. If clicking is not felt distinctly, the GEB is advanced further until it “holds up” at the carina or when it comes in contact with a peripheral airway of a smaller diameter [5]. Advancement always must be gentle. The laryngoscope blade is left in place as the ETT is inserted over the GEB and into the trachea. It is important to rotate the ETT 90 degrees counterclockwise before the tip of the ETT passes through the vocal cords. This maneuver prevents the beveled tip of the ETT from catching on the right arytenoid process, aryepiglottic fold, right vocal cord, or epiglottis. Clicking and holding up are cardinal signs of tracheal insertion by the GEB, both of which were noted during the insertion of the GEB in our patient with the open zone II neck injury.

Possible complications from a bougie insertion are pharyngeal perforation, mediastinal emphysema, and pneumothorax. (JEM April 2003)

The obstruction is caused by impingement of the tube on the right vocal cord complex and arytenoids [2]. Cossham [3] described a pre-emptive 90° anti-clockwise rotation of the tube (90CCWR), the Cossham twist

Am J Emerg Med. 2004 Oct;22(6):479-82. Links Use of the endotracheal bougie introducer for difficult intubations. A difficult to intubate patient occurs infrequently in the emergency department. The endotracheal tube introducer or gum elastic bougie is a device used by British anesthesiologists in difficult airways. The device is inexpensive, has few complications and is easy to use. Similar to the Seldinger technique for gaining access to a large central vein, the endotracheal tube introducer is used to assist in cannulating the trachea and acts like the wire in central vein access. PMID: 15520943 [PubMed - indexed for MEDLINE]

Anaesthesia. 1988 Jun;43(6):437-8.Links Successful difficult intubation. Use of the gum elastic bougie. Kidd JF, Dyson A, Latto IP. Department of Anaesthesia, University Hospital of Wales, Heath Park, Cardiff. The reliability of two signs of tracheal placement of a gum elastic bougie was studied. These signs were clicks (produced as the tip of the bougie runs over the tracheal cartilages) and hold up of the bougie as it is advanced (when the tip reaches the small bronchi). Ninety-eight simulated and two genuine Grade 3 difficult intubations were attempted with the aid of a gum elastic bougie. Seventy-eight tracheal and 22 oesophageal placements of the bougie resulted. No clicks or hold up occurred with the bougie in the oesophagus. Clicks were recorded in 89.7% of tracheal placements of the bougie. Hold up at between 24-40 cm occurred in all tracheal placements. We conclude that these signs are reliable and that they should be taught as part of any difficult intubation drill in which the gum elastic bougie is used.

From Seth Manoach “

From an abstract Julio and colleaugues wrote and sent me a few years
ago I learned the tricks of using the larygoscope to lift the
epiglottis enough during ETT placement so the lip of the epiglottis
does not catch the ETT as it is railroaded over the bougie. With this
the more often described corkscrewing of the ETT during introduction
to sneak the beveled edge of the tube under the epiglottis. Both of
course are ways to contend with the main bougie problem,
circumferential bougie:tube size mismatch.  These tricks changed my
relationship to the device and are to me like the up and down and
chandy maneuvers with the fastrach/ilma — shouldn’t really talk about
success rates without them.”

Combitube

Hold right above yellow balloon

Use thumb to press tongue out of way

Place until teeth between two black lines

Inflate blue cuff until lower black line moves above the teeth (relative amount)

Inflate white for 12 cc (absolute amount)

Blue is first for everything (inflation, deflation, ventilation)

Combitube Video

I agree that DL is the best way to place a SGA, also Combitube /Easytube. Just to line out a few points for alleviating elective use/training of Combitube /Easytube:1) Use DL2) Insert Combitube /Easytube “flat” along the tongue parallel to outer surface of patients’ body (not along the hard palate) 3) Inflate upper balloon (blue pilot balloon No. 1) with 25 to 75 ml in 10 ml incremental steps until you get a tight seal as described by Dr. Gaitini several years ago.This “minimal volume inflation technique” minimizes the stress to the pharyngeal mucosa. However, prevention of accidental extubation is also reduced.When using Combitube /Easytube in a manikin, make sure the device is well lubricated. Combitube /Easytube work best in manikins such as SimMan, Bill, VBM manikin, and/or Laerdal.Ambu is not suitable for Combitube /Easytube. Then, insertion and first ventilation are possible within 15 to 30 seconds.Michael FrassInventor of Combitube

Trach Light

·        Cut Tube to 27 cm and reattach connector.  Lube wire and lube stylet

·        Bulb should be flush with distal part of bevel, it should just touch your finger.

·        Hold like a cup of tea (between thumb and index finger, pinky up is your choice)

·        In Peds, only pull back 2-3 cm on wire

·        Must bend 90 or it will not work

·        Touch it to the patient’s chest in midline and then rotate it in while performing a jaw thrust.

·        Patient’s head can be in neutral position

Several tips have been suggested in the literature for improving the success of Trachlight®-guided intubation. These include lifting the tongue with the thumb of the nondominant hand or having an assistant pull the tongue while the intubator continues to provide a jaw thrust, lubricating the wand and the stylet,1 dimming operating room lights, using smaller size endotracheal tubes, inserting the wand side-on, or providing at least a 90° bend to the wand.2 Others have suggested gauging the appropriate “bent length” by measuring the distance from the thyroid prominence to the angle of the mandible.3 Patients with buck teeth may benefit from the addition of another bend to the wand at the level of the buck teeth.4 Following repeated use, the internal rigid stylet sometimes assumes a “snake-like” bend that poses difficulty in retraction of the wand. In such situations, it has been suggested that the stylet be straightened, if possible, before reuse, failing which it needs to be disposed. 5 We have also encountered a similar situation leading to difficulty in withdrawing the wand along with the rigid internal stylet after successfully negotiating the endotracheal tube-Trachlight® assembly into the trachea. We have noticed that the snake-like bend of the stylet poses a problem when it crosses the endotracheal tube connector, which happens to be not only the narrowest, but also the most rigid portion of the endotracheal tube-connector assembly. We have successfully overcome “hold up” at this level by separating the endotracheal tube connector from the endotracheal tube prior to withdrawal of the wand-stylet assembly. The distal 90° bent portion of the wand-stylet assembly is the other point at which difficulty is encountered during withdrawal of the stylet, especially in the pediatric age group due to the small size of the tube and its connector. Our suggestion provides a solution to this problem also. We therefore recommend that the connector be routinely separated from the endotracheal tube to facilitate smooth removal of the stylet and possibly prolong the life of the stylet. We have applied this technique of removal of the endotracheal tube connector to aid in Trachlight®-guided oral intubation using the Ring Adair Elwyn (Mallinckrodt Medical, Athlone, Ireland) tube also. In obese individuals, the midline tissues of the neck may be obscured by folds of fat arising either from a double-chin above, or from the anterior chest wall below, posing difficulty in appreciation of the circumscribed glow in front of the neck. Dimming the operating room lights and placing a support under the shoulder to extend the neck often improves success of Trachlight®-guided intubation in obese patients. We have found that having an assistant retract the fold of fatty tissue down and away from the neck so as to avoid formation of skin folds over the neck helps in shortening the time to obtain the classical well-circumscribed midline glow. Since its introduction in 1959, the lightwand has proven its utility in several clinical situations. Our experience gleaned from the use of the Trachlight® for more than 350 intubations has prompted us to share some of the practical solutions that we have used to overcome problems that we have commonly encountered during its use. (Can J Anesth 2007;54:398-399)

Glidescope

More maneuvers to facilitate tracheal intubation with the GlideScope® David C. Kramer, MD and Irene P. Osborn, MD Mount Sinai Medical Center, New York, USA, E-mail: david.kramer@msnyuhealth.org To the Editor: The GlideScope® (Diagnostic Ultrasound Corporation,Bothell, WA, USA), is a videolaryngoscope, whichincorporates a fibreoptic and digital camera systeminto the blade.1 The blade displays a video output to adedicated monitor. The flange of the blade has a 60°angulation, which facilitates better exposure of the larynxthan traditional Macintosh blades.2,3 Some authorshave reported difficulty intubating the trachea despitethe superior view offered by the GlideScope®.1 In thelargest series of Glidescope use (728 patients), 14 ofthe 26 failed intubations occurred in spite of achievinga Cormack-Lehane grade 1 view.4 In that study,failures resulted not from an inability to view the larynx,but in directing the endotracheal tube throughthe glottic opening. In our experience, the device hasbeen successful in over 500 patients, especially thosewith large tongues, relatively small mouths, and inpatients with limited neck mobility. We have used thedevice for conventional induction, in rapid sequenceintubation, and for awake intubation. Because theGlideScope lifts the tongue rather than displacing itinto the submental space, patients with Mallampaticlass III and IV airways are usually afforded Cormack-Lehane grades 1 or 2 glottic views. We have found the following maneuvers to be helpful when intubating the trachea with the GlideScope

• Using a stylet, bend the endotracheal tube (ETT) into a “hockey stick” shape; this usually facilitates tracheal intubation if one obtains a Cormack-Lehane grade 1 view. If the larynx appears anteriorly, bending the ETT into a steeper curve is helpful. This can be achieved by emulating the bend of the GlideScope® flange and handle.
• Introduce the ETT through the mouth in a horizontal plane, and once the tube has passed the flange of the GlideScope®, rotate the ETT to the vertical position.
• If the ETT advances posteriorly to the arytenoids, the following is helpful: With the ETT held between the fingertips, pull it superiorly, rotate the ETT over the left arytenoid, and gently twist the tube over the epiglottic aperture.
• If the ETT abuts the glottic lip, rotate the ETT clockwise into the glottic aperture, while with-drawing the stylet.5
• A midline approach and positioning to achieve an optimal laryngeal view is also important. The described maneuvers have helped the authors facilitate introduction of the ETT into the mouth, past the GlideScope®, and decrease the risk of trauma to the posterior larynx and tracheal glottis. These approacheshave also been very helpful in teaching proper use of the GlideScope®, and in managing failed tracheal intubations at our institution.

Can J Anaesth. 2007 Nov;54(11):891-6.

The GlideScope-specific rigid stylet and standard malleable stylet are equally effective for GlideScope use.

Letter to editor on glidescope use (Journal of Clinical Anesthesia, Volume 22, Issue 2, Pages 152-154)

Look down, up, down, up (Anesth Anal 2007;104:1611)

Video Laryngoscopy

Anaesthesia. 2010 Sep 30. Comparison of three videolaryngoscopes: Pentax Airway Scope, C-MAC™, Glidescope(®) vs the Macintosh laryngoscope for tracheal intubation*

All work same

LMAs

CLINICAL SKILLS FOR THE PREHOSPITAL USE OF THE LMA Similar to the first laryngoscopy,41 the first LMA insertion attempt should be optimized. Is the Correct LMA Size Selected? The LMA Classic is available in six sizes. The manufacturer recommends two size selection criteria: weight based (for adults patients: size 3, 30 to 50 kg, size 4, 50–70 kg, size 5, 70–100 kg, and recently size 6 for >100 kg) and gender based (size 4 for female and size 5 for male adults). The manual also recommends that clinical judgment should be used in selecting the size. Is the LMA Ready to Use? The device is prepared (deflation and lubrication of the dorsal surface with a water soluble lubricant), stored, and used in an uncontrollable and unpredictable environment. The LMA, water soluble lubricant and a syringe should be packaged together. The disposable LMA-Unique (sizes #3, #4, and #5) (LMA North America, San Diego, Calif.) offers this advantage. Is the Patient Ready to Accept the LMA? Insertion of the LMA during inadequate level of anesthesia is a common mistake. A patient who is not “deep enough” (gagging, coughing …) will fight the LMA insertion and discourage the rescuer from inserting the index finger deep into the mouth resulting in misplacement of the device. A misplaced LMA is more likely to be dislodged or to trigger reflexes (laryngospasm, glottic closure, vomiting, or hiccups).42 In the OR the loss of motor response to the “jaw thrust” is considered more reliable to assess adequate “depth” than the loss of verbal contact with the patient.43 Unwanted effects of the jaw thrust may include cervical spine mobilization and stimulation of the patient. Optimal Insertion of the LMA The rescuer will insert the LMA in variable positions: standing (emergency room), kneeling (scene, ambulance), sitting (helicopter), and from the patient’s side (difficult extrication). Experienced anesthesiologists need at least 2 cm distance between the upper and the lower incisors to insert the LMA.44 The kneeling position is suboptimal for the ETT placement but advantageous for the LMA insertion. The standard index finger technique is used when standing or kneeling at the patient’s head. This technique is superior to any other insertion techniques.45 The thumb technique is useful when the victim is trapped (motor vehicle crash) or difficult to reach from above the head. The rescuer standing by the side of the patient will use the thumb of the dominant hand that substitutes the index finger to guide the LMA along the palato-pharyngeal path. The insertion success rate of the thumb technique is lower than the index finger technique.46 The most common error made during the early learning phase with the standard technique is the insertion of the LMA straight into the mouth without using the hard palate as a slide and with the index finger not inserted deep enough into the mouth, misplacing the LMA. Other reasons for failure are: choice of wrong LMA size, incomplete cuff deflation, inability to get the mask past the teeth, inability to advance the cuff past the base of the tongue, insufficient air, or overinflation of the LMA cuff.47 An automated voice advisory manikin may correct these predictable mistakes.48 Neutral head position, CP, and MILS can complicate the LMA insertion. Insertion of the LMA should be attempted with the anterior half of the cervical collar removed and MILS applied. Brimacombe recommends that LMA insertion with CP applied should be attempted only if the oxygen saturation (SpO2) is >95%. If insertion fails, CP should be released for the second attempt. If the SpO2 is <95% initial insertion should be with CP released as ventilation/oxygenation is more important than preventing aspiration.13 Optimal Cuff Inflation Inflate the cuff with two-thirds of the maximum volume recommended (marked on the LMA tube), then, add 3 to 5 mL of air, as needed up to the maximum volume recommended. A rigid over inflated cuff will loose its ability to mold on the soft periglottic tissues: over inflation will not compensate for malposition but will further compromise the seal and the use of PPV. The manufacturer recommends the use of a pressure gauge for optimal cuff inflation. All current literature pertinent to supraglottic airway devices (SGD) standardizes cuff inflation pressure to 60 cm H2O. LMA Ventilation Pharyngeal and esophageal leaks are expected with airway pressure over 20 cm H2O. Overzealous ventilation with no airway pressure monitoring can lead to a “misperceived” leak in an otherwise correctly placed LMA. Chest movement with small TV may be difficult to evaluate in a dressed victim, with chest trauma or strapped chest. Auscultation (chest, neck, and epigastrum) with small TV in a noisy environment may be deceiving. The use of the inflatable bulb (esophageal detector device) with the LMA is discouraged.49 In the OR the most specific test to detect LMA misplacement (defined fiberoptically) was the ability to generate airway pressure of 20 cm H2O without a leak whereas, the ability to ventilate manually (movement of the chest, condensation of expired gases, adequacy of expired gas volume and the feel of the bag) had the highest overall accuracy. Is the Patient Ready for Transport? Tape the LMA firmly in the midline to the upper jaw without bending the tube toward the forehead; keep the LMA tube in a neutral position (bended toward the chin) being vigilant not to dislodge the device during transport or manipulation of the resuscitation bag. A bite block will increase the device’s stability.50 Asai et al. considers that although CP applied after correct placement of the LMA significantly decreases the incidence of gastric insufflation, it also decreases the adequacy of ventilation.51 Ventilation should be reassessed after the application of the anterior cervical collar. If monitored, the airway pressure should be kept under 20 cm H2O. Regurgitation in the LMA Tube Brain considers the LMA cuff protective by filling the pharyngeal space otherwise filled with aspirate and should not be removed; also the LMA tube represents a path of minimal resistance, an alternative to the trachea.52 In the event of regurgitation/aspiration disconnect the breathing tube and allow regurgitated material to drain, and then gently ventilate using small tidal volumes (TV) with 100% Fio2. Place the patient with cervical spine precautions in Trendelenburg position. Sedate and/or paralyze the patient that is “too light.” Oxygenation should be maintained during the incident. Suction the LMA tube. There is no predictable continuum between the LMA tube and the glottic opening.53 A suction catheter will most likely not penetrate the trachea (for the same reason rescue medications administered through the LMA will not reach consistently the trachea). If the LMA fails (reduced chest wall movement, deteriorating O2SAT and ETCO2, increased airway pressure) other airway management options should be considered.

LMA Seal Breakdown

25 cm H20

BVM

100

Combitube 45

Incredibly low aspiration rate when LMA used for general (Anaes 2009;64:1289)

opening pressure ~21 with LMAS (21 J.F. Heuer, M. Stiller and J.Rathgeber et al., Evaluation of the new supraglottic airway devices Ambu AuraOnce and Intersurgical I-gel. Positioning, sealing, patientcomfort and airway morbidity, Anaesthesist 58 (2009), pp. 813–820

Inflate LMAs to less than 44 mmHg (60 cm H20)

Sizing

Evaluation of the LMA Supreme™: A Sizing and Troubleshooting Study   *  Allan J. Goldman, M.D., Daniel Langille, C.R.N.A., Peter Freund, M.D., Michael Flacco, M.D.Department of Anesthesiology, University of Washington Medical Center, Seattle, Washington Introduction: The LMA Supreme(TM) (SLMA) is a new disposable supraglottic airway, which combines the features of the LMA Proseal(TM) (gastric access tube) and Fastrach(TM) (fixed curve shaft). All LMA manufacturers’ sizing recommendations are based upon patient weights. Early in our SLMA evaluation, we experienced occasional failures using those weight guidelines. We then observed that the shape and length of the SLMA fixed curve shaft is similar to a Guedel oral airway [fig. 1]. We proposed that using an oral airway-sizing guide might offer a better method for selecting the correct SLMA size. A secondary outcome from our sizing study was identifying which maneuvers improved the SLMA’s fit. Method: We prospectively collected insertion data from 100 patients. After a propofol induction, we waited till there was lack of response to a jaw thrust before inserting the SLMA. The SLMA size was chosen according to traditional oral airway size selection (angle of jaw to corner of the mouth). 80 mm oral airway = #3 Supreme 90 mm oral airway = #4 Supreme 100 mm oral airway = #5 Supreme If the choice was between two sizes, we chose the smaller device. If after inserting and taping the SLMA in place, the fixation tab was pressing on the upper lip, we then changed the SLMA to the next bigger size. A proper fit was determined to be [1]: fixation tab .5-2.5 cm from upper lip, tidal volume > 8ml/kg, oropharyngeal leak pressure > 20 ml/kg, and a positive suprasternal notch test [2]. If the fit was poor, one of the following maneuvers was performed: deeper insertion, an up-down maneuver (slowly withdrawing the inflated mask 5-6cm and reinserting) [3], or exchanging the device for a different size. Results: Size #3 was chosen for women 77% of the time, and size #4 was chosen for men 77% of the time (table 1). In the remainder of patients, the next larger size was chosen. In 5 patients (5%) the device was removed and exchanged for another size (table 1). The SLMA was an effective airway in all patients in this study. The up-down maneuver gave a better fit in 27% of the patients.

~ The rigid connection of the respiratory gas tubing(with respect to the bowl of the mask) is the culprit behindthe inability to get the mask fully around the corner,as evidenced by the success with the LMA Unique.The connection between the respiratory gas tubing andthe bowl of the mask needs to flex (to a variable degree,depending on the patient’s anatomy) for the final phaseof LMA insertion to be complete. Solution? Mac 3 toelevate the base of tongue and flatten the “angle of attack”to mask insertion. Mac 3…. the ultimate tonguedepressor for the most Supreme airway. James DuCanto, MD

Systematic Review of advantages of LMA over ETT and Facemask (Can J Anaesth 1995;42(11):1017)

Troubleshooting Article by Osbourne

ILMA

·        Lubricate the tip of the tube.

·        Hold et tube at black line and insert and withdraw until lube on tube is totally spread, so there is no resistance.

·        Lift and tilt back on handle until minimum air leak when ventilating, this is the position the tube should be passed in.

ILA

Klein Maneuver

Pull back a few cm, jaw thrust, push forward

Chandy Maneuver

The Chandy maneuver (Figure 2) was developed by Dr. Chandy Verghese and significantly improves the effectiveness of the ILMA (25). It incorporates two maneuvers that improve lung ventilation and tracheal intubation using the ILMA. Part one of the Chandy maneuver facilitates positioning of the ILMA in the upper airway so that lung ventilation is maximized through the device. This is done by grasping the ILMA by the handle and moving it back and forth in the sagittal plane while observing the patient’s tidal volume and/or the capnographic waveform (if ventilation is being controlled manually). However, if the patient is breathing spontaneously, an airway whistle (e.g., Patil intubation guide [Anesthesia Associates, San Marcos, CA] or Beck Airway Airflow Monitor [Great Plains Ballistics, Lubbock, TX]) can be attached to the proximal portion of the ILMA to optimize ventilation through it. The whistle will sound with each breath the patient takes. The ILMA is then moved slowly back and forth in the sagittal plane using part one of the Chandy maneuver until maximal whistling is attained. Maximal whistling indicates optimal positioning of the ILMA. The second part of the Chandy maneuver involves aligning the ILMA to facilitate smooth passage of the endotracheal tube (ETT) into the trachea.

A special Euromedical ETT is provided with the ILMA. The ETT has a longitudinal line, which should be oriented to face the patient’s nose superiorly. Proper orientation of the longitudinal line causes the ETT to exit the ILMA at an angle that eases its passage into the trachea. The ETT also has a circumferential line at a distance from the distal tip of the ETT that is equal to the length of the ILMA from the proximal to the distal port. At the point where the circumferential line is advanced to the proximal port of the ILMA, the distal tip of the ETT will be in contact with the epiglottic elevator bar (which covers the distal port of the ILMA). The epiglottic elevator bar raises the epiglottis so that the ETT can enter the glottis unimpeded. Just before the distal tip of the ETT contacts the epiglottic elevator bar, the second part of the Chandy maneuver is performed. This involves lifting the handle of the ILMA at a 45° angle to the patient’s chest. This helps align the trajectory of the ETT into the trachea inferiorly and usually facilitates smooth passage of the ETT into the trachea. If the patient is breathing spontaneously, an airway whistle attached to the proximal end of the ETT will sound with each ventilation. As the tip of the ETT enters the trachea, the volume of the whistle increases. When the cuff of the ETT is inflated, the volume of the whistle will increase even more, heralding the sealing of the ETT within the trachea and securement of the patient’s airway. Tracheal intubation should always be confirmed with an evidence-based method, using a carbon dioxide detector if the patient has a perfusing cardiac rhythm or a self-inflating bulb if the patient does not have a perfusing cardiac rhythm (39). Additionally, auscultation of bilateral breath sounds will confirm that the ETT is lying in a midtracheal position. The ILMA can then be removed over the ETT using the stabilizing rod (Figure 1) or left in place with the mask deflated until the trachea is extubated. (Proc Bayl Univ Med Cent 2005 July; 18(3): 220–227. James M. Rich, CRNA, MA)

The two steps of the Chandy maneuver. (a) After insertion of the LMA-Fastrach, optimal ventilation is established by slightly rotating the device in the sagittal plane, using the metal handle, until the least resistance to bag ventilation is achieved. This helps to align the internal aperture of the device with the glottic opening, (b) Just before blind intubation, the LMA-Fastrach is slightly lifted (but not tilted) away from the posterior pharyngeal wall using the metal handle. This prevents the endotracheal tube (ETT) from colliding with the arytenoids and facilitates the smooth passage of the ETT into the trachea. Reprinted from reference 25 with permission.

The ABC of the LMA

The LMA needs no introduction as a supraglottic device for airway control. It exists in a variety of designs, safe and successful use of which can be enhanced by well practiced use of the following manoeuvres that can easily be remembered as the ABC of the LMA.

A is the Archie Manoeuvre, or the up-down manoeuvre. After LMA insertion, the apex of the mask can occasionally “down fold” the epiglottis, or rarely the tip of the mask folds back on itself, both resulting in airway obstruction. The manoeuvre involves withdrawing the LMA by 5cm followed by reinsertion. This has a high first time success rate of relieving airway obstruction by correcting both of these occurrences.

B is the Bailey Manoeuvre. This technique allows extubation under deep anaesthesia by substituting an oral endotracheal tube for an LMA. The LMA is inserted over the ET tube, and the cuff is inflated. The cuff on the ET tube is then deflated and the tube is removed. The manoeuvre allows the LMA to maintain the airway during emergence with minimal stimulation, avoiding the coughing and bucking that is often undesired after certain surgical procedures.

C is the Chandy manoeuvre. This 2 stage technique is used to increase the first time success rate of tracheal intubation with an ILMA by aligning the internal aperture of the device with the glottic opening. After the ILMA is inserted, the first part of the manoeuvre is to grasp its handle and rotate it in a saggital plane until optimal ventilation is achieved. The second part involves lifting the device to an angle of 45 degrees to the patients’ chest, aligning the distal aperture of the device with the trachea.

For blind placement, 1 study indicates that Fastrach is better than Air-Q (Anaesthesia 2011;66:185)

King LT/Laryngeal Tube Airways

sort of of a simplified combitube (Brit Journal Anaes 2005;95(6):729)

1.  Insert connector to teeth
2. add 10-20 cc of air
3. pull back until good compliance
4. add 30- 40 cc of air
5. secure

AirTraq

Anaesthesia Volume 64, Issue 3, pages 315–319, March 2009

Fiberoptic Stylet

ours is the bonfils

from Levitan course:

turn tube 90 clockwise off stylet pull stylet not straight back 20 minute cidex scope Follow the existing passage, don’t try to make you’re own with fiberoptic devices Perspective Step back

Fiberoptic Scope

Cricothyrotomy (Surgical)

1. Stand at pt’s right (if you are right hand dominant, otherwise reverse all sides)
2. Left  hand holds thyroid cartilage with index finger touching membrane.
3. Make a vertical incision from thyroid cartilage to above jugular notch.
4. Make horizontal stab incision through cricothyroid membrane
5. Drop trach hook into incision with pointy hook facing towards the ceiling
6. Then turn the hook to grasp thyroid cartilage and hand it to an assistant
7. Put in trousseau dilator with blades at caudad/cephalad positions.
8. Dilate the airway.
9. Put tube between blades of the trousseau with the tube lumen facing towards the patient’s left.
10. Rotate the trousseau with the tube so that the lumen faces the patient’s feet.

The trach kit supplied at EHC is good, in case you accidentally cut off the patients head and have to sew it back on.  Otherwise you are probably better off taking out the scalpel, trousseau, and trach hook and repackaging them.

Minimum training for successful cric should include mannequin practice for 5 attempts or until the procedure can be performed in less than 40 seconds or less (Anesthesiology 98(2):349, Feb 2003)

Homemade Cric trainer (Anaesthesia 2004;59:1012)

Article showing wire cric is incredibly slow (Anaesth Anal 2010;110(4):1083) and (Anaesth 2006;61:565)

bougie

-guided cric is faster than standard (ACADEMIC EMERGENCY MEDICINE 2010; 17:666–669)

Cricothyrotomy (Needle)

Can use nasal canula c 02 on 15 lpm as jet insufflator.  Put one prong in catheter and the other as valve

aim flow perpendiculat to cannula to effect venturi effect–bench research (Anaest 2009;64:1353)

wall flow was better than bvm, no sig. difference between a 13G and 16G catheter (AMERICAN JOURNAL OF EMERGENCY MEDICINE Volume 22, Number 4 July 2004)

Or attach 3-0 ET tube adapter to 14 g angiocath for needle cric FOR PEDS ONLY

Or 3ml syringe barrel with 7-0 ET adapter (Am J Emerg Med 2004;22:37)

Or larger syringe barrel with ET tube inserted and cuff inflated

Article using anesthesia circuit with PEEP of 35-40 (Br J Anaesth 2011 Oct;107(4):642-3)

Resuscitation Volume 72, Issue 1 , January 2007, Pages 164-166 Manual specifically states the oxygen source must be high pressure (capable of a driving pressure of 50 psi). A wall oxygen flowmeter provides a maximum flow of 15 L/min at a pressure of up to 400 kPa (58 psi) dependant on the resistance to flow.  that connects directly to the piped oxygen supply at 400 kPa (58 psi) and provides sufficient flow for effective ventilation.Hospital wards have wall-mounted oxygen flowmeters or oxygen cylinders, from which the maximum driving pressure is 400 kPa (58 psi). Failure to connect the equipment described in Figure 1 to an appropriate oxygen source may waste valuable time following emergency needle cricothyroidotomy. We propose the following clarification to the information provided in the ALS Student Manual: “When performing emergency needle cricothyroidotomy the cannula should be connected to either the wall oxygen flowmeter directly to a jet ventilator or to an oxygen cylinder and not to the common gas outlet of an anaesthetic machine.”

Wall O2 flowmeters have enough pressure, but only if you turn them up way beyond 15 lpm (Anesth Anal 2010;110:94)

Extrapolated to the clinical situation, these data suggest that low-pressure devices will not deliver adequate MVs via a cannula cricothroidotomy and should no longer be advocated.Purpose-made devices should be available in all areas where anaesthesia is administered or airway interventions are performed. (Br J Anaesth 2009; 103: 891–5)

Trach

Possibility of using bedside percutaneous dilatational trachs (PERCUTANEOUS DILATATIONAL TRACHEOSTOMYFOR EMERGENT AIRWAY ACCESS. Ault MJ,Ault B, Ng PK. J Intensive Care Med 2003;18(4):222–226)

Random Tidbits

Push on chest to get air bubble if airway is full of secretions/blood

Ventilating through airway exchange caths can cause barotrauma/pneumo (Can J Anesth/J Can Anesth (2011) 58:560–568)

Sigma shape for ease of tube placement in difficult airway

anesth 2007-106-1069

Research

NEAR Database

Selective Intubation

Rotational technique can be used for L mainstem with 50% success rate. Rotate 90 towards bronchus you want to intubate, then advance. (Acad Emerg Med 2004;11(10):1105.

Trauma Intubation

Systematic Review (Emerg Med J 2006;23:3-11)

Use RSI (B)

In-line Stabilization with anterior portion of collar removed

Tracheal tube introducer for ALL intubations; use routinely, not as rescue (B)

Variety of sizes and shapes of blades should be available

LMA as temporary adjunct for failed airway

Review Article of intubation and its effects on c-spine injuries (Anesthesiology 2006;104(6):1293)

Head Injury Intubation

Now an article in the lit extolling ketamine as the ideal agent for head injury RSI (CJEM 2010;12(2):154)

Airway Carts

Open endotracheal tubes may be safely left on an ED airway cart for 48 hours. (Am J Emerg Med. 2005 Jul;23(4):548-51.) CONCLUSION: It appears that opening, preparing, and storing ETTs in an ED airway cart for up to 48 hours does not increase the risk of bacterial contamination of the ETTs.

Sterility of prepared drug syringes Driver et al (Anesth Analg 1998;86:994‑7) evaluated the sterility of drug syringes used in the obstetric operating room. Most anesthesia departments draw up these drugs fresh every 24 hours in order to be prepared for the emergent situation where general anesthesia has to be rapidly induced. Drugs commonly prepared are atropine, succinylcholine, thiopental, ephedrine and oxytocin. The authors of this study prepared 756 syringes and stored them for eight days. They then sampled 42 syringes of each drug randomly selected on days 1,4 and 8. None of the 756 drug syringes grew any organisms. The results of this study imply that one can retain drug syringes for longer periods of time than has been traditionally done. As the cost of the drugs that are daily prepared is minimal, and the risk of forgetting to change drugs if left for a longer period of time is considerable, I would not consider changing my pattern of practice.

Pediatric Airway

Ventilators

Extubation and Weaning

Rapid Sequence Airway

RSI but with SGA, possibly the best idea for the prehospital environment (from Darren Braude’s RSI/RSA Book)

Airway Intervention Study

A group of interventions for airway and post-intubation management improved severe complications

2 operators

fluid loading pre-tube

prep of post sedation beforehand

preox with bi-pap if needed

RSI

sellick

capnography

norepi if low diastolic bp (<35)

long-term sedation

lung protective vent

Review of Aspiration Pneumonia and Prevention

Anesthesia and Analgesia August 2001 vol. 93 no. 2 494-513

Obstructed Trachea

Push down with et into one of the mainstems and then pull the tube back (Emerg Med Australas. 2011 Dec;23(6):776-8)

References Not Cited in Body

1. Walls RM et al.  Manual of Emergency Airway Management.  Lippincott, 2000.
2. Shah SM et al.  Emergency Neurology.  CambridgeUniversity Press, 1999.
3. The Airway Site.  http://www.theairwaysite.com
4. Ovassapian, A et al.  Fiberoptic endoscopy and the difficult airway, 2nd ed.  Philadelphia : Lippincott-Raven, 1996.
5. Benumof J.  Airway management : principles and practice.  St. Louis ; New York : Mosby, 1996.
6. Brimacombe JR et al. The laryngeal mask airway : a review and practical guide. Philadelphia: W.B. Saunders, 1997.
7. Management of the difficult and failed airway Hung/Murphy

How to Handle Laryngospasm from Anaestricks

• 100% O2
• Laryngospasm notch pressure
• CPAP or positive pressure ventilation
• Lignocaine on the cords
• Induction dose of propofol
• Suxamethonium IV (1 to 2mg/kg) or IM (4mg/kg)

PS – Laryngeal notch pressure: Firm pressure to the notch behind
the earlobe, bounded by the mastoid process, base of skull and condyle
of mandible. Pressure on both sides in a cephalad and medial direction
can terminate laryngospasm. The jaw should move anteriorly. Mechanism
unknown.

Larson C. Anesthesiology. 1998 Nov,(5):1293-4

|      |      |

http://www.acidbase.org/ for analyzer http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php incredible online text   My Acid/Base SheetSodium Bicarb ReviewPharm induced AcidosisGreat Lactate Review

Best Sources

http://www.acidbase.org

http://www.acid-base.com

NEJM 1998;338(1):26

NEJM 1998;338(2):107

Quantitative Approach: (Crit Care 2005;9(2):204) and anaesthesia 2002;57(4):348

Anaesthesia Volume 57 Issue 4 Page 348-356, April 2002 Acid−base physiology: the ‘traditional’ and the ‘modern’ approaches

2.46 x 10-8 x pCO2 (mmHg)/10-pH

albumin (g/L) x (0.123 x pH – 0.631)

phosphate (mg/dL) x (0.309 x pH – 0.469)

bicarb is only an effective buffer at pH

at this pH, give 50% of bicarb deficit

HCO3 deficit=0.6 x wt (kg) x (15-current HCO3)

HCl Infusions

calculate H deficit

H (meq) deficit=0.5 x wt (kg) x (measured HCO3 – desired HCO3)

volume of 0.1N HCl (L) = H deficit/100

set desired at halfway between actual and normal

0.1N contains 100 mEq of H+ per liter

must go in central vein

infusion rate should not exceed 0.2 mEq/kg/hour

Interpreting ABGs

Corrected Aa Gradient=10+Age/10

Metabolic Acidosis

PCO2=(1.5xBicarb) + 8 (+-2)

Metabolic Alkalosis

PCO2=(0.7xBicarb) + 21 (+-1.5)

Respiratory Alkalosis

Acute Bicarb=((CO2-40)/10) + 24

Chronic Bicarb=((CO2-40)/3) + 24

Respiratory Acidosis

Acute Bicarb=((40-CO2)/5) + 24

Chronic Bicarb=((40-CO2)/2) + 24

Normal Anion Gap=2 (Albumin) + 0.5 (Phosphate)

Acidemia

impairs cardiac contractility

arterial dilation, venous constriction

hyperventilation

inhibits anaerobic metabolism

hyperkalemia

sympathomimetic release, but attenuates the response to catecholamines (consider in b-agonists in asthmatics)

decreases the uptake of glucose into cells and induces insulin resistance

Metabolic Acidosis

The body will buffer any acid load with proteins, Hb, and creatinine.  If the bicarb drops, it is b/c these buffers have been overwhelmed.

In disease states where tissue hypoxia causes the acidosis, exogenous bicarb administration is actually harmful, but if tissue hypoxia is not present, bicarb can be beneficial.

Bicarb can be harmful in 5 ways:

1. Venous hypercapnea with decreased tissue pH
2. A decline in the pH of CSF
3. Tissue Hypoxia
4. Hypernatremia
5. Hyperosmolality with resultant CNS dysfunction

Hypercapnic Metabolic Acidosis

increased CO2 not due to pulmonary dysfunction, so the PaCO2 will remain normal, but the mixed venous will not be.  ABGs are poorly representative of tissue acid/base status or oxygenation.  Central venous or mixed venous (pulmonary artery) are much more representative.

DKA

in this state the body has 400-500 mmol of available bicarb precursor in the form of lactate and ketoacid anions.  The addition of exogenous bicarb does not help, what helps is reversal of the process of ketosis with insulin allowing the liver to produce bicarb.

Severe acidemia will be associated with bicarb of

In keto or lactic acidosis, treat the underlying disorder because endogenous anions will be converted back to bicarb

In hyperchloremic, patient needs bicarb

Alkalizing salts like sodium lactate, citrate, or acetate depend on oxidation of salts to bicarb

NaBicarb Administration

Give Bicarb to get pH to 7.2, so bicarb must be increased to between 8 and 10

Consider bicarb space to be 50% of body weight as starting point

so give 8-Bicarb * kg * 0.5=mmol of bicarb needed

Bicarb normally comes as a 1N solution (1 mmol per cc)

Remember admin of bicarb increases CO2 so only give if intubated or patient has compensatory reserve to blow off excess

Lactic Acidosis

Best Review of Lactate

Most pathways to excess lactate are from decreased elimination as opposed to solely increased production

1/2 life of lactate is 3 hours

At pH

Type A (Anaerobic) caused by tissue hypoxia

and

Type B (Aerobic)  no evidence of hypoxia

Type B is seen in DKA, certain cancers, and congenital diseases of the liver.

Lactates >9 are associated with a mortality of >75%

Another review (Curr Opin Crit Care 2006;12:315)

D-lactic acidosis is the stereoisomer seen in patients with short gut syndrome.

Uribarri J, Oh MS, Carroll HJ: D-lactic acidosis. A review of clinical presentation, biochemical features, and pathophysiologic mechanisms. Medicine (Baltimore) 1998; 72: 73-82

D-Lactic acidosis Emergency physicians frequently are called upon to evaluate patients with an acute change in mental status. If the patient exhibits a metabolic acidosis, the clinician should consider D-Lactic acidosis as part of the differential diagnosis. Patients with this condition may complain of or appear to be drunk in the absence of ethanol intake. A unique form of lactic acidosis can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or another cause of the short bowel syndrome. In these settings, glucose and starch are metabolized in the colon into D-lactic acid, which is then absorbed into the systemic circulation. Patients typically present with episodic metabolic acidosis (usually occurring after high carbohydrate meals) and characteristic neurologic abnormalities including confusion, cerebellar ataxia, slurred speech, and loss of memory. It is not clear if these symptoms are due to D-lactate itself or to some other toxin produced in the colon and then absorbed in parallel with D-lactate. The diagnosis of D-lactic acidosis should be strongly considered in the patient presenting with an increased serum anion gap, normal serum concentrations of lactate, and one or more of the following: Short bowel or other malabsorption syndrome Acidosis that is preceded by food intake and resolves with its discontinuation Characteristic neurologic symptoms and signs The standard assay for lactate will not detect D-lactate, hence serum concentrations of lactate will appear normal. Confirmation of the diagnosis requires a special enzymatic assay specifically testing for D-lactate. Therapy in this disorder consists of acute sodium bicarbonate administration to correct the acidemia and oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) to decrease the number of D-lactate producing organisms in the gut.

D-Lactic AcidosisEmergency physicians frequently are called upon to evaluate patients with an acute change in mental status.  If the patient exhibits a metabolic acidosis, the clinician should consider D-Lactic acidosis as part of the differential diagnosis.  Patients with this condition may complain of or appear to be drunk in the absence of ethanol intake.A unique form of lactic acidosis can occur in patients with jejunoileal bypass or, less commonly, small bowel resection or another cause of the short bowel syndrome. In these settings, glucose and starch are metabolized in the colon into D-lactic acid, which is then absorbed into the systemic circulation. Patients typically present with episodic metabolic acidosis (usually occurring after high carbohydrate meals) and characteristic neurologic abnormalities including confusion, cerebellar ataxia, slurred speech, and loss of memory. It is not clear if these symptoms are due to D-lactate itself or to some other toxin produced in the colon and then absorbed in parallel with D-lactate. The diagnosis of D-lactic acidosis should be strongly considered in the patient presenting with an increased serum anion gap, normal serum concentrations of lactate, and one or more of the following:

• Short bowel or other malabsorption syndrome
• Acidosis that is preceded by food intake and resolves with its discontinuation
• Characteristic neurologic symptoms and signs

The standard assay for lactate will not detect D-lactate, hence serum concentrations of lactate will appear normal. Confirmation of the diagnosis requires a special enzymatic assay specifically testing for D-lactate.Therapy in this disorder consists of acute sodium bicarbonate administration to correct the acidemia and oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) to decrease the number of D-lactate producing organisms in the gut. References: (1) Stolberg, L, et al. D-Lactic acidosis due to abnormal gut flora  N Engl J Med 1982; 306:1344. (2) Halperin, ML, Kamel, KS. D-lactic acidosis: Turning sugars into acids in the gastrointestinal tract. Kidney Int 1996; 49:1. (3) Uribarri, J, et al. D-lactic acidosis. Medicine 1998; 77:73. (4) Mayne, AJ, et al. Dietary management of D-lactic acidosis in short bowel syndrome. Arch Dis Child 1990; 65:229. (5) Coronado, BE, Opal, SM, Yoburn, DC. Antibiotic-induced D-lactic acidosis.Ann Intern Med 1995; 122:839.

from emedhome

In the River’s study, 1/3 of folks with lactate>4 had bicarb >22 and anion gap≤15

References: (1) Stolberg, L, et al. D-Lactic acidosis due to abnormal gut flora N Engl J Med 1982; 306:1344. (2) Halperin, ML, Kamel, KS. D-lactic acidosis: Turning sugars into acids in the gastrointestinal tract. Kidney Int 1996; 49:1. (3) Uribarri, J, et al. D-lactic acidosis. Medicine 1998; 77:73. (4) Mayne, AJ, et al. Dietary management of D-lactic acidosis in short bowel syndrome. Arch Dis Child 1990; 65:229. (5) Coronado, BE, Opal, SM, Yoburn, DC. Antibiotic-induced D-lactic acidosis. Ann Intern Med 1995; 122:839.

Lactate Metabolism

(Current Anaesthesia & Critical Care (2006) 17, 71–76)

pH = pKa+ log (H A/HA)

7:4 = 3.85 + log lactate /lactic acid

lactate to lactic acid 3548:1 at pH 7.4

Diagram from resus.me

Shoshin Beri Beri

Most severe form; pt will have enormous degree of lactic acidosis with hyperdynamic cardiac function. Should respond immediately to 100 mg thiamine. (Intensive Care Med (2005) 31:1004)

Thiamine deficiency should be considered in every case of severe lactic acidosis without an obvious cause, especially in high-risk populations (malnourished, alcoholics, Far-East workers, etc). (Journal of Emergency Medicine Volume 26, Issue 3 , April 2004, Pages 301-303)

Alakalosis can cause lactate production because it stimulates glycolysis

Liver fx by itself can cause high blood lactate

Lactate ion itself in addition to the acidemia mat contribute to circulatory fx

If you give bicarb at all, give 1-2 mmol per kg by slow infusion

Drugs known to be associated with type B2 lactic acidosis: acetaminophen, alcohols and glycols (ethanol, ethylene glycol, methanol, propylene glycol), almitrine, antiretroviral nucleoside analogs (zidovudine, delavirdine, didanosine, lamivudine, stavudine, zalcitabine), beta-adrenergic agents : epinephrine, ritodrine, terbutaline – but not salbutamol…, biguanides (phenformin, metformin), cocaine, cyanogenic compounds (eg, cyanide, aliphatic nitriles, nitroprusside), diethyl ether, 5-fluorouracil, halothane, iron, isoniazid, nalidixic acid, propofol, sugars and sugar alcohols (fructose, sorbitol, and xylitol), salicylates (eg, Reye syndrome), strychnine, sulfasalazine, and valproic acid. As you see, beta adrenergics can cause it, but salbutamol seems not to be reported yet. (Claudia)

Cori Cycle

Aspirin

Anion Gap

=(Na (? + K)) – (Cl + Bicarb)

Correct for albumin by equation of Figge: AG + (0.25 x (42 – albumin))   g/L; if given in g/dL, the factor is 2.5 (Crit Care Med 1998; 26:1807-1810)

Normal Gap 8-12 mEq/L

Delta Gap=(AG-12)-(24-Bicarb) The increase in the AG should equate with the decrease in bicarb.

The concept is that there is a one to one relationship between the anion gap and decreased bicarb in pure anion gap acidosis.  If there is not then there is either a combined non-anion gap acidosis or a metabolic acidosis depending on whether the delta gap is positive or negative.

Anion Gap (AG)=2 x ALB + 0.5 (Phos)

one article showed no increased discriminatory ability from correcting the anion gap for hypoalbuminemia (Emerg Med J 2006;23:627)

With bicarbs>8 there should be a 1 mmHg drop in PaCO2 for every 1 meq/dl fall in Bicarb.  PCO2 can drop to ~12.

Sodium Dichloroacetate (DCA):  has the potential to decrease lactate levels and increase pH without the negative effects seen with bicarb.

Carbicarb:  equimolar mixture sodium bicarb and sodium carbonate.  Decrease CO2 instead of increasing it.

THAM

an exogenous buffer

Review (acta anaes scand 2000;44:524)

Guidelines

High Anion Gap (CAT MUDPILES)

Uremia-From H+ retention and from other organic acids

Salicylates-respiratory alkalosis, then met acidosis (uncoupling of oxidative phosporylation)

Methanol-wood alcohol.  Becomes Formaldehyde and Formic Acid (blindness)

Ethylene Glycol-antifreeze.  Urine will fluoresce.  Kidney failure

Paraldehyde-Old medication

Cyanide, Carbon Monoxide

Alcoholic Ketoacidosis

Toluene, theophylline

Methanol, Metformin, MetHb

Uremia (need BUN 50/Cr 5)

Diabetic Ketoacidosis, Starvation Ketoacidosis

Paraldehyde,  phenformin, Propylene Glycol

INH, Ibuprofen (high dose), IRON

Lactic Acidosis D (Blind GI Loops) and L (consider metformin, Type I), Lithium

Ethylene Glycol

Salicylates, strychnine

If gap from lactate, should be 1:1, if not other acids are present.

High-dose lorazepam infusion is associated with high propylene glycol concentration, which may cause adverse effects. Therefore, PG accumulation and toxicity should be monitored for all patients receiving high-dose lorazepam for more than 48 hours. Potential adverse effects associated with high doses of PG include hyperosmolar metabolic acidosis, renal dysfunction, and intramuscular hemolysis in critically ill patients with normal renal function.

Ativan and diazepam will cause propylene glycol toxicity causing anion gap and osmal gap acidosis. Anions are lactic acid. Versed does not need the propylene glycol because it is water soluble at low pH and fat soluble at body pH.

A good portion of anion gap acidosis is probably caused by circulating members of the krebs cycle. These low molecular weight molecules were found in patients with lactic acidosis and DKA (Critical Care 2005;9:R591)

Unknown Cause of High Sig in the Critically Ill

Sig in the critically ill

Normal Anion Gap

Any intestinal loss or RTAs

Renal Tubular Acidosis

physicochemical approach

I-Distal

Impaired distal hydrogen ion secretion. Often accompanied by hypokalemia, low urinary NH4+, and hypocitraturia. Nephrolithiasis often occurs. Transient or persistent (classic adult form is associated with bicarb wasting and nerve deafness.) Mineral metabolism, hyperglobulinemic states, renal disease Myeloma.  Urine pH

II-Proximal

impaired prox bicarb reabsorb. Vit d deficiency. Fanconi syndrome drugs like diamox, hyperparathyroidism, nephrotic syndrome   U pH>5.55 with bicarbonaturia. Bicarb is exhanged for Cl, which actually causes the acidosis

IV-Hyperkalemic

Intact acidification but impaired ammoniagenesis. Aldosterone deficienct. heparin, captopril, prostaglandin inhibitors. Increased K.  Diabetics.

get UA and U lytes.  Calculate urine anion gap.  Urine (Na+K)-Cl.  If negative then most likely a non-renal cause of non-anion gap acidosis.  If positive, consider RTA.

article on quant approach to RTA (crit care 2005;9)

In pure met acidosis c compensation, last two digits of pH should=CO2

If pH

Loss of HCO3 -

Diarrhea

Ureterosigmoidostomy

Cholestyramine

Proximal renal tubular-acidosis

Renal insufficiency

Acetazolamide (Diamox)

Inability to excrete H+

Obstructive uropathy

Pyelonephritis

Hypoaldosteronism

Distal-renal tubular acidosis

Ingestion of ammonium chloride

Hyperalimentation

The administration of sizable amounts of sodium bicarbonate is associated with certain risks. Infusion of the usual undiluted 1N preparation (containing 1000 mmol of sodium bicarbonate per liter) can give rise to hypernatremia and hyperosmolality. This complication can be avoided by adding two 50-ml ampules of sodium bicarbonate (each containing 50 mmol of sodium bicarbonate) to 1 liter of 0.25 N sodium chloride or three ampules to 1 liter of 5 percent dextrose in water, thereby rendering these solutions nearly isotonic. (NEJM 1998, 338(1), 26-34)

Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest 2000;117(1):260-7. Circumstances where it is appropriate to give bicarbonate:

• Hyponatraemic acidosis, without hypochloraemia (if respiratory system ok)
• Hyperchloraemic acidosis, without hypernatraemia (if respiratory system ok)
• And possibly, although evidence against mounting, rhabdomyolysis to alkalinize urine and prevent pigment nephropathy (as Tamm-Horsfall protein only precipitates at acid pH).

Low Anion Gap

Sources of Error: Pseudo-Met Acidosis

Increased AG

excessive exposure of sample to air causing carbonic acid decrease secondary to CO2 release

administration of poorly absorbed anionic abx (carbenicillin)

Decreased AG

halide, bromide, or iodide intox causing a false elevation of Cl

Hypertriglyceridemia causing false elev of Cl

Poorly absorbed cationic abx (polymyxin B)

hypoalbuminemia

Strong Ion Approach

proof that stewart is much better than conventional s albumin correction (Crit Care Med 2007;35:1264)

Articles

Reunification of Acid-base physio (Critical Care 2005;9(5): )

Best Article on utility of Stewarts (Crit Care 2005;9(2):204)

Effects of Fluids

Acid Base in the ICU

1. Is there an acid base problem?
2. Is it primarily respiratory or metabolic?
3. Is the compensation appropriate [using the rules of thumb for expected pCO2 resoponse to a metabolic problem and expected HCO3 change in response to a respiratory problem]?
4. Are there any gaps? [calculate the anion gap and osmolar gap] 5. Do things not add up? [look at delta AG: delta HCO3, calculate the Na/Cl effect, calculate the albumin effect]

Obeserved BE + (sodium/cl effect) – (albumin correction)=true base excess

When albumin is decreased, blood becomes more alkaline b/c it is a weak acid

BE in whole blood, defined as the quantity (mM) of strong acid needed to restore pH to 7.4 in a blood sample equilibrated at PaCO2 = 40 mm Hg using the Van Slyke equation

narrow Na Cl gap acidosis

It doesn’t change the H ion concentration. It causes more of the H ions to get dissociated. In other words the total H ions remain the same, but the free H ion activity increases. This changes the pH Lets imagine a container of pure water. Unlimited number of H ions, but almost no H is dissociated. Unlimited number of OH ions, but almost no OH is dissociated. Neutral pH . Neutral as in chemically neutral, not physiologically neutral. Add some strong ions to this pure water, say NaCl. Being strong ions, these will dissociate. The free Na will cause some OH to dissociate & the free Cl will cause an equal amount of H to dissociate. The amount of H & OH dissociated will be the same & hence the pH will still be “neutral”. Now take a fluid like blood with more Na (135) than Cl (100). More OH (135) is dissociated compared to H (100) & the pH will be alkalotic. Say the pH is 7.4. This is chemically alkalotic, but taken as the physiological neutral value. If this solution now had more Cl, with the same Na, relatively more H will be dissociated & the pH will fall, maybe to 7.3. The fall of the SID resulted in the pH becoming more acidic. This is because there were relatively more free or dissociated H ions are present in the solution after the SID decreased.

It does not use ATP. The equilibrium between lactate and pyruvate depends on the pH. If H+ concentration is high the equilibrium shifts to more lactate, if low, more pyruvate. Pyruvate is reduced to lactate by LDH (changes NADH to NAD) pH is -log[H+]

Br J Anesthesia 2004;92(1):54-60

Am J Respir Crit Care Med 2000;162:2246.

Lactic Acid (HLa) = Lactate- + H+ (99% disassociated at physiologic pH)

Heart and Brain can take up lactate and use for energy

RBCs shuttle lactate and take it to other areas of the body

Plasma carries 70% while RBCs carry 30%

lactic acid metabolism (j applied physio  558(1):29)

About erythrocyte metabolism. Erythrocytes use the Pentose Phosphate shunt (PPS) because it is the only way they can generate NADPH. Erythrocytes need NADPH to maintain a ready supply of reduced gluthathione, which is needed to combat oxidative stress. If the erythrocytes cannot use the PPS, they hemolyze. This is why people with G6PD deficiency (which is part of the PPS) hemolyze. Both Glycolysis and the PPS produce 3-P-glyceraldehide, which can be either converted to 2,3 DPG, or to Pyruvate and lactate. But the erythocyte contains as much 2,3 DPG as it does hemoglobin. So it produces relatively small quantities of lactate, as most of the 3-P-glyceraldehide is converted to 2,3 DPG.

In patients with hepatic fx, lactate in solutions can increase serum lactate levels. Liver can process 100 mmol/hour (Clin Endocrinol Metab 1980;9:513)

Most commercial solutions have racemic lactate mixtures, the D-form is not measured by serum assay

Lactate in Sepsis

(Curr Opin Crit Care 1999;5(6):452)

is not a reliable indicator of anaerobic glycolysis

Dichloroacetate stims pyruvate dehydrogenase which converts pyruvate to acetyl CoA. This decreases lactate in septic patients without increasing oxygenation

another theory is regional anaerobiosis

more likely is that lactate metabolism is decreased in sepsis

Hyperventilation triples lactate in normal individuals: this is because cells do not take up lactate not b/c of increased prod.

lungs may be source of excess lacate in sepsis

production may be aerobic representing cell stress from catecholamines

Hyperchloremic Acidosis

(Anesth Analg 2003;96:919)

Massive NaCl infusion causes met acidosis (J Trauma 2001;51(1):175)

Acid Base Physiology of Crystalloids

(Curr Opin Crit Care 1999;5(6):436)

water is a weak acid (pKa 13.5 at 40 C) as temp goes up, it gets more acidic

free water therefore causes acidosis when given to correct hyponatremia

This is because free water causes Na to fall in greater degree than Cl

Dextrose makes solutions even more acidic, b/c it forms acid after oxidation. That is until it is metabolized

Multicarbon ions such as acetate and gluconate are usually taken up by cells within minutes. The actual metabolism of these ions may further decrease acidosis.

If packaging is in bags instead of glass, CO2 will diffuse in, which alters bicarb concentrations; this is why multicarbons are used

Acid Base of Colloids

(Curr Opin Crit Care 1999;5(6):440)

colloid is a state of matter that is neither solution or suspension; defined by ability to move molecules across membranes

Albumin 20% has a mild acidifying effect (Intensive Care Med (2005) 31:1123–1127)

Acid Base and Renal Failure, CVVH  and Hemodialysis

(Curr Opin Crit Care 1999;5(6):443)

In patients with liver failure, multicarbon anions will not be metabolized and CVVH will cause acidosis. In these folks, bicarb solutions must be used

Lactate is not cleared by hemofilter, so serum levels are still accurate if substitution fluid is not lactate containing

Bicarb solutions can be kept shelf-safe by using two bags, one with 4.75 L of bicarb-free solutions and a 250 cc glass bottle of bicarb solution containing 160 mmol NaBicarb (Hemosol) Double spike delivers bicarb to bag just before use.

Acid Base of HD (Curr Opin Crit Care 1999;5(6):468)

four defense mechanisms to our daily acid load:

ion transport across cell membranes

removal of co2 by lungs

kidney ion elimination

liver metabolism

renal failure causes hyperchloremic acidosis and then high anion gap acidosis

this causes decreased cardiac contractility

and altered response to drugs

SID of HD dialysate is usually 40

Lactate and the Kidney (Critical Care 2002;6(4))

kidney second only to the liver in the ability to remove lactate from the circulation and metabolizing it

very little is actually excreted in the urine confined to cortex; medulla actually creating lactate from glycolysis

Diamox works by excretion of sodium without chloride (Critical Care 2006;10:R14)

Formulas

SBE = 0.9287 × (HCO3- – 24.4 + 14.83 × [pH - 7.4])

Corrected Base Excess=BE-(Na-Cl-38)-(2.5(4.2-Albumin in g/dl))

Each 1 g/dl albumin has a charge of 2.8 mEq/l at pH 7.4 (2.3 mEq/l at 7.0 and 3.0 mEq/l at 7.6), and each 1 mg/dl phosphate has a charge of 0.59 mEq/l at pH 7.4 (0.55 mEq/l at 7.0 and 0.61 mEq/l at 7.6). Thus, in much the same way that the corrected SBE equation (Eqn 5) updates BE to allow for changes in ATOT, the AG may be corrected to yield a corrected AG (AGc)

SIG = ([Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate-]) – (2.46 × 10-8 × PCO2/10-pH + [albumin (g/dl)] × [0.123 × pH - 0.631] + [PO4- (mmol/l) × (pH - 0.469)])

SIDm=Na + K + 2(Mg) +2(Ca) – Cl – lactate – urate

Importantly, all the strong ions are expressed in mEq/l and only the ionized portions of Mg2+ and Ca2+ are considered (to convert total to ionized Mg2+, multiply by 0.7). Note also that we do not consider lactate as unmeasured. Because the concentration of unmeasured anions is expected to be quite low (

Br J Anaesth 2004;92(1):54-60)

Sodium Cl effect (meq/l)=Na – Cl – 38

Albumin Effect (meq/l)=(0.123 x pH – 0.631) x (42-albumin (g/l))

=0.25 x (42-albumin (g/l)

=2.5 x (4.2 – albumin (g/dl)

Corrected Base Excess (meq/l)=BEm – (Na – Cl – 38) – (2.5 x (4.2-albumin)

Am J Respir Crit Care Med 2000;162:2246

Pi-=(Pi) x (0.309 x pH -0.469)

XA-=other strong ions: lactate, ketoacids, sulfate

1.8 (Pi mmol/L)

Mixing Dialysis fluids can use NaAcetate or NaBicarb to balance NaCl

In massive fluid resus such as cardiopulmonary bypass priming, then move closer to 24 for SID to make up for dilution of albumin

Hyproteinemia, SID, and acid base in the crit ill (J appl physio 1998;1740)

serum acid-base may be misaltered b/c of compensation for csf acid-base

so hypoproteinemia may actually result in hyperventilation

Fundamental Principles of Acid-Base (Critical Care 2005;9(2):)

SIG=AG – [albumin (g/dl)] (1.2 × pH-6.15) – [phosphate (mg/dl)] (0.097 × pH-0.13)

Method IV Fencl-Stewart

see above

Disease states classified according to the Stewart approach  Acid–base disturbance   Disease state   Examples   Metabolic alkalosis   Low serum albumin   Nephrotic syndrome, hepatic cirrhosis     High SID+   Chloride loss: vomiting, gastric drainage, diuretics, post-hypercapnea, Cl- wasting diarrhea due to villous adenoma, mineralocorticoid excess, Cushing’s syndrome, Liddle’s syndrome, Bartter’s syndrome, exogenous corticosteroids, licorice Na2+ load (such as acetate, citrate, lactate): Ringer’s solution, TPN, blood transfusion  Metabolic acidosis   Low SID+ and high SIG   Ketoacids, lactic acid, salicylate, formate, methanol     Low SID+ and low SIG   RTA, TPN, saline, anion exchange resins

gelatin from some colloids is a weak acid

free water is an acid, b/c it has a SID of 0

SBE=0.93 x ((Bicarb) + 14.84 x (pH – 7.4) – 24.4)

Equivalent strong ion difference reductions by adding 1 l water or 1 l of 0.15 mol/l NaCl to a 3 l sample of mock extracellular fluid    ‘ECF’   After saline dilution   After water dilution   [Na+]   140   142.5   105  [Cl-]   100   112.5   75  [A-] + [HCO3 -]   40   30   30  SID   40   30   30

If met alkalosis is assoc c decreased serum K, then KCl is a great way to correct as it has a SID of 0 which actually becomes neg as k is taken up

‘Balanced’ crystalloids To avoid crystalloid induced acid–base disturbances, plasma SID must fall just enough during rapid infusion to counteract the progressive ATOTdilutional alkalosis. Balanced crystalloids thus must have a SID lower than plasma SID but higher than zero. Experimentally, this value is 24 mEq/l [23,43]. In other words, saline can be ‘balanced’ by replacing 24 mEq/l of Cl- with OH-, HCO3 – or CO3 2-. From this perspective, and for now ignoring pH, solutions 1 and 3 in Table 4 are ‘balanced’. However, it is noteworthy that, unless stored in glass, solutions 1 and 3 both become solution 2 by gradual equilibration with atmospheric CO2 (Table 4). Solution 2 is also ‘balanced’. To eliminate the issue of atmospheric equilibration, commercial suppliers have substituted various organic anions such as L-lactate, acetate, gluconate and citrate as weak ion surrogates. Solution 4 (Table 4) is a generic example of this approach (for actual examples, see Table 5). L-lactate is a strong anion, and the in vitro SID of solution 4 is zero. However, solution 4 can also be regarded as ‘balanced’, provided L-lactate is metabolized rapidly after infusion. In fact, in the absence of severe liver dysfunction, L-lactate can be metabolized at rates of 100 mmol/hour or more [44,45], which is equivalent to nearly 4 l/hour of solution 4. The in vivo or ‘effective’ SID of solution 4 can be calculated from the L-lactate component subject to metabolic ‘disappearance’. If the plasma [lactate] stays at 2 mmol/l during infusion, then solution 4 has an effective SID of 24 mEq/l. Hence, despite wide variation in pH, solutions 1–4 in Table 4 have identical effective SID values. They are all ‘balanced’, with identical systemic acid–base effects. However, other attributes must be considered. Solution 1 (pH 12.38) is too alkaline for peripheral or rapid central administration. The situation for solution 2 is less clear. Atmospheric equilibration has brought the pH to 9.35, which is less than that of sodium thiopentone (pH 10.4) [46] – a drug that is normally free of venous irritation. Similarly Carbicarb, a low CO2TOT alternative to NaHCO3 preparations [47], has a pH of 9.6 [48]. Thus, the pH of solution 2 may not preclude peripheral or more rapid central administration. On the downside, and like Carbicarb, solution 2 contains significant concentrations of carbonate, which precipitates if traces of Ca2+ or Mg2+ are present. A chelating agent such as sodium edetate may be required.

Four balanced crystalloids (see text)    Solution 1   Solution 2   Solution 3   Solution 4   [Na+]   140   140   140   140  [Cl-]   116   116   116   114  [HCO3 -]     19.2   24    [CO3 2-]     4.8      [OH-]   24        [L-lactate]         26  PCO2 (mmHg)   0   0.3a   760   0.3a  pH   12.38   9.35   6.04   6.49  Effective SID   24   24   24   24

Six colloid solutions    Albumex 4   Haemaccel   Gelofusine   PENTASPAN   HESpan   Hextend   [Albumin]b   40 g/l            [Gelatin urea-linked]b     35 g/l          [Gelatin succinylated]b       40 g/l        [Pentastarch]         100 g/l      [Hetastarch]           60 g/l   60 g/l  [Na+]   140   145   154   154   154   143  [K+]     5.1         3  [Ca2+]     12.5         5  [Mg2+]             0.8  [Cl-]   128   145   120   154   154   124  [L-lactate]             28  [Glucose]             5.5  [Octanoate]   6.4            Effective SID   12   17.6   34   0   0   26a   aAssumes stable plasma lactate concentrations of 2 mmol/L (see text). bWeak acid. Electrolyte concentrations are given in mEq/l. SID, strong ion difference.

Blood At collection, blood is mixed with a preservative, normally CPDA-1 [68], providing approximately 17 mEq trivalent citrate anions per unit, and a small amount of phosphate [69]. The accompanying sodium cation adds about 40 mEq/l to the effective SID of whole blood. For this reason it is not surprising that large volume whole blood transfusion commonly results in a post-transfusion metabolic alkalosis (following citrate metabolism). With packed red cells, the standard red cell preparation in most countries, the preservative load per blood unit is reduced. Nevertheless, large volume replacement with packed red cells still produces metabolic alkalosis [69]. Conversely, if liver dysfunction is severe enough to block or grossly retard citrate metabolism, then the problem becomes ionized hypocalcaemia and metabolic acidosis [70]. sulphates are the strong anions in renal failure

ng suction without proton pump inhibition cause alkalosis from cl loss

lactic acidemia vs. hyperlactatemia

acidosis screws up coagulation

van slyke is accurate in vivo (crit care med 2000;28(8):2932)

Acid Base of RRT

phosphate x (0.309 x (pH-0.469))

1000 x 2.46 x 10-11 x PCO2/( 10-pH )

possible unmeasured anions in uremia are sulfate, urate, hydroxypropionate, oxalate, furanpropionate

if pt’s liver can not metabolize citrate, it will stay in the blood stream and chelate calcium and act as a strong anion causing met acidosis

CVVH may have a sieving constant of >1 causing met alkalosis even with well designed fluids

Acidosis of Cardiac Arrest

not due to hyerlactatemia alone, a good portion is from organic acids such as: phosphate, sulphate, urate, oxo acids. This response is attenuated by hypochloremia, hyperkalemia, hypermagnesemia (Critical Care 2005;9:R357-62)

Technologic advances in the measurement of electrolytes have an influence on how quantitive acid–base parameters are calculated. Currently, there are three techniques commonly used to measure quantitive acid–base variables: flame photometry and potentiometry using direct ion selective electrodes (ISEs) or indirect ISEs. Flame photometry is used infrequently in developed countries. It is the measurement of the wavelength of light rays emitted by excited metallic electrons exposed to the heat energy of a flame. The intensity of the emitted light is proportional to the concentration of atoms in the fluid, such that a quantitative analysis can be made on this basis. Examples are the measurements of sodium, potassium, and calcium. The sample is dispersed into a flame from which the metal ions draw sufficient energy to become excited. On returning to the ground state, energy is emitted as electromagnetic radiation in the visible part of the spectrum, usually as a very narrow wavelength band (e.g. sodium emits orange light, potassium purple, and calcium red). The radiation is filtered to remove unwanted wavelengths and the resultant intensity measured. Thus, the total concentration of the ion is measured. Flame photometry has several limitations, one of the more common being the influence of blood solids (lipids). These lipids have been shown to interfere with the optical sensing (due to increased turbidity) and by causing short sampling errors (underestimating true sample volume) [75]. Flame photometry also measures the concentration of ions, both bound and unbound, whereas newer techniques (ISEs) measure the disassociated form (or ‘active’ form) of the ion. An ISE measures the potential of a specific ion in solution, even in the presence of other ions. This potential is measured against a stable reference electrode of constant potential. By measuring the electric potential generated across a membrane by ‘selected’ ions and comparing it with a reference electrode, a net charge is determined. The strength of this charge is directly proportional to the concentration of the selected ion. The major advantage that ISEs have over flame photometry is that ISEs do not measure the concentration of an ion; rather, they measure its activity. Ionic activity has a specific thermodynamic definition, but for most purposes it can be regarded as the concentration of free ion in solution. Because potentiometry measures the activity of the ion at the electrode surface, the measurement is independent of the volume of the sample, unlike flame photometry. In indirect potentiometry, the concentration of ion is diluted to an activity near unity. Because the concentration will take into account the original volume and dilution factor, any excluded volume (lipids, proteins) introduces an error (usually insignificant). When a specimen contains very large amounts of lipid or protein, the dilutional error in indirect potentiometric methods can become significant. A classic example of this is seen with hyperlipidemia and hyperproteinemia resulting in a pseudo-hyponatremia by indirect potentiometry. However, direct potentiometry will reveal the true sodium concentration (activity). This technology (direct potentiometry) is commonly used in blood gas analyzers and point-of-care electrolyte analyzers. Indirect ISE is commonly used in the large, so-called chemistry analyzers located in the central laboratory. However, there are some centralized analyzers utilizing direct ISE. The methodologies can produce significantly different results [72-74,76]. Recent evidence reinforces how technology used to measure acid–base variables affects results and may affect interpretation of clinical studies. Morimatsu and colleagues [77] have demonstrated a significant difference between a point-of-care analysis and the central laboratory in detecting sodium and chloride values. These differences ultimately affect the quantitative acid–base measurements. The study emphasizes that differences in results may be based on technology rather than pathophysiology. One reason may be related to the improving technology of chloride and sodium specific probes. On a similar note, it also appears that there is variation in the way in which the blood gas analyzers calculate base excess [78]. Unfortunately, many studies evaluating acid–base balance have failed to report details of the technology used to measure these variables. This limitation was discussed by Rocktaeschel and colleagues [24] in 2003. Since then, detailed methods sections that include specific electrode technology have become more common when acid–base disorders are evaluated [23,40,79,80]. (Critical Care 2005;9(5):508)

Lactate and increased SIG assoc with mortality (Gunnerson Crit Care 2006,10:R22)

Unidentified Strong Acids associated with increased mortality in severe malaria (Crit Care Med 2004;32(8):1683)

Urinary SID

Unfortunately, it is not easy to consider the urinary SID. In

fact, although 40–42 mEq/l of plasmatic negative charge may

–], [HCO

2PO

+], [Na+] and [Cl–

+] + [K+] + [Un+] = [Cl–] + [Un–

+ and Un–

+] + [K+] – [Cl–] = [Un–] – [Un+

+] + [K+] – [Cl–

+] and [K+

–] and [Un+

, which is a way to augment elimination of Cl–

+

(Crit Care 2006;10:137)

Acid–base patterns observed in humans   Disorder   HCO3- (mEq/l)   PCO2 (mmHg)   SBE (mEq/l)   Metabolic acidosis     = (1.5 × HCO3-) + 8 = 40 + SBE    Metabolic alkalosis   >26   = (0.7 × HCO3-) + 21 = 40 + (0.6 × SBE)   >+5  Acute respiratory acidosis   = ([PCO2 - 40]/10) + 24   >45   = 0  Chronic respiratory acidosis   = ([PCO2 - 40]/3) + 24   >45   = 0.4 × (PCO2 – 40)  Acute respiratory alkalosis   = 24 – ([40 - PCO2]/5)     = 0  Chronic respiratory alkalosis   = 24 – ([40 - PCO2]/2)     = 0.4 × (PCO2 – 40)   Adapted with permission from Kellum [7]. PCO2, partial carbon dioxide tension; SBE, standard base excess. Am J Surg. 1996 Feb;171(2):221-6.

Serial blood lactate levels can predict the development of multiple organ failure following septic shock.Bakker J, Gris P, Coffernils M, Kahn RJ, Vincent JL. Department of Intensive Care, Erasme University Hospital, Brussels, Belgium. BACKGROUND: Despite successful initial resuscitation, septic shock frequently evolves into multiple system organ failure (MSOF) and death. Since blood lactate levels can reflect the degree of cellular derangements, we examined the relation between serial blood lactate levels and the development of MSOF, or mortality, in patients with septic shock. PATIENTS AND METHODS: In 87 patients with a first episode of septic shock, we measured initial lactate (at onset of septic shock), final lactate (before recovery or death), “lactime” (time during which blood lactate was > 2.0 mmol/L, and the area under the curve (AUC) for abnormal values (above 2.0 mmol/L). These measurements were correlated with survival and organ failure and scored for four systems (ie, respiratory, renal, hepatic, and coagulation), adding to a maximal score of 8. RESULTS: Thirty-three (38%) patients survived. Of the 54 (62%) nonsurvivors, the 13 patients who died during the first 24 hours of septic shock had higher initial blood lactate levels than those who died later (mean +/- standard deviation 9.6 +/- 5.3 mmol/L versus 5.6 +/- 3.7 mmol/L, P

Crit Care Med. 2004 Aug;32(8):1637-42  Early lactate clearance is associated with improved outcome in severe sepsis and septic shock.Nguyen HB, Rivers EP, Knoblich BP, Jacobsen G, Muzzin A, Ressler JA, Tomlanovich MC. Department of Emergency Medicine (HBN), Loma Linda University and Medical Center, 11234 Anderson Street, Loma Linda, CA 92354, USA. hbnguyen@ahs.llumc.edu OBJECTIVE: Serial lactate concentrations can be used to examine disease severity in the intensive care unit. This study examines the clinical utility of the lactate clearance before intensive care unit admission (during the most proximal period of disease presentation) as an indicator of outcome in severe sepsis and septic shock. We hypothesize that a high lactate clearance in 6 hrs is associated with decreased mortality rate. DESIGN: Prospective observational study. SETTING: An urban emergency department and intensive care unit over a 1-yr period. PATIENTS: A convenience cohort of patients with severe sepsis or septic shock. INTERVENTIONS: Therapy was initiated in the emergency department and continued in the intensive care unit, including central venous and arterial catheterization, antibiotics, fluid resuscitation, mechanical ventilation, vasopressors, and inotropes when appropriate. MEASUREMENTS AND MAIN RESULTS: Vital signs, laboratory values, and Acute Physiology and Chronic Health Evaluation (APACHE) II score were obtained at hour 0 (emergency department presentation), hour 6, and over the first 72 hrs of hospitalization. Therapy given in the emergency department and intensive care unit was recorded. Lactate clearance was defined as the percent decrease in lactate from emergency department presentation to hour 6. Logistic regression analysis was performed to determine independent variables associated with mortality. One hundred and eleven patients were enrolled with mean age 64.9 +/- 16.7 yrs, emergency department length of stay 6.3 +/- 3.2 hrs, and overall in-hospital mortality rate 42.3%. Baseline APACHE II score was 20.2 +/- 6.8 and lactate 6.9 +/- 4.6 mmol/L. Survivors compared with nonsurvivors had a lactate clearance of 38.1 +/- 34.6 vs. 12.0 +/- 51.6%, respectively (p =.005). Multivariate logistic regression analysis of statistically significant univariate variables showed lactate clearance to have a significant inverse relationship with mortality (p =.04). There was an approximately 11% decrease likelihood of mortality for each 10% increase in lactate clearance. Patients with a lactate clearance> or =10%, relative to patients with a lactate clearance

Surg Today. 2001;31(10):853-9.  Serial measurement of arterial lactate concentrations as a prognostic indicator in relation to the incidence of disseminated intravascular coagulation in patients with systemic inflammatory response syndrome.Kobayashi S, Gando S, Morimoto Y, Nanzaki S, Kemmotsu O. Department of Anesthesiology and Critical Care Medicine, Hokkaido University School of Medicine, Sapporo, Japan. To demonstrate the prognostic value of measuring blood lactate concentrations and to investigate the mechanisms of lactate production in patients with systemic inflammatory response syndrome (SIRS), we conducted a prospective cohort study. Among 22 patients with SIRS, there were 9 survivors and 13 nonsurvivors. Serial arterial lactate concentrations were measured on the day of admission to the intensive care unit (day 0). then on days 1-4. The subjects of this study consisted of 14 patients with SIRS, 6 with severe sepsis, and 2 with septic shock. On admission, the lactate concentrations did not differ between the two groups, but remained high in the nonsurvivors throughout the study period, while they progressively decreased in the survivors. The incidence of disseminated intravascular coagulation (DIC) was significantly higher in the nonsurvivors than in the survivors. The nonsurvivors had persistently higher DIC scores and lower platelet counts than the survivors. The changes in lactate concentration over time were statistically different between the patients with DIC and those without DIC. The findings of this study clearly demonstrated that serial arterial lactate measurements can predict a poor outcome in patients with SIRS, severe sepsis, or septic shock. DIC might play an important role in the pathogenesis of lactate production in these newly defined critically ill patients.

Respiratory Acidosis

Winter’s Formula:  PCO2=(1.5 x HCO3) + 8 ± 2

Respiratory acidosis

Acute

a. HCO3- increases 1 (range: 0.25 to 1.75) mEq/L for every 10 mm Hg increase in P CO2 .

b. pH drops 0.08 for every 10 mEq/L rise in HCO3- .

Chronic (greater than 5 days of hypercapnia)

a.HCO3- increases 4 mEq/L for every 10 mm Hg increase in P CO2 (±4).

Limit of compensation: bicarbonate will rarely exceed 45 mEq/L.

Metabolic acidosis:

Note: It may take 12 to 24 hours for maximal respiratory response to develop:

a. Pa CO2 =(1.5×HCO3- ) +8±2.

b. Pa CO2 is equivalent to the last 2 digits of the pH (i.e., if P CO2 is 20, the pH should be 7.20).

c. Delta P CO2 =1-[1.3×(DeltaHCO3- )].

d. For a pure anion gap acidosis; the rise in the anion gap should be equal to the fall in the bicarbonate concentration (i.e., the Deltagap should equal 0).

e. For a pure non-anion gap (hyperchloremic) acidosis, the fall in the bicarbonate should be equal to the rise in the chloride concentration (i.e., Delta bicarb= -Delta chloride).

Limit of compensation: Pa CO2 will not fall below 10 to 15 mm Hg.

a. P CO2 =0.9(HCO3- )+9

b. P CO2 increases 0.6 mm Hg for each mEq/L increase in HCO3- .

Limit of compensation: P CO2 rarely exceeds 55 mm Hg.

pH>7.55 associated with mortality of >45%

suppresses respiration with increased O2/Hb binding decreasing tissue available O2

Consider contraction alkalosis from volume depletion

Many times, merely correcting the contraction alkalosis with NaCl can correct KCl levels if the patient is put into K sparing drugs like ACE inhibitors and spironolactone, and offered the basic K daily minimum K recquirements on the diet or on IV hydration.However, as I stated before, below 2.5 serum K levels, sinoventricular conduction ensues and there is AV node and His-Purkinje conduction depression. Risk of heart block – and below 2.0 sinusal arrest.I would take a good look at the patient?s EKG, start NaCl administration, and decide upon her clinical signs of dehydration whether I would give her a 3% solution NaCl or saline infusion

Pyroglutamic Acidemia

High anion gap metabolic acidosis is frequently encountered in critical care practice. Recently, there have been several reports of high anion gap acidosis resulting from excess production of 5-oxoproline, and termed “pyroglutamic acidaemia”.1-5 This acidaemia is most frequently reported with paracetamol therapy,1 but has also been associated with flucloxacillin2 and vigabatrin,3 particularly in the setting of severe sepsis, renal or hepatic dysfunction.4

The reported inciting dose of paracetamol has been variable: 8 g of paracetamol daily for 3 weeks in one study,6 and a cumulative dose of 20.8 g of paracetamol over 2 weeks in another.7 In a series of 11 patients with transient oxoprolinuria, all patients were taking paracetamol, with most receiving therapeutic dosages.8 A serum paracetamol level of > 200 μmol/L was seen in only one of the eight patients in whom paracetamol levels were checked. Our patient received a cumulative dose of 8 g of paracetamol over 4 days, and it is likely that PGA was precipitated by a combination of factors, including sepsis, renal dysfunction, and co-administration of flucloxacillin.

Primary Versus Mixed ConditionsThis is guaranteed to keep coming up on every exam for the rest of your life, so you might as well learn it.

This page provides two ways to consider acid-base disturbances:

Method I.  A rigorous method which involves calculation of the expected compensations. Method II.  A quick and dirty method to tell from a blood gas if a respiratory condition is simple or compensated. Method III.  Look on a nomogram.

Also see the discussion of how to interpret the base deficit on a blood gas.

Method I.  Expected compensations

Condition HCO3- pCO2Metabolic Acidosis Lower LowerRespiratory Acidosis higher if chronic HigherMetabolic Alkyosis Higher higherRespiratory Acidosis lower if chronic LowerAdapted from Peds Nephrol 42:1365-1395

In acid-base disorders, there are expected compensatory mechanisms.  For instance, bicarbonate is lost the primary process is metabolic alkalosis and the normal response is compensatory respiratory acidosis (retention of CO2).  If the change in pCO2 or HCO3- is equivalent to the expected compensatory response, the disorder is “simple”.  However, if the compensation is outside the normal range, it is a mixed disorder; that is, two primary processes are taking place simultaneously.  The expected compensation is for each condition is defined below:

Metabolic

Acidosis

Expected pCO2 = 1.5 x [HCO3-] + 8 ± 2

Alkalosis

Expected pCO2 = 6 mmHg per 10 mEq/L  in HCO3-

Respiratory

Acidosis

  Acute  Expected HCO3- = 1 mEq/L for each 10 mm pCO2Chronic  Expected HCO3- = 3.5mEq/L for each 10 mmHg pCO2

Alkalosis

  Acute  Expected HCO3- = 2 mEq/L for each 10 mm Hg pCO2Chronic  Expected HCO3- = 5 mEq/L for each 10 mmHg pCO2

Some examples:

1.  If the bicarbonate is 10 due to a purely metabolic acidosis, it would be expected that the pCO2 would be about 23.  If, however, it were measured as 30, there must a component of respiratory acidosis complicating the matter.

2.  pH=7.08, pCO2=14, HCO3-=4, Na=140, Cl=104:

• Primary disorder is a metabolic acidosis
• The pH is low indicating the primary disorder is acidosis.
• The pCO2 is low, the expected compensation, trying to “blow off” CO2.
• The compensation does not fully correct the primary problem.
• The predicted pCO2 by the above equation is 1.5*4+8 = 14.
• This is the observed pCO2
• The anion gap is 140 – (104 + 4) = 32, thus elevated.

Therefore, this is a simple increased anion gap metabolic acidosis.

3.  pH 7.08, pCO2=14, HCO3-=4, Na=140, Cl=124:

• AG = 140 – (124 + 4) = 12
• Same situation as above, but chloride has replaced bicarbonate.

4.  pH 7.37, pCO2=18, HCO3-=10, Na=140, Cl=114

• For the pH to be normal, this must be mixed disorder (respiratory compensation can never fully correct a simple metabolic acidosis).
• The anion gap is 16, thus increased.
• Expected pCO2 is 1.5*10+8 = 23 (21 at minimum).
• Thus, there must be an element of respiratory alkalosis too.

Therefore, this is a combination of increased anion gap metabolic acidosis and a respiratory acidosis.

5.  In a patient with severe BPD, cor pulmonale, and who is diuretics, the pH=7.42, pCO2 = 65, HCO3-=41, Na 143, K 3.1, Cl 88:

This chronic condition can be approached from either the viewpoint of a a respiratory acidosis, or a metabolic alkalosis — it doesn’t matter which one you start with, the result is the same: this is a mixed condition.  To prove it:

A)  Start with a metabolic alkalosis, the patient has too much bicarbonate…

• The expected compensation would be retention of CO2, 6 mmHg for each 10 mEq/L HCO3-.
• Given a HCO3- of 41, with normal of 24: 41-24 = 17
• Therefore, pCO2 should be 1.7 * 6 + 40 = 50.2 mmHg
• However, pCO2 is measured at 65
• Thus, there is a respiratory acidosis (due to CO2 retention) which complicates the metabolic alkalosis which has come about secondary to diurectic use.

B)  Start with respiratory acidosis, the patient is a CO2 retainer…

• The expected renal compensation would be a 3.5 mEq/L increase for every 10 mmHg increase in pCO2.
• Thus, 65-40=25
• The HCO3- should be 2.5*3.5+24 = 32.75
• However, it is measured as 41
• Thus, there is a metabolic alkalosis (due to diuretic use) which complicates the respiratory acidosis due to CO2 retention.

Method II.  Estimating by pH and pCO2

This method relies on following observation which is consistently true for uncompensated respiratory conditions: The pH varies by 0.008 units for every 1 mmHg change in pCO2.

In children

• the normal pH ranges from 7.35 to 7.45
• the normal pCO2 ranges from 35 to 45

For a given condition, if the pCO2 makes sense in light of the pH, the condition is of uncompensated respiratory origin.  Metabolic compensation for a primary respiratory condition usually takes between 8 and 48 hours to occur.

This is a useful way to analyze the situation when all you have is a blood gas, and the bicarbonate value is not directly measured as in the above examples.

Examples:

1.  Given the ABG of 7.5/29/94/25 (pH/pCO2/pO2/HCO3-)

• Since it is alkalemia, start at the upper end of normal, 7.45
• Add 0.008 for each mmHg that the pCO2 differs from normal
• The lower limit of normal pCO2 is 35, so
• (35 – 29) = 6 mmHg less than normal pCO2
• 6  * 0.008 = 0.048
• thus, predicted pH is 7.45 + 0.048 = 7.498
• this jibes well with the measured 7.5
• thus, this is an uncompensated respiratory alkalosis

2.  Given the ABG of 7.2/64/75/25

• Since it is acidemia, start at the lower limit of normal, 7.35
• Subtract 0.008 for each mmHg that the pCO2 differs from normal
• The upper limit of normal pCO2 is 45, so
• (64-45) = 19 mmHg more than normal pCO2
• 19 * 0.008 = 0.152
• thus, predicted pH is 7.35 – 0.152 = 7.198
• this agrees well with the measured 7.2
• thus, this is an uncompensated respiratory acidosis

3.  Given the ABG of 7.31/72/52/35

• Start with 7.35 because it is acidemia
• The pCO2 differs from the maximum by (72 – 45) = 27
• Expected pH = 7.35 – (0.008 * 27) = 7.13
• Thus, this is not a simple respiratory acidosis; some compensation is present

4.  Given the ABG of 7.50/59/60/41

• The pH is elevated but the pCO2 is also elevated.  This cannot be a primary respiratory problem, but must be a metabolic alkalosis.  The degree to which each contribute requires additional information, either a serum bicarbonate and the application of method one (above) or interpretation of the base deficit.

Method III.  Acid-Base Nomograms

The following nomogram can be used to classify a condition based on blood gas measurements:

BD = – [(HCO3) - 24.8 + (16.2 × (pH - 7.4))].

Alterations of consciousness with pH. 7.2 drowsy, 6.98 stuporous, 6.9 comatose (pediat diabetes 2006;7:11)

Bicarb use in acidosis

In clinical practice, particularly in critically ill patients, lactic acidosis is essentially always an adverse finding. Elevated lactate in these patients generally results from a combination of increased production (also known as type A lactic acidosis) and impaired clearance (type B lactic acidosis).

Lactate clearance has been well characterized, with metabolism to pyruvate in the liver responsible for over 50% of the clearance [5,6], while the kidney and to a lesser extent skeletal muscle, red blood cells and the heart metabolize the remainder. Due to resorption in the proximal convoluted tubule, urinary excretion of lactate is normally under 2%, rising to at least 10% with markedly elevated lactate levels [7]. While lactate clearance in healthy individuals is well understood, the mechanism behind impaired clearance in critically ill patients remains only partly defined. When confronted with hypoperfusion resulting in outright organ dysfunction such as ‘shock liver’, impaired hepatic clearance is easily attributable to the hepatic manifestation of global organ impairment. However, lactic acidosis can occur in patients who are hemodynamically normal but suffering from systemic inflammatory states such as early sepsis. It appears as though circulating inflammatory mediators change the liver from an organ which extracts lactate to one which actually produces excess lactate [8,9].

Internal homeostasis is fundamental for maintaining life, so significant deviations from normal biochemical concentrations of electrolytes and other molecules generally indicate a physiologically important abnormality in homeostatic function. Hydrogen ion concentration is particularly tightly regulated both intracellularly and extracellularly. Normal hydrogen ion concentration is approximately 40 nmol/l. Interestingly, the life sciences have adopted the practice of expressing hydrogen ion concentration as -log10([H+]) = pH from the physical sciences in which hydrogen ion concentrations vary so dramatically that a logarithmic scale was required. This has the effect of obscuring the extent of deviations from normal. For example, a change in pH from a normal value of 7.4 to 7.2 results in a 60% increase in hydrogen ion concentration from 40 to 63 nmol/l and a further increase to 100 nmol/l at a pH of 7.0.

When we consider other tightly regulated cation concentrations such as Na+ or K+, this H+ ion concentration increase is substantial. Changes in ion concentrations depend upon the flux in to and out of the volume of distribution of the ion and, importantly, the size of the volume of distribution. As a result, Na+ concentrations can change only slowly. For example, infusion of 250 ml of 3% saline over 1 h (a very high Na+ flux) will contribute ~80 mEq compared with a total body pool of typically ~6000 mEq (140 mEq/l × 60% × body weight) so that Na+ concentration changes only slightly. Thus, Na+ concentrations depend on the large size of total body Na+ and water pools, and only very marginally on hourly or daily Na+ or water fluxes through these pools. When Na+ concentration is abnormal, is the problem with Na+ flux or Na+ or water pools? Clearly, it is a problem with the Na+ or water pools.

In contrast the H+ pool of 40 nmol/l in the extracellular space and approximately the same concentration in the intracellular space totals less than 0.01 mEq. Extensive extracellular and intracellular buffer systems increase the effective H+ pool substantially to about 1000 mEq. In comparison, the flux of H+ through this pool of normal health is high (see below) and can easily increase 10-fold during stress and muscle exertion. Thus, production and clearance of H+ become dominant mechanisms of regulation. When H+ concentration is abnormal, is the problem with H+ flux or H+ and buffer pools? In acidoses that are stable over days and weeks, the problem may be with the buffer pool but in lactic acidosis due to shock the problem is clearly with H+ flux.

H+ titrated by bicarbonate administration: in context

The primary source of H+ production is simply metabolism. For example, approximately 200 ml of CO2 is produced per minute by a typical human, which is the same amount of CO2 produced by bicarbonate buffering of 9 mEq H+ per minute or 540 mEq H+ per hour. For higher metabolic rates (which can increase 10-fold or more), the effective rate of acid production increases proportionately. For anaerobic metabolism, this same acid flux no longer is manifest solely as CO2 production but is also converted into lactic acid production, where clinicians consider bicarbonate administration to increase the buffer pool size.

The problem is not in the buffer pool size. The buffer pool size is overwhelmed by the H+ flux in to the pool. The 50 mEq per ampule of bicarbonate is small in comparison to the H+ flux in to the pool. Thus, in the context of the magnitude of the acid flux that is associated with metabolism (hundreds of mEq per hour), it is clear that use of buffers will never keep up and, ultimately, always fails unless aerobic metabolism is restored.

While H+ and HCO3-, as charged ions, do not readily diffuse across cell membranes, CO2 does readily diffuse. In the intracellular compartment, the high CO2 concentration will drive this same equation in reverse and generate intracellular H+ (Fig. 1 [10]). Thus, bicarbonate administration will cause intracellular acidosis unless PCO2 can be controlled by increased ventilation. One ampule of bicarbonate fully reacted will generate over 1 l of CO2. As normal CO2 production is about one fifth of a liter per minute this means that one ampule of bicarbonate should be infused over 5 min or more if alveolar ventilation can be doubled – which is often challenging in a critically ill patient. Increasing alveolar ventilation up to five-fold to allow infusion of bicarbonate over 1 min is generally not possible. The practice of bolus infusion of an ampule of bicarbonate will result in mixing of the bicarbonate with a relatively small volume of blood, which will then have a very high local PCO2. When this volume of blood transits the lungs and heart and perfuses the coronary arteries, the cardiac myocytes will be transiently exposed to this very high local PCO2. This high PCO2 will decrease myocardial contractility [11] and, in anecdotal animal experiments, can cause cardiac arrest.

Table 1 Change in blood chemistry 15 min following 2 mmol/kg bicarbonate infusion [10] From:   Boyd: Curr Opin Crit Care, Volume 14(4).August 2008.379–383

The increase in pH was transient so that much of the bicarbonate effect was gone after 30 min. As all patients were being treated with catecholamines, the observed lack of clinical sensitization following substantial reversal of the acidosis was puzzling, given good evidence that acidosis significantly attenuates the effect of catecholamines [13]. This led the authors to suggest that the 10% decrease in plasma ionized calcium countered any positive inotropic effect conferred from an increase in pH [10]. This hypothesis has yet to be tested clinically.

A summary in 12 short points

1. An acid is a proton donor  — it’s conjugate base  accepts the proffered proton!
2. pH is a convenient logarithmic way of representing large changes in hydrogen ion activity.
3. Exam candidates should probably learn how the glass pH electrode works.
4. The body tightly regulates pH, to maintain normal metabolic functions and trap certain ions inside cells, at least, this is what we believe!
5. In examinations, an FAQ (by examiners) is buffering, especially buffering by haemoglobin (and the role of this protein in CO 2  transport). Know this.
6. The terms acidosis and alkalosis are general terms that refer to states where the pH has changed, and either been compensated for, or not! If the blood pH is outside the normal limits of 7.36–7.44, then only are we justified in using the terms acidaemia or alkalaemia.
7. The lungs, kidney and liver are crucial to maintenance of acid-base homeostasis. For example, metabolic alkalosis doesn’t usually persist unless the kidneys are somewhat whacked!
8. Derangement in lung function/control results in respiratory acidosis/alkalosis; metabolic derangement due to renal dysfunction, gastrointestinal abnormalities, or ingestion, production or failure of removal of acids (or alkali) results in metabolic acidosis/alkalosis. The body usually compensates as best it can.
9. Conventional lore lays great emphasis on the Henderson-Hasselbalch equation, and exam candidates ignore it and its derivation at their peril.
10. The anion gap is the amount of unmeasured negative ions that make up the difference (balances charge) between the measured concentrations of positive and negative ions in plasma. Normally the AG is mainly due to albumin, and about 8–12 mmol/l. The AG is important in the evaluation of metabolic acidosis , but beware of missing a high anion-gap acidosis masked by hypoalbuminaemia!
11. Compensation for acid-base derangement can be simply guesstimated using the Boston formulae: The Boston formulae* State Rule Formula Range metabolic acidosis 1.5+8 PCO 2  (mmHg) = 1.5*bicarbonate + 8 ± 2 metabolic alkalosis 0.7+20 PCO 2  (mmHg) = 0.7*bicarbonate + 20 ± 5 acute respiratory alkalosis 2 for 10 bicarbonate (mmol/l) drops 2 mmol/l     for every 10 mmHg PCO 2  drop ? chronic respiratory alkalosis 5 for 10 likewise, but 5 mmol/l ? acute respiratory acidosis 1 for 10 bicarbonate (mmol/l) increases 1 mmol/l     for every 10 mmHg ? chronic respiratory acidosis 4 for 10 likewise, but 4 mmol/l ? * The values are derived from Brandis
12. The Stewart approach seems a little more complex, but may well be better than the conventional approach, especially for cutting through confusion. With Stewart, a low SID , high albumin concentration and/or high PCO 2  may all contribute to acidosis; the reverse for alkalosis.

NaOH (sodium hydroxide) has the same effects as sodium bicarb, but its alkalinity precludes clinical use (pH 14)Bicarb is just carbonated NaOHwe can metabolize 100 mMol/h of lactate with healthy liversNaOH and THAM are CO2 consuming, bicarb is CO2 generatingGive bicarb slowly to avoid delerterious effectsformate and glycolate cause cerebral edemasevere perturbations of pH alter A- component of AtotSID + H+ – HCO3- – CO3– – A- – OH- = 0HCO3 = SID – A-CO2 is present in bicarb vial to lower the pH, if bicarb is in plastic, it will become NaOH pH (8-9.4)unless bicarb disappears, the SID of NaBicarb is 0 and it is an acidic solutionplasmalyte is very basicliver metabolzies citrate blood products are acidoticpyruvate + NADH + H+ L-Lactate + NAD+ to excrete Cl-, the kidney also excretes NH4+acidosis=liver increases glutamine allowing greater Cl- excretionRenal Fx acidosis=Citrate, Acetate, Fumurate, hyperphosphatemiaIf SID is negative, incrasing CO2 has no effect on pH, if positive, dramatic effectCO2 + H20 = H2CO3 = H+ + HCO3-CO2 + OH- = HCO3-Dissolved CO2 is several hundredfold greater than H2CO3Only because of carbonic anhydrase is CO2 to bicarb near instantaneouspressure of CO2 in blood is independent of SID changespH = 7.6 + log10 {SID/Pc} meq/l/mmHgHCO3 IS INDEPENDENT of PcCO2 has no chargeCO2 + H20CO3– + H+ + H+As CO2 decreases CO3– increases and chelates calciumhence the hyperventilation syndrome5% change in either Pc or SID yields 5% change in H+ or 0.3% change in pHBicarb seemed important to the old folks b/c it was the only way to measure PaCO2CO2 + H20 = CO2 (dissolved) or H2CO3 or HCO3- or CO3++CO2 dissolved and H2CO3 is proportional to the PcHCO3- and CO3– determined by SIDcarbonic acid is present in only inconsequential amountspH = 7.6 + log10 {SID / Pc} mEq/liter/mm HgFor positive [SID] values, [OH-] is always larger than [H+] and be`haves qualitatively in the opposite way to [H+], as Figures 6.1 and 6.3 show. The effect of the added CO2 is to decrease [OH-] for it is no longer the only weak anion present, so that some, in fact most, of the excess strong ion positive charge measured by [SID] can be balanced by [CO3 2-] and [HCO3-]. Another puzzling feature of Equation (6.4.9) is that it says that [HCO3-] is independent of Pc. This is clearly counterintuitive, but Figure 6.2 shows it to be true. A deeper view is provided by Figure 6.3, which shows that [HCO3-] does indeed vary with Pc but only when Pc is very small, well below any physiological value. For all biological purposes, [HCO3-] in ISF is indeed independent of Pc and just equal to [SID]. This conclusion means that if [SID] is constant, but Pc changes, [CO3 2-], [OH-] and [H+] will all change, but [HCO3-] will not. [HCO3-] is therefore not a very useful quantity in the analysis or understanding of interstitial fluids.

Bicarbonate Challenge

(Current Anaes and Crit Care 2009;20:259)

when the pt is acidotic, urinary pH should be < 5.5

complete renal fx with RRT leads to only 100 mmol acid clearance per day. This much can be made per hour in hypoperfusion

1. correct hypoperfusion

2. achieve buffer baseline with bicarb admin to BD <5

3. Observe after 1-2 hours to see if ongoing process. If < 5 rise in 2 hours then not ongoing

weight in kg x 0.2 x BD = NaBicarb dose in mmol

Treating Non-Anion Gap

from Centor’s blog

3. Would you treat, and how?

We did decide to treat acutely to return the bicarbonate to approximately 22.  Since he weighed 70 kg, and is a relatively young man, we estimated that his total body water was around 40 liters.  Remember that the “bicarbonate space” is the total body water.  Given a deficit of 6 mEq per liter, we assumed that we needed to provide approximately 240 mEq of bicarbonate.

As a rule we try to correct halfway over the first day.  We added 2 amps of bicarbonate to a liter of D5/0.5 NS.  The next day his bicarbonate was 19.  We repeated on day 2.  His electrolyte panel after repletion:

Electrolyte panel Na 145 Cl 114 BUN 22 K 2.9 HCO3 23 creat 2.1 Blood Sugar 99

4. Will he need long term treatment?

I believe that we should treat long term. I know of 3 reasons to treat persistent normal gap acidosis in CKD patients:

1. Decrease bone destruction
2. Improve overall nutrition – Some research data show a correlation between chronic acidosis and malnutrition.  This reason may be soft, but the treatment is very benign.
3. Delay dialysis – a recent study suggests that treating metabolic acidosis delays dialysis.  The article and the abstract:

Bicarbonate Supplementation Slows Progression of CKD and Improves Nutritional Status

Bicarbonate supplementation preserves renal function in experimentalchronic kidney disease (CKD), but whether the same benefit occursin humans is unknown. Here, we randomly assigned 134 adult patientswith CKD (creatinine clearance [CrCl] 15 to 30 ml/min per 1.73m2) and serum bicarbonate 16 to 20 mmol/L to either supplementationwith oral sodium bicarbonate or standard care for 2 yr. Theprimary end points were rate of CrCl decline, the proportionof patients with rapid decline of CrCl (>3 ml/min per 1.73m2/yr), and ESRD (CrCl <10 ml/min). Secondary end pointswere dietary protein intake, normalized protein nitrogen appearance,serum albumin, and mid-arm muscle circumference. Compared withthe control group, decline in CrCl was slower with bicarbonatesupplementation (5.93 versus 1.88 ml/min 1.73 m2; P < 0.0001).Patients supplemented with bicarbonate were significantly lesslikely to experience rapid progression (9 versus 45%; relativerisk 0.15; 95% confidence interval 0.06 to 0.40; P < 0.0001). Similarly, fewer patients supplemented with bicarbonate developed ESRD (6.5 versus 33%; relative risk 0.13; 95% confidence interval0.04 to 0.40; P < 0.001). Nutritional parameters improvedsignificantly with bicarbonate supplementation, which was welltolerated. This study demonstrates that bicarbonate supplementationslows the rate of progression of renal failure to ESRD and improvesnutritional status among patients with CKD.

I would treat this patient to maintain a bicarbonate of 22.  I would start either with 5 tablets of sodium bicarbonate each day.  Remember that a 650 mg bicarbonate tablet has 7.7 mEq of bicarbonate.  I usually start with approximately 0.5 mEq per kg.  This assumes a normal diet of 1 mEq per kg of acid that needs buffering and some remaining buffering from phosphate.

If the patient cannot tolerate sodium bicarbonate I use sodium citrate (Shohl’s solution or Bicitra) and would start with 15 cc twice a day.  Each cc converts to 1 mEq of bicarbonate.

Regardless of our starting point, we need to follow the patient closely and titrate our therapy to maintain the bicarbonate around 22.

I would appreciate comments, especially from those nephrologists who frequent this blog.  If any of my discussion remains obtuse, please call me out and I will try to explain better.

________

Study which corrects the SBE for the changes in chloride from PaCO2 buffering in erythrocytes (when CO2 goes up, it changes chrloride (chloride tide) in plasma with RBCs) Journal of Crit Care 2009;24:484)

|      |      |

Lacunar/small vessel strokes-usually eithe risolated sensory or isolated motor

Cortical/large vessel=alterations of cosciousness, thinking, language

Ant=leg, Arm/face=MCA, Homonymous hemianopsia=PCA

Must, must do sensory exam inthese patients, often times they will not complain fo sensory c/o

NNT

from Michael Liao

NINDSNNT 6 (42.7% vs 26.5%)NNH 17 (6.4% vs 0.6%)ECASSIIINNT 14 (52.4% vs 45.2%)NNH 47 (2.4% vs 0.2%)…. 23 (7.9% vs 3.5% with NINDS definitions)NNT is based on mRS <= 1 at 3 moNNH is based on symptomatic ICHI use all the NINDS data as it appears they skewed both part 1 andpart 2 (artificially(?)) to have approx half of the patients in the0-90min time windows. I find NINDS a bit trickier to piece back together than ECASS3.

—

Expansion of TPA window to 4.5 hours by AHA (Stroke 2009;40:)

ECASS III

Table 1 ECASS III Exclusion Criteria

• Age < 18 or > 80 years
• Onset of stroke > 4.5 hours before drug administration or symptom onset unknown
• Stroke symptoms present < 30 minutes or significantly improving before treatment
• Intracranial hemorrhage
• Severe stroke as defined by NIHSS > 25 or imaging (CT or MRI) displaying > 1/3 of middle cerebral artery territory involved
• Seizure at the onset of stroke
• Stroke or serious head trauma within the previous 3-months
• Combination of previous stroke and diabetes mellitus
• Heparin within the preceding 48 hours with PTT above normal limit
• Platelet count < 100,000 mm3
• Systolic blood pressure > 185 mm Hg or diastolic > 110 mm Hg or aggressive treatment (intravenous medication) to reduce blood pressure to these limits
• Glucose < 50 mg/dL or > 400 mg/dL
• Symptoms suggestive of subarachnoid hemorrhage even if CT normal
• Oral anticoagulation therapy
• Major surgery or severe trauma within 3-months
• Other major disorders with an increased risk of bleeding

The Evidence Thrombolysis with Alteplase 3 to 4.5 Hours after Acute Ischemic Stroke, N Engl J Med 2008; 359: 1317-1329.                                                        t-PA       Placebo    NNT    NNHGood Recovery at 90 Days              52.4%     45.2%       14        N/A Symptomatic ICH                            2.4%       0.3%         N/A     47Death                                              7.7%       8.4%         N/A     N/A

 Tenecteplase vs. Alteplase-New inclusion criteria, manufacturer supported, (N Engl J Med 2012;366:1099-107.)

Acute Stroke with NIHSS Score of 0

Physicians rely on the National Institutes of Health Stroke Scale (NIHSS) to evaluate patients with suspected acute stroke and to make decisions about acute treatment. The NIHSS correlates with infarct size, clinical severity, and long-term outcome. It is important to recognize, however, that ischemic stroke may cause symptoms that are not captured by the NIHSS scale.

The NIHSS scale is highly weighted toward deficits caused by anterior circulation strokes, whereas deficits caused by posterior circulation strokes receive fewer points (1-3).  Within the anterior circulation, the scale underestimates the degree of right versus left hemisphere injury (1,4). It is possible that some patients with persistent symptoms on arrival to ED and an NIHSS score of 0 still have an infarct (1).

In a recent study, stroke patients with an NIHSS score of 0 most commonly presented with nausea, vomiting, and headache, all of which are associated with posterior circulation ischemia (1). Midline lesions of the cerebellum cause truncal ataxia, which is not part of the NIHSS.  In addition, decreased visual acuity, Horner’s syndrome, and memory impairments are neurologic deficits not captured by the NIHSS.  Subtle limb weakness (4/5) in an upper motor neuron pattern (extensors of the arms or flexors of the legs) may not be observed on the motor component of the NIHSS.

These data reinforce that the NIHSS cannot replace history and a thorough neurologic exam to diagnose acute stroke and that the NIHSS alone cannot be used to rule out a stroke in patients with acute persistent symptoms.

References:
(1) Martin-Schild S, et al.   Zero on the NIHSS Does Not Equal the Absence of Stroke Ann Emerg Med 2010 Sep 8. [Epub ahead of print]
(2) Libman RB, et al. Differences between anterior and posterior circulation stroke in TOAST Cerebrovasc Dis 2001;11:311–316.
(3) Sato S, et al. Baseline NIH stroke scale score predicting outcome in anterior and posterior circulation strokes Neurology 2008;70:2371–2377.
(4) Fink JN, et al. Is the association of National Institutes of Health Stroke Scale scores and acute magnetic resonance imaging stroke volume equal for patients with right- and left-hemisphere ischemic stroke? Stroke 2002;33:954–958.

(Source Unknown Sorry!!!!!)

2009 AHA Stroke Imaging Recs

Acute Stroke, Neuroimaging, and Thrombolysis

• MRI is at least equal in efficacy to CT for detection of ICH in the hyperacute stroke patient, and both appear to have very high sensitivity and specificity. MRI is superior to CT for demonstration of subacute and chronic hemorrhage and hemorrhagic transformation of an acute ischemic stroke.

• MR-DWI (diffusion weighted imaging MR) is far superior to unenhanced CT and routine MRI in the detection of acute ischemia, with very high sensitivity and specificity. For a patient within 3 hours of symptom onset, MRI can be used if it does not unduly delay the timely administration of IV tPA since a more definitive diagnosis will be obtained with MR-DWI and it is far more effective than CT for excluding some mimics of acute cerebral ischemia.

• For patients beyond 3 hours from onset of symptoms, either MR-DWI or CTA should be performed, especially if mechanical thrombectomy or intra-arterial thrombolytic therapy is contemplated.

• Frank hypointensity on CT, particularly if it involves more than one third of an MCA territory, is a strong contraindication to treatment with thrombolysis. Early signs of infarct on CT, regardless of their extent, are not a contraindication to treatment.

• Gradient-echo MR can detect microhemorrhage, both old and new, better than CT, indicating the presence of amyloid angiopathy, hypertension, small vascular malformations, and other vascular diseases. The presence of a small number of these microhemorrhages (< 5) does not contraindicate intravenous thrombolysis.

Reference: Latchaw RE,et al. Recommendations for imaging of acute ischemic stroke: a scientific statement from the American Heart Association Stroke 2009;40(11):3646-78.

_____

Advanced Stroke Imaging References

• CTP future CVA imaging ann Neurol 2009
• CTP CT in AIS neurorad 2010
• CTP AIS TPA imaging review 2007

Early CT Signs of Ischemic Stroke

from emedhome
The NINDS Study found a 31% sensitivity for early signs of ischemic stroke on noncontrast CT within 3 hours of symptom onset. The rate of detection increased to 82% at 6 hours (1).

Early signs of cerebral ischemia on CT:

• Hypoattenuation of brain tissue – with ischemia, cytotoxic edema develops resulting in increased brain water content. There is a loss of gray-white differentiation because of the increase in the relative water concentration within the ischemic tissues.
• With edema, swelling of the gyri produces sulcal effacement, which may lead to ventricular compression.
• Hyperdense MCA sign - a result of thrombus or embolus in the MCA.
  
• Obscuration of the lentiform nucleus (also called blurred basal ganglia) is seen in MCA infarction and is one of the most frequently seen signs.
• Insular Ribbon sign refers to hypodensity and swelling of the insular cortex (the center of the cerebral cortex deep between the temporal lobe and the frontal lobe).

The sooner these signs become evident, the more profound is the degree of ischemia (1,2). Typically, at 6-12 hours sufficient edema is recruited into the stroke area to produce significant regional hypodensity on CT; a large hypodense area present within 3 hours of reported symptom onset should prompt careful review regarding the time of stroke symptom onset.

There is controversy as to whether early signs of infarct on CT are a contraindication to thrombolysis. The presence of CT evidence of infarction early in presentation has been associated with poor outcome and increased propensity for hemorrhagic transformation after thrombolytics in some studies (3,4).  In the NINDS trial, there was no interaction between early infarction signs and tPA treatment for any clinical outcomes. Currently early signs of ischemia on CT are not generally considered to be a contraindication to use of tPA.  However, “frank hypointensity” on CT, particularly if it involves more than one third of an MCA territory, is a strong contraindication to treatment (1).

References:
(1 ) Latchaw et al.  Recommendations for imaging acute ischemic stroke:  A scientific statement from the American Heart Association  Stroke 2009;40:3646-78.
(2) Patel SC, et al. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Lack of clinical significance of early ischemic changes on computed tomography in acute stroke JAMA. 2001;286: 2830–2838.
(3) von Kummer R, et al. Acute stroke: usefulness of early CT findings before thrombolytic therapy Radiology1997;205(2):327-33.
(4) Dzialowski I, et al. Extent of early ischemic changes on computed tomography (CT) before thrombolysis: prognostic value of the Alberta Stroke Program Early CT Score in ECASS II Stroke 2006;37(4):973-8.

80-85% of strokes

majority are thrombotic vs. embolic (Mitral Stenosis, MI, A-Fib)

Hallmark of stroke is sudden onset of focal neurological derangement in a vascular area

Differential

Hemorrhage Migraine Hyperglycemia Carotid Dissection Todd’s Paralysis Bell’s Encephalitis/Abscess Temporal Arteritis Hypoglycemia Hyponatremia Hypertensive Encephalopathy Air Embolism Multiple Sclerosis Dementia

Common Major Stroke Syndromes

Anterior Circulation

Frontoparietal Lobes

Anterior Aspect of Temporal Lobes

Optic Nerve and Retina

Deep Gray Matter Structures

Posterior Circulation

Medial Aspect of Temporal Lobes

Visual Occipital Cortex

Thalamus

Brainstem

Upper Spinal Cord

Cerebellum

Auditory and Vestibular Aspects of the Ear

Anterior cerebral artery

Paralysis mainly of opposite leg and mild arm involvement

Sensory deficits paralleling paralysis

Altered mentation, confusion, judgment, and impaired insight

Gait apraxia (clumsiness)

Bowel and bladder incontinence

Middle cerebral artery

Paralysis of opposite side of body; arm and face worse than leg

Sensory deficits paralleling paralysis

Blindness in half of visual field (hemianopsia)

Aphasia (if dominant hemisphere involved, usually left)

Hemineglect (If non-dominant hemisphere, usually right)

Inability to recognize known objects (agnosia)

If Gaze preference, patients look towards the lesion

Posterior cerebral artery

Blindness in one half of visual field (hemianopsia)

Third nerve paralysis

Lack of visual recognition (visual agnosia)

Altered mental status with impaired memory

Cortical blindness

Brainstem/Cerebellum

Crossed Signs-face one side, body the other

Hemiparesis or quadriparesis (or worse yet locked in syndrome)

Sensory loss, hemi or all 4 extremities

Diplopia

Dysconjugate Gaze

Nystagmus

Dysarthria/Dysphagia

Vertigo

Decreased LOC or syncope

Ataxia

Vomitting

Patients presenting with pontine infarction may describe a preceding transient pain radiating from the unilateral eye to the nose, following which they developed numbness or ataxic hemiparesis on the side contralateral to the pain.4 The “beauty parlor syndrome” has been described in elderly patrons receiving shampoo treatments. Mechanical impingement by neck rotation and hyperextension decreases vertebral artery flow and produces hypoperfusion at the atlanto-occipital-distal vertebral artery junction. Patients may present with vertigo and ataxia.5

Evaluation

Stroke notification

Check Glucose

Consider Aortic Dissection or if neck pain in the absence of trauma, consider arterial dissection of neck vessels

Obtain a BP in both arms

NIH Stroke Scale (FERNE) , but remember it leaves out some CN, gait, and nystagmus

EKG

Draw Labs-CBC, PT/PTT, Lytes, C-XR, Consider ABG, C-Spine, LFTs

Get a stat CT Minus Head

multimodal MRI including gradient echo is at least as and probably more sensitive for bleeds than CT (J Neuro Neurosurg Psych 2001 Apr;70 suppl 1:I7-11)

Management

BP

One study showed cardene/labetalol lowering of BP before TPA may be assoc. with higher adverse events, but it may just be that patients with HTN do worse (Arch Neurol 2008;65:1174)

Keep MAP<130

Positioning

Hob flat may increase CPP (Neurology 2005;64:1354)

Cerebral Edema

Elevate head of bed to 30º

Hyperventilation or Mannitol only if acute deterioration

Seizures

Only to prevent recurrent seizures

Anticoagulation

ASA well proven (huge Chinese study)

No harm if you give it in hemorrhagic stroke, but still not advised (Stroke, 2000;31:1240-1249)

No benefit to other anticoagulants unless concerns over pt with current A.Fib (Stroke 33:856, 2002)

TPA

lytics up to 4.5 hours (NEJM 2008;359(13):1317)

Must be read by neuroradiologist (Neurologists, general radiologists, and certainly ER docs are not qualified)

BP must be less than 185/110

The NINDS trial was divided into two parts; in both parts, patients were randomized to receive tPA, 0.9 mg/kg, or placebo within three hours after onset of stroke symptoms. Patients in the treatment arm were given 0.9 mg/kg tPA (maximum dose, 90 mg) in a 10% bolus followed by a constant infusion of the remaining 90% over 60 minutes. The first part enrolled 291 patients and measured whether they had improvement in their NIHSS score of four points or more over baseline or resolution of deficits within 24 hours of onset of stroke. In this portion of the trial, there was no statistical difference between the tPA group and the placebo recipients (P = 0.21). However, in post hoc analysis, the authors point out that the median NIHSS scores were two points lower in the 0- to 90-minute range and four points lower in the 90- to 180-minute range when the tPA group was compared with placebo (P value not provided). The second part enrolled 333 patients and assessed clinical outcomes at three months. Patients who received tPA were at least 30% more likely to have minimal or no disability based on four measures of neurologic disability (NIHSS, modified Rankin, Glasgow outcome scale, and Barthel Index). The primary hypothesis in part two was tested with a global statistic to simultaneously test for effect in all four outcome measures. Symptomatic intracerebral hemorrhage occurred in 6.4% of tPA recipients but only 0.6% of placebo recipients (P < 0.001). Mortality at three months was 17% in the tPA group and 21% in the placebo group (P = 0.30). A number-needed-to-treat analysis of the NINDS trial indicates that for every eight acute stroke patients treated, one will benefit. One patient in 17 will suffer an intracranial hemorrhage, and one in 40 will die. These numbers may be helpful in explaining risks and benefits to patients who are eligible for thrombolytic treatment.

Meta-analysis of current thrombolytic for stroke data Symptomatic ICH 6.2% Absolute Risk Increase Fatal ICH 2.5% Absolute Risk Increase (Stroke. 2003 Jun;34(6):1437-42.)

The major risk of t-PA is symptomatic intracerebral hemorrhage, which occurred in 6.4 percent of patients who received t-PA, as compared with 0.6 percent of patients who received placebo.1 These figures represent an absolute difference in the risk of symptomatic intracerebral hemorrhage of 6 percent. Seventy-five percent of the patients with a symptomatic intracerebral hemorrhage were dead at three months. Yet despite the risk of intracerebral hemorrhage, the mortality at three months was insignificantly lower in patients treated with t-PA (17 percent) than in placebo-treated patients (21 percent). Two reasons may underlie the similar mortality of t-PA­treated and placebo-treated patients despite a higher risk of symptomatic intracerebral hemorrhage among patients treated with t-PA. First, most patients who had an intracerebral hemorrhage had large strokes and were likely to do poorly regardless of the presence of intracerebral hemorrhage within the damaged brain. Secondly, t-PA probably makes some “big” strokes much smaller. The patients with small strokes are less likely to die. Patients treated with t-PA who have very large strokes (very severe neurologic deficits, meaning an NIH stroke scale score greater than 20) and who already have evidence of a large acute ischemic stroke on baseline CT have an increased risk of symptomatic intracerebral hemorrhage. 17 However, patients in these two subgroups who receive t-PA are more likely to return to normal than patients who are treated with placebo. The decision to use t-PA in these patients should be made only after frank discussion of the potential risks and benefits with both the patient and the family. Figure 1 adapted from Marx J. Classification system for stroke patients. Proceedings of the National Symposium on Rapid Identification and Treatment of Acute Stroke, December 13, 1996. Washington, D.C.: National Institute of Neurological Disorders and Stroke (NINDS), November 1997.

Contraindications to TPA

Get TEE, eval ekg for A-Fib.  Carotid dopplers.

ASA or plavix

Site for NINDS Group Guidelines for TPA

editorial on why it has not been adopted more widely (Lancet 2006;5:722)

ECASS-III

Cerebellar Stroke

Neurosurgery consult

Misc.

Elevated CK-MB after stroke are not necessarily indicative of AMI, need elevated Troponin to properly eval. (Stroke 33:286 2002)

Giving ASA even to hemorrhagic stroke did not cause additional mortality or increased bleeds (Stroke 2000; 31:1240-9)

Old Stroke Patients

may still be safe to lyse patients > 80 y/o (BMJ 2010;341:c6046)

Andy has editorial as well (ACEP News Feb 2011)

Young Stroke Patients

Strokes in Younger Patients (EMEDhome)

When evaluating a younger patient in the Emergency Department with a stroke, keep in mind the following:

• Cardiac causes including Right-to-Left shunts from a patent foramen ovale (PFO) or occult atrial septal defect (ASD).
• Cocaine and amphetamine use
• Atrial myxoma
• Cervical artery dissections.   Approximately 20% of strokes in the young are caused by carotid artery and vertebral artery dissections in the neck, compared to 2.5% in older patients.

As transesophageal echocardiography (TEE) is considered the most sensitive method to date to detect PFO (1), think to suggest a TEE as part of the evaluation.

“In the absence of other causative conditions, an ASD or PFO may be presumed to be the underlying cause of cerebrovascular thromboembolism. The search for these defects will be more cost-effective in younger stroke patients who, unlike older patients, rarely have the cardiovascular conditions associated with advanced age that commonly cause strokes in the elderly” (2).References: (1) Horton SC, Bunch TJ. Patent foramen ovale and stroke  Mayo Clin Proc 2004;79(1): 79-88. (2)  Jaber WA, et al. Suspect an atrial septal defect if a young patient has a stroke Cleveland Clin J Med  2001; 68: 954-956. (3) Cabanes L, et al.  Atrial septal aneurysm and patent foramen ovale as risk factors for cryptogenic stroke in patients less than 55 years of age. A study using transesophageal echocardiography. Stroke 1993; 24:1865-1873. (4)  Jones J, Geninatti M. Cardiology  Emerg Med Clin North Am 1997;15(2):341-63.

from emedhome.com

Think Endocarditis in Young Patients With Apparent Stroke Neurologic complications occur in approximately one-third of cases of infective endocarditis and typically present as a stroke syndrome.

Valvular vegetations can embolize to the brain and causes cerebral infarction, usually in a branch of the middle cerebral artery, causing contralateral motor or sensory symptoms. However, infarction can occur anywhere in the cerebral circulation, producing a myriad of possible neurologic symptoms. Infectious vegetations can embolize to branch points in the cerebral vascular tree, causing the formation of mycotic aneurysms. A mycotic aneurysm is an aneurysm that results from an infectious process that involves the arterial wall. These are noted in up to 2% of patients with infective endocarditis, causing symptoms due to mass effect, vascular leakage, or sudden rupture. This can lead to a broad spectrum of clinical presentations ranging from subarachnoid hemorrhage to meningitis to coma.

Infective endocarditis is therefore an important consideration when a young person who has no risk factors for premature cerebrovascular disease who presents to the ED with stroke symptoms, particularly when the patient has risk factors for the development of infective endocarditis, such as IV drug use or valvular heart disease, or presents with a fever. References:  (1) Mattu A, Goyal D. Emergency Medicine: Avoiding the Pitfalls and Improving the Outcomes Â© Blackwell, 2007  (2) Crawford MH, Durack DT. Clinical presentation of infective endocarditis Cardiol Clin 2003;21: 159-66.  (3) Tunkel AR, Kaye D. Neurologic complications of infective endocarditis Neurol Clin 1993;11: 419-40.

Exam

(Jama 2005;293(19):2391)

LR of the absence of facial paresis, arm drift, and abnormal speech is 0.39

Oxfordshire Classification of Subtypes of Cerebral Infarction*

Totalanterior circulation infarction syndrome (TACS)

A combinationof new higher cerebral dysfunction (ie, dysphasia, dyscalculia, visuospatial disorder); homonymous visual field defect; and ipsilateral motor and/or sensory deficit of at least 2 areasof the face, arm, and leg.  

Partial anterior circulation infarction syndrome (PACS)

Only 2 of the 3 components of theTACS syndrome are present, with higher cerebral dysfunction alone, or with a motor/sensory deficit more restricted thanthose classified as LACS (ie, confined to 1 limb or to faceand hand, but not to the whole arm).

Lacunar infarctionsyndrome (LACS)

Pure motor stroke, pure sensory stroke, sensori-motorstroke, or ataxic hemiparesis.

Posterior circulation infarction syndrome (POCS)

Any of the following: ipsilateral cranial nervepalsy with contralateral motor and/or sensory deficit; bilateralmotor and/or sensory deficit; disorder of conjugate eye movement; cerebellar dysfunction without ipsilateral long-tract deficit(ie, ataxic hemiparesis); or isolated homonymous visual fielddefect.

*Based on data from Bamford et al.54

Sub-Arachnoid Hemorrhage (SAH)

Posterior Circulation Stroke

posterior circ stroke

Neurologists have described acute confusional states and acute agitated delirium with several sites of infarction [4, 5 and 6]. Some have been bilateral, others on the right (non-dominant) or the left (dominant) specifically. Restlessness, agitation and disorientation are common with posterior artery infarctions. Forced crying out, cursing and unintelligible speech often have been reported in these cases, as they were in our patient [2]. Hypertension and generalized slowing on EEG are described in some patients, whereas others have normal CT scans for some time before changes of density can be identified [2]. The course of delirium can last several weeks with varying outcomes. Older age, comorbidity, and extent of the infarction have significant impact. Our patient had a history that included diabetes mellitus, hypertension, adenocarcinoma, and psychiatric disorders, all of which could have produced some of the initial symptoms. It is unlikely that her fever was due to medications, because she had been taking them for weeks, or that it was due to infection, because an organism could not be cultured and the white blood cell count was persistently normal. The maximum outside temperature on that day was 76°C.

The Amitriptyline and Nortriptyline levels were less than 10 ng/ml. It is known that acute strokes can cause elevated temperature, agitation and hypothermia. Although total CK level was not obtained, it is unlikely that agitation caused the fever, as it persisted even after agitation resolved with sedation. The ultimate cause of her fever was puzzling, but the most likely etiology was the stroke. Whether or not the antibiotics prescribed at the onset eradicated an undetected infection was never resolved. The confirmed diagnosis of left posterior cerebral artery infarction certainly could have explained the majority of her signs and symptoms as well as the course.

It is quite important to consider this diagnosis early as it carries a high mortality, particularly in the elderly [2]. Rapid intervention with TPA is increasingly initiated to spare neuronal damage when it can be administered shortly after an event. It would not have been given to this patient 11 h post infarction. Because initial CT scans may not be diagnostic, an MRI or MRA is more definitive. Plan for workup depends on initial clinical evaluation, although in most hospitals the first imaging study would be a CT scan. A CT scan can exclude unexpected large lesions or the presence of bleeding but other investigations are necessary to identify the stenotic or occluded artery. Abnormal diffusion weighted imaging (DWI) is a very sensitive and specific identifier of ischemic stroke in patients presenting within 6 h of stroke. Although DWI can detect areas of ischemia within 15–30 min of onset after only 3 s of imaging, its availability is limited. CT scans are more available, easily obtained and cheaper than MRIs or DWIs, so they are usually ordered first. But when non-diagnostic and at the earliest suspicion of ischemic stroke, the alternatives should be considered. Once the delirium clears, post-stroke depression should be reassessed. Untreated depression has a negative impact on both rehabilitation and long-term prognosis, and a premorbid history for depression significantly increases the risk for recurrence. Post-stroke depression is a well-known phenomenon and consistent with our patient’s symptoms [7]. When the anterior limbic system is disconnected from the destroyed posterior, the amygdala and anterior hippocampus can also induce confusion, fever, anger and amnesia. The infarct will also disrupt connections between the temporal neocortex and the limbic system, making it extremely difficult to use language-encoded memories. As time progresses to allow for collateral circulation, the symptoms may resolve if the infarction is not so large that it causes devastating destruction.

In conclusion, infarction of the posterior cerebral artery, whether unilateral or bilateral, may present first as delirium without many focal findings. When suspected, an MRI should be immediately obtained to help clarify a diagnosis. Intervention with TPA in all non-hemorrhagic strokes remains controversial but patients treated within 90 min definitely have improved outcomes. Early identification of the patients who may benefit from this approach is essential [8]. The affected limbic structures can produce early psychiatric symptoms involving delirium and altered affect and the later development of post-stroke depression.

ATLANTIS trial:  Mild to moderate strokes 79% completely recover at 90 days vs. 56% for placebo.  In moderate to severe, 33% TPA vs. 5% placebo.  22% change of intracranial hemorrhage.  All symptomatic hemorrhages were fatal. (Stroke 2002, 33:493-496)

ANTIPLATELET DRUG DISCONTINUATION IS A RISK FACTOR FOR ISCHEMIC STROKESibon, I., et al, Neurology 62:1187, April 2004

BACKGROUND: Prophylaxis with antiplatelet drugs is effective for the secondary prevention of cardio- and cerebrovascular disease. Only limited information is available concerning the occurrence of ischemic stroke in the setting of discontinuation of such treatment.

METHODS: These French authors interviewed 320 patients (or surrogates) hospitalized for a transient ischemic attack (TIA) or stroke, regarding their use of an anti- platelet drug (almost always aspirin), and any changes in that treatment, in the month before hospitalization.

RESULTS: Of the minority (31, 9.7%) with a hemorrhagic stroke, none had discontinued an antiplatelet drug during the previous month, while six were being anticoagulated. Of 289 patients with an ischemic infarction, antiplatelet drug therapy was discontinued during the month before the episode in 13/103 who had been receiving it. The interval between discontinuation of anticoagulation and the occurrence of stroke was always 6-10 days, which is consistent with the timing of aspirin’s effect on platelets. In seven of the 13 cases, discontinuation of treatment was ordered by a physician prior to surgery, while in six it occurred due to “negligence” or based on the belief that treatment was not clinically relevant.

CONCLUSIONS: There may be an increased risk of stroke fairly shortly after discontinuation of antiplatelet drug prophylaxis. 8 references (igor.sibon@chu-bordeaux.fr)

NINDS study: inclusion criteria—ischemic stroke with clearly defined time of onset; measurable deficit on National Institutes of Health (NIH) stroke scale; no evidence of intracranial hemorrhage on computed tomography (CT) of brain; treatment—t- PA 0.9 mg/kg for maximum of 90 mg (10% given as bolus, 90% as constant infusion over 60 min [smaller than cardiac dose]); patient not to receive anticoagulants or antiplatelet drugs for 24 hr after treatment; strict protocol for blood pressure monitoring and control; exclusion criteria—prior stroke or head trauma within 3 mo; major surgery in previous 14 days; history of intracranial hemorrhage; hypertension; suspected transient ischemic attack (TIA); hypothesis—consistent and persuasive difference between t-PA and placebo in patients who recover with minimal or no deficit 3 mo after treatment; outcome—t-PA group had higher percentage of favorable outcomes; no increase in severe disability or death resulting from administration of t-PA; however, “you were ten times more likely to develop a symptomatic intracranial hemorrhage resulting from your stroke if you got t-PA than if you didn’t”; mortality from symptomatic intracranial hemorrhage 45% higher than mortality from disease process itself; t-PA patients 32% to 55% more likely to have complete recovery from stroke than placebo group (11%-13% more patients have complete recovery with t-PA than without it); must treat 8 to 9 patients to obtain one additional complete recovery; all patients with ischemic stroke benefited equally, regardless of size; these results held at 6 mo and 1 yr Recommendations of Stroke Council of American Heart Association: published in 1996; t-PA should be given according to NINDS protocol by physicians with expertise in diagnosis of stroke and interpretation of CT; streptokinase should not be used; do not treat if CT signs suggest major infarct or treating facility cannot handle complications of intracranial hemorrhage (need neurosurgery backup plan); use caution in severe strokes (score >22 on NIH stroke scale); obtain informed consent

NIH stroke scale: fairly reliable and reproducible; primarily identifies lateralizing findings; evaluates 11 criteria; takes 5 to 8 min to perform; patient must have score >4 but <22 CT criteria: must be done within 3 hr of symptom onset; parenchymal hypodensity indicates large stroke or long interval between time of stroke and patient’s arrival; study showed correct interpretation of CT by emergency physicians in 66% of cases, 83% for neurologists and radiologists; only 70% of emergency physicians interpreted CT correctly 100% of time, 40% of neurologists and 50% of radiologists

Comparison of MRI and CT for Detection of Acute Intracerebral Hemorrhage

JAMA. 2004;292:1823-1830. Results The study was stopped early, after 200 patients were enrolled, when it became apparent at the time of an unplanned interim analysis that MRI was detecting cases of hemorrhagic transformation not detected by CT. For the diagnosis of any hemorrhage, MRI was positive in 71 patients with CT positive in 29 (P<.001). For the diagnosis of acute hemorrhage, MRI and CT were equivalent (96% concordance). Acute hemorrhage was diagnosed in 25 patients on both MRI and CT. In 4 other patients, acute hemorrhage was present on MRI but not on the corresponding CT—each of these 4 cases was interpreted as hemorrhagic transformation of an ischemic infarct. In 3 patients, regions interpreted as acute hemorrhage on CT were interpreted as chronic hemorrhage on MRI. In 1 patient, subarachnoid hemorrhage was diagnosed on CT but not on MRI. In 49 patients, chronic hemorrhage, most often microbleeds, was visualized on MRI but not on CT.

Prognosis and Decision Making in Severe Stroke

JAMA 2005;294(6):725

Our analysis suggests that EICs are prevalent within 3 hours of stroke onset and correlate with stroke severity. However, EICs are not independently associated with increased risk of adverse outcome after rt-PA treatment. Patients treated with rt-PA did better whether or not they had EICs, suggesting that EICs on CT scan are not critical to the decision to treat otherwise eligible patients with rt-PA within 3 hours of stroke onset. (JAMA. 2001 Dec 12;286(22):2830-8.)

Optimal stroke scale to lyse 10-20

Dizziness and Stroke

Stroke Among Patients With Dizziness, Vertigo, and Imbalance in the Emergency Department: A Population-Based Study Kerber KA, Brown DL, Lisabeth LD, et al. Stroke 2006;37:2484–7 Catherine Ambrose MDa aDenver Health Medical Center, Denver, Colorado Available online 30 March 2007. As part of the Brain Attack Surveillance in Corpus Christi (BASIC) project, this study sought to determine the percentage of stroke patients who presented to the Emergency Department (ED) with the complaints of dizziness, vertigo, or imbalance. This large population-based study examined all patients over the age of 44 years who presented to the ED or were directly admitted to the hospital between January 2000 and June 2003 with the previously mentioned isolated dizziness symptoms (DS) in Nueces County, Texas. The association of age, sex, race/ethnicity, and isolated dizziness symptoms with stroke or transient ischemic attack (TIA) was then determined using multivariable logistic regression. A total of 1666 patients were included in the study, with 3.2% (53 of 1666) ultimately diagnosed with stroke/TIA. Of those diagnosed, 23 presented with dizziness as the chief complaint, 18 with vertigo, 11 with imbalance, and 1 with more than one of the above symptoms. Isolated DS without additional neurological findings was a strong negative predictor of stroke/TIA (odds ratio [OR] 0.05; 95% confidence interval [CI] 0.02–0.11), whereas male sex was associated with an increased association with stroke/TIA (OR 2.5; 95% CI 1.4–4.4). Patients diagnosed with stroke/TIA were also found to be significantly older (69.3 ± 11.7 vs. 65.3 ± 12.9, p = 0.02). No significant difference in race/ethnicity was found between the stroke and non-stroke groups. When compared to dizziness, patients with imbalance were found to have an increased risk of stroke/TIA (OR 3.7; 95% CI 1.3–10.7), whereas no increased risk was found between those with vertigo versus dizziness (OR 0.9; 95% CI 0.4–2.0). The authors acknowledge several limitations to this study, including lack of evaluation of the majority of study patients in the ED by a neurologist, lack of magnetic resonance imaging on most study patients leading to possible undiagnosed strokes, and lack of comparison of symptom onset, duration, aggravating/alleviating factors, headache, and auditory symptoms between groups. The authors conclude that dizziness and vertigo are not associated with stroke/TIA, whereas patients who present with imbalance, those with additional neurologic findings, male gender, and older age are at the highest risk for possible stroke/TIA.

Rapid approach to NIHSS

The NIHSS as formulated by the National Institute of Neurological Disorders and Stroke has been applied at our medical center as the SQS and is shown here with maximal deficit scores clustered into 3 groups having a total of 7points each (Fig. 1). The level of consciousness section to the NIHSS is grouped together in the frontal regions with an aggregate deficit score totaling 7 for deficits in alertness, ability to answer questions, and obey commands. A second cluster of 3 consisted of deficits in sensation, extinction, and language being clustered along the motor strip and temporal-parietal regions; the extinction category tests inattention with complete neglect scoring 2. In regards to sensory deficits, this can be tested as withdrawal to noxious stimuli, with a severe loss scoring 2 points. A third cluster was placed in the posterior regions and included the maximal visual deficit score of 3 for bilateral hemianopia, and the near to unintelligible deficit score of 2 for dysarthria was placed alongside the maximal limb ataxia score of 2 in the cerebellar region; although speech dysarthria can be a result of ischemic damage to the motor strip, an alternative possibility would be dysarthria of a cerebellar origin and for convenience is grouped here in the posterior fossa region. The maximal motor deficit score of 4 for each of 4 extremities is grouped together (green circle, Fig. 1). Miscellaneous items that are not part of the 322 groupings are separated by a line parallel to the catho-metal line: best gaze (forced deviation of the eyes scores 2 points) and facial palsy (complete facial palsy scores 3 points). 3. Discussion Although not yet formally tested under controlled conditions, the SQS diagram may accelerate the time factor in reaching an accurate score, but formal testing of this hypothesis is needed. Although the NIHSS attempts to comprehensively include all regions of the brain that could be affected by stroke, the weighting factors for each functional item might need reassessment. The current equal weighting for arms vs legs remains reasonable for now, because 1 study showed very good reliability for these items with the 15-item NIHSS [6]. However, the same study found the least reliable items to facial palsy and dysarthria with low intraclass correlation coefficients being less than 0.40, and advocated a modified 11-item version of the NIHSS. In summary, the presented SQS diagram shown in Fig. 1, or similar versions, may facilitate training of examiners to comprehend the overall structure of the NIHSS system. The SQS diagram is intended only to serve as a supplement and not a replacement for current methods of scoring. However, further testing of a single visual composite for the NIHSS as an ancillary tool is needed to determine its actual usefulness. (AJEM 2008;26:189)

From EP Monthly:The year’s top stroke advances by Bobby Desai, MD

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Lacunes & Lacunar Infarcts

The terms “lacune”, “lacunar infarct” and “lacunar stroke” are often used interchangeably, but they are not the same thing. Lacunes are 3 to 15 mm cerebrospinal fluid (CSF)-filled cavities in the basal ganglia or white matter, frequently observed coincidentally on imaging in older people, often not clearly associated with discrete neurological symptoms. “Lacunar stroke” describes a clinical stroke syndrome with the typical symptoms and signs referable to a small subcortical or brain stem lesion.1,2 “Lacunar infarct” should refer to a clinical stroke syndrome of lacunar type where the underlying lesion is an infarct on brain-imaging. On CT or MR T2-weighted and fluid-attenuated inversion recovery (FLAIR) imaging, an acute lacunar infarct can look just like a white matter lesion (WML), difficult to distinguish from an asymptomatic WML without diffusion-imaging to show a hyperintense signal (reduced on ADC), or a prior scan for comparison, especially in patients with WMLs. Some clinically evident acute lacunar infarcts may evolve with time into lacunes. These points are well-established.

Less well-established is how many clinically evident lacunar infarcts ever cavitate to become “lacunes”. It seems generally assumed that all lacunes start life as an infarct, even if the patient did not notice anything, and therefore share the same risk factors, etiology, prognosis, pathogenesis, etc, as clinically evident lacunar infarcts.3–5 However, suppose only a proportion of lacunar stroke lesions, perhaps as few as a third, ever cavitate, with the majority that fail to cavitate retaining the appearance of a WML?6 Counting lacunes could result in spurious risk factor and etiologic associations for lacunar stroke. We should not assume that the pathogenesis of clinically evident lacunar stroke is the same as for clinically silent lacunes. Equally, similarity in appearance between WMLs and clinically evident acute lacunar infarct could imply similar causation. However, surely the fact that one has caused symptoms (lacunar stroke/infarct) and the other not (WML/lacune) is important in itself and should lead to their careful distinction in any research at least until we know more.

Hemicraniectomy for Malignant Middle Cerebral

(Review)

Bleck:

Perhaps I’m missing something, but as I read the case the patient was being treated with enoxaparin for secondary stroke prevention, presumably from a cardiac source since there would not be an indication to do so without a suspected cardiac source (excepting hospitals with the initials Must Give Heparin).  Many stroke neurologists would think that four days is too early to start anticoagulation because of the risk of hemorrhagic transformation.  This is an area of considerable controversy and little data, but a two week delay is commonly suggested.  I didn’t think this should go by without comment.  Now for a statement that may label me as a heretic, or an old guy to be ignored: I don’t think that the ease of use of enoxaparin justifies its use in this circumstance.  I only use unfractionated heparin by intravenous infusion without a bolus in this setting, and keep the PTT about 70 sec.  I don’t want a drug that may be too effective as an anticoagulant, or that I can’t reverse quickly.  And I would not send a patient home this quickly when starting anticoagulation.  Sorry, but this case demonstrates why.

Regarding treatments to stabilize the patient in order to get to the OR (or theatre for some of you, or operating department for people who object to the term room), this is one of the few circumstances in which more than modest hyperventilation is reasonable in the setting of ischemia; I might even hyperventilate more than David suggests, into the low to mid 20s for a brief period in order to get the patient to the OR.  Regarding the mannitol dose, no one knows this either, but I’d probably start with 1 gm/kg on the theory that I want a high osmotic gradient and am not worried about rebound since the surgeon will make room for more swelling later.  In recent years I have used a lot more hypertonic saline, but I realize that the literature is mixed in this regard; this would be a circumstance in which 30 – 60 mL of 23.4% saline (sodium quadrate in pharmacy parlance) over 10 min might be best because it seems to work most quickly.  Coplin, what do you think as the holder of the IND for salt?  Raise the head of the bed and give neuromuscular junction blockade so there is no coughing (boy am I old-fashioned!); there’s no point in ‘following the exam’ any longer.  Turn the FiO2 up to 1.0 try to get some oxygen in without having to raise the blood pressure pharmacologically, although it is probably going up pretty high on its own (and if it isn’t, or is falling, the game is probably over already).  Although there is no question that lowering core temperature lowers ICP, there isn’t time to do it here; the patient needs to be decompressed before any modality would work.  I suppose I might start running in some chilled saline, which we keep around for post-cardiac arrest hypothermia, on the way to the OR, but I wouldn’t do anything that would delay transit.

I think the real question is whether to put in an external ventricular drain while the OR is being prepared.  There is likely to be obstructive hydrocephalus here, and one might lower the ICP substantially by relieving it.  The downside of this is the risk of upward herniation, which I have seen enough times to believe in and fear.  Some folks will put one in prophylactically and clamp it to have it in place already when the patient’s exam deteriorates.  If one does place an EVD, it shouldn’t be allowed to drain to atmospheric pressure; just take off a small amount of fluid.  Since in the emergent situation the fluid will initially gush out, this is another argument for placing it before the patient is trying to die.

Basilar Artery Occlusion (BAO)

From Google Knol

Administered IV Tpa up to 24 hours (48 hours if fluctuating) (Stroke 2011;42:2175)

TPA in patients on Coumadin

retrospective study showed increase post-tpa bleed rate even with INR < 1.7 (Arch Neurol 2010;67(5):  Prabhakaran)

Critical Review Of Decomp Crani for Middle Cerebral Infarct

The Neurologist Issue: Volume 17(1), January 2011, p 63–66

Posterior circulation stroke

Ischaemic stroke of the posterior circulation may cause mild or non-specific acute symptoms that are not captured on the National Institutes of Health Stroke Scale (NIHSS). A study published in the Annals of Emergency Medicine (2011;57:42–5) reveaed that patients with an NIHSS score of 0 and a documented infarct on diffusion-weighted imaging, frequently presented with headache, vertigo, nausea and truncal ataxia. This highlights the need to be alert to this pattern of symptoms in order to investigate further and rule out a posterior circulation stroke.

Neutrophilia

Stroke. 2008 Feb;39(2):355-60. Epub 2007 Dec 27.Early neutrophilia is associated with volume of ischemic tissue in acute stroke.

Good Care for Post-Stroke is most Important Factor

From EM Lit of Note Blog:

This is a prospective interventional study in which acute stroke units
in New South Wales Australia were randomized to either no protocolized
intervention, or an intervention with nursing protocols named above.  At
the end of the three-year intervention period, 42% of the control group
had mRS 0 or 1 at 90 days, and 58% of the intervention group had mRS 0
or 1 at 90 days.  There were small differences in the type of stroke,
education level, and prior ability to work that probably favored the
intervention group, but the differences at baseline were far smaller
than the magnitude of the treatment effect.  In short, a basic nursing
protocol intervention improved outcomes more than any other intervention
for acute stroke.

“Implementation of evidence-based treatment protocols to manage fever,
hyperglycemia, and swallowing dysfunction in acute stroke (QASC): a
cluster randomised controlled trial.”
(Lancet, Volume 378, Issue 9804, Pages 1699 – 1706, 12 November 2011)

Crossed Leg Sign

Leg crossing is an easily obtained clinical sign and is independent of additional technical
examinations. Leg crossing within the first 15 days after severe stroke indicates a favorable
outcome which includes less neurologic deficits, better independence in daily life, and lower rates
of death. Neurology® 2011;77:1453–1456

Heart Failure (Dropsy, Hydropsy)

APE

best review by Hermann

evidence based guidelines for patients with acute decomp heart failure (Crit Care Med 2008;36(Suppl):S129)

Ejection fraction most important determinant

Pt’s c APE may still be intravascularly depleted

Always think valvular problem in new CHF

Always think valve thrombosis in CHF with a prosthetic valve

Do not give vasodilators in AS, but yes in MR

***A-Line in CHF c decreased CO (cuff bp more representative of mean than systolic)***

Decline in cardiac output leads to increased sympathetic tone, increased peripheral resistance (afterload), and increased renin/angiotensin/aldosterone axis.

Review: Postgrad Med 103:2, 1998

Retrospective Study:  Am J EM 17:6

X-Rays

VPW>70 and CTR>.55 has good correlation with PAOP>18 (Chest 122:6, Dec 2002)

but small heart does not mean no heart failure (Eur J Heart Fail 5:117, March 2003)

High Dose Nitro Drip

Start at 50 mcg/min, can rapidly titrate to 200-400 mcg/min. You must stand at the bedside to use these doses.

Need >120 mcg/min to get sig decreased PCWP(Am J Cardio 2004;93:237)

Nitro Bolus

is very effective, give 0.8 mg over 2 minutes=400 mcg/min for 2 minutes.  (Annals EM 1997, 30:382)

Run normal drip setting (10 mcg/min=3cc/hr) at 120 cc/hr for 2 minutes to get same dose.

High dose nitroglycerin for severe decompensated heart failure–2mg at a time (Ann Emerg Med 2007;50:144)

Low nitrates c high lasix vs., the opposite, shows nitrates more effective (Lancet 1998 351:389-393)

BP lowering as long as the patient can mentate, ambulate, and urinate.

Cotter gave isosorbide 3 mg q 5 minutes with good results in his study.  This is equivalent to nitro 600 mcg/min. (Lancet 1998 351:9100, 389-393)

The Feasibility of Treating Severe Acute Congestive Heart Failure With Bolus Intravenous Nitroglycerin Zalenski RJ, Levy P, Compton S, Delgado G, Welch R, Waselewsky D/Wayne State University, Detroit Receiving Hospital, Detroit, MI Study objectives: Bolus intravenous nitroglycerin is a potential innovation for the management of severe acute decompensated heart failure (ADHF) but has undergone limited clinical evaluation. Although previous studies have demonstrated improved outcomes, the effect of adding bolus intravenous nitroglycerin to standard American Heart Association (AHA) treatment of severe ADHF has not been defined. Our primary objective is to evaluate the feasibility of using this novel therapeutic approach in the management of severe ADHF. Secondary objectives include an assessment of the safety and efficacy of bolus intravenous nitroglycerin. Methods: This study was designed as an unblinded pilot intervention trial of the addition of bolus intravenous nitroglycerin to standard AHA treatment for ADHF. The eligible study population included all adult patients (age $18 years) presenting to the emergency department of Detroit Receiving Hospital (Detroit, MI: annual census ;85,000) or Sinai-Grace Hospital (Detroit, MI: annual census ;62,000) with a clinical diagnosis of acute cardiogenic pulmonary edema. The prespecified goal was to enroll 30 patients. The main inclusion criterion was a systolic blood pressure of 160 mm Hg or greater or a mean arterial pressure of 120 mm Hg or greater. Patients with a suspected or proven right ventricular infarction, known or suspected pregnancy, or a history of intolerance to nitroglycerin and those requiring immediate intubation or cardiopulmonary resuscitation were excluded. The study was approved by the institutional review board of Wayne State University, and written informed consent was obtained from all patients (or proxy) before initiation of the protocol. On enrollment, baseline hemodynamic values and a serum brain natriuretic peptide level were obtained. Initial treatment of all patients consisted of 100% oxygen (by nonrebreather), 3 doses of sublingual nitroglycerin (0.4 mg), and intravenous furosemide (60 to 100 mg). Administration of morphine sulfate (3 to 5 mg) was permitted but not encouraged. Patients without improvement were then started on the intervention protocol, which included initiation of a nitroglycerin infusion (0.3 to 0.5 mg/kg per minute) with concurrent administration of a dose of bolus intravenous nitroglycerin (2 mg). Titration of the infusion (#400 mg/min) and repeated dosing of bolus intravenous nitroglycerin (2 mg) was allowed every 3 to 5 minutes, up to a total of 10 doses, at the discretion of the treating physician. Ventilatory assistance with endotracheal intubation or biphasic positive airway pressure and administration of additional pharmacologic therapy was permitted at any point at the discretion of the treating physician. The primary efficacy endpoint was rate of endotracheal intubation. Secondary efficacy endpoints included the need for ICU admission and total hospital length of stay. Primary safety endpoints included the incidence of cardiac or neurovascular complications and symptomatic hypotension. Descriptive statistics are provided. Results: Twenty-eight patients were enrolled. Mean age was 61.57 years (615.01 years); 89.3% were black and 64.3% were men; 89.3% had a history of heart failure, 92.9% had hypertension, and 35.7% had coronary artery disease; 76.5% were noted with New York Heart Association heart failure classification III or IV, and the median brain natriuretic peptide level was 1,849 pg/mL. Baseline vital signs (mean6SD) were as follows: mean arterial pressure 155.11 mm Hg (623.49 mm Hg); pulse rate 114.93 beats/min (624.85 beats/min), and respiratory rate 31.07 breaths/min (66.77 breaths/min). Mean protocol intervention time was 18.21 minutes (614.97 minutes). Symptom improvement was reported in 24 patients (85.7%). Mean dosing of bolus intravenous nitroglycerin was 6.50 mg (63.47 mg). Mean nitroglycerin infusion rate was 38.82 mg/min (628.04 mg/min), and mean intravenous furosemide was 85.00 mg (624.11 mg). Other administered medications included morphine (11 patients), angiotensin-converting enzyme inhibitors (10 patients), and b-blockers (3 patients). Patients were monitored for a mean period of 75.46 minutes (669.84). During this time, significant reductions from baseline vital signs were noted (mean D [95% confidence interval (CI)]: pulse ANNALS OF EMERGENCY MEDICINE 4 4 : 4 OCTOBER 2004

ACEI

• Captopril SL (12.5-25 mg) (Current Ther Res 1991 29:2) (Acad Emerg Med 3:3, 1996) (Crit Care Med 23:5, 1995) (Int J Cardio 27:3, p.351)
• Enalapril 1.25-2.5 mg (Circulation 94:6, 1996)

ACEI best (tested SL Captopril) (Sacchetti AM J Emerg Med Oct 1996 17 (6))

Diuretics

Do not help and may cause further decline in the acute phase of APE (J Am Soc Nephrol 4:2, 1993) (Am J Med 96:3, 1994)

Vasoconstrictor Response initially by IV furosemide (Ann Intern Med 1985; 103:1-6)

Worsening of outcome when used in prehospital setting (Chest. 1987; 92:586-593)

Head to head nitrites vs. furosemide (Lancet 1983;i:730-32)

Typically requires high dose diuretics Indirect effects of diuretics may be counterproductive Increase neurohormonal activation 1,2 Reflex vasoconstriction, ↓ cardiac output 1 Worsening of renal function 3 1. Francis GS, et al. Ann Int Med. 1985;103:1-6. 2. Bayliss J, et al. Br Heart J. 1987; 57:17-22. 3. Mehta RL, et al. JAMA. 2002;288:2547-2553

Consider furosemide infusion at 20-40 mg/hr

after the first hour of treatment.

Vasodilatory effect of loop diuretics Vasodilation is mediated through prostaglandins Effect is blunted in patients taking ASA Majority of HF patients take ASA because of concomitant CAD

Jhund PS, et al. J Am Coll Cardiol. 1999;33:572-575

Morphine

Increases ICU admits (Am J EM 17:6 571-574)

When given in prehospital, results in deterioration and subjective increase in distress (Chest 92:4, 1987)

Milrinone

Not very effective. (J Am Coll Cards 2002, 39:798-803)

Natrecor

Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial. SO – JAMA 2002 Mar 27;287(12):1531-40. CONTEXT: Decompensated congestive heart failure (CHF) is the leading hospital discharge diagnosis in patients older than 65 years. OBJECTIVE: To compare the efficacy and safety of intravenous nesiritide, intravenous nitroglycerin, and placebo. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind trial of 489 inpatients with dyspnea at rest from decompensated CHF, including 246 who received pulmonary artery catheterization, that was conducted at 55 community and academic hospitals between October 1999 and July 2000. INTERVENTIONS: Intravenous nesiritide (n = 204), intravenous nitroglycerin (n = 143), or placebo (n = 142) added to standard medications for 3 hours, followed by nesiritide (n = 278) or nitroglycerin (n = 216) added to standard medication for 24 hours. MAIN OUTCOME MEASURES: Change in pulmonary capillary wedge pressure (PCWP) among catheterized patients and patient self-evaluation of dyspnea at 3 hours after initiation of study drug among all patients. Secondary outcomes included comparisons of hemodynamic and clinical effects between nesiritide and nitroglycerin at 24 hours. RESULTS: At 3 hours, the mean (SD) decrease in PCWP from baseline was -5.8 (6.5) mm Hg for nesiritide (vs placebo, P<.001; vs nitroglycerin, P =.03), -3.8 (5.3) mm Hg for nitroglycerin (vs placebo, P =.09), and -2 (4.2) mm Hg for placebo. At 3 hours, nesiritide resulted in improvement in dyspnea compared with placebo (P =.03), but there was no significant difference in dyspnea or global clinical status with nesiritide compared with nitroglycerin. At 24 hours, the reduction in PCWP was greater in the nesiritide group (-8.2 mm Hg) than the nitroglycerin group (-6.3 mm Hg), but patients reported no significant differences in dyspnea and only modest improvement in global clinical status. CONCLUSION: When added to standard care in patients hospitalized with acutely decompensated CHF, nesiritide improves hemodynamic function and some self-reported symptoms more effectively than intravenous nitroglycerin or placebo.

Not that I have anything against the industry or anything, but an interesting twist has twisted in the ‘life after death’ aftemath of the Nesiritide scandal.   A study designed and funded by Scios for the purpose of addressing the furor that followed the publication of a provocative meta-analysis in JAMA (2005;293:1900-1905) has now been published in J Emerg Med (2005; 29:243-252). The JAMA SR reported a RR for death, nesiritide compared to control, of 1.7 (95% CI 0.97, 3.1), just missing statistical significance. The JEM study reported an all-cause mortality rate of 5/120 (4%) in the nesiritide group and 1/117 (1%) in the standard care group with a resulting p value of  0.213 (also not significant).  Now, as reported in our own ACEP News of February 2006, it turns out that 2 extra deaths, both in the nesiritide group, were first lost, and now found (Funny how things happen).  This would convert the death toll to 7/120 nesiritide versus 1/117 in the control.    ACEP News reports that both the PI on the study and a Scios spokesman ‘downplayed’ the ‘significance’ of the two additional deaths, emphasizing that one died of CO poisoning and the other in a traffic accident.  This raises an interesting issue- all cause versus disease specific mortality.    The stakes are a bit high.  Whatever the PI and the Scios rep mean by ‘significance’, it is apparently not to do with statistical significance.  A quick visit to the useful online free access calculator site (http://members.aol.com/johnp71/ctab2x2.html) reveals that when the new numbers are plugged into a standard formula we have a RR for death, nesiritide compared to control, of   6.8 I(95% CI 1.1, 42).  In short, accepting these results, we now have a statistically significant increase in all cause death in patients treated with nesiritide.   So the issue is all-cause mortality.  Should we reject the deaths of the 2 extra patients in the nesiritide as ‘insignificant’.  One might speculate that they were probably not ‘insignificant’ to the patients and their families, particularly considering that one was functional enough to be taking a ride in a car or walking across the street and the other perhaps being poisoned in a car or in a closed space running a fuel driven device.  One might also speculate that perhaps one drifted off due to uremic encephalopathy due to after effects of nesiritide (which another SR, published in Circulation, showed worsened renal function) and that the other collapsed from flash pulmonary edema while driving.    Speculative certainly.  However, the fantasies illustrate why all cause mortality is actually the preferred outcome with respect to adverse effects of drugs. When looking at direct effects of drugs, disease specific mortality may have a case for preference.  For example, screening mammography may effectively and significantly lower mortality from breast cancer without altering all cause mortality, simply because most women do not die from breast cancer.  However, when the effect is statistically significant and when ‘wild card’ consequences of adverse effects pertain, all cause mortality wins all.   Again, this is just for teaching purposes.  Purely objective science….   Peter

Another negative nesiritide study (Ann Emerg Med 2008;51:571)

BiPAP

Lancet 356:2126, December 23/30, 2000

Systematic Review (Ann Emerg Ned 2006;48:260)

CPAP

Eur Heart Journal 2002, 23:1379

In one study (Emerg Med J 2004; 21:155-161) survival to hospital discharge was improved with CPAP (10 mm/Hg) over BiPap (Ipap 15 Epap 5) and conventional therapy.

CPAP was just as good as PSV (Intens Care Med 2005;31:807)

New York Heart Association Classification

Class   Functional state        Symptoms

I             No limitation                    Asymptomatic during usual daily activities

II            Slight limitation             Mild symptoms (dyspnea, fatigue, or chest pain) with

ordinary daily activities

III          Moderate limitation       Symptoms noted with minimal activity

IV           Severe limitation             Symptoms at rest

Common Precipitants Of CHF Decompensation

• Medication noncompliance

• Dietary indiscretion (salt)

• Uncontrolled hypertension

• Myocardial ischemia/infarction

• Acute valvular dysfunction

• Cardiac arrhythmias

• Pulmonary and other infections

• Administration of inappropriate medications (e.g., negative inotropes)

• Fluid overload

• Missed dialysis

• Thyrotoxicosis

• Anemia

• Alcohol withdrawal

Substantial subset of elderly pts presenting with CHF have near-normal LV systolic function and their underlying cause may be dysrhythmia, ischemia, or valvular abnormalities.  Early echo should be considered.  (Am J Med Sci 323(5), 2002)

Diastolic Dysfunction

decreased ventricular distensibility

Multicenter rct showed better avoidance of intubation and resolution of symptoms (Intensive Care Med (2011) 37:1501–1509)

B-Natriuretic Peptide

Use cut off of 100 pg/ml.  Not much different than cardiomegaly on C-XR

(N Engl J Med 347(3):161, July 18, 2002 manufacturer funded)

B-type Natriuretic Peptide as a Marker for CHF

The symptoms and signs of heart failure are neither sensitive nor specific and considerably overlap those of pulmonary disease. B-type natriuretic peptide (BNP) is a polypeptide secreted by the cardiac ventricles in response to myocyte stretch, resulting from ventricular volume expansion and pressure overload. BNP levels are elevated in patients with left ventricular dysfunction, and the levels correlate with both the severity of symptoms and the prognosis.

In the largest study to date, the Breathing Not Properly Multinational Study, BNP levels were more accurate than any historical or physical finding or laboratory value in identifying heart failure as the cause of dyspnea. The diagnostic accuracy of BNP at a cutoff value of 100 pg/ml was 83%, with a sensitivity of 90% and a specificity of 76% (1,2).

There is a high negative predictive value of a low level of BNP with respect to the diagnosis of heart failure. A BNP level below 100 pg/ml in a patient with acute dyspnea makes the diagnosis of heart failure very unlikely and can help clinicians focus on alternative diagnoses, whereas a level above 500 pg/ml makes the diagnosis of CHF highly likely. For intermediate levels, use of clinical judgment and adjunctive testing are encouraged (4).

It should be noted that in patients with severe renal disease, B-type natriuretic peptide levels are increased. Therefore, higher cutoff values need to be identified for this important patient population.

References:

(1) Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med 2002;347:161-167.

(2) McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation 2002;106:416-422.

(3) Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. N Engl J Med 2004;350:647-654.

(4) Mark, D. B., Felker, G. M. (2004). B-Type Natriuretic Peptide — A Biomarker for All Seasons?. N Engl J Med 350: 718-720

Comparison of BNP vs. ECHO.  (J Am Coll Card 40(10):1794, Nov 20,2002)  Use <80 no CHF, >300 CHF, in between grey zone.  BNP 12% missed, physical exam 15% miss.

Remember that either ventricle failing will produce BNP so any patient with cor pulmonale from copd will also have elevated bnps.

Anterior Q waves or Left BBB both have specificity of ~90% but lack sensitivity (Ann Emerg Med 41:4, April 2003)

B-type is so named because it was first isolated from porcine brains, mostly secreted from ventricles.

Patients with PE can have levels from 200-300 (Ibid) COPDers with cor pulmonale can have levels of 300-600 (Ibid)

New NEJM study (N Engl J Med 2004 Feb 12)

I use the BNP both to rule in and to rule out CHF. So, in the example of the patient who has chronic lung disease and who has rales that might be “wet” or “dry” and a chest x-ray that shows interstitial markings that could represent fibrosis or fluid (and no priors for comparison, of course): a BNP less than 100 satisfies me that the patient probably does not have CHF, while one greater than 500 (or, better yet, 1,000) strongly suggests that the patient does, indeed, have CHF. Values between 100 and 500 are not very useful. Although our lab reports the results with a cut-off of 100 between normal and abnormal, I consider values between 100 and 500 to be indeterminate.

Patient Oriented Evidence on BNP

Less than 100 no CHF, >500 definitely CHF, in between use clinical judgment

Knowing the level of B-type natriuretic peptide during initial evaluation in the emergency department is associated with more rapid initiation of appropriate treatment, less needfor hospitalization and intensive care, a shorter length ofstay, and lower costs. The next question is whether the BNPcan replace other tests like the chest x ray or echocardiogramfor some patients. (Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriureticpeptide in the evaluation and management of acute dyspnea. NEngl J Med 2004;350: 647-54) and POEM (BMJ  2004;328 (29 May))

There us a delay of several hours after onset of symptoms before excess BNP is produced

Physical Diagnosis

(JAMA 2005;294(15):1944)

Data Synthesis Many features increased the probability of heart failure, with the best feature for each category being the presence of (1) past history of heart failure (positive LR = 5.8; 95% confidence interval [CI], 4.1-8.0); (2) the symptom of paroxysmal nocturnal dyspnea (positive LR = 2.6; 95% CI, 1.5-4.5); (3) the sign of the third heart sound (S3) gallop (positive LR = 11; 95% CI, 4.9-25.0); (4) the chest radiograph showing pulmonary venous congestion (positive LR = 12.0; 95% CI, 6.8-21.0); and (5) electrocardiogram showing atrial fibrillation (positive LR = 3.8; 95% CI, 1.7-8.8). The features that best decreased the probability of heart failure were the absence of (1) past history of heart failure (negative LR = 0.45; 95% CI, 0.38-0.53); (2) the symptom of dyspnea on exertion (negative LR = 0.48; 95% CI, 0.35-0.67); (3) rales (negative LR = 0.51; 95% CI, 0.37-0.70); (4) the chest radiograph showing cardiomegaly (negative LR = 0.33; 95% CI, 0.23-0.48); and (5) any electrocardiogram abnormality (negative LR = 0.64; 95% CI, 0.47-0.88). A low serum BNP proved to be the most useful test (serum B-type natriuretic peptide <100 pg/mL; negative LR = 0.11; 95% CI, 0.07-0.16). Conclusions For dyspneic adult emergency department patients, a directed history, physical examination, chest radiograph, and electrocardiography should be performed. If the suspicion of heart failure remains, obtaining a serum BNP level may be helpful, especially for excluding heart failure.

Electrolyte Disturbances

Hypomagnesemia very common in CHF and can cause dysrhythmia.  Check Mg or empirically replace if there are dysrhythmias (Eur J Heart Failure 4:167 2002)

Swimming Induced

yes you can get APE just from swimming (Annals EM 41:2, 2003)

Unilateral Pulmonary Edema Common teaching states that a unilateral alveolar or interstitial infiltrate is most likely a result of pneumonia, and not pulmonary edema.  However, unilateral pulmonary edema has been well documented, and can result from a myriad of causes.  Described causes of unilateral pulmonary edema include congestive heart failure (1), severe mitral valve insufficiency (2), upper airway obstruction (3), pulmonary artery compression from aortic dissection (4,5), pulmonary venous obstruction from mediastinal fibrosis (6) neurogenic pulmonary edema (7), and amiodarone-related (8) and heroin-related (9) pulmonary edema. Thus, even if the pulmonary opacities are unilateral – and even though radiology may read the x-ray as exhibiting llikely pneumonia – if the clinical manifestation is compatible with pulmonary edema and not with pneumonia, early and aggressive treatment should be initiated for pulmonary edema. References: (1) Nitzan O, et al. Unilateral pulmonary edema: a rare presentation of congestive heart failure  Am J Med Sci  2004;327:362–364. (2) Legriel S, et al. Unilateral pulmonary edema related to massive mitral insufficiency  Am J Emerg Med  2006;24: 372. (3) Morisaki H, et al. Unilateral pulmonary edema following acute subglottic edema  J Clin Anesth  1990;2: 42–44. (4) McTigue C, et al.  Unilateral pulmonary edema associated with pulmonary arterial compression  Australas Radiol  1988;32: 390–393. (5) Takahashi M, et al.  Unilateral pulmonary edema related to pulmonary artery compression resulting from acute dissecting aortic aneurysm  Am Heart J  1993;126: 1225–1227. (6) Routsi C, et al.  Unilateral pulmonary edema due to pulmonary venous obstruction from fibrosing mediastinitis   Int J Cardiol  2006;108: 418–421. (7) Perrin C, et al.  Unilateral neurogenic pulmonary edema. A case report  Rev Pneumol Clin  2004;60(1):43–45. (8) Herndon JC, et al.   Postoperative unilateral pulmonary edema: possible amiodarone pulmonary toxicity  Anesthesiology  1992;76: 308–312. (9) Sporer KA, Dorn E.  Heroin-related noncardiogenic pulmonary edema: a case series  Chest  2001;120: 1628–1632.

Morphine screws up decomp heart fx patients (EMJ 2008;25:205)

Neurogenic Pulmonary Edema

(CHEST March 2012 vol. 141 no. 3  793-795)

phentolamine may fix neurogenic APE

• Resuscitation and General Principles
  • Management
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    • A New Airway Curriculum
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      • Basic Vent Stuff
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This site represents my opinions only. See here for full disclaimer

• TEG Based Protocol
• Another for using FIBTEM for prediction, but Hb and PT seemed as good (Crit Care 2001;15:R265)
• BET for Mass Trans
• Review of 1:1 (Transfusion Medicine Reviews 2009;23(4):255)

Coagulopathy in Trauma

The mechanism of coagulopathy in trauma is complex and multifactorial: Dilutional coagulopathy results from the dilution of coagulation factors and platelets caused by the infusion of large volumes of crystalloids, colloids, or blood products, which are administered to improve oxygen delivery. The severity of dilutional coagulopathy is determined by both the volume and type of fluids infused. Whereas permissive hypotension and reduced fluid volume in the prehospital setting and early in-hospital treatment may decrease the extent of such coagulopathy, newly developed types of fluids, such as hypertonic saline (with or without dextran), new colloids, and artificial oxygen carriers, may exacerbate it [710]. Hypothermia is a common complication of both civilian and combat injuries, leading to severe coagulation impairment. This is due to the decline in both platelet and coagulation enzyme activities [1113]. These effects are often underestimated as most laboratories re-warm blood samples to 37°C before testing for clotting assays, i.e. PT, PTT. Even if these plasma-clotting assays were performed at the patient’s body temperature, they would still underestimate the magnitude of the coagulopathy, as these assays do not reflect the in vivo coagulation process occurring on cell membranes, such as tissue factor (TF)-bearing cells and activated platelets [14]. Furthermore, platelet functions, which are significantly impaired by hypothermia [15], are not monitored routinely, contributing to the underestimation of the hemostatic defect. Acidosis resulting from decreased perfusion and production of anerobic metabolism leading to the accumulation of lactic acid is common among trauma victims. Even a slight decrease in pH compromises the function of both coagulation enzymes and platelets, particularly in the presence of hypothermia [11]. A decrease in pH from 7.4 to 7 reduces prothrombin (FII) activation by the prothrombinase complex (FXa/FVa) by 70% [15]. Hyperfibrinolysis may be more common in trauma patients than was previously realized. The failure to detect this condition stems from the lack of routine laboratory tests for fibrinolysis. A recent study using rotational thromboelastography (roTEG) has shown that approximately 20% of multi-trauma patients suffering from massive bleeding have marked hyperfibrinolysis (M. Vorweg and M. Doehn, Personal Communication). The reproduction of these findings in larger patient series would support the theory that early administration of antifibrinolytic agents may be beneficial for hemorrhage control in trauma. Treatment with recombinant activated factor VII (rFVIIa), which reduces clot susceptibility to fibrinolysis partly by the induction of thrombin-activated fibrinolytic inhibitor (TAFI), may also be of value in hyperfibrinolysis [16]. Anemia-induced coagulopathy: In addition to their role in oxygen delivery, red blood cells (RBC) provide important mechanical and biochemical functions in the coagulation process. Therefore, anemia causes prolongation of the bleeding time, which can be corrected with a RBC transfusion [1719]. Furthermore, reduction of the hematocrit (Hct) inhibits platelet adhesion and aggregation, e.g. Hct of 20% restricts aggregation to a degree similar to that observed with 20 000 platelets mL1 [20]. Consumption coagulopathy is induced by exposure of TF at the site of injury, leading to activation of the coagulation cascade at this site. Massive injury may cause extensive consumption with depletion of platelets and coagulation factors. This process results in laboratory findings resembling disseminated intravascular coagulation (DIC), such as prolonged PT and aPTT, low levels of platelets and fibrinogen, and high levels of D-dimers and other markers of coagulation and fibrinolysis activation. However, in most cases, these findings do not reflect DIC, as there is no evidence of microthrombi formation and, thus, no intravascular clotting [21].     hypothermia is an independent risk factor for trauma mortality (J Trauma 2005;59(5):1081)   hypocalcemia is also a cause of coagulopathy increased fibrinolysis as well whole blood is used in iraq Best Review (Brit J Anaes 2005;95(2):130   Acidosis impairs coagulopathy as well (J Trauma 2006;61:624, J Trauma 2003;55:886)   European Surgical Bleeding Guidelines (Management of bleeding following major trauma: a European guideline Critical Care 2007, 11:R17)   Acidosis massively increases risk of coagulopathy, Impairs factor VIIa/tissue factor complex. Clot formation can be normalized with a buffer (J Neurosurg Anesth 2006;18:200)

Massive Transfusion

For every 4 packed cells – 2 FFP For every 8 packed cells and – 4 FFP: 6 Random platelets For every 16PC / 8 FFP – 12 Random platelets plus add a unit of cryoprecipitate   mortality benefit shown (J Trauma 2008;64:1177) It also reduces overall blood usage   Survey of world centers (J Trauma 2006;60:s91)   need plasma coag at least 40% of normal for clotting   >5 units PRBC, you get dilutional coagulopathy need 1:1:1 ratio after ~8 units PRBC At 10 units, you need platelts send fibrinogen levels, may need cryo   can’t clot when acidotic       (Anesth Analg 2007;105:905) fibrinogen is probably the reason for dilutional coagulopathy colloids interfere with clotting by fibrinogen concentration and polymerization blood loss causes fibrinogen to drop first maintaining fibrinogen at at least 150 mg/dL may be the key to trauma bleeding <50 no clot <75 weak clot   linear improvement in clot strength up to 300 OB study with <200 shows 100 % predictive value for postpartum bleeding   Study from Iraq shows 1:1 probably best, but just retrospective. Also has most of the massive transfusion references (J Trauma 2007;63:805)   Two from AAST FFP:PRBC Transfusion Ratio of 1:1 is assoc with sig lower risk of mortality following massive transfusion Early Achievement of a 1:1 ratio of FFP:PRBC reduces mortality in patients receiving massive transfusion   acidosis causes RBC swelling which increases viscosity   Mathematical model of FFP transfusion strategy shows 1:1 is the only way to avoid dilutional coagulopathy (Can J Surg 2005;48(6):470)   We were talking about this yesterday with Peter Shirley who is one of our intensivists and a Royal Air Force anaesthesia/critical care doctor who has recently returned from Camp Bastion in Afghanistan.  The British military have deployed ROTEM for the past 12+ months – initially as a research tool but now used to guide therapy. Peter’s experience is entirely descriptive, but he describes 3 phases of care for the exsanguinating, coagulopathic patient: 1. Identification of active exsanguination, severe shock, Acute Traumatic Coagulopathy (ROTEM 5-minute Clot Amplitude (CA5) less than or equal to 35mm)  = empiric (blind) aggressive transfusion/component therapy.  (Ross Davenport from our unit has done some truly excellent work on ROTEM diagnosis of ATC which was presented at TSIS2010 and is currently in submission) 2. Resuscitation continues, coagulopathy worsens, A ROTEM-guided phase where component therapy is based on clotting profiles 3. Correction of shock state (base deficit normalised) = ROTEM correction may lag behind visible clotting capability and patients have a tendency to overtransfusion if ROTEM is used as a guide in this phase and the “brakes” aren’t put on. There’s no data yet for phase 3 but we’ll see. Note we have presented data to show that a normal CA5 on admission has a 99% negative predictive value for massive transfusion – so ROTEM may be useful to stop massive haemorrhage protocols early and avoid waste / reduce transfusion -related complications. Karim Brohi retrospective support for high plasma rations when >4 <10 units used (J Trauma 2011;70:81)

Prothrombin Complex Concentrate

see also reversal section in Hematology   500 units of Beriplex=2 L of FFP (Eur J of Cardio Surgery 2001;19:219)   Best review (Eur J Anaes 2008;25:784)   New observational trial included 38 patients who got pcc just for bleeding not anti-coagulant (Crit Care)   BJA: British Journal of Anaesthesia Volume 102, Number 3Pp. 345-354  Haemodilution markedly prolonged prothrombin time and reduced peak thrombin generation. PCC, but not FFP, fully reversed those effects. Compared with 15 ml kg–1 FFP, PCC shortened the time to haemostasis after either bone (P=0.001) or spleen (P=0.028) trauma and reduced the volume of blood lost (P<0.001 and P=0.015, respectively). Subsequent to bone injury, PCC also accelerated haemostasis (P=0.003) and diminished blood loss (P=0.006) vs 40 ml kg–1 FFP. Conclusions: PCC was effective in correcting dilutional coagulopathy and controlling bleeding in an in vivo large-animal trauma model. In light of its suitability for more rapid administration than FFP, PCC merits further investigation as a therapy for dilutional coagulopathy in trauma and surgery. Keywords: blood, haemodilution; complications, haemorrhagic disorder; complications, trauma; fresh frozen plasma; prothrombin complex concentrate   FFP compared to PCC and fibrinogen for trauma patients. No mortality benefit. There was morbidity benefit (Injury, Int. J. Care Injured 42 (2011) 697–701)

First trauma study of 3-factor (profilnine SD on average 35 units/kg) showed good reversal of coagulopathy (J Trauma 2012;72(4):828)

Fibrinogen

ABC Score

Abstract from the EAST showed sens 87 spec 85       Case report (anaesthesia 2010;65:199)

European Bleeding in Trauma Guidelines

recommend teg not pt/ptt amongst other good recs

Factor VIIa

If the clot amplitude at 5 minutes is <=35 on rTEG (Crit Care Med 2011;39:2652)

Tranexamic Acid

Crash 2 (Lancet 2011) Review from J Trauma Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study showed mortality benefit, esp in patients who were massively transfused (Morrison Arch Surg 2011)

In AAA

Effect of Early Plasma Transfusion on Mortality in Patients with Ruptured Abdominal Aortic Aneurysm: Well MW, O’Neil AS, Callcut RA, et al. Surgery 2010;148:955–62.

Platelets

Old Platelets are bad from Kenji (Volume 71(6), December 2011, pp 1766-1774)

Arterial Lines

1 unit/cc of heparin, take air out of IV bag first.  Must have line open to air in order to zero.

risks:  thrombosis/embolism, distal ischemia, infection

the brachial artery has much higher rates of thrombosis

can use radial, ulnar, axillary, dorsalis pedis, femoral,

upper extremity wave form has a dichrotic cleft

SPV systolic pressure variation examines the min to max variation is one respiratory cycle.  The change down pressure is the 1st drop with inspiration.  The change u

A significant change down=inadequate preload, no change down =CHF

dominant change up=CHF or hypervolemia

In conclusion, there is no significant difference between heparinized and nonheparinized flush solutions for the maintenance of perioperative radial artery catheter patency. (Anesth Analg 2005;100:1117-1112)

and ICU a-lines (Intensive Care Medicine 1432-1238Volume 34, Number 2 / February, 2008)

MA of ultrasound showed benefit (Chest 2011;139;524-529)

Trick from Anaesthesia 2010

In patients on vasopressors, radial arterial lines underestimate central arterial pressure (I would posit the same phenomena in sick vasoconstricted trauma patients) (Crit Care Med 1998;26:1646)

Intraaortic Balloon Pump

Tracheostomy

Consider when > than 14 days of intubation are planned.

Risks include:

• Tracheoinnominate Artery Fistula (TIA)-causes severe airway bleeding which can be fatal.  Consider hyperinflating the cuff to tamponade bleeding as temporizing measure.  In differential of any bleeding >48 hours after placement.
• Tracheoesophageal Fistula (TEA)-may require methylene blue in esophagus to diagnose if not seen on endoscopy.  Consider barium swallow.  Esophagus will have air in it on x-rays.
• Tracheal Stenosis

Portex trach tube is far superior to the Shiley trach tube which comes in the Cook kit, and, at least to me, the superiority of Portex’s trach tube outweighs the superiority of the Cook/Shiley Blue Rhino PDT kit.  The solution may be that Portex is already marketing a ‘White Rhino’ kit in Europe, and we’re hoping to see it here soon, so that will allow us the best of both worlds.

 

Severe reactive airway disease: use pretreatment

Coagulopathy

 

Keep extra clamp to pull out dilator

 

Early may be better (Crit Care Med 2004 Vol 32 #8 1689-1693)

 

Change tubes over 4.5 pediatric endotracheal tube

 

 

Technique for Crash Trach (Injury 2008;39:375)

Percutaneous Tracheostomy

We tried the Ciaglia and the Fantoni techniques and we prefer the Ciaglia/ Blue Rhino set.

 

Changing a Perc Trach

1. Check the size currently in situ and ensure that you have the correct size and one size smaller, just in case. 2. Mentally walk through the procedure, like say oxygenate, deflate the cuff, remove and suction…….. 3. Demonstrate to all what a magnificent operation has taken place, that one can see with a light into the trachea and that the patient can easily breath through the hole.

there is no need for positive pressure then there is no need for a cuff, and I try to change tubes to uncuffed before the patient leaves ICU. It is pretty clear that cuffs do NOT prevent aspiration – we know that one factor in VAP is continuous microaspiration past the cuff, and we deliberately keep cuff pressure less than mucosal capillary pressures so a good vomit will go past the cuff anyway. Cuffs do interfere with swallowing, however because of pressure on the cricopharyngeus. I find that if I don’t aggressively change to uncuffed tubes before the patients goes to the ward the patient gets caught in a vicious cycle of ‘leave the cuff up to prevent aspiration ….. look he has failed his swallow test you had better leave the cuff up to protect his airway ….” and nobody every gets around to taking the rotten tube out.

 

Just below thryoid for incision. Can enter sub-cricoid

Cut trach tie 1/3 and 2/3 then put slit 1 cm down to pull end through

 

can put saline into angio to see if it sprays when pt ventilated

put finger in hole, use it to guide the needle

 

Details on technique by the man, Ciaglia (Chest 1996;110(3):762)

 

 

Perc Trach without Bronch (Chest 2004;126(3):869)

 

The use of the bronchoscope is felt by some to be mandatory but many including myself, Sedar, and some of the Intensivists in the Silvester series prefer to perform the procedure with the bronchoscope on standby only to be used if needed. We have developed a technique using a bronchoscopy adapter on the endotracheal tube through which we place a 5 mm Cooktube changer which extends 10 cm beyond the tip of the endotracheal tube allowing easy rescue of the air way if needed. The tube changer is small enough not to impair ventilation (important for ICP control) during the procedure or interfere with accessing the trachea and placing the tracheostomy. PT is now really a misnomer since most operators use a modified technique creating a 1.5–2 cm horizontal incision a fingers breadth below the cricoid cartilage. Blunt dissection is carried out to the anterior tracheal wall with a hemostat and gloved finger. Our preference is to leave the cuff on the endotracheal tube inflated as it is drawn back 8 cm from its original position.

We place the needle for canulation on the trachea while it is splinted by the cuff of the endotracheal tube. When the cuff passes under the gloved finger held on the trachea beside the needle, the needle is inserted and air is aspirated and the guide wire is passed, etc.

 

 

(Curr Opin in Crit Care 2005;11:326)

We buy the small Blue Rhino kit without the Shiley Trach tube, and use the Portex Trach tube separately.  I do not like the Shiley tube – if you don’t position it properly on the loading dilator, there is a gap between the tube and the dilator. I have had this rip on the tracheal ring, making it impossible to advance and having to get a new tube.  It just does not slide in nearly as easily as the Portex.  So, by unbundling, we are able to get the best of both worlds.  It does cause us to have to scurry around sometimes to make sure that all the things we need are present, but it is much more preferable than having to use a sub-standard Trach tube.  What bothers me is that I have many times talked to both the Cook and Shiley people about it – they each point a finger and blame the other company, then point the finger at me and tell me that we are doing something wrong because “nobody else complains about the trach tube!!”.  If the Blue Rhino were not so superior, I would stop using it also, based on their attitude!

Open Tracheostomy

Prep out to both shoulders up to chin and down to nipple line

Mark Thyroid, Cricoid and Sternal Notch

Incise from above notch to just below cricoid ~2.5 cm

Grab with pickups in tissue

Use coag setting on bovie to cut through fascia

Insert wheatleys

Go down to strap muscles using a small kelly or right angles to spread for the bovie

Switch to debakeys

Find isthmus of thyroid

Place straight clamp with jaws facing up. Put two kellys in jaws with concave facing in

cut with bovie or mets

Tie off with vicryl

Feel for depth of innominate

Deflate cuff

Make square cut, can mark with bovie

Johnson uses horizontal slit with two 45 degree extensions into ring

Insert dilator

Put obstructing cannula into trach

Grab cricoid with hook

Pull tube back

Put trach in horizontally and rotate

Close skin with two nylons

then suture trach through the plastic, not through the hole

Pull a drain gauze through

Get trach tray or suture Kit

Prep

Place table over patient’s waist and cover with drape

Hyperextend neck

Mark Cricoid and sternal notch. Entry point is usally two finger breadths above notch

Inject with lido c epi before setting up the kit to increase hemostasis

Incision

Spread with two mosquitoes all the way down to the trach

Feel for between 1st and 2nd ring

Deflate cuff and pull back to 18, you should feel the loss of resistance

Reinflate cuff

Put needle against trach

Put finger in hole to feel

Insert needle and withdraw until air bubbles

Hold cath and pull out needle

Reinsert syringe and verify placement

Advance wire, remove needle, dilate three times with small dilator

Put on white with dilator

From this point forward, always have knob in between your fingers

Dilate three times

Put on trach with inner cannula

Pull out wire, white, and dilator. May need kelly

Hold Trach

Put in inner cannula

Attach vent, look for return of expiratory

Inflate Cuff

After sutured, then pull ET tube

put iv bag between shoulder blades

put head in head ring

consider laryngoscopy

reinflate cuff after pulling back

Laryngoscope. 2005 Oct;115(10 Pt 2):1-30. Related Articles, Links Endoscopic percutaneous dilatational tracheotomy: a prospective evaluation of 500 consecutive cases. Kost KM. Department of Otolaryngology, McGill University, Montreal, Quebec, Canada. kmkost@yahoo.com OBJECTIVES/HYPOTHESIS: An evaluation of 500 adult, intubated, intensive care unit patients undergoing endoscopic percutaneous tracheotomy using the multiple and single dilator techniques was conducted to assess the feasibility and safety of the procedure as it compares with surgical tracheotomy. Endoscopy was used in all cases and evaluated as an added safety measure in reducing complications. STUDY DESIGN: A prospective evaluation of endoscopic percutaneous dilatational tracheotomy in 500 consecutive adult, intubated intensive care unit patients. METHODS: Between 1990 and 2003, endoscopically guided percutaneous dilatational tracheotomy (PDT) was performed in 500 consecutive adult, intubated patients in the intensive care units (ICU) of three tertiary care adult hospitals. The first 191 patients underwent PDT using the Ciaglia Percutaneous Tracheostomy Introducer Kit (Cook Critical Care Inc., Bloomington, Indiana) and in the remaining 309 patients the Ciaglia Blue Rhino Single Dilator Kit (Cook Critical Care Inc., Bloomington, Indiana) was used. The procedure was contraindicated in the following situations: 1) children, 2) unprotected airway, 3) emergencies, 4) presence of a midline neck mass, 5) inability to palpate the cricoid cartilage, and 6) uncorrectable coagulopathy. The following parameters were recorded preoperatively: age, sex, diagnosis, American Society of Anesthesia (ASA) class, body mass index (BMI), and number of days intubated. Recorded hematologic parameters included hemoglobin (Hgb), platelets, prothrombin time (PT), partial thromboplastin time (PTT), and the international normalized ratio (INR) since it became available in 1998. All patients were ventilated on 100% oxygen and vital signs were continuously monitored. Tracheotomy was carried out under continuous endoscopic guidance using a series of graduated dilators in the first 191 cases, and a single, tapered dilator in the remaining 309 patients. The preoperative data on each patient, along with the type of dilator used, the size of the tube, the intraoperative and postoperative complications, and blood loss information were recorded prospectively and maintained in a computer spreadsheet. Univariate analyses were used in each group separately for each type of dilator to assess the risks of a complication within subgroups defined by each parameter/characteristic, and the statistical significance assessed with a chi test, or Fisher exact test. RESULTS: The total complication rate was 9.2% (13.6% in the multiple dilator group, and 6.5% in the single dilator group), with more than half of these considered minor. Overall, the two most common complications were oxygen desaturation in 14 cases and bleeding in 12 cases. The absence of serious complications such as pneumothorax and pneumomediastinum are attributable to the use of bronchoscopy. There was no significant association between the rate of complications and age, gender, ASA, weeks intubated, tracheostomy tube size, Hgb levels, platelets, PT, PTT, or INR. There was a statistically significant relationship between experience and the likelihood of complications in the multiple dilator group (P < .0001), with a higher rate of complications in the first 30 patients (40%) compared with 8.7% in the remaining 161 patients. This relationship did not exist for the first 30 patients in the single dilator group. Patients with a BMI of 30 or higher experienced a significantly greater (P < .05) number of complications (15%), compared with an 8% complication rate in patients with a BMI of less than 30. This risk was even more significant for patients with a BMI of 30 or greater who were also in ASA class 4 (11/56 or 20%) (P < .02). CONCLUSIONS: Endoscopic PDT is associated with a low complication rate and is at least as safe as surgical tracheotomy in the ICU setting. Bronchoscopy significantly decreases the incidence of complications and should be used routinely. While embraced by critical care physicians, endoscopic PDT has been infrequently performed by otolaryngologists. As the airway experts, otolaryngologists are in the best position to learn and teach the procedure as it should be done. Publication Types: 2006/2/14, Marek Nalos <mareknalos@mediclub.cz>: > Chest. 2004 Aug;126(2):547-51. Related Articles, Links Percutaneous tracheostomy is safe in patients with severe thrombocytopenia. Kluge S, Meyer A, Kuhnelt P, Baumann HJ, Kreymann G. Department of Medicine, University Hospital Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. skluge@uke.uni-hamburg.de STUDY OBJECTIVES: Severe thrombocytopenia has been described as a contraindication for percutaneous tracheostomy (PT). The objective of this study was to assess the safety of PT in mechanically ventilated patients with severe thrombocytopenia (defined by a platelet count of < 50 x 10(9) cells/L). DESIGN: Retrospective, single-center cohort study. SETTING: Medical ICU of the University Hospital Hamburg-Eppendorf, Germany. PATIENTS: Forty-two medical patients with acute respiratory failure and severe thrombocytopenia. INTERVENTIONS: Bedside PT under bronchoscopic guidance using the Griggs guidewire forceps technique.Measurements and main results: The mean (+/- SD) intubation time prior to undergoing PT was 6.7 +/- 3.9 days (range, 1 to 20 days). The mean platelet count was 26.4 +/- 11.6 x 10(9) cells/L (range, 1 x 10(9) to 47 x 10(9) cells/L). The median transfusion of platelets before the procedure in 40 of the 42 patients was 6 +/- 2.5 U (range, 3 to 12 U). Twenty-two patients (52%) had an additional coagulopathy (activated partial thromboplastin time [APTT], > 40 s; international normalized ratio, > 1.5). PT was safely performed in all 42 patients. Only two (5%) patients developed major postprocedural bleeding complications that required suturing. Both of these patients had an elevated APTT due to heparin therapy. CONCLUSIONS: When performed by experienced personnel, PT with bronchoscopic guidance has a low complication rate in patients with severe thrombocytopenia, provided that platelets are administered beforehand. However, in order to minimize bleeding complications heparin infusions should be temporarily interrupted during the procedure. PMID: 15302743 [PubMed - indexed for MEDLINE] Chest. 2003 May;123(5):1595-602. Related Articles, Links Comment in: Chest. 2003 May;123(5):1336-8. Percutaneous dilatational tracheostomy in the ICU: optimal organization, low complication rates, and description of a new complication. Polderman KH, Spijkstra JJ, de Bree R, Christiaans HM, Gelissen HP, Wester JP, Girbes AR. Departments of Intensive Care, University Medical Center, Amsterdam, the Netherlands. k.polderman@tip.nl STUDY OBJECTIVES: To assess short-term and long-term complications of bronchoscopy-guided, percutaneous dilatational tracheostomy (PDT) and surgical tracheostomy (ST) and to report a complication of PDT that has not been described previously. DESIGN: Prospective survey. SETTING: University teaching hospital. PATIENTS: Two hundred eleven critically ill patients in our ICU. INTERVENTIONS: PDT was performed in 174 patients, under bronchoscopic guidance in most cases. ST was performed in 40 patients. RESULTS: No procedure-related fatalities occurred during PDT or ST. The incidence of significant complications (eg, procedure-related transfusion of fresh-frozen plasma, RBCs, or platelets, malpositioning or kinking of the tracheal cannula, deterioration of respiratory parameters lasting for > 36 h following the procedure, or stomal infection) in patients undergoing PDT was 4.0% overall and 3.0% when bronchoscopic guidance was used. No cases of paratracheal insertion, pneumothorax, pneumomediastinum, tracheal laceration, or clinically significant tracheal stenosis occurred in patients undergoing PDT. We attribute this low rate of complications to procedural and organizational factors such as bronchoscopic guidance, performance by or supervision of all PDTs by physicians with extensive experience in this procedure, and airway management by physicians who were well-versed in (difficult) airway management. In addition, an ear-nose-throat surgeon participated in the procedure in case conversion of the procedure to an ST should become necessary. We observed a complication that, to our knowledge, has not been reported previously. Five patients developed intermittent respiratory difficulties 2 to 21 days (mean, 8 days) after undergoing PDT. The cause turned out to be the periodic obstruction of the tracheal cannula by hematoma and the swelling of the posterior tracheal wall, which had been caused by intermittent pressure and chafing of the cannula on the tracheal wall. In between the episodes of obstruction, the cannula was open and functioning normally, which made the diagnosis difficult to establish. CONCLUSIONS: Bronchoscopy-assisted PDT is a safe and effective procedure when performed by a team of experienced physicians under controlled circumstances. The intermittent obstruction of the cannula caused by swelling and irritation of the posterior tracheal wall should be considered in patients who develop unexplained paroxysmal respiratory problems some time after undergoing PDT or ST.

Trach emergencies

Hyperextend the neck as first step

Incise as big as you need all the way down the midline

CUT TO AIR bleeding is a good thing, it tells you your patient is still alive

Meta Analysis of Early Trach shows reduced ICU time and Vent days (BMJ 2005 Griffiths J, Barber VS, Morgan L)

Canadian Journal of Anesthesia 54:321-322 (2007) Use of the “Aretube” to facilitate ventilation during percutaneous tracheostomy

Tracheostomy protocol (Crit Care Med 2008;36:1742)

The PWA is performed by the nursing and respiratory therapy staff and determines whether a patient’s level of ventilatory support is appropriate for weaning attempts (i.e., Fio2 <=0.5, positive end-expiratory pressure <=8 cm H2O, minute volume <15 L/min) and whether acute physiologic derangements (i.e., increased intracranial pressure, significant hemoptysis, active gastrointestinal hemorrhage, evolving myocardial infarction, elevated minute ventilation) might preclude successful weaning. Ventilator settings are then adjusted to provide a continuous positive airway pressure of 5 cm H2O and Fio2 = 0.4. If after 2 mins patients manifest no evidence of respiratory or hemodynamic derangement (i.e., dyspnea, use of accessory muscles, SpO2 <92%, tachypnea, tachycardia, bradycardia, hypotension), SBT is performed. Patients displaying evidence of respiratory or hemodynamic distress during this 2-min trial are categorized as PWA failures and returned to pretrial ventilatory support. During SBT, patients receive minimal ventilatory support (pressure support 5–8 cm H2O, positive end-expiratory pressure 5 cm H2O, Fio2 = 0.4) for 30 mins. Patients exhibiting signs of respiratory or hemodynamic distress are categorized as SBT failures and returned to pretrial ventilatory support. Patients passing the SBT are considered extubation candidates. SBT results are conveyed to the physician staff responsible for decision for extubation. Timing of extubation following successful SBT completion is at the discretion of the physician staff.

Use of ultrasound in the perc trach procedure

Critical Care 2011, 15:R67

perc trach ultrasound Critical Care 2011, 15:147

Trach Emergencies

patent upper airway

post-laryngectomy

Extracorporeal Support (ECMO) and Bypass

Two modes

venousarterial provides cario and pulmonary support

venous-venous provides only respiratory support

venous-venous is usually done with inflow to pump from IVC and blood retrun via the femoral vein

Bronchoscopy

simulator online

http://www.bronchoscopy.org/ for training

and maybe even better

http://www.thoracic-anesthesia.com/?page_id=2&langswitch_lang=en

need 2mm larger ET tube than diameter of scope, so 8mm tube to use adult size bronchoscope

Procedure from Practical Bronchoscopy

Some bronchoscopists prefer to face the sitting or lying patient whilst others stand behind the head of the lying               Of patient (Fig. 3.7). Face to face contact with the frontal approach generally proves valuable to maintain rapport between patient and bronchoscopist. An advantage of standing behind the head of the supine patient is that the spatial orientation of the bronchial tree is then the same for both flexible and rigid bronchoscopes, which may be of importance for bronchoscopists who practise both methods but have difficulty in transposing images.

Fibrescopy procedure

The patient is seated comfortably with legs horizontal and trunk and head supported at 30‑45′ with a pillow under the head. The bronchoscopist stands to the right of the couch and the assistant behind the patient’s head.

Lignocaine solution (4 or 10%) is sprayed from an atomizer into each nostril, the fauces and posterior pharyngeal wall, the patient having been first warned that the initial effects are an unpleasant stinging and taste. Within 2‑3 minutes the fibrescope lubricated with lignocaine gel can be introduced into the nose or mouth. Once the bronchoscope has passed through the nose or mouth, supplemental oxygen can be given through a nasal cannula into the unoccupied nostril.

The bronchoscopist should wear a clean gown and disposable gloves. If the gloves have been dusted with powder this must first be washed off to prevent starch granules contaminating the trap specimen and causing confusion in interpretation of the speci­ mens at microscopy.

The fibrescope should be inspected and if necessary the lens cleaned with sterile gauze moistened with sterile saline. The flexible fibrescope is a delicate and expensive apparatus. It must at all times be handled with care to avoid damage to the fibres. Knocking the shaft or tip against furniture and bending or kinking the shaft or tip with undue force must be avoided. The central channel and the polythene connecting tube should be flushed by aspirating sterile saline. To reduce fogging the distal lens can be wiped with silicone or soapy water. The fibrescope shaft should be lubricated with sterile 2% lignocaine jelly and some of this jelly can also be applied into the nostril through which the instrument is to be passed.

The technique of holding the fibrescope depends on the type of instrument available. The Olympus type is most widely used in Britain and can be held and operated by either the left or the right hand (Fig. 3.8). The body of this instrument is held by the 2nd, 3rd and 4th fingers and palm and the control knob can then be moved up and down by the thumb. The index finger is placed near the proximal end of the suction channel to seal it for aspiration as and when necessary. Rotation of the tip is achieved by rotating the wrist and thus the whole instrument (Fig. 3.9). The free hand is used to hold steady, advance and withdraw the shaft as well as to manoeuvre the biopsy forceps and cytology brushes to their targets (Fig. 3. 10). This can greatly reduce nasal discomfort for the patient.

The Machida type of fibrescope is held in the left hand reserving the right hand to operate the various handles at the proximal end as well as supporting, advancing and withdrawing the shaft of the fibrescope. Angulation and rotation of the tip are both achieved by rotating the proximal eyepiece which twists the distal end to the right and anti­clockwise twists it to the left. Rotation can also be achieved by rotating the left wrist.

For all types and makes of instrument the bronchoscope tip is inserted gently into the nostril under direct vision and passed into the widest part of the nasal passages. This is usually the inferior meatus between the inferior turbinate and the floor of the nose. Lignocaine does not abolish pressure sensitivity and so the bronchoscope should not be forced as this will cause discomfort. The flexible tip of the bronchoscope is its widest part and once this has passed through any passage the shaft will follow more easily. If the bronchoscope will not pass comfortably through either nasal passage then it should be inserted through the mouth using the guard as described.

Once the posterior pharyngeal wall is reached the fibrescope is angulated downwards following the shape of the pharynx and into the oropharynx behind the uvula. At this stage it should be possible to see the epiglottis and the glottis in the distance. It may be necessary to aspirate secretions obscuring the view. Care should be taken to ensure that the shaft of the instrument is straight and the patient’s chin well forward. Asking the patient to protrude his tongue or to swallow may also help to reveal the epiglottis.

Once the epiglottis has been identified the glottis is usually visible behind and beyond it. If difficulty is encountered in getting behind the epiglottis it may be possible to pass the fibrescope tip laterally and posteriorly alongside the epiglottis and then turn the tip in medially to curl over onto the dorsal surface of the epiglottis. The glottis and the vocal cords are sensitive areas and care should be taken to avoid undue irritation by the bronchoscope tip whilst anaesthetizing this area. Watch for the effects of cardiac dysrhythmias induced by vagal stimulation.

Next, vocal cord mobility should be checked during normal inspiration and expiration by asking the patient to adduct his cords in saying ‘see’. Inequality of movement of the cords suggests recurrent laryngeal nerve palsy. The patient should be warned that the next step will cause coughing. This occurs as the vocal cords are anaesthetized by injecting 2 ml of 4% lignocaine (80 mg) onto them in their adducted position via the central channel of the fibrescope.

For purpose of regional anaesthesia via the fibrescope lignocaine should be drawn up as 2 ml aliquots in 5 ml syringes with 3 ml of air in the syringe. The bronchoscope should be positioned with the suction channel uppermost so that the local anaesthetic is injected first and flushed through the central channel by the following air from the syringe.

Two or three minutes are allowed for the lignocaine to have maximum effect and this time should be spent examining the pyriform fossae and the area between the vocal cords and the ary‑epiglottic folds. During deep inspiration 2 ml of 2% lignocaine (40 mg) is next injected through the vocal cords into the trachea. The fibrescope tip should be quickly withdrawn a few centimetres during the coughing which will follow. Another 2 ml of the 2% lignocaine is usually required to anaesthetize the trachea adequately.

Before the fibrescope is inserted between the cords into the trachea the patient must be warned that this will make him cough, cause transient breathlessness and that he should not attempt to speak. The patient is advised to resist the impulse to take large breaths but rather to continue with shallow breaths which he should be reassured are sufficient.

During quiet inspiration the bronchoscope is passed gently between the cords through the posterior part of the glottis where the opening is the widest (Fig. 3M). The patient should be instructed that although the sensation is odd, he can breathe and swallow normally. A minute or so should be allowed for the patient to become accustomed to the presence of the fibrescope

the trachea. Further boluses of 2% lignocaine may be required if much coughing occurs.

The trachea should be inspected for the appearance of the mucosa and abnormally increased or decreased mobility of the walls should be noted. Similarly the carina should be examined for its sharpness and mobility. Normally the carina becomes shorter and thicker during coughing. Abolition of this variability may indicate infiltration by carcinoma or enlargement of the s ubcarinal lymph glands.

Further boluses of 2 ml of 2% lignocaine are injected through the suction channel as necessary but the total dose administered should be kept to a minimum by avoiding contact with the bronchial walls thus reducing irritation. If the coughing induced is more than slight it is worth withdrawing the bronchoscope and injecting more lignocaine because once coughing is allowed to become severe it is difficult to control. There is considerable variation in sensitivity of the bronchial mucosa between patients and certainly smokers cough more easily and excessively. Encouragement and keeping the patient informed of what is happening with instructions to keep both eyes open will help to make the examination more comfortable for the patient and easier for the operator.

Both right and left bronchial trees must be systematically examined even if the chest radiograph suggests a unilateral lesion. Opinions vary as to whether the normal or abnormal side should be examined first. It is recommended that the normal side should be inspected first. If examined last it is more likely to be inadequately explored as both patient and bronchoscopist may be tired and secretions and blood may have spilled from the abnormal side following inspection and sampling.

Right Lung

To examine the right bronchial tree, the black notch in the visual field is turned to the right side of the patient. This ensures that the fibrescope tip has maximum manoeuvrability for examination of the bronchi on this side. The right upper lobe orifice usually lies just below the carina on the opposite lateral wall; it leads off at an angle of 80‑90′. It is helpful to give an extra 2 ml of 2% lignocaine into the upper lobe before it is inspected as the previous doses of lignocaine frequently fail to reach it due to its angulation. The orifice is now entered and the segments and subsegments are examined. The anterior segment which lies ventrally and the posterior segment lying dorsally are relatively easy to inspect without too much manipulation of the fibrescope tip. The apical segmental bronchus is more difficult to enter. To help this manoeuvre, the patient is asked to take a few deep breaths and then to hold the breath at full inspiration when the apical segmental orifice will be more easily seen with the tip of the fibrescope bent maximally upwards towards the head.

The right middle lobe bronchus arises ventrally from the intermediate bronchus and extends obliquely downwards. The notch in the visual field of the fibrescope should be placed in the anterior position to aid manoeuvrability in this bronchus which can usually be inspected to subsegmental level.

The fibrescope is then withdrawn back into the intermediate bronchus, the notch rotated dorsally until the orifice of the apical, segment of the right lower lobe is seen lying at the same level as the middle lobe. This segmental bronchus branches at 90′ from the intermediate bronchus and once again entry into it can be aided by asking the patient to hold the breath in full inspiration.

The remaining segmental orifices of the right lower lobe lie several centimetres distal to the apical segment. They all extend downwards and really are an extension of the main bronchus so little difficulty is usually encountered in entering them.

Left lung

After withdrawing the fibrescope back to the carina, the left bronchial tree is next examined by having the notch in the visual field rotated to the left side of the patient. The left main bronchus is longer than the right and also deviates more laterally or horizontally in the erect subject. The secondary carina between the upper and lower lobe orifices is a useful landmark.

The lingular bronchus is usually an extension of the upper lobe bronchus and descends downwards dividing into superior and inferior segments.

The upper division of the upper lobe bronchus is next examined by withdrawing the fibrescope back into the upper lobe bronchus and turning its tip upwards (headwards) with maximum flexion. This is perhaps the most difficult bronchus to enter. This can be made easier by asking the patient to take a deep breath. The anterior and apico­posterior segments are then examined in turn.

The fibrescope is withdrawn back to the secondary carina and the left lower lobe is examined by rotating the notch in the visual field towards it. The apical segmental bronchus arises dorsally almost at the level of the secondary carina. It is located by turning the notch posteriorly and again if difficulty is encountered in entering it, the patient is asked to hold the breath in deep inspiration. The basal segments of the left lower lobe should present no difficulty to examination, noting that the anterior and mediobasal segments are usually combined into a single orifice.

Examination of an average ‘normal’ tracheobronchial. tree has been described. Variations in the branching of the bronchi are frequently encountered and should be borne in mind if apparent abnormalities occur, especially if the mucosa looks normal. At more peripheral levels, individual bronchi or combinations of bronchial orifices cannot be recognized by individual appearances alone because they usually look alike and variations are common. They can only be identified by remembering the route the bronchoscope has taken to get to that point in the bronchial tree. Occasionally it may be necessary to retrace the route to a more central and recognizable bronchus.

A routine of systematic examination of the airways should be adopted to prevent mistakes through omission. In addition to the bronchial tree an orderly inspection of the extrathoracic airways must also be completed. It is valuable to re‑inspect bronchi as the fibrescope is being withdrawn to confirm observations made when the instrument was advancing.

Manipulating the fibrescope

The ability to use a fibrescope comes only with practice. Although many useful hints are often given there is no substitute for time spent handling the instrument. The period of time that the novice can spend on a patient is limited and it can be helpful to use the various lung models available. Eventually, operating the instrument should become a subconscious act, like driving a motor car. The experienced bronchoscopist comes to know the position and orientation of the fibrescope tip as a form of extended proprioception, just as a good motorist knows the limits of the front or back of his car. Similarly guiding the instrument with coordinated movements of the wrist, thumb and fingers of the right hand as well as the forward and backward motion of the left hand will begin to occur at a subconscious level.

ThoracicAnesthesia.com is an internet based education, information, and reference service for issues related to Anesthesia for Thoracic Surgery.

This service is a free not-for-profit continuing medical education activity which is offered to all practitioners of Anesthesia and related areas of Medicine and Surgery. By clicking on the “Bronchial Anatomy Quiz” tab readers can complete a needs assessment of their knowledge of tracheo-bronchial anatomy

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Best Review of Reversal of coumadin

another pretty good review

Pts did better with PCC reversal in terms of outcome and hematoma enlargement (Cerebrovasc Dis. 2011;31(2):170-6. Epub 2010 Dec 3.)

Patients on Plavix and ASA do worse than patients on ASA alone (World Neurosurg. 2011 Jul-Aug;76(1-2):100-4; discussion 59-60.)

Semin Neurol. 2010 Nov;30(5):565-72.

Anticoagulated Patients

All patients on warfarin should have an INR performed, and a CT scan should be done in most anticoagulated patients. All supratherapeutically anticoagulated patients, as well as any anticoagulated patient with a traumatic CT abnormality, should be admitted for neurologic observation and consideration given to short term reversal of anticoagulation. Routine repeat CT scanning at 12 to 18 hours or when even subtle signs of neurologic worsening occur is a strong recommendation. A multi-institutional, prospective trial using these guidelines would be a first step toward demonstrating improved outcomes in the anticoagulated patient population after head trauma. Semi-SR (J Trauma 2006;60(3):553)

Vitamin K 24 hours

FFP 6 hours

VIIa 3-4 minutes

Coumadin bleeds into head and surg site

heparin generally does not cause much bleeding, though it can

protamine

protamines do not work on fondaparinex

asa is irreversible, but out of serum in 45 minutes, so give platelets

dDAVP will reverse ASA effect

Plavix causes moderate to severe bleeding

irreversibly alters platelets but stays in serum for 8 hours, so can not give more PLT

dDAVP does not work

Emergency Reversal of Anticoagulation after ICH (Stroke 1992;23:972)retrospec 17 pts ~5 hrs with PCC; ~7.3 hrs with FFP 10 cc of PCC equiv to 600 FFP pts received on average 0.43 cc (25.8 IU) /kg of PCC or 8 cc/kg of FFP

Timing of FFP and rapid correction of coagulopathy in ICH (Stroke 2006;37:151) Odds of reversal of INR in 24 hours was directly related to how quickly the FFP was administered. Each delay of 30 minutes to first dose lead to 20% decrease in odds of successful reversal

Hematoma growth and outcome in pts with ICH on anticoags (stroke 2006;37:1465) PCC worked better than FFP or Vit K 3 groups 1 PCCS +-ffp and vak 2 FFP +- vak 3 VAK alone retrospective PCC was better but only compared to pts who were not reversed in 2 hrs by other means

Ultra-early hemostatic therapy for primary intracerebral hemorrhage (Can J Neurol Sci 2005;Suppl. 2-S31-S37) review article of factor VII

Phase II trial of VIIa in non-coagulopathic patients (NEJM 2005;352:777) Mayer Trial 7% vs 2% thromboembolic complications ? if this was combined endpoint would it still be as bad

VIIa to reverse coagulopathy in pts going to surgery (Neurosurg 2003;53:34)

Best Review article of oral anticoag assoc ICH (Stroke 2006;37:256)

Hematoma expansion occurs in ~40% of pts in early hours following onset

Vitamin K It takes at least 2 to 6 hours, and often more than 24 hours,to achieve an effective response to vitamin K administration, although vitamin K alone is often inadequate to completely normalizethe international normalized ratio in that time frame. Concomitantadministration of coagulation factors is therefore required.Nevertheless, because of the short HLT of transfused coagulationfactors (factor II: 48 to 60 hours; factor VII: 5 to 6 hours;factor IX: 20 to 24 hours; factor X: 24 to 48 hours), the administrationof 5 to 20 mg of vitamin K is necessary to achieve a sustainedreversal of anticoagulation.42–46 The effect of vitaminK is more rapid when given intravenously. Although there havebeen concerns regarding allergic and anaphylactic reactionsto intravenous vitamin K, the risk of this complication appearsto be quite low,47 with an incidence in one study of 3 per 10000 doses (95% CI: 0.04 to 11 per 10 000 doses).48 Subcutaneousadministration may be safer but does not correct the INR asrapidly or as reliably as intravenous use.49

Fresh Frozen Plasma FFP contains all coagulation factors in a nonconcentrated form; hence, to achieve effective hemostasis a large volume (up to several liters) is required.9,50,51 In principle, 1 mL of FFP/kgbody weight increases the levels of coagulation factors by 1to 2 International Units (IU)/dL.52 The traditional dose of10 to 15 mL of plasma/kg body weight may have to be exceededin massive bleeding.53 However, the standard of an FFP unitis based on its factor VIII content; the actual levels of vitaminK-dependent coagulation factors are not specified and vary considerably.50,54Our routine experience, and that of others, suggests that FFPvolumes required to reduce the INR below 1.4 may vary considerably:for example, between 800 and 3500 mL.39,55

FFP requires compatibility testing and thawing before transfusion.Furthermore, the large volume required and a rapid transfusionrate can lead to circulatory overload. In cases of life-threateningbleeding such as ICH, or in patients with impaired cardiac function,FFP is therefore a less than ideal treatment option. In addition,FFP transfusion is associated with several potential adversereactions, including transfusion-related acute lung injury, blood-borne infection, citrate toxicity, and allergic reactions.56,57

PCC PCC contain coagulation factors VII, IX, X, and prothrombinas well as proteins C, S, and Z in a concentrated form, and,unlike FFP, can be given without waiting for compatibility testingand thawing. The potency of PCC is expressed as factor IX contentin IU, varying between preparations,58 and a dose consists of50 to 150 mL of reconstituted product. Based on data obtainedfrom patients with hemophilia B, a dose of 1 IU of factor IX/kgbody weight increases the level of plasma factor IX by 1 IU/dL.59

Studies of small numbers of patients suggest that PCC corrects a prolonged INR more rapidly than FFP.38,50,60 However, a retrospectivestudy comparing vitamin K, FFP, PCC, and no treatment in 151patients with OAT-ICH, found no difference in 90-day mortality.61The main concerns with PCC-use focus on the potential to inducethrombosis and disseminated intravascular coagulation.62–66

10 mg of Vit K/50 U/kg of PCC or 15 cc/kg of FFP

Time Window for Treatment In SICH, evidence suggests that significant hematoma expansion tends to occur during the first 4 hours after onset, and thisis likely to be the critical time window for a hemostatic treatment.30,37In OAT-ICH, the natural course of hematoma expansion is probablymore prolonged, perhaps up to 24 or 48 hours,1,18,79 raisingthe possibility that patients presenting as late as 24 hours(or even later) may benefit from effective hemostatic treatment.

Dose Regimen Administration of an effective hemostatic agent at an earlystage of SICH appears to accelerate the formation of a fibrinclot, which stops the bleeding.37 In this case, it seems thata single dose is sufficient. However, in OAT-ICH, the underlyingcoagulopathy may require a higher dose or repeated dosing.

Monitoring Hemostasis During the Reversal of Anticoagulant Effect PT-INR is routinely used for regulating OAT as well as monitoring the reversal of its anticoagulant effect. The test is sensitive to decreased levels of factor VII and factor X, and prothrombin, but not to decreased levels of factor IX.50,53,80,51,75 BecauseFFP contains variable amounts of factor IX, the correction ofthe INR with FFP may not be accompanied by a correction of factorIX levels.50 For example, Makris et al found that administrationof 800 mL FFP decreased the mean INR from 6.73 to 2.38, whereasthe mean factor IX levels were essentially unchanged (from 26.45IU/dL to 27.36 IU/dL).50 Thus, the INR may be normalized butthe patient remains at risk of further bleeding.

The use of the INR for monitoring patients treated with rFVIIa is also problematic. Pharmacological doses of rFVIIa will always lower the INR regardless of the levels of other coagulation factors. Hence, when monitoring the reversal of anticoagulant effect, INR values should be interpreted with caution as they might not reflect the actual status of all vitamin K-dependent coagulation factors.53,51

Thromboelastography may provide a more meaningful measure of coagulation status. This system records a profile of clot formationin whole blood, providing an overall picture of hemostatic function.81,76Based on 7 patients with central nervous system bleeding duringOAT who were treated with rFVIIa, Sørensen and colleagues showed that it may be feasible to use thromboelastography to monitor hemostatic status.71 Nevertheless, more data are neededto prove the clinical utility of the measure.

Does VIIa cause hydrocephalus in ICH pts (Neurology 2006;67:1096)

Br J Surg. 1993 Jun;80(6):723-4. Links Use of desmopressin to prevent bleeding complications in patients treated with aspirin. Flordal PA, Sahlin S. Department of Surgery, Karolinska Institute, Danderyd Hospital, Sweden. Aspirin induces a haemorrhagic diathesis that persists for at least 1 week after discontinuation of the drug. The effect of the vasopressin analogue desmopressin was studied in 12 patients treated with aspirin who were undergoing cholecystectomy. Desmopressin was given to six of these patients. There were five postoperative bleeding complications; all occurred in patients who had not received desmopressin (P < 0.05). The bleeding time was prolonged in aspirin-treated patients and normalized by desmopressin (P < 0.05). Desmopressin can be used safely to prevent bleeding induced by aspirin.

Anesth Analg. 1997 Dec;85(6):1258-67. Links Drugs to minimize perioperative blood loss in cardiac surgery: meta-analyses using perioperative blood transfusion as the outcome. The International Study of Peri-operative Transfusion (ISPOT) Investigators. Laupacis A, Fergusson D. Clinical Epidemiology Unit, Loeb Research Institute, University of Ottawa, Canada. alaupacis@Lri.ca Concern about the side effects of allogeneic red blood cell transfusion has increased interest in methods of minimizing perioperative transfusion. We performed meta-analyses of randomized trials evaluating the efficacy and safety of aprotinin, desmopressin, tranexamic acid, and epsilon-aminocaproic acid in cardiac surgery. All identified randomized trials in cardiac surgery were included in the meta-analyses. The primary outcome was the proportion of patients who received at least one perioperative allogeneic red cell transfusion. Sixty studies were included in the meta-analyses. The largest number of patients (5808) was available for the meta-analysis of aprotinin, which significantly decreased exposure to allogeneic blood (odds ratio [OR] 0.31, 95% confidence interval [CI] 0.25-0.39; P < 0.0001). The efficacy of aprotinin was not significantly different regardless of the type of surgery (primary or reoperation), aspirin use, or reported transfusion threshold. The use of aprotinin was associated with a significant decrease in the need for reoperation because of bleeding (OR 0.44, 95% CI 0.27-0.73; P = 0.001). Desmopressin was not effective, with an OR of 0.98 (95% CI 0.64-1.50; P = 0.92). Tranexamic acid significantly decreased the proportion of patients transfused (OR 0.50, 95% CI 0.34-0.76; P = 0.0009). Epsilon-aminocaproic acid did not have a statistically significant effect on the proportion of patients transfused (OR 0.20, 95% CI 0.04-1.12; P = 0.07). There were not enough patients to exclude a small but clinically important increase in myocardial infarction or other side effects for any of the medications. We conclude that aprotinin and tranexamic acid, but not desmopressin, decrease the number of patients exposed to perioperative allogeneic transfusions in association with cardiac surgery. Implications: Aprotinin, desmopressin, tranexamic acid, and epsilon-aminocaproic acid are used in cardiac surgery in an attempt to decrease the proportion of patients requiring blood transfusion. This meta-analysis of all published randomized trials provides a good estimate of the efficacy of these medications and is useful in guiding clinical practice. We conclude that aprotinin and tranexamic acid, but not desmopressin, decrease the exposure of patients to allogeneic blood transfusion perioperatively in relationship to cardiac surgery.

Anesth Analg. 2004 Mar;98(3):578-84, table of contents. Links Prophylactic treatment with desmopressin does not reduce postoperative bleeding after coronary surgery in patients treated with aspirin before surgery. Pleym H, Stenseth R, Wahba A, Bjella L, Tromsdal A, Karevold A, Dale O. Departments of Anesthesiology, St Olav University Hospital, Trondheim, Norway. hilde.pleym@stolav.no The synthetic vasopressin analog desmopressin has hemostatic properties and may reduce postoperative bleeding after coronary artery bypass grafting (CABG). A study on the effects of recent aspirin ingestion on platelet function in cardiac surgery showed a greater impairment of platelet function in patients treated with aspirin <2 days before the operation. We evaluated the effects of desmopressin on postoperative bleeding in CABG patients who were treated with aspirin 75 or 160 mg until the day before surgery. The study was a prospective, randomized, double-blinded, placebo-controlled, parallel group trial. One-hundred patients were included and divided into two groups. One group received desmopressin 0.3 micro g/kg and the other received placebo (0.9% NaCl) after the neutralization of heparin with protamine sulfate. Postoperative blood loss was recorded for 16 h. The mean (SD) bleeding was 606 (237) mL in the desmopressin group and 601 (301) mL in the placebo group (P = 0.93), representing no significant difference (95% confidence interval, -107 to 117 mL). We conclude that desmopressin does not reduce postoperative bleeding in CABG patients treated with aspirin until the day before surgery. IMPLICATIONS: Continuation of aspirin until the day before coronary artery bypass grafting may increase postoperative bleeding. The administration of desmopressin to these patients after the neutralization of heparin with protamine sulfate does not reduce postoperative bleeding.

Blood. 2003 Dec 15;102(13):4594-9. Epub 2003 Aug 14. Links Desmopressin antagonizes the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors and aspirin. Reiter RA, Mayr F, Blazicek H, Galehr E, Jilma-Stohlawetz P, Domanovits H, Jilma B. Department of Clinical Pharmacology, University of Vienna, Wahringer Gurtel 18-20, A-1090 Vienna, Austria. Whereas bleeding is the most frequent adverse event encountered in patients receiving glycoprotein (GP) IIb/IIIa inhibitors, there are currently no recommendations for how to treat such patients. The present study tested the hypothesis that infusion of desmopressin (DDAVP) reverses the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors (+l-aspirin). Study group 1 (10 healthy volunteers) received a DDAVP infusion to establish dose-response curves for the in vitro inhibition of platelet function by eptifibatide, abciximab, and tirofiban together with l-aspirin before and after DDAVP. In a randomized, double-blind, placebo-controlled, crossover study (group 2) volunteers received l-aspirin and a standard eptifibatide infusion. Thereafter, DDAVP or a physiologic saline infusion was given over 30 minutes. In group 1, all GPIIb/IIIa inhibitors prolonged collagen-epinephrine (CEPI) and collagen-adenosine diphosphate (CADP) closure times (CTs), measured with the platelet function analyzer 100 (PFA-100). DDAVP caused a shift in the concentration response curves to the right of all 3 GPIIb/IIIa inhibitors. In group 2, DDAVP accelerated the normalization of CADP-CT and CEPI-CT after the stop of eptifibatide infusion with a maximum effect at 1.5 hours to 2 hours. In contrast, CEPI-CT remained above normal in the placebo group for more than 4 hours. In conclusion, DDAVP accelerates normalization of the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors (+l-aspirin).

Transfusion. 2005 Mar;45(3):420-6. Links Additive effects between platelet concentrates and desmopressin in antagonizing the platelet glycoprotein IIb/IIIa inhibitor eptifibatide. Reiter R, Jilma-Stohlawetz P, Horvath M, Jilma B. Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria. BACKGROUND: Platelet (PLT) glycoprotein (GP) IIb/IIIa receptor antagonists have demonstrated efficacy in decreasing ischemic complications of percutaneous coronary intervention and/or unstable angina. In case of bleeding, the drug can be stopped and PLT transfusions can be given. STUDY DESIGN AND METHODS: This crossover study tested the additive effects of PLT concentrates (PCs) after desmopressin (DDAVP) infusion in antagonizing the anti-PLT effects of GPIIb/IIIa inhibitors and aspirin. After eptifibatide and aspirin infusion (at standard dosages), 10 healthy volunteers received DDAVP or placebo. Thereafter, increasing amounts of PLTs from fresh single-donor apheresis concentrates were added in vitro to blood samples of all volunteers to increase PLT counts by 30 x 10(9), 60 x 10(9), or 120 x 10(9) per L. RESULTS: Adding platelets in vitro further improved PLT function after DDAVP: it shortened collagen-adenosine diphosphate closure times (p < 0.01), to normal ranges as measured by the PLT function analyzer (PFA-100). In contrast, normal PLT function could not be restored even when PLT counts were increased by 50 percent (120 x 10(9)/L) in the placebo group. CONCLUSION: Combined use of PLTs from fresh apheresis PC and DDAVP additively enhances recovery of normal PLT function after eptifibatide infusion. Such a strategy may help to avoid excessive transfusion of PC. PMID: 15752161 [PubMed - indexed for MEDLINE] Go to source: Entrez PubMed

Another review of reversal of anticoag in ICH (Mayo Clinic Proceed 2007;82(1):82)

Vit K takes 6-24 hrs to reverse and IX and X reversal takes longer than 24 hours

FFP 12-32 hours for reversal

PCC 15 min after infusion completed

FFP 15 min after bolus

Leo / Lou   Its my understanding that you are both about half correct.  Plavix irreversably inactivates the P2Y-12 ADP receptors on platelets, meaning that any circulating plavix will wreak havoc on any platelets being transfused.  Once the receptor is inactivated theres no reversing it, nor does there seem to be a way to subvert the blockade pharmacologically.  As far as I am aware, all activators of platelets independant of P2Y receptor binding (thrombin and TXA2) are locally relseased mediators, so I can’t think of a pharmacologic therapy worth attempting.  Now, if circulating clopidogrel levels are low, some platelets that are infused may not suffer from total P2Y inativation and thus promote clotting, but the effectiveness is potentially limited.  The Plavix people claim that 7 days is long enough without the drug on board to return clotting function and allow platelet transfusion to be effective, however many of the surgeons and anesthesiologists I have spoken to claim it is more on the order of two weeks in many patients.   As far as formal indications and contraindications for the platelets, I can’t speak, but thats the cliffs notes on the physiologic story behind it, as its been explained to me.   ~ Chris   Chris,   This is a very good answer to the question. The real issue is the presence or absence of residual active drug. The answer can be found in the pharmacokinetics of clopidrogel. Clopidrogel would be a lot less demonized and a lot safer it if didn’t have such a miserably long half life. I’ve pasted in a couple of abstracts below, and as you can the half life ranges from 275 to 433 hours in chronic dosing! That’s about 11-1/2 days for the shortest half life! The variation in half life seems to be do to variations in abortion as opposed to variations in metabolism.  The irreversible inactivation of P2Y-12 ADP receptors isn’t as much of a problem as the long circulating time of effective doses of the drug. Aspirin works by irreversibly acetylating platelets, however, it is rapidly eliminated which means that you can give unacetylated donor platelets and rapidly reverse the antiplatelet effect.   I have no idea why clopidrogel was selected as the prototypical P2Y-12 ADP receptor inhibitor. It would have seemed infinitely wiser to me to choose a compound which is much more rapidly metabolized. My prediction (absent anything but a hunch) is that you will see P2Y-12 ADP receptor inhibitors designed to have a much shorter half life released in the coming years. Clopidrogel will then fade away from routine use or disappear completely.   I am about the hard businesses of trying to master the mechanics of hemorheology. I scarcely see this discipline mentioned in CCM, but I predict that this will be a font of new insights and pharmaceuticals in the coming decade. Modulating RBC aggregability, as well as WBC and platelet adhesion and interactions has powerful therapeutic potential. Hopefully, they’ll do better with those drugs than they did with clopidrogel.   Semin Thromb Hemost. 1999;25 Suppl 2:29-33. Links Pharmacokinetic profile of 14C-labeled clopidogrel. Lins R, Broekhuysen J, Necciari J, Deroubaix X.   Biopharma Research, AZ Stuivenberg, Antwerpen, Belgium.   In order to obtain a global assessment of circulating clopidogrel-related products and of the excretion of the drug, the pharmacokinetic behavior and the excretion balance of 14C radioactivity following the administration of a single dose of 75 mg of 14C-labeled clopidogrel were compared in 6 clopidogrel-free healthy male subjects (Period I) and after 7 days of once daily therapy with the unlabeled drug in these subjects (at steady state) (Period II). The two study periods were separated by a 4-week washout period. For each administration of 14C-clopidogrel, blood samples were collected before and at regular intervals over 28 days after administration of the radiolabeled drug. Expired air samples were collected before and over 24 hours after the administrations of 14C-clopidogrel. All urine voided and all stools were collected before and for up to 120 hours after the administration of 14C-clopidogrel, in consecutive periods of 12 to 24 hours. The mean radiocarbon plasma concentration profiles after administration of 14C-clopidogrel given as a single dose (Period I) and during steady state (Period II) were superimposable. There were no statistically significant differences between the two treatments for any parameters. A Cmax of 3.9 mg-Eqv/L was reached after a median time of 1 hour (Tmax). The plasma elimination half-life, t1/2, ranged from 336 hours to 672 hours in Period I and from 275 to 433 hours in Period II. The radiocarbon excretion over 10 to 12 hours post-dose (time to last measurable radioactivity) in expired air represented 0.31 to 0.35% of the administered dose. Mean cumulative urinary excretion over 120 hours represented 41% of the dose after a single-dose administration and 46 % after administration at steady state. The cumulative fecal recovery over 120 hours ranged from 35 to 57% of the dose in Period I and from 39 to 59% of the dose in Period II. Mean total excretion of radioactivity was 92% of the dose during Period I and 93% during Period II. These data indicate that, following multiple-dose administration of clopidogrel, the biodisposition of the drug remains unaltered compared to a single dose.   PMID: 10440420 [PubMed - indexed for MEDLINE]   Semin Thromb Hemost. 1999;25 Suppl 2:25-8. Links Pharmacokinetics of clopidogrel. Caplain H, Donat F, Gaud C, Necciari J.   Institut Aster, Hopital Cognacq-Jay, Paris, France.   Clopidogrel is extensively metabolized, as evidenced by the absence of detectable amounts of unchanged clopidogrel in plasma samples in most clinical trials. The major circulating compound is the inactive carboxylic acid derivative SR26334, and information on the absorption and elimination of clopidogrel after oral administration is derived from the pharmacokinetics of this metabolite. Single-dose pharmacokinetics of SR26334 were investigated in a randomized, dose-proportionality study comparing single 50, 75, 100, and 150 mg oral doses of clopidogrel administered to 12 subjects. Multiple-dose pharmacokinetics of SR26334 were primarily derived from a study carried out in 18 subjects treated with clopidogrel 75 mg once daily for 14 days. Further data on multiple-dose pharmacokinetics were provided by the results of a long-term study carried out in a group of 35 subjects who received clopidogrel 75 mg once daily for 12 weeks. All subjects were healthy male volunteers and, in all cases, clopidogrel was taken in the morning after an overnight fast. The mean Cmax values (+/-SD) for SR26334 following single doses of 50, 75, 100, and 150 mg were 1.6+/-0.30 mg/L, 2.9+/-0.68 mg/L, 3.1+/-0.94 mg/L, and 4.9+/-1.22 mg/L, respectively. The ANOVA performed on dose-normalized Cmax showed no statistically significant dose effect, demonstrating a dose-proportional increase of Cmax in this range of clopidogrel doses. The urinary excretion of SR26334 was low-2.2 to 2.4% of the dose administered-and Cl(r-2-24) remained virtually constant at all four doses. Median T(max)(0.8-1.0 hour) and mean plasma t1/2 (7.2-7.6 hours) values were not significantly different between doses. Following repeated dosing with clopidogrel 75 mg, mean (+/-SD) C(trough) values (values before dosing) for SR26334 at steady state ranged from 0.8+/-0.04 mg/L to 0.11+/-0.07 mg/L. These values are similar to those observed during the 12-week administration of clopidogrel indicating that steady-state values are reproducible and that the esterasic biotransformation of clopidogrel into its carboxylic acid metabolite remains constant over a number of months of treatment.   PMID: 10440419 [PubMed - indexed for MEDLINE]   Mike Darwin

Louis M. Aledort, M.D. Professor, Medicine / Hematology And Medical Oncology E-mail: louis.aledort@mssm.edu Tel: (212) 241-7971

I just wanted to clarify that Dr. Aledort also gives some FFP (2 U typically) in bleeding liver disease patients along with the PCC, as PCC does not replace other important factors like V and VIII.

Ultrarapid Reversal of OAT

18 pts on coumadin, some supratherapeutic. All got 20 units/kg of PCC with full reversal within 3 minutes (inten care med 2007;33:721)

They gave the med over 2 minutes

 Feiba

 FEIBA for warfarin (Int J Emerg Med 2009;2:217)
 

DeZee KJ, Shimeall WT, Douglas KM, Shumway NM, O’Malley PG. Treatment of Excessive Anticoagulation With Phytonadione (Vitamin K): A Meta-analysis. Arch Intern Med. February 27, 2006 2006;166(4):391-397.

Crowther MA, Douketis JD, Schnurr T, et al. Oral vitamin K lowers the international normalized ratio more rapidly than subcutaneous vitamin K in the treatment of warfarin-associated coagulopathy. A randomized, controlled trial. Ann Intern Med. Aug 20 2002;137(4):251-254.

Riegert-Johnson DL, Volcheck GW. The incidence of anaphylaxis following intravenous phytonadione (vitamin K1): a 5-year retrospective review.

Ann Allergy Asthma Immunol. Oct 2002;89(4):400-406.

Shields RC, McBane RD, Kuiper JD, Li H, Heit JA. Efficacy and safety of intravenous phytonadione (vitamin K1) in patients on long-term oral anticoagulant therapy. Mayo Clin Proc. Mar 2001;76(3):260-266.

Fiore LD, Scola MA, Cantillon CE, Brophy MT. Anaphylactoid reactions to

vitamin K. J Thromb Thrombolysis. Apr 2001;11(2):175-183.

Dr Mattox & everybody,   First of all: There is a large individual heterogeneity in response of clopidogrel. This is endorsed by tests like TEG Platelet Mapping Assay,  PFA 100, Multiplate Platelet function analyzer, Ultegra P2Y12 and Chronolog model 700. All of them have developed tests to evaluate clopidogrel-loaded platelet response. And all of these assays demonstrate high interindividual variability, regardless of method used. In laboratory methods, optimum variability coefficients range around 5-6%. Clopidogrel resistance tests usually have the coefficients around 20%. So, I expect that patients under clopidogrel toxicity also have different responses to the treatment. Some will respond to platelet transfusions in the OR, others won´t. This is the result I expect from a larger cohort prospective study into this subject, which is presently lacking, and this is what I see in the ORs around here. Presently, platelet transfusion cannot be recommended as a STANDARD, since the rate of success is not over 40% in my biased clinical practice. I strongly believe that in such a case preoperative liver evaluation is very important. Also I believe that sources of extrinsic pathway factors have to be used if platelets alone are not working: PRP, FFP and Cryo.I suspect there can be some toxicity involving fibrin structure or ADAMTS 13 and other metalloproteinases activity together with pure hepatic and platelet dysfunction in the severe unresponsive cases. Of course that clopidogrel is a devil during surgery, but I cannot refrain the comment that clopidogrel plus a non-gifted surgeon is a serial killer. No one deserves it.So operating under clopidogrel is a task for senior Mattox-trained gentlemen, it´s not something for residents, OK? DDAVP might work at least temporarily in some patients, and antifibrinolytics will probably not be useful unless you detect active fibrinolysis at a TEG or ROTEM or SonoClot device during the procedure. Attached there is a small slide presentation about this subject. 1: Lethagen S. Related Articles,   Links Desmopressin–a haemostatic drug: state-of-the-art review. Eur J Anaesthesiol Suppl. 1997 Mar;14:1-9. Review. PMID: 9088828 [PubMed - indexed for MEDLINE] 2: Flordal PA, Sahlin S. Related Articles,  Links Use of desmopressin to prevent bleeding complications in patients treated with aspirin. Br J Surg. 1993 Jun;80(6):723-4. PMID: 8330156 [PubMed - indexed for MEDLINE] 3: Kam PC. Related Articles,  Links Use of desmopressin (DDAVP) in controlling aspirin-induced coagulopathy after cardiac surgery. Heart Lung. 1994 Jul-Aug;23(4):333-6. PMID: 7960860 [PubMed - indexed for MEDLINE] 4: Reiter RA, Mayr F, Blazicek H, Galehr E, Jilma-Stohlawetz P, Domanovits H, Jilma B. Related Articles,  Links Desmopressin antagonizes the in vitro platelet dysfunction induced by GPIIb/IIIa inhibitors and aspirin. Blood. 2003 Dec 15;102(13):4594-9. Epub 2003 Aug 14. PMID: 12920042 [PubMed - indexed for MEDLINE] 5: Chard RB, Kam CA, Nunn GR, Johnson DC, Meldrum-Hanna W. Related Articles,  Links Use of desmopressin in the management of aspirin-related and intractable haemorrhage after cardiopulmonary bypass. Aust N Z J Surg. 1990 Feb;60(2):125-8. Review. PMID: 2183746 [PubMed - indexed for MEDLINE] Go to source: Entrez PubMed

animal study showing ddavp reverses aspirin induced platelet dysfunction (British Journal of Haematology, 2002, 117, 658–663)

Factor VIIa was cost effective in trauma patients (J  Trauma Volume 66(1), January 2009, pp 63-75)

Ddavp is safe, no increased risk of thrombotic complications (Anesth 2008;109:1063)

CHANT study shows hematoma enlargement and worse outcomes with anticoag, but not so much with anti-plt (Hematoma growth in oral anticoagulant related intracerebral hemorrhage. Stroke. 2008;39:2993–6)

Plt transfusion improved plt function (3.Naidech AM, Jovanovic B, Liebling S, Garg RK, Bassin SL, Bendok BR, et al. Reduced platelet activity is associated with early clot growth and worse 3-month outcome after intracerebral hemorrhage. Stroke. 2009;40:2398–401.)

13.Naidech AM, Jovanovic B, Liebling S, Garg RK, Bassin SL, Bendok BR, et al. Reduced platelet activity is associated with early clot growth and worse 3-month outcome after intracerebral hemorrhage. Stroke. 2009;40:2398–401.14.Naidech AM, Bernstein RA, Levasseur K, Bassin SL, Bendok BR, Batjer HH, et al. Platelet activity and outcome after intracerebral hemorrhage. Ann Neurol. 2009;65:352–6.

Conclusions  A medication history does not reliably identify patients with reduced platelet activity after ICH, and this may explain studies that found no association between known aspirin use and outcomes. Future studies should screen for unknown use of anti-platelet medications after ICH. Neither assay perfectly identified patients who reportedly used anti-platelet medication before ICH.(Naidech AM, Bassin SL, Bernstein RA, Batjer HH, Alberts MJ, Lindholm PF, Bleck TP. Reduced platelet activity is more common than reported anti-platelet medication use in patients with intracerebral hemorrhage. Neurocrit Care. 2009. [Epub ahead of print])

Suboptimal effect of 3 vs. 4-factor PCC (Transfusion 2009;49:1171)

PCC Review including chart of all agents

and another one with chart of newer agents and a discussion of why factor II is probably the bad actor in thrombotic complications

Reversing Anti-platelet Agents

Best Review Article (Transfusion. 2011 Aug 19. How do I transfuse platelets (PLTs) to reverse anti-PLT drug effect? Sarode R.)

Orlando Regional Hospital Reversal of Anti-PLT Protocol

Aspirin can be reversed with dDAVP (European Journal of Anaesthesiology 2002; 19: 647–651)

1/2 life of ASA is ~20 minutes

First study to show outcome benefits from reversal of anti-platelet effects (Neurocrit Care 2012;16:82)

Plavix

In healthy volunteers, factor VIIa at 10-20 ug/kg will reverse plavix (Anesth Analg 2011;113:703–10)

Ocular

brace your hand on patient’s nose. Fan through eye in transverse and sag

can see vitreous bleed

retinal detachment

icp-optic nerve sheath

lens dislocation

retro-orbital bleed

Key question, does the ocular anatomy look normal

More and more, it looks like 5.7 is the magic cutoff (Crit Care 2008;12:150)

If the optic nerve sheath is >5mm at a point 3 mm behind the globe, then there is increased icp (ACAD EMERG MED d April 2003, Vol. 10, No. 4)

(2nd study Tayal VS Ann Emerg Med 2006)

Another study (Emerg Med J 2007;24:251)

Third Study (Annals of Emergency Medicine 2007;49(4):508-514)The sensitivity for the ultrasonography in detecting elevated intracranial pressure was 100% (95% confidence interval [CI] 68% to 100%) and specificity was 63% (95% CI 50% to 76%).

another ONSD uts study case control methods and weird endpoint make this one less compelling, but it bore out the technique they used a 5.77 mm cutpoint (Inten Care Med 2007;33:1704) Confirmation with real ICP measurements ((2008) Academic Emergency Medicine 15 (2) , 201–204) another real time showed nerve sheath but not nerve reflected ICP (Inten Care Med 2008;34:2062) Reply to Copetti and Cattarossi

Thomas Geeraerts1 , Olivier Bergès2, Sybille Merceron1, Yoann Launey1, Dan Benhamou1, Bernard Vigué1 and Jacques Duranteau1

(1)  AP-HP, Département d’Anesthésie-Réanimation Chirurgicale, Hôpital Bicêtre, Université Paris-Sud, Centre Hospitalier Universitaire Bicêtre, 94275 Le Kremlin-Bicêtre, France(2)  Service d’Imagerie Médicale, Unité Ultrasons, Fondation Ophtalmologique Adolphe de Rothschild, 25 rue Manin, 75019 Paris, France

Thomas GeeraertsEmail: thgeeraerts@hotmail.com

Accepted: 28 February 2009  Published online: 15 April 2009

Without Abstract This reply refers to the comment available at: doi:10.1007/s00134-009-1494-4

We thank Drs. Copetti and Cattarossi for their comments. We however disagree with the assumption that our results [1, 2] are related to artifacts.

Using ocular sonography, the optic nerve sheath diameter (ONSD) can be measured on coronal view (with the probe being vertical) or on axial view (horizontal probe). On axial view, the optic nerve sheath can appear fusiform, but not as a result of an acoustic artifact arising from the lamina cribrosa, but rather from unintended reconstruction when using an outdated ultrasound system, or from a meningeal shadow when the nerve does not run strictly straight. Blehar et al. [3] showed that measurements in the horizontal axis are consistently larger than those in the vertical axis. This could be related to a nonspherical ONSD, but also in some cases to this shadow. This discrepancy could become an issue when performing only one measurement in the horizontal axis, probably as Copetti and Cattarossi did. In both of our studies, this point has been considered. For each eye, we performed two measurements, one in coronal and one in axial view, the average being retained as the ONSD value. Nevertheless, to control this point, we performed an additional analysis of our second study [1]. We have now separated vertical and horizontal axis measurements of ONSD. We found a similar and significant relationship between intracranial pressure (ICP) and ONSD, with r = 0.65 (P < 0.0001) for horizontal ONSD and r = 0.71 (P < 0.0001) for vertical ONSD. Receiver operating characteristic (ROC) curves for the detection of raised ICP (>20 mmHg) show very similar patterns and best ONSD cutoff values for vertical, horizontal, and both averaged ONSD (5.88, 5.86, and 5.86 mm, respectively) (Fig. 1).Fig. 1 Receiver operating characteristic curves with respect to raised intracranial pressure (>20 mmHg) for optic nerve sheath diameter (ONSD) measured in vertical and horizontal axis, and for averaged horizontal and vertical axis. Curves are not significantly different

Moreover, we also disagree with the assumption that magnetic resonance imaging (MRI) and sonographic ONSD values strongly differ. We recently performed a study in 38 traumatic brain injury patients with invasive ICP monitoring, measuring ONSD with MRI [4]. Interestingly, we found a strong relationship between ICP and ONSD (r = 0.71, P < 0.0001) and a best cutoff value for raised ICP (5.8 mm) very close to the values obtained using ocular sonography.

We do not support the fact that color Doppler imaging of retrobulbar arteries can help in the ONSD measurement. There is no justification in the literature for this statement. Figure 2 is not convincing. The left cursor (mark 1) is 1–2 mm too lateral, resulting in a falsely enlarged ONSD. This could be related to the probe used by Copetti and Cattarossi. The frequency of the probe has to be superior to 7.5 MHz for enough precision [5]. Such a probe was used in our studies, but not in Copetti and Cattarossi’s work. Finally, ONSD values presented in their comments are not in the correct units. ONSD are probably 5.9 and 3.5 mm rather than 59 and 35 mm.

We strongly believe that the method we applied is appropriate. Data appear to be controlled, reproducible, and robust. Larger studies are certainly needed to confirm the accuracy and real-life feasibility of this method. This measure appears, however, to be interesting to rule out raised ICP.

A new study showing accuracy at 5.2 and rapid normalization when ICP is brought down (Neurocritical Care Dec 2009)

Results  Ninety-four ONSD measurements were analyzed. 5.2 mm proved to be the optimal ONSD cut-off point to predict raised ICP (>20 mmHg) with 93.1% sensitivity (95% CI: 77.2–99%) and 73.85% specificity (95% CI: 61.5–84%). ONSD–ICP correlation coefficient was 0.7042 (95% CI for r = 0.5850–0.7936). The median interobserver ONSD difference was 0.25 mm. CSF drainage to control elevated ICP caused a rapid and significant reduction of ONSD (from 5.89 ± 0.61 to 5 ± 0.33 mm, P < 0.01).Conclusion  Our investigation confirms the reliability of optic nerve ultrasound as a non-invasive method to detect elevated ICP in intracranial hemorrhage patients. ONSD measurements proved to have a good reproducibility. ONSD changes almost concurrently with CSF pressure variations.

Emerg Med J. 2010 Aug 15. [Epub ahead of print]Ultrasound measurement of optic nerve sheath diameter in patients with a clinical suspicion of raised intracranial pressure.Emergency Medicine, Norfolk and Norwich University Hospital, Norwich, UK.Abstract Background To assess if ultrasound measurement of the optic nerve sheath diameter (ONSD) can accurately predict the presence of raised intracranial pressure (ICP) and acute pathology in patients in the emergency department. Methods This 3-month prospective observational study used ultrasound to measure the ONSD in adult patients who required CT from the emergency department. The mean ONSD from both eyes was measured using a 7.5 MHz ultrasound probe on closed eyelids. A mean ONSD value of >0.5 cm was taken as positive. Two radiologists independently assessed CT scans from patients in the study population for signs of raised ICP and signs of acute pathology (cerebrovascular accident, subarachnoid, subdural or extradural haemorrhage and tumour). Specificity, sensitivity and kappa values, for interobserver variability between reporting radiologists, were generated for the study data. Results In all, 26 patients were enrolled into the study. The ONSD measurement was 100% specific (95% CI 79% to 100%) and 86% sensitive (95% CI 42% to 99%) for raised ICP. For any acute intracranial abnormality the value of ONSD was 100% specific (95% CI 76% to 100%) and 60% sensitive (95% CI 27% to 86%). kappa Values were 0.91 (95% CIs 0.73 to 1) for identification of raised ICP on CT and 0.84 (95% CIs 0.62 to 1) for any acute pathology on CT, between the radiologists. Conclusions This study shows that ultrasound measurement of ONSD is sensitive and specific for raised ICP in the emergency department. Further observational studies are needed but this emerging technique could be used to focus treatment in unstable patients.

Review Article (Acta Anaesthesiol Scand 2011;55:644)

prospective obs (emerg med j 2011;28:679)

finally the article that shows with treatment, ONSD resolves to normal (J Trauma 2011;71:779)

Another study in a neurocritical care unit (Neurocrit Care 2011;15:506)

Retinal Detachment

(Acad Emerg Med 2002;9:791 and Annals Emerg Med 2005;45(1):97)

ACEP News Article By Nate Teismann, M.D. , Sachita Shah, M.D. , and Arun Nagdev, M.D.

Learning Objectives

After reading this article, the physician should be able to:

• Understand the normal ultrasound anatomy of the eye, specifically the location of the retina.
• Know which probe is needed for ultrasound scans of the eye, and the method to accurately and safely perform the exam.
• Visualize an example of a retinal detachment diagnosed by ultrasound.

Acute retinal detachment is a sight-threatening condition requiring urgent diagnosis and treatment.

The most common type of retinal detachment (RD) is termed “rhegmatogenous” (from the Greek rhegma, meaning “tear”), which refers to a break or tear in the retinal epithelium. The majority of these cases result from age-related vitreous detachment, which can create tiny, horseshoe-shaped holes that allow fluid to pass into and accumulate in the subretinal space.1 In patients who are younger, direct trauma is the most common etiology.2

Less common types of RD include “tractional,” in which the vitreous contracts and pulls the neural retina off the underlying pigmented layer but does not cause a break in the epithelium, and “exudative,” in which serous fluid accumulates beneath the retina because of inflammatory conditions such as sarcoid uveitis.3

Regardless of the cause, RD must be diagnosed and treated rapidly to prevent monocular vision loss.

Traditionally, diagnosis of RD has relied on direct examination of the retina using an ophthalmoscope. However, a number of factors may make this difficult or impossible, including 1) contraindications to the use of mydriatics such as narrow-angle glaucoma or the need to follow pupillary exams in a head-injured patient; 2) significant periorbital trauma or soft tissue swelling; and 3) inability to visualize the posterior segment of the eye because of hyphema, lens opacification, or vitreous hemorrhage. In such cases, bedside ultrasound is critical to the timely diagnosis of RD.

Already in use for decades by ophthalmologists, ocular ultrasound is a relatively recent addition to emergency ultrasonography. Since 2002, a number of studies have demonstrated that emergency physicians using general-purpose, high-frequency transducers can accurately identify a variety of ocular pathologies, including retinal detachment.4,5,6 Bedside ultrasound is an indispensable tool for evaluating this potentially vision-threatening condition.

Procedure

Here is a simple mnemonic to help you with each CASE of potential retinal detachment: 1) Close and cover the eye; 2) place the transducer in the axial plane; 3) scan the retina; and 4) evaluate the periphery.

1) Place the ultrasound machine at the head of the bed with the patient supine. Ask the patient to close his or her eyes, and place a liberal amount of gel over the eyelid. A bio-occlusive dressing may be used to shield the eye from the gel.

2) Gently place the high-frequency linear (7.5-10 MHz) transducer over the patient’s closed eye. In order to obtain a stable image, the fourth and fifth digits of the examiner’s hand should rest against the bridge of the patient’s nose. The probe should be placed in a transverse orientation to scan in the axial anatomic plane. The probe marker should face the patient’s right side, which will correspond to the marker on the ultrasound screen (see image 1).

3) Carefully scan the eye for evidence of pathology. The normal retina is continuous with the other posterior elements of the globe and is not visible as a distinct structure. With retinal detachment, fluid enters the potential space beneath the retinal epithelium and accumulates, forcing the retina away from the outer surface of the globe. Sonographically, retinal detachment is seen as a thick, undulating, hyperechoic membrane that appears to have been lifted off the posterior surface of the eye (see images 2A and 2B).

4) Make sure to evaluate the entire globe in order to avoid missing a small RD at the periphery of the retina. Because the anterior-most attachment of the retinal epithelium is just lateral to the ciliary bodies, care must be taken to interrogate its entire surface. This may require asking the patient to gaze upward and downward while tilting the transducer accordingly to achieve adequate visualization.

Findings

In general, RD will appear as a prominent, continuous linear density rising from the fundus. Depending on the timing and severity of the detachment, the retinal separation may be visible only as a small peripheral convexity or, with an extensive detachment, as a complex array of bright, intersecting lines (see image 3A). Because the retina is fixed firmly to the optic disc, even a complete detachment will often appear tethered to this point, giving a “funnel” appearance (see image 3B).

Differentiation From Other Ocular Pathology

Other ocular processes may appear similar to RD on sonography, especially posterior vitreous detachment (PVD) and vitreous hemorrhage (VH). PVD may also appear as a hyperechoic linear density that has been lifted off the posterior globe; however, it typically appears as a thinner and smoother structure compared to RD. VH typically appears as nonlayering, low-level echoes within the vitreous body that are unattached to periphery of the globe (see image 4).

Because it can be difficult even for the expert ocular sonographer to differentiate these diagnoses from RD, we recommend prompt follow-up in any case with equivocal findings, especially when clinical features (e.g., photopsia) suggest RD.

Other findings such as retinal breaks or tears–which, as already addressed, are often the inciting event leading to RD–may be seen with ultrasound and are visible as small, echodense tufts elevated off the fundus.8 Given their small size, however, these structures typically require specialized ophthalmologic transducers for visualization. Thus, we do not believe this diagnosis should be considered within the scope of emergency sonography.

Discussion

Ocular ultrasound is emerging as a promising technique to diagnose RD. Sonography is especially helpful in cases where an adequate eye exam is impossible, or when the emergency physician does not have the luxury of time or expertise to perform a thorough, dilated fundoscopic exam.

If RD is identified, the patient should be referred to an ophthalmologist on an emergent basis, ideally within 24 hours. Because the sensitivity of this technique in the hands of emergency physicians using general-purpose portable ultrasound machines has yet to be determined, we recommend that any cases with high-risk clinical features, such as the presence of flashes of light or vision loss, also be referred on an urgent basis regardless of sonographic findings.

With this simple guide to ocular ultrasound, we hope more physicians will learn and incorporate ultrasound into their evaluation of ocular complaints in the emergency setting. We believe that ocular ultrasound is fast, safe, and easy to teach and learn. We hope you will remember to pick up the ultrasound probe for each CASE of potential retinal detachment you encounter.

References

1. D’Amico DJ. Clinical practice. Primary retinal detachment. N Engl J Med. 2008;359(22):2346-54.
2. Byer NE. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment. Ophthalmology. 1994;101(9):1503-13; discussion 1513-4.
3. Gariano RF, Kim C. Evaluation and management of suspected retinal detachment. Am Fam Physician. 2004;69(7):1691-8.
4. Blaivas M, Theodoro D, Sierzenski PR. A study of bedside ocular ultrasonography in the emergency department. Acad Emerg Med. 2002;9(8): 791-9.
5. Elia J, Borger R. Diagnosis of retinal detachment in the ED with ultrasonography. J Emerg Med. 2008. (Article in Press) Available at: www.ncbi.nlm.nih.gov/pubmed/18547771
6. Winter K, Baker T. Images in emergency medicine. Retinal de-tachment. Ann Emerg Med. 2007;50(1):89, 95.
7. DiBernardo CW, Greenberg, EF. Ophthalmic Ultrasound: A Diagnostic Atlas. 2nd ed. Thieme Medical Publishers; 2007.
8. Lorenzo-Carrero J, Perez-Flores I, Cid-Galano M, et al. B-scan ultrasonography to screen for retinaltears in acute symptomatic age-related posterior vitreous detach-ment. Ophthalmology. 2009;116(1):94-9.

For More Great Evidence and Resources on Sepsis,
See our Sepsis Collaborative Page at EMCrit.org

Review of all current lit (Annals Emerg Med 2006;48(1):28)

Loma Linda Toolkit from Nguyen (http://www.llu.edu/llumc/emergency/patientcare/)

ICU Sepsis Screen

Sepsis Definitions

Systemic Inflammatory Response Syndrome (SIRS)

The hallmark clinical manifestations of both sepsis and SIRS are two or more of the following conditions:

1.     Temperature >38ºC or <36ºC

(100.4/96.8)

2.     Tachycardia >90 beats per minute 3.     Respiratory rate >20 per minute or a PaCO2 <32 mm Hg 4.     White blood cell count >12,000 mm3 or <4,000/mm3 or >10% immature (band) forms (“left shift”). SSC Criteria   Infection plus any two, get lactate Temp >101 or <96.5 Altered Mental Status Chills with Rigors Tachy>90 RR>20 WBC>12000 or <4000 Sugar>120 mg/dl in absence of diabetes   signs of severe sepsis, any of the following distinct from the source of infection SBP<90 or MAP<65 or SBP decrease > 40 from baseline Cr > 2.0 or UO < 0.5 cc/kg/hour Billi > 2 mg/dl PLT < 100,000 Lactate >4 INR > 1.4 or PTT > 60 bilat infiltrates with criteria for ALI or need for increased supplemental O2 to maintain SpO2>90

Sepsis

2 or more SIRS plus infection

from the ancient Greeks, who used “sepsis” to describe putrefaction and a bad smell

Severe Sepsis

Sepsis c organ dysfunction, hypoperfusion, hypotension, AMS, acidosis, oliguria, ARDS

Septicemia

pathogens in the blood stream

Septic Shock

Hypotension after 2L of fluid

ARDS

PaO2/FiO2<200

B pulmonary infiltrates

PAWP<18

Bone’s criteria define septic shock as systolic BP <90 mm Hg or >40-mm drop in standard BP; organ perfusion based on mean arterial BP, which is determined by diastolic, not systolic, BP; patients whose BP usually 170/100 mm Hg who present with BP of 110/60 mm Hg have septic shock (ie, >40-mm Hg drop in baseline BP; do not treat with fluids); precipitous drop in mean arterial BP causes change in mental status, hemodynamic embarrassment, renal dysfunction, gastrointestinal (GI) tract hypoperfusion, and liver hypoperfusion (DeBlieux)

Types of Hypoxia

hypoxemic hypoxia (low paO2)

Anemic Hypoxia

Stagnant Hypoxia (low CO)

Cytopathic Hypoxia (Cell machinery can not use O2)

Who has Severe Sepsis?

Infection plus any two, get lactate Temp >101 or <96.5 Altered Mental Status Chills with Rigors Tachy>90 RR>20 WBC>12000 or <4000 Sugar>120 mg/dl in absence of diabetes   signs of severe sepsis, any of the following distinct from the source of infection SBP<90 or MAP<65 or SBP decrease > 40 from baseline Cr > 2.0 or UO < 0.5 cc/kg/hour Billi > 2 mg/dl PLT < 100,000 Lactate >4 INR > 1.4 or PTT > 60 bilat infiltrates with criteria for ALI or need for increased supplemental O2 to maintain SpO2>90

Fluids in Sepsis

(Chest 2008;133:252)

In early sepsis, we pour in the fluids as proven by EGDT studies

AFter the resus period, fluid management is very different

Pts have a normal or supranormal oxygen delivery. Even after fluids and blood, pts may have decreased MAPs; the temptation is to keep administering fluids, but this is often counterproductive.

Fluids can be harmful:

Normal ICU care gives patients a ton of extraneous fluid already–med infusions

Figure 1 Cardiac output (CO) [and, similarly, venous return] depend on Pra. However, this relationship depends critically on where the heart is operating on its function curve. For example, when the heart is at point A, small increments in Pra raise cardiac output greatly. In contrast, augmenting Pra when the heart is at point B has little impact on cardiac output.

Figure 2. Venous return function curve superimposed on the cardiac function curve. For this heart, the current state is described by the intersection point of the cardiac function and venous return function curves (arrow 1). Raising mean systemic pressure (for example, by infusing fluids or raising the legs) shifts the venous return function curve rightwards. The new state (higher Pra and higher cardiac output) is represented by the new intersection point (arrow 2).

Dynamic Measures

Spont inspiration will transiently raise the transmural Pra and shift CO curve to the left, increasing CO

Passive Mech Vent Inspiration shifts the CO curve to the right and temporarily decreases CO

Figure 3. The effect of spontaneous breathing is to shift leftwards the cardiac function curve (solid line to dotted line), shifting the intersection point from arrow 1 (end-expiration) to arrow 2 (end-inspiration). When the heart is operating on the steep portion of the cardiac function curve (top, a), this leftward shift moves the intersection point significantly (ie, Pra falls and cardiac output rises). However, if cardiac function is depressed or the circulation is fluid loaded (bottom, b), the respiratory shift (from arrow 1 to arrow 2) has only a trivial impact on Pra and cardiac output.

Figure 4. Passive ventilation shifts the cardiac function curve rightwards. The solid line represents end-expiration (intersection point 1), and the dotted line end-inspiration (intersection point 2). If the heart is preload responsive (top, a), the intersection point shifts and the resulting decrease in cardiac output will reveal itself in changing pulse pressure, stroke volume, and aortic or brachial artery peak flow velocity. If the heart is not preload responsive (bottom, b), there will be little respiratory-related decrease in cardiac output (as the intersection point shifts from arrow 1 to arrow 2).

Figure 5. Relationship of arterial pressure wave and passive respiration. Compared to end-expiration, the systolic pressure and pulse pressure rise during inspiration (INSP), then fall during expiration. PPmax = maximal pulse pressure; PPmin = minimal pulse pressure.

Recommendations for Fluid Management in Severe Sepsis For the first 6 h of severe sepsis, infuse fluids liberally, targeting SvO2 or ScvO2 > 70% Subsequently, do not use “maintenance” fluids Judge the intravascular volume daily (at least) For new hypotension, tachycardia, or unexplained oliguria, ascertain the cause and consider a fluid challenge:  When fluid challenge is of low risk, administer 500 to 1,000 mL of crystalloid;  When the risk of fluid challenge is not trivial (ALI/ARDS; oliguria; right ventricular dysfunction), use a dynamic predictor to guide fluid boluses   PLR for those with some measure of cardiac output;   PPV for those with regular rhythm and lack of spontaneous breathing;   Change in Pra for those with substantial inspiratory effort Reassess the patient frequently because the hemodynamic state changes often

Table 3. How To Measure PPV* Check that cardiac rhythm is regular Raise the tidal volume to 10 mL/kg of predicted body weight Ensure that the patient is receiving ventilation passively or adjust further the rate, tidal volume, or degree of sedation to achieve this Display or print the arterial pressure waveform for 30 s Measure the minimum and maximum pulse pressure Calculate PPV (PPmax – PPmin)/([PPmax + PPmin]/2) x 100% A value  13% predicts fluid responsiveness

* See Figure 5 legend for expansion of abbreviations.

A Bedside Approach

We summarize here our recommendations for management of fluids in septic patients (Table 2 ). In the first 6 h of acute resuscitation, fluids should be infused urgently to restore perfusion, guided by the ScvO2. Although infusing fluid until the Pra reaches 8 to 12 mm Hg is commonly recommended, the only basis for this is expert opinion.1281 We are concerned that excessive focus on Pra will lead to underresuscitation or overresuscitation, emphasize again that ScvO2 should be the target, and recommend that dynamic predictors be used (even at this early time) to gauge the likely impact of fluids.

Once the patient has been resuscitated, fluid infusion should be ceased and no maintenance fluids should be prescribed. The intravascular and total body volume state should be judged periodically (daily in a rather stable patient, more frequently in the newly admitted or unstable patient) using conventional means such as clinical examination, intake and output records, changes in weight, adequacy of urine output and perfusion, and other measures. Generally, such assessment should be followed by diuretic administration because the typical septic patient is hypervolemic. When persistent or recrudescent hypotension, tachycardia, or oliguria raise the question as to whether fluids would be helpful, the intensivist should estimate the probability of harm from a fluid bolus. For many patients, the risks of fluid expansion are trivial and, in such a case, an adequate fluid bolus should be infused rapidly while measuring clinically relevant outcomes. For others, however, the risks of fluid infusion may be real. Pulmonary or cerebral edema, abdominal compartment syndrome, acute right-heart strain, or oliguria are all conditions that raise the potential risk. Especially when these conditions are present, the clinician should attempt to identify patients unlikely to benefit from fluids, in order to spare them potential harm. Depending on the monitoring available (arterial line, PAC, ScvO2, echocardiography, Doppler ultrasound), one of the dynamic predictors of fluid responsiveness should be used to guide any fluid therapy. Most often this will involve PPV, as described in Table 3 . Technology is available to display PPV, but care must be taken that the preconditions for reliable measurement are adhered to (passive patient, tidal volume of 8 to 12 mL/kg, regular rhythm). The patient must be assessed carefully for respiratory activity, taking into account the ventilator pressure and flow waveforms, hemodynamic tracings, and the clinical examination. We recommend that the arterial pressure wave be printed on paper, preferably along with measures of airway pressure or chest volume, for careful assessment and measurement of pulse pressures. Visually and with the aid of a ruler, we find the tallest and shortest pulse waves, ensuring that these represent the typical cyclic pattern in a long strip. Further, it is essential to be certain that the cardiac rhythm remains regular, especially when choosing values of minimum and maximum pulse pressure. We then simply measure the pulse heights in millimeters on a ruler because there is no need to perform the arithmetic in millimeters of mercury. The equation for calculating PPV is provided in Table 3.32   If the PPV is > 13%, a fluid bolus should be administered. Some reliable indicator of perfusion should be measured before and after the bolus in order to determine the effect. If the bolus is effective, the patient should be assessed again for fluid responsiveness, and the procedure repeated until dynamic measures predict no further response. If the initial bolus is not effective, the intensivist should ask whether this is because the bolus was inadequate or the patient is simply unresponsive to fluid.

Article I have no idea what to with about positive fluid balance, uncontrolled for a billion variables (Crit Care Med 2011;39:259) did the patients have heart dysfunction giving high cvp, did they have kidney dysfunction leading to positive fluid balance

Albumin

Intensive Care Medicine

Volume 37, Number 1, 86-96, DOI: 10.1007/s00134-010-2039-6

Original

Impact of albumin compared to saline on organ function and mortality of patients with severe sepsis

The SAFE Study Investigators

and SR/MA (Crit Care Med 2011;39:386)

Vasopressors in Septic Shock

Xigris (Protein C)

Antibiotics

Retrospective study showed 6% absolute mortality benefit to pts who received abx that covered the bugs within 60 minutes (Crit Care Med 2006;34:1589)

time to abx from outset of hypotension is assoc with mortality

Elapsed times from triage and qualification forearly goal-directed therapy to administration of appropriate antimicrobialsare primary determinants of mortality in patients withsevere sepsis and septic shock treated with early goal-directedtherapy. (Crit Care Med 2010; 38:1045–1053)

(Chest. 2009 Nov;136(5):1237-48)Initiation of inappropriate antimicrobial therapy results in a fivefold reduction of survival in human septic shock. Kumar

When other varaibles are controlled for, the actual pathogen or infection site doesn’t seem to matter, only getting appropriate abx in early (Crit Care Med 2011;39:1886)

Resuscitation Endpoints

Trends of vital signs are not sufficient endpoints to determine an adequate response to therapy. Rady et al114 showed that 31 of 36 patients presenting with shock and resuscitated to normal vital signs continued to have global tissue hypoxia, as evidenced by decreased ScvO2 and increased lactate levels. A post hoc analysis of the early goal-directed therapy study5 in patients with mean arterial pressure greater than 100 mm Hg showed that control patients with persistently abnormal ScvO2 and lactate levels at 6 hours had a significantly higher mortality rate compared with the early goal-directed therapy patients whose values had reached therapeutic goals (60.9% versus 20.0%, P<.05).122 Other studies have also showed that a persistently high lactate is associated with increased mortality.74, 77, 123 and 124 Therefore, continuous ScvO2 and serial lactate measurements during resuscitation may help identify patients requiring continued intensive therapy.

114 114 M.Y. Rady, E.P. Rivers and R.M. Nowak, Resuscitation of the critically ill in the ED responses of blood pressure, heart rate, shock index, central venous oxygen saturation, and lactate, Am J Emerg Med. 14 (1996), pp. 218–225. SummaryPlus | Full Text + Links | PDF (850 K) | Abstract + References in Scopus | Cited By in Scopus

Surviving Sepsis Campaign Guidelines

Critical Care Medicine Volume 36(1), January 2008, pp 296-327

Surviving Sepsis Campaign Explanations (Crit Care Med 2004;32(11) suppl Nov 2004)

Steroids & Adrenal Insufficiency

Statins

correct microcirculatory flow abnormalities through Statins in the intensive care unit. Curr Opin Crit Care. 2006 Aug;12(4):309-14 Association of statin therapy and increased survival in patients with multiple organ dysfunction syndrome. Intensive Care Med. 2006 Aug;32(8):1248-51. Statins and sepsis. Lancet. 2006 May 20;367(9523):1651

Review

Brit J Anaes 2007;98(2):163

Lactate

Serum Lactate as a Predictor of Mortality in Emergency Department Patients with Infection (Ann of Emerg Med 2005;45(5):524-528)

Early lactate clearance assoc c decreased mortality and apache II (crit care med 2004;32(8):1637)

Blueprint for Sepsis (Acad Emerg Med 2005;12(4):352)

Lactate Predicts Death in Emergency Department Patients with Infection

Nathan I. Shapiro, Larry A. Nathanson, Michael Howell, Daniel Talmor, Alan Lisbon, Richard E. Wolfe and J. Woodrow Weiss

Beth Israel Deaconess Medical Center: Boston, MA

CONCLUSIONS: The serum lactatelevel shows initial promise as a predictor of death in patientswith infection, and may be useful as a risk stratification tool.Continued enrollment and the addition of clinical variableswill assist in risk assessment. Further study is necessary todetermine if early lactate-guided intervention can alter outcome.

As lactate increases from 2.0 to 8.0, mortality increases from 10-90% (Crit Care Med 1992;20:80)

venous and arterial is essentially equivalent in the ed population (Acad Emerg Med 1996;3:730)

but another article (1: Ann Emerg Med. 1997 Apr;29(4):479-83) suggests only real if low.

Lactate predicts death regardless of shock/organ failure (Crit Care Med Volume 37(5), May 2009, pp 1670-1677)

Even Lactates between 2-4 were predictive of mortality (Crit Care Med 2009 Vol. 37, No. 5,1670)

Now even >0.75 may be bad (Critical Care 2010, 14:R25)

point of care lactate improves pts getting goal-directed therapies (Am J Resp Crit Care 2010;181:A6141)

Shock. 2009 Jul;32(1):35-9. Multicenter study of early lactate clearance as a determinant of survival in patients with presumed sepsis. 79% of pts who didn’t clear their lactate had an ScvO2 > 70

Less severe sepsis progresses to severe sepsis with some regularity (Acad Emerg Med 2010;17:383)

StO2

The prognostic value of muscle StO2 in septic patients (Intensive Care Medicine 2007;33(9))

Early Goal Directed Therapy

River’s Study (NEJM 345:19 11/8/01)

RCT—263 Patients Post-ED Blinded Control=”Standard Care” ARR Mortality 16% NNT=~6 Patients

follow-up with rationale (Chest 2006;130:1579)

Also benefited post-op major surgery pts, though not in mortality (Crit Care 2005;9:R687)

Nguyen Retrospectively reviewed the feasibility of EGDT, steroids, and Xigris (Acad Emerg Med 2006;13(1):109)

Mortality benefit proven again by Trzeciak 1 year experience with egdt (Dellinger Chest 2006;129(2):225)

22 patients with 16 historical controls. Mortality rate 43% in pre group `8% in EGDT but not stat sig.

before and after review (Crit Care Med 2006;34:2707)

and another (Crit Care Med 2006;34:943)

Bryant’s How to get it done (Acad Emerg Med 2007;14:1079)

Economics

$5000 less per patient due to decreased LOS (Shorr AF. CCM 2007;35(5) POLF)

More on it costing less (Crit Care Med 2007;35:1257) and (35:2090)=Dave Huang’s

In another study, not cost-saving, but cost effective given QALY saved (Crit Care Med 2008;36:1168)

Jones showed it costs more but cost effective with QALY (Crit Care Med 2011;39:1306)

River’s Protocol

If SIRS and SBP<90 or Lactate >4

• Central venous catheter capable of measuring central venous oxygen saturation (ScvO2)
• A-Line
• 500-mL bolus of crystalloid every 30 minutes to achieve a CVP of 8-12 mm Hg
• Vasopressors or vasodilators to achieve MAP > 65 mm Hg or < 90 mm Hg, respectively
• If ScvO2 was < 70%, patients received red blood cell transfusions to achieve a hematocrit of at least 30%.
• If at that hematocrit, ScvO2 was still < 70%, patients were infused an escalating dose of dobutamine to a maximum dose of 20 mcg/kg/min.
• Patients then unable to achieve goals were intubated and ventilated

nguyen’s study (Crit Care Med 2007;35(4):1105) if entire bundle, mortality benefit

If using SvO2, 65% should be the target. (CCM Volume 32(7) July 2004 pp 1627-1628)

another prospective validation (Chest 2007;132:425)

intermittent sampling seems almost as good as cont. (Inten Care Med 2007;Online first Author Sakka SG)

Chest. 2007 Aug;132(2):425-32. Epub 2007 Jun 15. Links Prospective external validation of the clinical effectiveness of an emergency department-based early goal-directed therapy protocol for severe sepsis and septic shock. Jones AE, Focht A, Horton JM, Kline JA. Assistant Director of Research, Department of Emergency Medicine, 1000 Blythe Blvd, MEB 304e, Carolinas Medical Center, Charlotte, NC 28203, USA. alan.jones@carolinas.org OBJECTIVE: To determine the clinical effectiveness of implementing early goal-directed therapy (EGDT) as a routine protocol in the emergency department (ED). METHODS: Prospective interventional study conducted over 2 years at an urban ED. Inclusion criteria included suspected infection, criteria for systemic inflammation, and either systolic BP < 90 mm Hg after a fluid bolus or lactate concentration >/= 4 mol/L. Exclusion criteria were age < 18 years, contraindication to a chest central venous catheter, and need for immediate surgery. We prospectively recorded preintervention clinical and mortality data on consecutive, eligible patients for 1 year when treatment was at the discretion of board-certified emergency physicians. We then implemented an EGDT protocol (the intervention) and recorded clinical data and mortality rates for 1 year. Prior to the first year, we defined a 33% relative reduction in mortality (relative mortality reduction that was found in the original EGDT trial) to indicate clinical effectiveness of the intervention. RESULTS: We enrolled 79 patients in the preintervention year and 77 patients in the postintervention year. Compared with the preintervention year, patients in the postintervention year received significantly greater crystalloid volume (2.54 L vs 4.66 L, p < 0.001) and frequency of vasopressor infusion (34% vs 69%, p < 0.001) during the initial resuscitation. In-hospital mortality was 21 of 79 patients (27%) before intervention, compared with 14 of 77 patients (18%) after intervention (absolute difference, – 9%; 95% confidence interval, + 5 to – 21%). CONCLUSIONS: Implementation of EGDT in our ED was associated with a 9% absolute (33% relative) mortality reduction. Our data provide external validation of the clinical effectiveness of EGDT to treat sepsis and septic shock in the ED.

New meta-analysis of “quantitative” therapies for sepsis showed benefit if early but none if done late. (Crit Care Med 2008;36:2734)

We should probably add on ScvCO2-SaCO2>6 as a marker for need for further resus after ScvO2>70 (Inten Care Med 2008;34:2218)

ScvO2 > 64 indicated CI > 2.5 in an observational trial (Acta Anaes Scand 2010 54:98)

Low and High ScvO2 correlated with mortality (Ann Emerg Med 2010;55(1):40)

Can go non-invasive using 10% lactate clearance instead of ScvO2 in RCT (JAMA 2010;303(8):739)

More before and after shows ScvO2>70 actually has mortaliy benefit (Crit Care Med 2010 Vol. 38, No. 4)

Prognosis

Early changes in organ function predict survival

(Crit Care Med 2005;33(10):2194)

if you are not getting better, you are getting worse

baseline to day 1 improvement is the best predictor of outcome

MEDS Score

MEDS Score Crit Care Med 2007;35:192 Crit Care Med 2003;31:670 MEDS score was better than APACHE II for predicting mortality (Emerg Med J 2006;23:281-5)

Validated in SIRS patients (Crit Care Med 2008;36:421–6 )

e

Parameter

Finding

Points

terminal illness

absent

0

present

6

tachypnea or hypoxia

respiratory rate <= 20 breaths per minute and oxygen saturation >= 90%

0

respiratory rate > 20 breaths per minute and/or oxygen saturation <90%

3

septic shock

absent

0

present

3

platelet count

>= 150,000 per µL

0

< 150,000 per µL

3

percent bands in differential count

<= 5%

0

> 5%

3

age of the patient

<= 65 years

0

> 65 years

3

lower respiratory tract infection

absent

0

present

2

nursing home resident

no

0

yes

2

mental status

normal

0

altered

2

total score =

The higher the score, the more seriously ill the patient.

Total Score

Risk Group

Mortality Rate

0 to 4

very low

0.9 – 1.1%

5 to 7

low

2.0 – 4.4%

8 to 11

moderate

7.8 – 9.3%

12 to 15

high

16 – 20%

16 to 27

very high

39-50%

Performance:

SIRS did not improve mortality but severe sepsis or septic shock did (Ann Emerg Med 2006;48:583)

NNT for sepsis therapies

TABLE 1. Number Needed to Treat (NNT) to Prevent One Death: SALVAGE vs. Thrombolysis in Myocardial Infarction

1. Shapiro NI, Howell M, Talmor D. A blueprint for a sepsis protocol. Acad Emerg Med. 2005; 12:352–9.[Abstract/Free Full Text]
2. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomized trials of more than 1000 patients. Lancet. 1994; 343:311–22.[CrossRef][Medline]
3. Annane D, Sebille V, Charpentier C, et al. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA. 2002; 288:862–71.[Abstract/Free Full Text]
4. Bernard GR, Vincent JL, Laterre PF, et al. Efficacy and safety of recombinant human activated protein C for severe sepsis. N Engl J Med. 2001; 344:699–709.[Abstract/Free Full Text]
5. Warren BL, Eid A, Singer P, et al (KyberSept Trial Study Group). High-dose antithrombin III in severe sepsis: a randomized controlled trial. JAMA. 2001; 286:1869–78.[Abstract/Free Full Text]
6. Abraham E, Reinhart K, Opal S, et al (OPTIMIST Trial Study Group). Efficacy and safety of tifacogin (recombinant tissue factor pathway inhibitor) in severe sepsis: a randomized controlled trial. JAMA. 2003; 290:238–47.[Abstract/Free Full Text]
7. Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000; 342:1301–8.[Abstract/Free Full Text]
8. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001; 345:1359–67.[Abstract/Free Full Text]
9. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001; 345:1368–77.[Abstract/Free Full Text]

Intervention NNT

Early goal directed therapy 6-8 Drotrecogin alfa 16 (whole trial) 8 (APACHE II > 25) Intensive insulin therapy 29 Low dose steroids 7 Daily hemodialysis 5.5

Mottling Score

Fig. 1  Left: the mottling score is based on a mottling area extension on the legs.

Score 0 indicates no mottling;

score 1, a modest mottling area (coin size) localized to the center of the knee;

score 2, a moderate mottling area that does not exceed the superior edge of the kneecap;

score 3, a mild mottling area that does not exceed the middle thigh;

score 4, a severe mottling area that does not go beyond the fold of the groin;

score 5, an extremely severe mottling area that goes beyond the fold of the groin.

Six hours after inclusion,

oliguria [OR 10.8 95% CI (2.9, 52.8), p = 0.001],

arterial lactate level [<1.5 OR 1; between 1.5 and 3 OR 3.8 (0.7-29.5); >3 OR 9.6 (2.1-70.6), p = 0.01] and

mottling score

0-1 OR 1;

score 2-3 OR 16,

score 4-5 OR 74,

were strongly associated with 14-day mortality

(Intensive Care Med. 2011 May;37(5):801-7)

Equipment

Additional Equipment for EGDT (Crit Care 2005;9:349)

Physiology of Sepsis

Predisposition Predisposition to respond to therapy genetic comorbidities, environmental, social ie alcohol Infection Factors that may affect prognosis and likelihood of response to therapy identifiable infection source, severity, localized-disseminated (eg bacteraemia) organisms, appropriate/inappropriate initial antimicrobial therapy Response stratification of response based on: biomarkers conventional laboratory parameters eg WBC, procalcitonin, CRP, lactate Organ dysfunction number of organ dysfunctions specific organ dysfunctions magnitude of each organ dysfunction Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Crit Care Med 2003; 31:1250-1256 PIRO After an infectious insult, endothelial damage occurs. Activation of neutrophils increased vascular permeability with resulting tissue edema liberation of oxidants by the neutrophil. Tissue factor (TF) is expressed by monocytes and the damaged vascular endothelium Inflammatory cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 and IL-6, are secreted by the monocytes Coagulation activation finally release of thrombin and the formation of the fibrin clot “Walling off” infection Immune system overstimulation is not central Cytokines may actually be beneficial in sepsis Innate immune cells initiate responses via the Toll Like Receptors (TLR) TLR 4 is part of a recognition complex for bacterial lipopolysaccharide Modulation of tissue TLRs during the early phases of polymicrobial sepsis correlates with mortality Activation of nuclear factor kappaB a transcription factor involved in immediate early gene activation during inflammation Williams DL, Ha T, Li C, et al. Modulation of tissue Toll-like receptor 2 and 4 during the early phases of polymicrobial sepsis correlates with mortality. Crit Care Med 2003; 31:1808-1818 Hotchkiss RS, Karl IE. The pathophysiology and treatment of sepsis. N Engl J Med 2003; 348:138-150

Mental status changes – ANY KIND Confusion/delirium/compativeness Your pleasant grandpa is now pulling his lines out Decreased responsiveness, pt is less perky Lethargy Tachypnea and/or tachycardia WITHOUT fever (yet) Hypothermia – remember RECTAL temperature Dropping (slightly initially) blood pressure – beware of RELATIVE changes Your hypertensive granny with a BP of 100/82 may very well be septic Rising blood sugar – increasing insulin requirements

Cardiac Dysfunction

? from circulating factors tnf, IL 1b

intrinsic cellular alterations

nitric oxide induced mitochondrial damage

depressed contractility with preserved or initially increased CO

dobutamine may help~15% of pts initially

septic cardiomyopathy

recovers at day 7-10 with no lasting damage

(inten care med 2006;32:799)

~60% of patients have sepsis induced hypokinesia (Crit Care Med 2008;36:1701)

Source Control

Does the patient have a correctable source anywhere in his body? Abscess Liver Brain Retroperitoneum Lung-mediastinum Could the pleural effusion be an empyema? Can the dilated kidney represent an obstructive pyelonephritis? Are the paranasal sinuses/teeth filled with pus? Is there any dead bowel in the abdomen? Is the ascites infected? Is the hematoma infected? Is the gallbladder infected? Has this organ perforated?

Sublingual Capnometry

predicts microcirculatory changes and dobutamine reverses these changes in early sepsis (Intensive Care Medicine 2006;32:516)

shunting from stiffened endothelium closes down the microcirc. Increased cardiac output opens it back up

Opening the Microcirculation

Any pt with sepsis and some evidence of organ dysfunction derives mortality benefit from aggressive early therapies (Critical Care 2005, 9:R607-R622)

MEDS Score mortality in ed sepsis score (Crit Care Med 2003;31(3):670)

Economics of EGDT protocol. This study states it is cheaper for the ED or hospital (Crit Care Med 2007;35:1257)

sepsis timeline by Bryant (AJEM 2007;25:564)

Corticus

Bottom line: Hydrocortisone does not help in septic shock

European DB PRCT, 52 ICUs

1º outcome target decreased 28 day mortality in non-responders to ACTH (<9 rise)

2º outcome targets ICU and hospital mortalities, reversal of organ failures

Planned enrolment 800 patients to give a 80% power to detect a 10% reduction in mortality. Only 500 patients enrolled.

Inclusion           Infection within 72 hours

2+ SIRS criteria

Evidence of shock despite fluids and vasopressors

Organ dysfunction

ACTH test required

Exclusion          Prior steroids or immunosuppression

Dose of hydrocortisone: 50mg qid x4 days, 50mg bid x 3days, 50 mg once daily for 3 days

35 % of patients were medical

Source of infection was GI 49%, lungs 30%,

Non response to ACTH in 47% both groups

28 day mortality Steroid Placebo All patients 33.5% 31% ns Responders 28.8% 28.7% ns Non-responders 37.6% Missed it but ns difference

Steroid Placebo Reversal of shock 80% 74.6% p=0.14 Median time to reverse shock – all patients 3.1 days 5.7 days p=0.003 Median time to reverse shock – non-responders 3.7 days 6 days Median time to reverse shock – responders 2.8 days ? Secondary superinfection 33% 26.3% was sig ICU neuropathy 1% 2% RR 0.5 (0.09-2.68) Hyperglycemia >150 84% 72% RR 1.17 (1.06-1.28)

Conclusions:     Hydrocortisone does not decrease mortality in septic shock

Does not increase reversal of shock but shock reverses quicker

No polyneuropathy increase

More superinfection

ACTH is test not useful

Hydrocortisone should not be routinely used in septic shock.

There may be a role in those still hypotensive after 1 hour. I’ve no idea why they suggest this.

VASST

Vasopressin in Septic Shock Trial

Bottom line; mortality decreased with low dose vasopressin only in patients with less severe sepsis

1º hypothesis – Low dose vasopressin -0.03units/min will decrease 28 day mortality from 60% to 50% in septic shock compared to norepinephrine alone

2º stratification –           Severe septic shock = norepinephrine dose > 15 mcg/min

Less severe septic shock = norepinephrne 5-14 mcg/min

Resulted in 50% in each group

Inclusion           Severe septic shock

SIRS criteria 2/4

Infection

1 organ dysfunction

Exclusion          Septic shock > 24h, unstable heart, had received any vasopressin

Method            Blinded infusion of vasopressin 0.01units/min or norepinephrine 5mcg/min

Titrated to MAP 65-75 mmHg

If vasopressin reached 0.03units/min or norepi 15mcg/min then other pressors were added

Results             396 randomised to vasopressin, 382 to norepi, all were equally sick with 2.5 organ failures and were on 20mcg/min norepi

Measured vasopressin was very low in the noprepi group and 80-100picomol/L in the vaso group

28 day mortality Norepi Vasopressin p value Total 39.3% 35.4% 0.26 More severe sepsis 42.5% 44% 0.84 Less severe sepsis 35.7% 26.5% 0.04

90 day mortality, I couldn’t write the numbers fast enough, but overall the difference in mortality was not significant p= 0.11 but the less severe sepsis group had a mortality of 46.1% with norepi, and 35.8% with vasopressin which was significant at p=0.04.

BP was similar in both groups

No difference in adverse events in both groups except small increase in digital ischemia in the vaso group with p= 0.06

New SSC Recs in Review

early goal-directed resuscitation of the septic patient during the first 6 hrs after recognition (1B) blood cultures prior to antibiotic therapy (1C) imaging studies performed promptly to confirm potential source of infection (1C) administration of broad-spectrum antibiotic therapy within 1 hr of diagnosis (1B) reassessment of antibiotic therapy with microbiology and clinical data to narrow coverage, when appropriate (1C) a usual 7-10 days of antibiotic therapy guided by clinical response (1C) source control with attention to the balance of risks and benefits of the chosen method (1C) administration of either crystalloid or colloid fluid resuscitation (1B) aggressive fluid challenge to restore mean circulating filling pressure (1C) reduction in rate of fluid administration with rising filling pressures and no improvement in tissue perfusion (1D) vasopressor preference for norepinephrine or dopamine to maintain an initial target of mean arterial pressure > 65 mm Hg (1C) achieving a normal superior vena cava oxyhemoglobin saturation in the presence of evidence of tissue hypoperfusion (1B) dobutamine inotropic therapy when cardiac output remains low despite fluid resuscitation and combined inotropic/vasopressor therapy (1C) stress dose steroid therapy given only in septic shock after blood pressure is identified to be poorly responsive to fluid and vasopressor therapy (2C) recombinant activated protein C in patients with severe sepsis and clinical assessment of high risk for death (2B except 2C for post-operative patients).

In the absence of tissue hypoperfusion, coronary artery disease, or acute hemorrhage, target a hemoglobin of 7-9 g/dL (1B) a low tidal volume (1B) and limitation of inspiratory plateau pressure strategy (1C) for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) application of at least a minimal amount of positive end-expiratory pressure in acute lung injury (1C) a semi-recumbent bed position unless contraindicated (1A) avoiding routine use of pulmonary artery catheters in ALI/ARDS (1A) to decrease days of mechanical ventilation and ICU length of stay, a conservative fluid strategy for patients with established ALI/ARDS who are not in shock (1C) protocols for weaning and sedation/analgesia (1B) using either intermittent bolus sedation or continuous infusion sedation with daily interruptions or lightening (1B) avoidance of neuromuscular blockers, if at all possible (1B) institution of glycemic control (1B) targeting a blood glucose < 150 mg/dL after initial stabilization ( 2C ) equivalency of continuous veno-veno hemofiltration or intermittent hemodialysis (2B) prophylaxis for deep vein thrombosis (1A) use of stress ulcer prophylaxis to prevent upper GI bleeding using H2 blockers (1B) or proton pump inhibitors (1C) and consideration of limitation of support where appropriate (1C).

SSC Campaign Results

Data from 15,022 subjects at

165 sites were analyzed to determine the compliance with bundle

targets and association with hospital mortality. Compliance with the

entire resuscitation bundle increased linearly from 10.9% in the first

site quarter to 31.3% by the end of 2 yrs (p < .0001). Compliance

with the entire management bundle started at 18.4% in the first

quarter and increased to 36.1% by the end of 2 yrs (p .008).

Compliance with all bundle elements increased significantly, except

for inspiratory plateau pressure, which was high at baseline. Unadjusted

hospital mortality decreased from 37% to 30.8% over 2 yrs

(p .001). The adjusted odds ratio for mortality improved the longer

a site was in the Campaign, resulting in an adjusted absolute drop of

0.8% per quarter and 5.4% over 2 yrs (95% confidence interval, 2.5–8.4).

Conclusions:

The Campaign was associated with sustained,

continuous quality improvement in sepsis care. Although not

necessarily cause and effect, a reduction in reported hospital

mortality rates was associated with participation. The implications

of this study may serve as an impetus for similar improvement

efforts. (Crit Care Med 2010; 38:367–374)

Pentastarch and Intensive Insulin

(NEJM 2008;358(2):125) Intensive Insulin Therapy and Pentastarch Resuscitation in Severe Sepsis Background The role of intensive insulin therapy in patients with severe sepsis is uncertain. Fluid resuscitation improves survival among patients with septic shock, but evidence is lacking to support the choice of either crystalloids or colloids. Methods In a multicenter, two-by-two factorial trial, we randomly assigned patients with severe sepsis to receive either intensive insulin therapy to maintain euglycemia or conventional insulin therapy and either 10% pentastarch, a low-molecular-weight hydroxyethyl starch (HES 200/0.5), or modified Ringer’s lactate for fluid resuscitation. The rate of death at 28 days and the mean score for organ failure were coprimary end points. Results The trial was stopped early for safety reasons. Among 537 patients who could be evaluated, the mean morning blood glucose level was lower in the intensive-therapy group (112 mg per deciliter [6.2 mmol per liter]) than in the conventional-therapy group (151 mg per deciliter [8.4 mmol per liter], P<0.001). However, at 28 days, there was no significant difference between the two groups in the rate of death or the mean score for organ failure. The rate of severe hypoglycemia (glucose level, 40 mg per deciliter [2.2 mmol per liter]) was higher in the intensive-therapy group than in the conventional-therapy group (17.0% vs. 4.1%, P<0.001), as was the rate of serious adverse events (10.9% vs. 5.2%, P=0.01). HES therapy was associated with higher rates of acute renal failure and renal-replacement therapy than was Ringer’s lactate. Conclusions The use of intensive insulin therapy placed critically ill patients with sepsis at increased risk for serious adverse events related to hypoglycemia. As used in this study, HES was harmful, and its toxicity increased with accumulating doses. (ClinicalTrials.gov number, NCT00135473 [ClinicalTrials.gov] .)

Blood

analysis from SOAP study seems to show no increased mortality in pts receiving blood transfusions (Anesthes 2008;108:31)

Barriers to Implementation

National survey of ED directors and nursing directors (CCM 2007;35 POLF Carlbom DJ)

Infection + any two, get lactate

Temp >101 or <96.5

Altered Mental Status

Chills with Rigors

Tachy>90

RR>20

WBC>12000 or <4000

Sugar>120 mg/dl in absence of diabetes

signs of severe sepsis, any of the following distinct from the source of infection

SBP<90 or MAP<65 or SBP decrease > 40 from baseline

Cr > 2.0 or UO < 0.5 cc/kg/hour

Billi > 2 mg/dl

PLT < 100,000

Lactate >4

INR > 1.4 or PTT > 60

bilat infiltrates with criteria for ALI or need for increased supplemental O2 to maintain SpO2>90

Intubation for ScvO2

Intubating will increase the ScvO2 if it is low (Impact of emergency intubation on central venous oxygen saturation in critically ill patients: a multicenter observational study Critical Care 2009, 13:R63)

Digoxin in Sepsis

Digoxin at a dose of 10 mcg/kg IV over 3 minutes may have a strong inotropic response for septic patients (Chest 1989;95:612)

measured maximum response in a 6 hour period

Heme Stable Sepsis Patients progress to Badness

(Acad Emerg Med 2010;17:383)

StO2

ScvO2 kinda matches but not so much StO2

(Acad Emerg Med 2010;17:349)

Femoral ScvO2 does not correlate with Neck ScvO2

CHEST July 2010 vol. 138 no. 1 76-83

CO2 A/V for ScvO2 > 70

intra-op optimization using ScvO2 and Art/Ven CO2 differencePcv-aCO2 decreased tissue blood flow (tissue hypoxia) causes increased values for this marker> 6 mmHg seems to be cut-off in this trialCO2 stagnation phenomenonCritical Care 2010, 14:R193

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elmhurst oraquick advance HIV 1/2 rapid test.

5 microliters blood or plasma or swab teeth/gums both upper and lower one time around (but not cheeks) push until hit bottom of vial

takes 20 minutes

if you use the loop, stir around in the vial

solution should appear pink

if from blood tube, can use lavendar (edta), green (sodium heparin), or sodium citrate (Light blue)

Elisa to elisa to western blot

New rapid test with 20 min turnaround:  OraQuick Rapid HIV by Abbott uses fingerstick blood.

MAI-gi c/o, biaxin, ribabutin, ethabutol.  Zithromax for prophylaxis

PCP-non-productive cough.  Prednisone 40 BID if PaO2<70 or Aa>35

Encephalitis-toxo, crypto (indolent course, do LP with pressures after CT on HIV CD4<200 c headache), HSV, lymphoma, PML

Esophagitis-candida, HSV, CMV

Acute HIV Presentation

Fever/Fatigue/Rash/Oral Ulcerations/Lymphadenopathy looks like mono

Quick and Dirty CD4 Count

A CD4 count less than 200/mm3 leads to more advanced disease. It is important to identify patients in this category, because they are at much higher risk of opportunistic infections, including Pneumocystis carinii pneumonia (PCP), tuberculosis (TB), toxoplasmosis, cryptosporidiosis, isosporiasis, esophageal candidiasis, cryptococcosis, and histoplasmosis. Disseminated Mycobacterium avium complex (MAC) or cytomegalovirus (CMV) infection tend to occur in patients with CD4 counts of less than 50/mm3

new study on cut-offs

<950 or >1700 for cut-offs for ALC for CD4<200 prediction

• Blatt SP, Lucey CR, Butzin CA, Hendrix CW, and Lucey DR.  “Total lymphocyte count as a predictor of absolute CD4+ count and CD4+ percentage in HIV-infected persons.”  JAMA. 1993 Feb 3;269(5):622-6.
• Crowe S, Turnbull S, Oelrichs R, and Dunne A.  “Monitoring of human immunodeficiency virus infection in resource-constrained countries.”  Clin Infect Dis. 2003 Jul 1;37(Suppl 1):S25-35.
• Srirangaraj Sreenivasan and Venkatesha Dasegowda.  “Comparing Absolute Lymphocyte Count to Total Lymphocyte Count, as a CD4 T Cell Surrogate, to Initiate Antiretroviral Therapy.”  J Glob Infect Dis. 2011 Jul-Sep;3(3):265–268.
• Srithanaviboonchai K, Rungruengthanakit K, Nouanthong P, Pata S, Sirisanthana T, and Kasinrerk W.  “Novel Low-Cost Assay for the Monitoring of CD4 Counts in HIV-Infected Individuals.”  JAIDS. 2008 Feb 1; 47(2):135-9
• Academic Emergency Medicine Volume 18, Issue 4, pages 385–389, April 2011

HIV infection is a known risk factor for neuroleptic malignant syndrome and should be considered in any seropositive patient who takes an implicated antipsychotic medication, especially if they present with fever and some combination of cogwheeling, diaphoresis, disorientation, or rigidity.36 The antiretroviral drug abacavir (Ziagen) can cause a hypersensitivity reaction characterized by malaise, fever, and nausea, with or without vomiting. In such cases, the drug must be stopped and never restarted as fatal reactions may occur.

ALC = total white blood cell count X lymphocyte percentage

An ALC less than 1000 cells/mm3 was 91% predictive in identifying patients with CD4 counts less than 200 cells/mm3 (sensitivity only 67%, but specificity 96%), while an ALC greater than 2000 cells/mm3 was 95% predictive in identifying CD4 counts greater than 200 cells/mm3 (Ann Emerg Med 1998 32(3 Pt 1))

Prophylactic therapy with trimethoprim-sulfamethoxazole (TMP-SMX) or dapsone does not rule out PCP infection, as about one-fifth of compliant patients will suffer breakthrough infections. Nearly one-third of those using aerosolized pentamidine will also develop disease (NEJM 332(11))

About 35% of those with TB had no infiltrate, while 12% had a normal chest x-ray. (NEJM 340:5)

Resp

Although radiographic findings of many pulmonary complications may be nondiagnostic, certain patterns may be suggestive of specific disorders.  A focal infiltrate on plain chest radiography suggests bacterial pneumonia. A diffuse infiltrative process on chest radiography, especially in the absence of leukocytosis, is associated with PCP. PCP is suggested by increased serum LDH and hypoxia, which may be more severe than expected from radiographic findings. Hilar adenopathy with diffuse pulmonary infiltrates suggests cryptococcus, histoplasmosis, mycobacterial infection, or neoplasm. KS can exhibit cough, fever, and dyspnea, and the chest radiograph may mimic that seen with PCP.

PCP

non-productive cough, exertional dyspnea, weight loss.  LDH>220.  Give steroids if PO2 less than 70 or Aa>35 (Prednisone 40 mg PO BID).

3 Amps Bactrim Q 6 or Trimeth plus Dapsone or Pentamidine or Atovaquone or Clinda + Primaquine

Oral 2DS Tabs TID

Prone to pneumothorax

non-productive cough, exertional dyspnea, weight loss.  LDH>220.  Give steroids if PO2 less than 70 or Aa>35 (Prednisone 40 mg PO BID).  3 Amps Bactim Q 6.

Prone to pneumothorax

93 PCP cases: 63% had elevated LDH, hypoxemia in 57%, C-XR normal in 39%, interstitial 36%, and acinar infiltrates in 25%. (J Acquir Immune Defic Syndr 1994;7(1):39-45)

Eye

CMV retinitis occurs in 10% to 30% of HIV-infected patients, and is the most common cause of blindness in AIDS patients. With advances in HAART, reduced incidences of CMV retinitis have been observed, but discontinuation of HAART may result in intraocular inflammation.[i]  CMV retinitis typically produces severe necrotic vasculitis and retinitis. When present, it may be asymptomatic or may present as change in visual acuity, photophobia, scotoma, redness, or pain. It is diagnosed by its characteristic appearance on indirect ophthalmoscopy of fluffy white retinal lesions, often perivascular. Differential diagnosis includes toxoplasmosis, syphilis, HSV infection, VZV infection, and tuberculosis

CNS

Any HIV patient presenting with neuro complaints gets CT then an LP

Consider CT + and – or MRI c gadolinium

Serum vdrl, toxo serology, and crypto antigen

With LP, get VDRL, Crypto Antigen, Opening Pressures, TB, Use PCR if available for toxo, cmv, and EBV

Cryptococcus

May present as focal cerebral lesions of diffuse meningoencephalitis

The most common presenting symptoms are fever and headache, often accompanied by nausea and vomiting.  Less common are visual changes, dizziness, seizures and cranial nerve deficits.  The diagnosis depends on identifying organisms in CSF.  Cryptococcal antigen in the CSF is nearly 100% sensitive and specific; less definitive are India ink staining  (60-80% sensitive), fungal culture (95% sensitive) or serum cryptococcal antigen (95% sensitive).  Treatment of cryptococcal meningitis requires admission for IV amphotericin B (0.7 mg/kg/day); flucytosine (100 mg/kg/day) may be added to this regimen. A response can be expected approximately 60% of the time.

Toxoplasmosis

Toxoplasmosis tends to have a greater number of lesions with a predilection for the basal ganglia and corticomedullary area, versus lymphomas which are more often singular lesions located in the periventricular matter or corpus callosum.  Tuberculosis is characterized by an  inflammatory appearance on CT, with a thick isodense exudate filling the basal cisterns.     Patients with suspected toxoplasmosis should be admitted and treated with pyrimethamine (100-200 mg po loading dose, followed by 50-100 mg po/day), plus sulfadiazine (4-8 gm po/day) with folinic acid (10 mg po/day) to reduce the incidence of pancytopenia.  Short courses of high-dose steroids are beneficial in cases where significant edema or mass effect is noted; seizure prophylaxis with phenytoin, may also be used in these cases.

Differential of Masses on CT

with mass effect

toxo

primary lymphoma

tuberculoma

brain abscess

without mass effect

encephalopathy

HIV encephalopathy

GI

Patients with esophagitis usually complain of pain and difficulty swallowing. Candida albicans is most often responsible for esophagitis in AIDS patients, causing about 60%-75% of cases.119 Other etiologies include CMV and herpes simplex virus. The antiretroviral drug ddC can produce esophageal ulcers, and some patients with HIV have idiopathic esophageal ulcers that respond to steroids.120 Those using topical solutions for oral candidiasis, such as clotrimazole troches or nystatin suspensions, may not have visible evidence of oral or pharyngeal thrush but still have esophageal disease; topical solutions are effective for oral candidiasis but not for esophageal infection.

Diarrhea

Diarrhea is the most common gastrointestinal complaint in AIDS patients and is estimated to occur in 50% to 90%. Diarrhea can vary in severity from a few loose stools per day to massive fluid loss with prostration, fever, chills, and weight loss. Potential pathogens include parasites (Cryptosporidium parvum, Enterocytozoon bieneusi, Isospora belli, Giardia lamblia, Entameba histolytica, Microsporidia, Cyclospora, and others), bacteria (Salmonella, Shigella, Campylobacter, Helicobacter pylori, Mycobacterium tuberculosis, Mycobacterium avium complex, Clostridium difficile, and others), viruses (cytomegalovirus, herpes simplex, HIV, and others), and fungi (Histoplasma capsulatum, cryptococcus neoformans, coccidiodes imitis, and others). Significant gastrointestinal bleeding and dehydration have been associated with many pathogens, particularly CMV. Salmonella infection can be of particular concern in HIV-infected patients, often producing recurrent bacteremia and other significant clinical disease. Neoplastic GI involvement with KS or lymphoma may produce dysphagia, obstruction, intussusception, or diarrhea. Cryptosporidium and Isospora infections are commonly associated with HIV infection, and both organisms may produce prolonged watery diarrhea.[ii]112-113 Diagnosis may be sought using acid-fast staining of stool samples, or by monoclonal antibody, or enzyme-linked immunoabsorbent assays.  Treatment of these disorders is clinically variably successful.  Symptoms may be treated with diet modification or loperamide.  Cryptosporidium infections may be treated with some success with paromomycin (500 to 750 mg, PO, 4 times daily for 2 to 4 weeks), or azithromycin (2,400 mg/day on day 1, followed by 1,200 mg/day for 4 weeks, followed by 600 mg/day).[iii]114-115 Isospora infections are often successfully treated with TMP-SMX (1 DS tablet, PO, 3 times daily for 10 days, followed by twice weekly therapy for 3 weeks).[iv]1[v]16 Pyrimethamine or metronidazole may be used as alternative therapy.   ED management should include repletion of fluid and electrolytes and obtaining of appropriate diagnostic studies. These may include microscopic examination of stool for leukocytes and of stool samples for bacterial culture, acid-fast stain, ova, and parasites. If indicated, outpatient anoscopy, proctoscopy, or sigmoidoscopy (with or without biopsy) may be arranged for patients who require further evaluation but do not require immediate admission.  Management of symptoms of severe diarrhea not requiring specific therapy may include attapulgite (Kaopectate), psyllium (Metamucil), diet modification, or diphenoxylate hydrochloride with atropine (Lomotil).

Skin

Scabies

treat with 5% permethrin, single application

better yet Ivermectin 200 mcg/kg x 1 PO dose, as more effective and easier to take than lindane. (J Derm 28:481 2001)

Fever

PCP, pneumonia, MAC, lymphoma, toxo, line sepsis,

Send a cryptococcal antigen, blood cx for AFB, gallium scans or induced sputum for PCP

Lactic Acidosis

stavudine and didanosine when coadministered

didanosine and ribavarin coadministration

anecdotal reports of benefit from

thiamine 100 mg/day

riboflavin 50-200 mg/day

L-carnitine 990 mg tid

CoQ10 at least 50 mg/day

levels may be slow to normalize

Warm Line National HIV consultation 8am-8pm (800-933-3413)

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Otolaryngology (ENT)

Sensory supply to the ear

trigem=ant canal

VII=post canal

IX=lower canal

X=TM

II,III=post auricular region

Hearing Testing

Rinne

Use 512 Hz against mastoid ask which is louder, it should be air.

Weber

Place in middle of forehead

Conductive loss ear will hear better

Opposite of the sensorineural ear will hear better

Acute Otitis Media

Caused by Eustachian tube dysfunction.  S. Pneumo, H. flu, m. catarrhalis

Clear wax c 3% Hydrogen Peroxide.  In kids diagnose with pneumatic otoscopy

Amoxicillin, Bactrim (kernicterus if <2 mo.)  10 day course

Document no mastoid tenderness

Mastoiditis

Classic is from an untreated AOM

CT Scan c contrast

Trial of IV ABX and ENT consult for myringotomy

Bullous Myringitis

clear or hemorrhagic vesicles on TM

Viral or from mycoplasma

Sx treatment

Otitis Externa

pseudomonas and staph aureus

Presents with itching, pain, fullness in ear, redness and swelling, white cheesy or watery green d/c

Cleanse the ear and fully suction

2% acetic acid (VoSol Otic Solution or VoSol HC) or just have folks mix supermarket white vinegar half and half with warm tap water

If severe give the vinegar and then topical abx (polymyxin B, neomycin, with HC=cortisporin otic solution or suspension.)   If TM is perfed, use only the suspension.

A wick may need to be inserted to allow ABX access

Avoid wetting the canal for 2 weeks

If cellulitis is present, give systemic abx as well

Objective To compare the clinical efficacy of ear drops containingacetic acid, corticosteroid and acetic acid, and steroid and antibiotic in acute otitis externa in primary care.Participants 213 adults with acute otitis externa.Conclusions Ear drops containing corticosteroids are more effectivethan acetic acid ear drops in the treatment of acute otitisexterna in primary care. Steroid and acetic acid or steroidand antibiotic ear drops are equally effective.(BMJ  2003;327:1201-1205 (22 November), doi:10.1136/bmj.327.7425.1201)

Malignant Externa

It is actually pseudomonas osteo of the external canal and temporal bone.  ENT and IV ABX.

can be seen in diabetics and immuno-compromised folks

pain on the bony/cart border in front of tragus

30% of ct scans can be neg

give iv cipro

Perichondritis

infection of auricular cartilage

swollen red pinna

Ciprofloxacin or Augmentin

to cover pseudomonas, proteus, and staph

TM Perforation

give abx only if AOM or debris present

follow-up c ENT

Use only suspension

Foreign Bodies or Wax

it is safe to use syringe with canulla to spray eardrums for FB or wax (Emerg Med J 2005; 22:266-268)

Insects: Kill the insect before attempting to remove it Mineral oil or lidocaine (2%), or isopropyl alcohol (Suggest baby oil, isopropyl alcohol, or cooking oil if patient is frantically calling the ED)

Insecticidal activity of common reagents for insect foreign bodies of the ear Antonelli PJ, Ahmadi A, Prevatt A, Laryngoscope. 2001;111:15-20 Conclusion: Many agents commonly available in the EMS may be used to kill insect foreign bodies in the ear canal. Antiseptic agents and microscope oil were the most effective against the most common insect foreign body, the cockroach. Ticks were the most resistant to all agents tested. Comment: What is the best agent to grab when you have a distraught patient severely agitated by the presence of a live insect in the ear? Mineral oil has been commonly recommended, but it tends to create a gooey mess, making foreign body removal more difficult. Isopropyl alcohol would be my drug of choice. Although it is only number 2 on the quick-kill list, it is probably more readily available than the number 1–ranked ethyl alcohol. Liquid anesthetics are a nice thought, but take at least 3 or 4 times longer to achieve the desired lethal effect on the bug. (From ACEP)

Epistaxis

Greater understanding and visualization of nasal anatomy revealed that the nose receives blood from many different sources and a large amount of vascular redundancy exists.  The external carotid artery divides into the maxillary and superficial temporal arteries.  The maxillary artery has many branches including the sphenopalatine artery.  The sphenopalatine artery emerges from the sphenopalatine foramen and further divides into four branches: the posterior septal, inferior turbinate, middle turbinate, and nasopalatine arteries.  The inferior and middle turbinate arteries depart from the sphenopalatine artery at right angles.  Through its four divisions, the sphenopalatine artery supplies the majority of the blood to the nose (43).  The sphenopalatine infuses the posterior aspect of the nose, the septum, and the lateral wall from the middle turbinate caudally.  In the anterior region of the septum at about the same level as the middle turbinate is Little’s area and within it is Kiesselbach’s plexus, a area of vascular anastomosis that is often the site of anterior epistaxis.(Emedhome.com)

Little’s Area=Kiesselbach’s plexus.  The anteroinferior portion of the nasal septum.  most common ant bleeds.

Posteroinferior turbinate is the most common source of posterior bleeds

Hold for 15 minutes

Silver nitrate if can have 4-5 sec s bleed.  Never use for more than 15 sec.  Can also try surgicel/gelfoam

Afrin (oxymetazoline) a few squirts up the nose

Soak cotton swabs in lidocaine with epi, put as many as possible into nares (4-5) leave for 10 minutes.

4% Cocaine (still the best, comes in a slurry)

4% Lidocaine mixed 1:1 with 1% phenylephrine

Oxymetazoline 0.05% (Afrin – nasal spray) and 4% lidocaine 1:1

A few mils of 1:10,000 epi mixed with some 4% lidocaine

Leave anterior pack for 48 hrs, send home with Keflex

Unless severe hypertension is a problem, first squirt a nasal decongestant

into the affected nares, then have patient hold pressure on anterior nares

for 15 minutes by the clock.

If bleeding persists, using a headlamp, Frasier suction, and speculum put arms in vertical position to avoid compressing the septum)

illuminate the nares and if a bleeding site is apparent, cauterize it with a silver nitrate stick.

If bleeding continues (usually from a site inaccessible for cautery),

pack the anterior and middle nasal passage with an expandable sponge

(Merocel or similar), expanding it with more decongestant or cocaine spray.

May need more than one

If bleeding persists, then usually from a posterior source, remove the

anterior/middle packing, place a small Foley catheter through the nose into

the nasopharynx, blow up the balloon, pull it anteriorly to occlude the

posterior nares and direct all bleeding anteriorly, then repack the entire

nares with petroleum gauze strips using bayonet forceps. Clamp the Foley

where it exits the nose and tape the end of the gauze and Foley to the cheek

in a way that doesn’t pull against the skin of the nares.

Prophylaxis with TMP/SMX or keflex for sinusitis prevention (don’t know

the evidence, but ENT always asks me to), and admit the patient to a

monitored bed.

patients may become hypoxic and bradycardiac and can have actual syncope following posterior packing believed to be from a nasopulmonary reflex.

For patients with severe coagulopathies, also consider giving FFP

TECHNIQUE

A loop of BIPP-coated ribbon gauze is inserted into

the nose using Tilley dressing forceps. The forceps

are withdrawn and reinserted below the loop of

BIPP. The dorsal surface of the forceps is then used

to guide the loop into the superior nasal cavity and

to compress it into position. The next loop is

inserted into the nose and likewise compressed,

and this cycle is repeated until the whole nose is

filled by BIPP, extending from the superior limit of

the nose to the floor. This method has two

advantages over the traditional method: the internal

nasal valve does not limit the insertion of BIPP

and with each loop of BIPP inserted the cribriform

plate is further protected from trauma that could

otherwise be inflicted using the forceps.

(Emerg Med J 2009;26:52.)

Laryngeal Dyskinesia

review article (emerg med australia 2007;18 by lawrence sg)

Spasmdomic Dysphonia

irritable larynx disease.  May have benefit from heliox.  May need to be tubed

Paradoxical Vocal Cord Movement

young women

start on PPI

benzos

Lidocaine 2% 2 cc in 2 cc NS, nebulize

Cool Mist Nebs

Tell them to sniff, may disappear. May also disappear when reading from a book

Muscle Tension Dysphonia

On scoping, you will see vocal cord adduction

THE DIFFERENTIAL DIAGNOSIS OF PARADOXICAL VOCAL CORD MOVEMENT

Jamie Koufman, MD

This article is reprinted from THE VISIBLE VOICE Vol. 3, No. 3. (July 1994).

ABSTRACT

Paradoxical vocal cord movement (PVCM) producing airway obstruction is a relatively uncommon, and sometimes confusing, condition that affects the larynx. PVCM occurs when there is inappropriate closure of the vocal cords during inhalation, and the resultant respiratory obstruction may be intermittent or continuous, mild or severe, depending on the cause. The differential diagnosis of PVCM also includes congenital, inflammatory, traumatic, neoplastic, and neurological causes. Contrary to popular belief, relatively few cases are “functional,” i.e., psychogenic. This article presents the clinician with a differential diagnosis for PVCM and the clinical features that differentiate its various causes.

INTRODUCTION

During the respiratory cycle of most higher animals and of human beings, the vocal cords partially abduct (open) with inhalation and partially adduct (close) with exhalation. This phasic vocal cord movement is physiologic, and it allows the unimpeded movement of air into the lungs during inspiration while helping to maintain the alveolar patency (of the lungs) by providing positive airway pressure during expiration. Thus, the larynx serves as an upper airway valve to help keep the lungs expanded.

Some patients who present with stridor (noisy breathing), dyspnea (difficulty breathing), and upper airway obstruction have paradoxical vocal cord movement (PVCM), characterized by inappropriate adduction (closure) of the vocal cords during inhalation. The persistence and the degree of inappropriate glottic closure determines the degree of the airway obstruction, and hence the severity of respiratory symptoms experienced by the patient. In some patients, the problem is constant and severe, requiring prompt remedial treatment, and in other patients, the problem is intermittent and relatively mild. Few articles1,2 address the differential diagnosis of this condition or provide an approach to the management of these challenging patients.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of PVCM is shown in Table 1. Three key elements of the history quickly limit the possibilities in each case: (1) Is the stridor constant or intermittent? (2) Is there any history of head trauma, stroke, or other brainstem problem? (3) Are there any other associated symptoms, such as hoarseness, dysphagia, globus pharyngeus, or cough? In addition, as discussed below, the findings on fiberoptic laryngeal examination are crucial in making the diagnosis.

TABLE 1: PARADOXICAL VOCAL FOLD MOVEMENT (DIFFERENTIAL DIAGNOSIS)

• Gastroesophageal (laryngopharyngeal) reflux
• Psychogenic stridor (usually in adolescents)
• Respiratory-type laryngeal dystonia
• Drug-induced laryngeal dystonic reactions
• Asthma-associated laryngeal dysfunction
• Abnormalities that affect the brainstem
  • Chiari malformation I & II, hydrocephalus, meningomyelocele
  • Cerebrovascular accident (stroke)
  • Severe closed head injury

Paroxysmal Laryngospasm and PVCM Due to Gastroesophageal Reflux Gastroesophageal reflux can cause a true intermittent type of PVCM, laryngospasm, or both, in which adduction predominates and abduction is temporarily lost during “attacks.”3-5 Thus, laryngospasm may be considered a specific variation of PVCM. Using this definition, reflux appears to be the most common cause of PVCM.5 In either case, the attacks of respiratory obstruction are paroxysmal and the result of direct contact of gastric fluids with laryngopharyngeal structures.5 It is postulated that some additional form of vagal dysfunction may prolong the episodes for minutes, hours, or sometimes days.6,7

Patients with this frightening condition describe intermittent, sudden-onset, noisy, obstructed breathing, which some describe as “choking episodes.” Attacks of stridor may follow a pattern, e.g., occurring after a meal, after the start of exercise, or after bending over. Sometimes, the attacks may awake the patient from sound sleep. Often, the attacks are truly paroxysmal, occurring without any pattern or identifiable precipitating events. Some patients have one or more attacks per day, and others have their attacks as infrequently as a few each year. The duration of attacks is variable, but “a few minutes” is typical.5

Two-thirds of the patients deny ever having heartburn; however, all complain of some other symptom(s) of laryngopharyngeal reflux, such as chronic or intermittent hoarseness, difficulty swallowing, a sensation of a lump in the throat, chronic throat clearing and cough, or simply too much throat mucus and/or “post-nasal drip.”5

Within the past two years, the author has diagnosed this condition in 15 adult patients.5 Of these, 12 underwent pH monitoring, which yielded abnormal findings in 11 (92%), five of whom had laryngopharyngeal reflux demonstrated by a pH probe in the hypopharynx behind the laryngeal inlet.5 All fifteen patients were treated with dietary and life-style modification as well as omeprazole 20 mg b.i.d., and, within four weeks, all attacks of laryngospasm had ceased in all patients.

H2-blockers appear to be inadequate treatment for reflux in this group of patients.5,8 For some patients under age 40 years, fundoplication should be considered as an alternative long-term treatment after the symptoms of laryngospasm have been initially corrected by omeprazole therapy; that is, antireflux surgery should be considered in patients who subsequently fail maintenance on H2 blocker therapy.5,8

Patients with the respiratory type of adductor laryngeal dystonia (discussed below), may also have reflux disease. When these two conditions occur together, the attacks of PVCM tend to be prolonged and severe, and the patient may require airway intervention, e.g. intubation or tracheotomy. Such a patient usually requires treatment with both botulinum toxin and omeprazole.

The clinician caring for patients with PVCM due to causes other that reflux should realize that reflux may be a secondary initiating or complicating factor. When laryngopharyngeal reflux is suspected, by the history or by the laryngeal findings, ambulatory 24-hour double-probe pH monitoring is indicated. Long-term medical treatment or surgical fundoplication is usually necessary in such patients.

Psychogenic Stridor

After reflux, psychogenic stridor appears to be the second most common cause of PVCM. (The author sees approximately 2 to 3 such cases each year.) Usually, this group of patients is easily diagnosed. First, almost all are teenagers. Second, PVCM occurs with a sudden onset and offset. Third, such patients are usually unconcerned (blase) about their noisy breathing and airway obstruction. Fourth, it is usual for the clinician to be able to “fool” the patient during fiberoptic examination, thus making the PVCM go away. (In most cases, when the patient is asked to read a long passage loudly, the stridor may disappear and phasic respiratory activity of the vocal cords may become normal.) Fifth, the PVCM attacks often can be precipitated and ameliorated by injections of placebo.9-13

The history of each patient will often suggest an underlying psychologic or psychiatric problem, manipulative behavior, and family problems, alone or in various combinations, and the stridor usually occurs at “times of significance” for the patient. In one patient, for example, the stridor only occurred when she was sent to the school principal’s office for misbehaving. Characteristically, her stridor was so loud and disturbing that it demanded medical attention.

A word of caution about this diagnosis. Even though the criteria for psychogenic stridor are fairly well-established — (1) periods of normal phasic vocal cord movement during the fiberoptic examination, (2) induction of stridor and response to placebo, and (3) a psychological or psychiatric disorder — still, this is almost a diagnosis of exclusion. A review of the literature makes clear that many cases of “psychogenic stridor” probably actually had an organic basis, e.g., reflux or dystonia.

Patients with presumed psychogenic PVCM should be approached by the otolaryngologist and the psychologist and/or psychiatrist as a team, and should be completely evaluated before the team reaches a final diagnosis.

In the author’s experience, none of the patients diagnosed as having psychogenic stridor have subsequently developed one of the other conditions associated with PVCM. On the other hand, patients with another presumed cause of PVCM, such as respiratory-type laryngeal dystonia, are sometimes eventually diagnosed as having psychogenic stridor. In other words, the differentiation between dystonia-related and psychogenic PVCM sometimes may be difficult.

Respiratory-Type Adductor Laryngeal Dystonia The most common type of focal laryngeal dystonia causes a voice disorder known as spasmodic dysphonia (SD). SD occurs in women five times more frequently than in men, is rarely seen in people under age 20 years, and usually affects the voice very severely, but does not affect respiration. The most common pattern is the adductor type, in which glottal overclosures create a “strain-strangled” sounding voice. Patients with this type of SD do not usually experience difficulty breathing, although some patients with severe non-focal dystonia involving the larynx and pharynx (Meige’s syndrome) do have severe, inappropriate laryngeal hyperadduction, which causes airway obstruction. There also is a small group of patients with a respiratory type of adductor laryngeal dystonia in whom the vocal cords inappropriately hyperadduct during inspiration but the voice is normal. Stridor in these patients is present throughout the day, but disappears during sleep, a characteristic of most dystonias.

Blitzer and Brin 14 reported a large series of patients with laryngeal dystonia, most of whom had the well-recognized adductor-type SD. However, they did report that approximately 1% had a respiratory type of adductor laryngeal dystonia, as described above.

Within the past five years, the author has seen five patients with this type of laryngeal dystonia; these patients represent 2% of the author’s laryngeal dystonia patient population.15 None of the five have significant abnormality of voice, but two actually presented with tracheotomy tubes in place.15 On fiberoptic examination, the vocal cords characteristically close during inspiration, and when the patient is asked “take a deep breath,” the degree of overclosure worsens, increasing the respiratory obstruction.

Of the five patients in the author’s series, all have responded well to treatment with botulinum toxin, although this group of patients appears to need larger doses of botulinum toxin than those required by typical SD patients.15

Drug-Induced Laryngeal Dystonic Reactions

Temporary drug-induced PVCM has been reported after administration of neuroleptic drugs, including chlorpromazine and haloperidol.16 (Obviously, this cause of PVCM needs to be considered only in patients receiving such medications.) The stridor is usually associated with extrapyramidal symptoms, muscle stiffness, and dystonias of the head and neck, e.g., torticollis. The airway obstruction (PVCM) and the other dystonias are relatively short-lived (hours), and are reversible with intravenous administration of an anticholinergic drug.16 (The author’s experience is in agreement with this report.)

Thiopental, an anesthetic, also may have some such effects at certain doses.17 This may explain the relatively high incidence of “laryngospasm” observed during the induction of anesthesia. It has been shown experimentally that such laryngospasm can be prevented by the administration of topical lidocaine.18

Asthma-Associated Laryngeal Dysfunction

Patients who present with PVCM are frequently misdiagnosed as having asthma as the cause of the airway obstruction, even though anti-asthma medications are ineffective. Nevertheless, there appears to be a subset of patients with asthma who also have PVCM.19 Although the mechanism of PVCM in these patients is unknown, glottal aperture changes have been observed in asthma patients20; and vagal reflex dysfunction may be the cause.20 In any asthma patient, when inspiratory stridor is present, the diagnosis of PVCM should be considered. The finding of PVCM on transnasal fiberoptic laryngoscopy is diagnostic.

Brainstem Abnormalities

Many central neurological (usually brainstem) abnormalities can cause PVCM, in addition to or complicated by bilateral abductor paralysis, apneic episodes, and central sleep apnea syndrome.21 23 Severe closed head injury, Chiari malformations I and II, meningomyelocele, and cerebrovascular accidents (strokes of the posterior circulation) may all produce PVCM. In these cases, the obstruction and inappropriate vocal cord movement may be inconsistent and variable, and may appear to change with multiple fiberoptic examinations; what is important, however, is that the stridor does not disappear during sleep. This point is critical, since with all the other causes of PVCM, the stridor is paroxysmal or improves during sleep. Early (days or weeks) after closed head injury, extubation may fail and the patient may require multiple intubations, and then, later on, a tracheotomy. With time, as the cerebral and brainstem edema subsides, the vocal cord movement may return to normal and the stridor will disappear. Similarly, some patients with congenital lesions of the brainstem may experience a normalization of vocal cord function after surgical treatment of the lesion.

In the evaluation of patients with PVCM due to brainstem abnormalities, computerized tomographic scanning, magnetic resonance imaging (or both), as well as neurologic consultation is recommended. The prognosis should be guarded. For instance, patients with Chiari malformations who undergo surgical treatment of the malformation may have improvement of their PVCM postoperatively, while others may require a permanent tracheotomy.

APPROACH TO THE PATIENT WITH PVCM

After a thorough history is obtained, the first examination of the stridulous patient should include transnasal fiberoptic laryngoscopy (TFL). During this examination, the patient should be asked to: (1) alternatively phonate the vowel /i/ and sniff, in rapid alternating succession; (2) take deep breaths; (3) cough, throat clear, and chuckle; (4) count to fifty, rapidly and loudly; (5) read a written passage in a loud voice; and (6) sing.

These maneuvers may reveal a pattern of adduction and abduction consistent with PVCM and a specific diagnosis. Patients with an organic cause of the PVCM, that is, a non-psychogenic cause, usually demonstrates consistent fiberoptic findings, whereas patients with psychogenic PVCM do not. Patients with psychogenic stridor, for example, will often revert to normal phasic vocal cord movement when asked to count or read out loud.

PVCM is therefore usually diagnosed by TFL, and the diagnosis should be considered when there are findings of: (1) inappropriate vocal fold adduction during inspiration; (2) paroxysmal inability to abduct the vocal cords (“transient abductor paralysis”); or (3) a combination of these findings. There is, however, one group of patients that comprises a notable exception: patients with reflux-induced paroxysmal laryngospasm may have normal phasic vocal fold movement on TFL. In these patients, other findings characteristic of laryngopharyngeal reflux (edema, erythema, posterior commissure hypertrophy, and granulation) are almost always observed.

A firm diagnosis of reflux-induced PVCM can be made when the history (pattern and associated symptoms), the laryngeal findings, and the pH monitoring data all support the diagnosis. In addition, complete resolution of the laryngospastic episodes during a therapeutic trial of omeprazole (20 mg b.i.d.) confirms of the diagnosis.

Unlike patients in the other PVCM groups, patients with respiratory-type laryngeal dystonia describe a progressive onset of the PVCM over a period of days, weeks, or months. In addition, such patients usually deny having hoarseness or other reflux symptoms. On TFL, their PVCM is consistent and worsens when the patient is asked to take a deep breath, although the PVCM may improve when the patient reads a written passage or sings. However, improvement is only partial and transient.

On occasion, differentiating dystonic from psychogenic PVCM can be a difficult task. When the clinician is faced with this diagnostic dilemma, neuropsychological testing, psychiatric consultation, and trial injections of botulinum toxin may all be indicated. In some cases, it may take months for the clinical team to reach a diagnosis.

Except for patients in the brainstem abnormality group (who often require tracheotomy), patients with PVCM usually do not have respiratory obstruction severe enough to warrant emergency airway intervention. Of the other groups of patients with PVCM, dystonia patients appear next in terms of the frequency of need for airway support, followed in decreasing order by the psychogenic group, the asthma group, and the reflux group. Table 2 summarizes some of the differentiating features of PVCM.

The diagnostic work-up for each patient with PVCM should be individualized and may include some or all of the following: serial fiberoptic examinations, pH monitoring, neuropsychiatric evaluation, placebo injections, audio-recordings of the patient’s breathing during sleep, and radiographic examinations. In selected cases, therapeutic trials of omeprazole and/or laryngeal injections of botulinum toxin also may be used.

Finally, PVCM can be confused with other causes of laryngeal obstruction, at least on the initial clinical examination. Inspiratory stridor, for example, may be seen in patients with bilateral vocal cord paralysis, and in patients with laryngeal stenosis or fixation. These conditions may be differentiated from PVCM because, in the former group of conditions, examination shows that vocal cord abduction does not occur. Although abduction may be inconsistent, inappropriate, or incomplete, it must occur some of the time in order for the diagnosis of PVCM to be made.

TABLE 2 SOME DIFFERENTIATING FEATURES OF THE CAUSESOF PARADOXICAL VOCAL CORD MOVEMENT

Pattern

Duration

Hoarseness

Airway Support Needed

Reflux

paroxysmal

minutes

usually

almost never

Dystonia

daytime

hours

rarely

sometimes

Psychogenic

paroxysmal

variable

never

sometimes

Brainstem

continual

continual

sometimes

usually

SUMMARY

PVCM presents the clinician with an interesting and challenging differential diagnosis. Only abnormalities of the brainstem produce a constant (day and night) stridor and respiratory obstruction, whereas all of the other causes are intermittent or occur only during the daytime. The causes of PVCM, in the author’s experience, in order of frequency of occurrence are: gastroesophageal reflux, followed by psychogenic stridor, respiratory-type laryngeal dystonia, and abnormalities of the brainstem. In the last group, closed head injuries are most common.

The work-up of PVCM may require a multidisciplinary approach and a variety of diagnostic methods. Likewise, treatment often must be individualized. € Jamie Koufman, M.D.

REFERENCES

1. Ward PH, Hanson DG, Berci G: Observations on central neurologic etiology for laryngeal dysfunction. Ann Otol Rhinol Laryngol 90:430-441, 1981

2. Kellman RM, Leopold DA: Paradoxical vocal cord motion: an important cause of stridor. Laryngoscope 92:58-60, 1982

3. Chodosh PL. Gastro-esophageal reflux. Laryngoscope 87:1418-1427, 1977

4. Burton DM, Pransky SM, Kearns DB, et al.: Pediatric airway manifestations of gastroesophageal reflux. Ann Otol Rhinol Laryngol 101:742-749, 1992

5. Koufman JA, Loughlin C: Paroxysmal laryngospasm: an uncommon manifestation of gastroesophageal (laryngopharyngeal) reflux disease (Unpublished data)

6. Bauman NM, Sandler AD, Schmidt C, et al.: Reflex laryngospasm induced by stimulation of distal afferents. Laryngoscope 104: 209-214, 1994

7. Campbell AH, Mestitz H, Pierce R: Brief upper airway (laryngeal) dysfunction. Aust NZ Med 20:663-668, 1990

8. Koufman JA: Gastroesophageal reflux and voice disorders. In Diagnosis and Treatment of Voice Disorders Editors: Gould WJ, Rubin JS, Korovin G, Sataloff R. Igaku-Shoin Publishers, New York (In press)

9. Appleblatt KL, Baker SR: Functional airway obstruction. A new syndrome. Arch Otolaryngol 107:305-307, 1981

10. Snyder HS, Weiss E: Hysterical stridor: a benign cause of upper airway obstruction. Ann Emer Med 18:991-994, 1989

11. George MK, O’Connell JE, Batch AJ: Paradoxical vocal cord motion: an unusual cause of stridor. J Laryngol Otol 105:312-314, 1991

12. Skinner DW, Bradley PJ: Psychogenic stridor. [Review] J Laryngol Otol 103:383-385, 1989

13. Walker FO, Kilgo G, Hunt V, Koufman JA: Induction of psychogenic respiratory distress. (Unpublished data)

14. Blitzer A, Brin MF: Laryngeal dystonia: a series with botulinum toxin therapy. Ann Otol Rhinol Laryngol 100:85-89, 1991

15. Koufman JA, Blalock PD: Diagnosis and subclassification of spasmodic dysphonia: the value of “unloading” and of spectral analysis. Presented at the American Laryngological Association annual meeting, Los Angeles, California, April 18, 1993. (Submitted for publication)

16. Koek RJ, Pi EH: Acute laryngeal dystonic reactions to neuroleptics. Psychosomatics 30:359-364, 1989

17. Stoelting RK: Pharmacology and Physiology in Anesthetic Practice. page 112, Philadelphia, J. B. Lippincott Co., 1987

18. Henderson PS, Cohen JI, Jarnberg P-E, et al.: A canine model for studying laryngospasm and its prevention. Laryngoscope 102:1237-1241, 1992

19. Hayes JP, Nolan MT, Brennan N, FitzGerald MX: Three cases of paradoxical vocal cord adduction followed up over a 10-year period. Chest 104:678-680, 1993

20. Collett PW, Brancatisano T, Konno K: Changes in glottic aperture during bronchial asthma. Am Rev Respir Dis 128:719-723, 1983

21. Holinger PC, Holinger LD, Reichert TJ, Holinger PH: Respiratory obstruction and apnea in infants with bilateral abductor vocal cord paralysis, meningomyelocele, hydrocephalus, and Arnold-Chiari malformation. J Pediatrics 92:368-373, 1978

22. Hesz N, Wolraich M: Vocal-cord paralysis and brainstem dysfunction in children with spina bifida. Dev Med Child Neurol 27:528-531, 1985

23. Charney EB, Rorke LB, Sutton LN, Schut L: Management of Chiari II complications in infants with meningomyelocele. J Pediatrics 111:364-371, 1987

© Copyright, Center For Voice Disorders of Wake Forest University

Earlobe Lacs

Must cut both wound edges or will not heal well

Sore Throat

Negative rapid strep and worsening pharyngitis raises an interesting differential diagnosis.  Remember that the rapid strep test only has a sensitivity of 80-90%.  Sometimes we do not get an adequate throat swab.  Sometimes we have sampling error.  So a negative rapid test does not eliminate group A strep as a possibility.

Next, consider the non-group A strep – groups C and G.  In adolescents they cause approximately 1/3 as many sore throats as group A strep (this is not true for pre-adolescents.

Always consider infectious mononucleosis in adolescents with worsening pharyngitis.  Also remember that acute HIV infection can present as a sore throat.

Finally, we must consider peritonsillar abscess and Lemierre’s.  We should get clues from a careful physical examination.  We should examine the patient for neck swelling or asymmetric tonsillar swelling.

The key point is patient education.  We should tell patients that if they are worsening in 3-5 days that we should re-examine them, perhaps do further testing and generally view the patient as having a potentially serious infection.

Adult Epiglottitis

Can actually involve the supraglottic tissue and spare the epiglottis.  Muffled voice and anterior neck tenderness.  If there is no respiratory distress, you may perform laryngoscopy.  Start 3rd gen. Cephalosporin (or bactrim, zosyn).  Consider ICU admit or intubation.

Ducic and colleagues described the vallecula sign, which is easily learned and applied by practitioners at all levels of training [ix].  In this prospective, blinded study involving 26 laryngoscopically-proven cases of epiglottitis and 26 controls, staff emergency physicians, radiology and otolaryngology residents, and senior medical students were asked to evaluate randomly mixed radiographs for epiglottitis, both before and after a 5-minute tutorial on the vallecula sign.  The sign increased sensitivity and specificity from 78.5% and 82.8% to 98.2% and 99.5% respectively, with no difference between evaluator groups.  This sign is based on evaluating the vallecula, which appears as an air pocket at the level of the hyoid that should be roughly parallel to the pharyngotracheal air column.  To do this, first start at the base of the tongue, trace down to the hyoid bone where you should then find the epiglottis.  If the air column anterior to this is not deep, sharp, and roughly parallel to the pharyngotracheal air column, then epiglottitis is present.  In this study, the vallecula was deemed abnormal in all cases of epiglottitis, including those patients with minor symptoms, as well as those that needed urgent airway intervention.  Furthermore, the vallecula was deemed abnormal in cases where the epiglottis itself was difficult to evaluate (and hence signs like the thumb sign could not be applied).  A normal appearing vallecula accurately predicted a normal epiglottis (see Figure 4 below of a normal vallecula and an abnormal vallecula found with epiglottitis, both outlined in red). It is noted that the x-ray must be taken with the patient’s mouth closed, as an open mouth may artificially obliterate the vallecula by epiglottic repositioning.

The Vallecula Sign

Step 1:             Ensure that the patient’s mouth is closed for x-ray. Step 2:             Identify the base of the tongue. Step 3:             Trace the tongue to the level of the hyoid. Step 4:             Locate the epiglottis. Step 5:             Locate the air pocket extending nearly to the hyoid.   Is the vallecula deep and roughly parallel to the pharyngotracheal air column?      YES: No epiglottitis       NO: Epiglottitis present

crack or cocaine can cause it in the absence of infection

HIV folks are prone to it

Actinomyces

neck masses c sulfa granules.

Diphtheria

grey or white pseudomembrane.  Can be associated c polyneuritis, tubular necrosis, or myocarditis.

horse anti-toxin, erythromycin

From the Greek for skin or hide

C. diphtheriae (gram +)-humans are the only carriers

Resp tract and skin

Exotoxin induces grayish/brown membrane, which does not effect gingival.  Bleeding will occur if removal is attempted.

2-4 day incubation period

can cause cervical nodes extensive enough to give bull neck.

Myocarditis is possible 1-2 weeks after.

Can also give muscle weakness/paralysis 2° to exotoxin which looks like G. Barre

Indigent population can present c cutaneous presentation

Alert lab, b/c special cx is needed.

Give antitoxin (equine) 20000-400000 for pharyngeal disease and 80000-100000 for extensive disease

and 14 days erythromycin or PCN

Can get carrier state.

Booster immunizations every decade.

Pertussis (Whooping Cough)

Means violent cough.  Airborne transmission.  7-10 day incubation.

Bortedella pertussis

Catarrhal phase-non-specific uri. Most contagious

Paroxysmal-cough, decreased fever.  Post-tussive vomiting.  Lasts 2-4 weeks

Convalescent-can last months

Complications-aspiration pneumonia, CNS

Presents c very elevated WBC, get nasopharyngeal cx

Erythromycin may help, definitely give to non-immunized exposures

Pertussis component of DPT most likely to cause complications.

Strep Pharyngitis

cough is usually absent.

Give 60 mg POPrednisone x 1

(or Decadron)

Oral Dex helps subset of strep + kiddies, but only marginal improvement ((Ann Emerg Med. 2003 May;41(5):601-8))

im or oral dex helps pt >15 y/o (Laryngoscope. 2002 Jan;112(1):87-93)

A randomized clinical trial of oral versus intramuscular delivery of steroids in acute exudative pharyngitis. (Acad Emerg Med. 2002 Jan;9(1):9-14)  They are the same and help im dex. (Ann Emerg Med. 1993 Feb;22(2):212-5) Dexamethasone as adjuvant therapy for severe acute pharyngitis.  

only strep worth treating is group A B-hemolytic strep to decrease risk of RF and quinsy.  Antibiotics probably do not reduce risk of glomerulonephritis.

Centor criteria (Ann Int Med 2001;134:506)

• Fever (or reliable history thereof): 1 point
• Exudate: 1 point
• Cervical adenitis (tender enlargement of nodes): 1 point
• NO cough: 1 point

4 points: treat with penicillin (Bicillin 1.2 million units)

0,1 or 2 points: do not treat

3 points: flip a coin (trust your instinct, give an antibiotic if the patient

wants one, etc.)

If the Centor score is 4, the percentage of patients who have the disease is

50-70% depending on time of year, current outbreak in the community, etc.  Add

a scarletiniform rash (uncommon), and that takes the patient well into the 90′s%.

Sore throat score adds age

One point for age less than 15 years. One point is subtractedif the person is 45 years of age or older

Better than rapid strep (Can J Emerg Med 4 (3):178 2002)  Score had sensitivity of 97% and spec. of 78% while rapid strep testing was 75% and 99%.  Gold standard was throat cultures

Validated in Kids:

ACP Journal Club. v136(1):p.37, January/February, 2002.

Culture after Negative Rapid Strep is not necessary or cost effective (Preventative Medicine 35 25-257, 2002) Reviewed Source Attia MW, Zaoutis T, Klein JD, Meier FA. Performance of a predictive model for streptococcal pharyngitis in children. Arch Pediatr Adolesc Med. 2001 Jun;155:687-91.

cervical lymphadenopathy, tonsillar swelling (2-category severity scale: absent or mild and moderate or severe), coryza, and scarletiniform rash (present or absent)

218 children (37%) had positive culture results for GABHS. The prediction model did better than the physicians’ probability estimates and was comparable to the rapid antigen detection test . The model did not differ in performance according to setting (emergency department vs outpatient clinic) or study period (in season [January to March] vs off season [April to December]).

anti-streptolysin-O titers were not done leading to problem of differentiating carrier state

AAP standard evaluated vs. two rapids in a row. 

Single Rapid: Sens-88%, Spec 96.2%

Double Rapid:  92% and 95%

Rapid and Cx:  96% and 96%

(Pediatrics 111(6):666, June 2003)

Vincent’s angina

anaerobes, foul breath, pseudomembrane, sub-mandibular nodes.  From poor oral hygiene

Rx with Penicillin

STDs

gonorrhea and chlamydia

Mononucleosis

From Epstein Barr Virus (EBV), a herpesvirus

Tender, large anterior or posterior cervical lymph nodes

Get CBC c Diff, Monospot, throat culture and LFTs. Check for hepatosplenomegaly

Give prednisone 40 mg PO for 5 days

If you give ampicillin, they will get rash which is not allergic

Incubation period of 1-2 months, most occur 4-6 weeks after exposure. Can stay contagious for months after the infection.  (even years in a small percentage)

Three forms:

Anginose:  fever, sore throat, and adenopathy

Typhoidal:  prolonged fever, minimal pharyngitis, and delayed lymphadenopathy

Glandular:  dramatic LA, with minimal fever and pharyngitis

Complications:

Splenic Rupture:  1:1000 cases.

Airway Obstruction:  from hypertrophied tonsils and lymphoid tissues.  Steroid therapy is efficacious.

Lingual Tonsillitis

Occurs only post-tonsillectomy.  Pain worsens c tongue movement

Laryngitis

R/o epiglotittis, steroids help with quicker recovery

Laryngotracheitis

Viral

Bacterial

relatively  uncommon.  etiologies include staph, strep pneumo, and h. flu.  Diphtheria, TB, and syphyllis can also be causes.

Fungal

histoplamsosis, blastomycosis, coccidiomycosis (San Joaquin), and candidiasis

add four tabs (1 gm) of carafate to a bottle of ocean Use QID 3 sprays each time

From Centor

Most readers know that I have written extensively about pharyngitis.  After yesterday’s brief post about a letter I wrote, I received this comment:

so how should a culture be sent, just culture for any species? Our lab does STREP A culture only for throat/tonsil swabs.

Here are the problems for adolescent and adult pharyngitis (caveat – pre-adolescents are different in many ways so this rant only focuses on adolescents and adults):

1. The Group A strep rapid tests probably only have a sensitivity of around 75% in actual practice – this makes reliance on rapid tests less certain than most experts have suggested.  Fortunately the specificity is very high, so we can really believe positives but not negatives.
2. Group C (and group G) cause approximately 1/3 as many sore throats as group A – but I would favor treating those infections.  Some labs will culture for these infections, but most only culture for group A.
3. Fusobacterium necrophorum probably causes approximately 10% of pharyngitis in this age group.  We cannot currently test for this infection.
4. All these bacterial infections can cause serious sequelae.

So what is a conscientious clinician to do?  I have favored the empiric therapy approach for those patients who look sick.  I define looking sick as pharyngitis scores of 3 or 4 (I am still embarrassed to type the eponym).

I tell all patients that they should be improved in 3-5 days. If their symptoms worsen or if they develop neck swelling they should return for further evaluation.

And that’s my story – and I am stickin

Angioedema

Deep Space Infections

Masticator Space Abscess

bounded by masseter and internal pterygoid muscles

from extension of anterior space infection

lateral face swelling and trismus

Ludwig’s Angina

from the Latin angere: to strangle

odontogenic infections

Progressive cellulitis of mouth and neck beginning in the submandibular space.

Ludwig’s angina is a cellulitis involving the submandibular (sublingual, submaxillary, submental) spaces, rather than simply any perimandibular infection as often erroneously described

Dental disease is the most common cause.  Can cause airway obstruction.  Neck tenderness, sub-Q emphysema.  Cellulitis of connective tissue, not glands.  Bilateral.

Microbes associated with Ludwig’s angina

Viridans streptococci

Streptococci species

Bacillus fragilis