Neglected phases of TBI-apneic and catecholamine surge
Suspect elevated ICP if:
GCS ≤ 10 and:
Hematoma volume > 30 ml (A,B,C,/2)
Midline Shift > 1 cm
Pineal shift > 5 mm
Compression of the Lateral VentriclesBack to top
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 38 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
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.Back to top
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)Back to top
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)Back to top
brain hits opposite wall first. Air bubble in soda bottle (Neurocritical Care 2004;1:384)
Diffuse Axonal Injury
Widespread structural failure of axonsBack to top
Who Needs Surgery?
A Simple Tool To Predict The Need To Operate On A Subdural Hematoma
- Measurements of the maximum thickness of the lesion, its volume, and the degree of midline shift were taken.
- Reasonable attempts were made to ensure inter-rater reliability.
- The total pool of scans studied was 483. 44% were judged to need surgical management.
- Maximum SDH thickness of 10mm or more, or a midline shift of 1mm or more were found to accurately predict 100% of surgical lesions.
- The best predictor of the need for surgery was midline shift.
- Adding hematoma thickness did not significantly improve the ROC curve.
Single center experience: Injury 46(1):76-79, 2015.
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 gcsBack to top Back to top
ICP Monitor, either ventriculostomy or bolt (parenchymal strain gauge) if abnormal CT or normal CT c 2 of 3: SBP<90, Age>40, posturing
(BEST TRIP TRIAL) No benefit in this one RCT of camino monitoring vs. neuro exam and imaging by Chestnut et al. (N Eng J Med 367;26:2471-2381) and then Chestnut wrote his own editorial of the paper (Intens Care Med 2013;39:771)Back to top
Cerebral Perfusion Pressure
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 lessBack to top
HerniationBack to top
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
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
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)Back to top
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)Back to top
A recent review demonstrated that perhaps we should consider hypertonic, not mannitol the gold standard for ICP measurement (Crit Care 2012;16:113)
Another great review (Neurocrit Care. 2012 Aug;17(1):117-30. Hyperosmolar therapy for intracranial hypertension.)
And a meta-analysis of Hypertonic Saline (J Neurosurg 2012;116:210)
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
Meta-Anal of Hypertonic vs. Mannitol shows hypertonic is better (Crit Care Med 2011;39:554)
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
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; 31:16831687
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; 36:795800
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; 33:196202, discussion 257198
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; 60:494498
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; 35:344348
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:R530R540
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; 12:334344
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; 51:324325
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
23.4% will reduce intracranial hypertension even when serum and CSF osmolality is high (Neurocrit Care 2012;17:204)
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)Back to top
ICP Monitoring Waves
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
IVC if not already placed
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
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)
ICP and IAP are correlated (Inten Care Med 2005;31:1577)
THAM may lower ICP as well
GHB may be better than barbsBack to top
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 15Back to top
Intracranial Volume Targeted (Lund Concept)
Ways its been described:
Antihypertensive and intracranial volume-targeted therapy
Physiological volume regulation of the intracranial compartments
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
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)
The modified Lund concept, directed at bedside real-time monitoring of brain biochemistry by CM showed better results compared to CPP-targeted therapy in the treatment of comatose patients sustaining SBI after aneurysmal SAH and severe TBI. (Clin Neurol Neurosurg. 2012 Feb;114(2):142-8.)Back to top
Brain Tissue Oxygen Monitoring (PbtO2)
should be pvO2 > 15-20 mm Hg
Licox will give readings 5 mm Hg lower than Neurotrend (anecdotal)
Midline shift>5mm or mass effect
Large or enlarging hematoma
Depressed skull fracture
Posterior fossa mass lesion
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)
Excellent Review Article (Crit Care Med 2009; 37:2057–2063)Back to top
Lactate/Pyruvate Ratio should be >40
Back to top
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-injuryBack to top
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)Back to top
Transfusion in Head Injury
keep crit between 30-35 to maximize oxygen delivery but minimize decreased blood flow due to viscosityBack to top
for 1st week. Dilantin may cause drug fever.
Keep on for the first week
Free dilantin should be 1-2Back to top
feed glutamine containing immune diet for 5-10 days if GCS<8
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)Back to top
Hold for 72 hours post-injury, post change in status, or post procedureBack to top
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 pinpointBack to top
Pulmonary and Cardiac Sequelae
usually seen in Subarachnoid Hemorrhage (Inten Care Med 2002;28:1012)
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 injuriesBack to top
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.Back to top
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)Back to top
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
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 perfusionBack to top
in post hoc analysis of SAFE, albumin was assoc. with higher mortality (NEJM 2007;357:874)Back to top
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 (email@example.com)Back to top
Signs of Herniation
Unilateral or bilateral unreactive, dilated pupil Extensor posturing (decerebrate) A sharp decline in GCS
decerebrate posturing=brainstem dysfunction
decorticate posturing=brainstem functioningBack to top
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. firstname.lastname@example.org 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 35 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
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 email@example.com
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) 35:56878.[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) 100:8416.[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) 105:8190.[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) 100:11606.[CrossRef][ISI][Medline] 24 Fay T. Observations on generalized refrigeration in cases of severe cerebral trauma. Assoc Res Nerv Ment Dis Proc (1943) 24:61119. 25 Franks NP, Honore E. The TREK K2P channels and their role in general anaesthesia and neuroprotection. Trends Pharmacol Sci (2004) 25:6018.[CrossRef][Medline] 26 Gentile NT, Seftchick MW, Huynh T, Kruus LK, Gaughan J. Decreased mortality by normalizing blood glucose after acute ischemic stroke. Acad Emerg Med (2006) 13:17480.[Abstract/Free Full Text] 27 Gluckman PD, Wyatt JS, Azzopardi D, et al. Selective head cooling with mild systemic hypothermia after neonatal encephalopathy: multicentre randomised trial. Lancet (2005) 365:66370.[ISI][Medline] 28 Goldstein A Jr, Wells BA, Keats AS. Increased tolerance to cerebral anoxia by pentobarbital. Arch Int Pharmacodyn Ther (1966) 161:13843.[ISI][Medline] 29 Gray JJ, Bickler PE, Fahlman CS, Zhan X, Schuyler JA. Isoflurane neuroprotection in hypoxic hippocampal slice cultures involves increases in intracellular Ca2+ and mitogen-activated protein kinases. Anesthesiology (2005) 102:60615.[CrossRef][ISI][Medline] 30 Harada H, Kelly PJ, Cole DJ, Drummond JC, Patel PM. Isoflurane reduces N-methyl-D-aspartate toxicity in vivo in the rat cerebral cortex. Anesth Analg (1999) 89:14427.[Abstract/Free Full Text] 31 Hellstrom-Westas L, Forsblad K, Sjors G, et al. Earlier Apgar score increase in severely depressed term infants cared for in Swedish level III units with 40% oxygen versus 100% oxygen resuscitation strategies: a population-based register study. Pediatrics (2006) 118:e1798804.[Abstract/Free Full Text] 32 Higgins RD, Raju TN, Perlman J, et al. Hypothermia and perinatal asphyxia: executive summary of the National Institute of Child Health and Human Development workshop. J Pediatr (2006) 148:1705.[CrossRef][ISI][Medline] 33 Hoffman WE, Charbel FT, Edelman G, Ausman JI. Thiopental and desflurane treatment for brain protection. Neurosurgery (1998) 43:10503.[CrossRef][ISI][Medline] 34 Jastremski M, Sutton-Tyrrell K, Vaagenes P, Abramson N, Heiselman D, Safar P. Glucocorticoid treatment does not improve neurological recovery following cardiac arrest. Brain Resuscitation Clinical Trial I Study Group. JAMA (1989) 262:342730.[Abstract] 35 Kaisti KK, Langsjo JW, Aalto S, et al. Effects of sevoflurane, propofol, and adjunct nitrous oxide on regional cerebral blood flow, oxygen consumption, and blood volume in humans. Anesthesiology (2003) 99:60313.[CrossRef][ISI][Medline] 36 Kammersgaard LP, Jorgensen HS, Rungby JA, et al. Admission body temperature predicts long-term mortality after acute stroke: the Copenhagen Stroke Study. Stroke (2002) 33:175962.[Abstract/Free Full Text] 37s: comparison with plain film examinations. Am J Roentgenol (1987) 148:117985.[Abstract/Free Full Text] 2 Adams JH, Doyle D, Ford I, Gennarelli TA, Graham DI, McLellan DR. Diffuse axonal injury in head injury: definition, diagnosis and grading. Histopathology (1989) 15:4959.[ISI][Medline] 3 Alderson P, Roberts I. Corticosteroids in acute traumatic brain injury: systematic review of randomised controlled trials. Br Med J (1997) 314:18559.[Abstract/Free Full Text] 4 Andrews BT, Levy ML, Pitts LH. Implications of systemic hypotension for the neurological examination in patients with severe head injury. Surg Neurol (1987) 28:41922.[CrossRef][ISI][Medline] 5 Arango MF, Mejia-Mantilla JH. Magnesium for acute traumatic brain injury. Cochrane Database Syst Rev (2006) 4. doi:10.1002/14651858. CD005400.pub2. 6 Balestreri M, Czosnyka M, Chatfield DA, et al. Predictive value of Glasgow Coma Scale after brain trauma: change in trend over the past ten years. J Neurol Neurosurg Psychiatry (2004) 75:1612.[Abstract/Free Full Text] 7 Bernard F, Menon DK, Matta BF. Corticosteroids after traumatic brain injury: new evidence to support their use. Crit Care Med (2006) 34:583.[CrossRef][ISI][Medline] 8 Berne JD, Velmahos GC, El-Tawil Q, et al. Value of complete cervical helical computed tomographic scanning in identifying cervical spine injury in the unevaluable blunt trauma patient with multiple injuries: a prospective study. J Trauma (1999) 47:896902.[ISI][Medline] 9 Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med (1994) 331:11059.[Abstract/Free Full Text] 10 Blumbergs PC, Jones NR, North JB. Diffuse axonal injury in head trauma. J Neurol Neurosurg Psychiatry (1989) 52:83841.[Abstract] 11 Boto GR, Gomez PA, De La Cruz J, Lobato RD. Severe head injury and the risk of early death. J Neurol Neurosurg Psychiatry (2006) 77:10549.[Abstract/Free Full Text] 12 Bouma GJ, Muizelaar JP, Choi SC, Newlon PG, Young HF. Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg (1991) 75:68593.[ISI][Medline] 13 Bouma GJ, Muizelaar JP, Stringer WA, Choi SC, Fatouros P, Young HF. Ultra-early evaluation of regional cerebral blood flow in severely head-injured patients using xenon-enhanced computerized tomography. J Neurosurg (1992) 77:3608.[ISI][Medline] 14 Braakman R, Gelpke GJ, Habbema JD, Maas AI, Minderhoud JM. Systematic selection of prognostic features in patients with severe head injury. Neurosurgery (1980) 6:36270.[ISI][Medline] 15 Brain Trauma Foundation. Guidelines for Prehospital Management of Traumatic Brain Injury (2000) New York: Brain Trauma Foundation. 16 Brain Trauma Foundation. Management and Prognosis of Severe Traumatic Brain Injury (2000) New York: Brain Trauma Foundation. 17 Canavero S, Bonicalzi V, Narcisi P. Safety of magnesium-lidocaine combination for severe head injury: the Turin lidomag pilot study. Surg Neurol (2003) 60:1659.[CrossRef][ISI][Medline] 18 Chesnut RM, Gautille T, Blunt BA, Klauber MR, Marshall LE. The localizing value of asymmetry in pupillary size in severe head injury: relation to lesion type and location. Neurosurgery (1994) 34:8405.[ISI][Medline] 19 Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma (1993) 34:21622.[ISI][Medline] 20 Chesnut RM, Marshall SB, Piek J, Blunt BA, Klauber MR, Marshall LF. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochir Suppl (Wien) (1993) 59:1215.[Medline] 21 Choi SC, Barnes TY, Bullock R, Germanson TA, Marmarou A, Young HF. Temporal profile of outcomes in severe head injury. J Neurosurg (1994) 81:16973.[ISI][Medline] 22 Choi SC, Narayan RK, Anderson RL, Ward JD. Enhanced specificity of prognosis in severe head injury. J Neurosurg (1988) 69:3815.[ISI][Medline] 23 Clifton GL, Ziegler MG, Grossman RG. Circulating catecholamines and sympathetic activity after head injury. Neurosurgery (1981) 8:1014.[ISI][Medline] 24 Cochran A, Scaife ER, Hansen KW, Downey EC. Hyperglycemia and outcomes from pediatric traumatic brain injury. J Trauma (2003) 55:10358.[ISI][Medline] 25 Cohan P, Wang C, McArthur DL, et al. Acute secondary adrenal insufficiency after traumatic brain injury: a prospective study. Crit Care Med (2005) 33:235866.[CrossRef][ISI][Medline] 26 Davis DP, Dunford JV, Ochs M, Park K, Hoyt DB. The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma (2004) 56:80814.[ISI][Medline] 27 Davis DP, Heister R, Poste JC, Hoyt DB, Ochs M, Dunford JV. Ventilation patterns in patients with severe traumatic brain injury following paramedic rapid sequence intubation. Neurocrit Care (2005) 2:16571.[CrossRef][ISI][Medline] 28 Davis DP, Idris AH, Sise MJ, et al. Early ventilation and outcome in patients with moderate to severe traumatic brain injury. Crit Care Med (2006) 34:12028.[CrossRef][ISI][Medline] 29 Davis DP, Peay J, Sise MJ, et al. The impact of prehospital endotracheal intubation on outcome in moderate to severe traumatic brain injury. J Trauma (2005) 58:9339.[ISI][Medline] 30 Davis DP, Serrano JA, Vilke GM, et al. The predictive value of field versus arrival Glasgow Coma Scale score and TRISS calculations in moderate-to-severe traumatic brain injury. J Trauma (2006) 60:98590.[ISI][Medline] 31 Davis DP, Stern J, Sise MJ, Hoyt DB. A follow-up analysis of factors associated with head-injury mortality after paramedic rapid sequence intubation. J Trauma (2005) 59:48690.[Medline] 32 Demetriades D, Kuncir E, Velmahos GC, Rhee P, Alo K, Chan LS. Outcome and prognostic factors in head injuries with an admission Glasgow Coma Scale score of 3. Arch Surg (2004) 139:10668.[Abstract/Free Full Text] 33 DeWitt DS, Jenkins LW, Prough DS. Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury. New Horiz (1995) 3:37683.[Medline] 34 Diringer MN. Is aggressive treatment of hyperglycemia for everyone? Crit Care Med (2006) 34:9301.[CrossRef][ISI][Medline] 35 Eisenberg HM, Gary HE Jr, Aldrich EF, et al. Initial CT findings in 753 patients with severe head injury. A report from the NIH Traumatic Coma Data Bank. J Neurosurg (1990) 73:68898.[ISI][Medline] 36 Excellence, National Institute of Clinical. Head Injury Triage, Assessment, Investigation and Early Management of Head Injury in Infants Children and Adults. Clinical Guideline 4 (2003) London: NICE. 37 Farin A, Deutsch R, Biegon A, Marshall LF. Sex-related differences in patients with severe head injury: greater susceptibility to brain swelling in female patients 50 years of age and younger. J Neurosurg (2003) 98:326.[ISI][Medline] 38 Fearnside MR, Cook RJ, McDougall P, McNeil RJ. The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre-hospital, clinical and CT variables. Br J Neurosurg (1993) 7:26779.[ISI][Medline] 39 Forsyth RJ, Jayamoni B, Paine TC. Monoaminergic agonists for acute traumatic brain injury. Cochrane Database Syst Rev (2006) 4. doi:10.1002/14651858. CD003984.pub2. 40 Gale JL, Dikmen S, Wyler A, Temkin N, McLean A. Head injury in the Pacific Northwest. Neurosurgery (1983) 12:48791.[ISI][Medline] 41 Gausche M, Lewis RJ, Stratton SJ, et al. Effect of out-of-hospital pediatric endotracheal intubation on survival and neurological outcome: a controlled clinical trial. JAMA (2000) 283:78390.[Abstract/Free Full Text] 42 Gennarelli TA, Spielman GM, Langfitt TW, et al. Influence of the type of intracranial lesion on outcome from severe head injury. J Neurosurg (1982) 56:2632.[ISI][Medline] 43 Gentry LR, Godersky JC, Thompson B, Dunn VD. Prospective comparative study of intermediate-field MR and CT in the evaluation of closed head trauma. Am J Roentgenol (1988) 150:67382.[Abstract/Free Full Text] 44 Gill MR, Reiley DG, Green SM. Interrater reliability of Glasgow Coma Scale scores in the emergency department. Ann Emerg Med (2004) 43:21523.[CrossRef][ISI][Medline] 45 Glass TF, Fabian MJ, Schweitzer JB, Weinberg JA, Proctor KG. The impact of hypercarbia on the evolution of brain injury in a porcine model of traumatic brain injury and systemic hemorrhage. J Neurotrauma (2001) 18:5771.[CrossRef][ISI][Medline] 46 Goldstein B, Kelly MM, Bruton D, Cox C. Inflicted versus accidental head injury in critically injured children. Crit Care Med (1993) 21:132832.[ISI][Medline] 47 Graham DI. The pathology of brain ischaemia and possibilities for therapeutic intervention. Br J Anaesth (1985) 57:317.[Free Full Text] 48 Graham DI, Ford I, Adams JH, et al. Ischaemic brain damage is still common in fatal non-missile head injury. J Neurol Neurosurg Psychiatry (1989) 52:34650.[Abstract] 49 Group ALS. Advanced Paediatric Life Support: the Practical Approach (2005) London: BMJ Books/Blackwell. 50 Helmy A, Vizcaychipi M, Gupta AK. Traumatic brain injury: intensive care management. Br J Anaesth (2007) 99:3242.[Abstract/Free Full Text] 51 Harders A, Kakarieka A, Braakman R. Traumatic subarachnoid hemorrhage and its treatment with nimodipine. German tSAH Study Group. J Neurosurg (1996) 85:829.[ISI][Medline] 52 Hare GMT, Kavanagh BP, Mazer CD, et al. Hypercapnia increases cerebral tissue oxygen tension in anesthetized rats. Can J Anaesth (2003) 50:10618.[Abstract/Free Full Text] 53 Hartl R, Gerber LM, Iacono L, Ni Q, Lyons K, Ghajar J. Direct transport within an organized state trauma system reduces mortality in patients with severe traumatic brain injury. J Trauma (2006) 60:12506.[ISI][Medline] 54 Havill JH, Sleigh JW, Davis GM, et al. Observer error and prediction of outcomegrading of head injury based on computerised tomography. Crit Care Resusc (2001) 3:158.[Medline] 55 Haydel MJ, Preston CA, Mills TJ, Luber S, Blaudeau E, DeBlieux PM. Indications for computed tomography in patients with minor head injury. N Engl J Med (2000) 343:1005.[Abstract/Free Full Text] 56 Healey C, Osler TM, Rogers FB, et al. Improving the Glasgow Coma Scale score: motor score alone is a better predictor. J Trauma (2003) 54:6718.[ISI][Medline] 57 Heiden JS, Small R, Caton W, Weiss M, Kurze T. Severe head injury. Clinical assessment and outcome. Phys Ther (1983) 63:194651.[ISI][Medline] 58 Hodgkinson DW, Berry E, Yates DW. Mild head injurya positive approach to management. Eur J Emerg Med (1994) 1:912.[CrossRef][Medline] 59 Hogan GJ, Mirvis SE, Shanmuganathan K, Scalea TM. Exclusion of unstable cervical spine injury in obtunded patients with blunt trauma: is MR imaging needed when multi-detector row CT findings are normal? Radiology (2005) 237:10613.[Abstract/Free Full Text] 60 Holly LT, Kelly DF, Counelis GJ, Blinman T, McArthur DL, Cryer HG. Cervical spine trauma associated with moderate and severe head injury: incidence, risk factors, and injury characteristics. J Neurosurg (2002) 96:28591.[ISI][Medline] 61 Hukkelhoven CWPM, Steyerberg EW, Rampen AJJ, et al. Patient age and outcome following severe traumatic brain injury: an analysis of 5600 patients. J Neurosurg (2003) 99:66673.[ISI][Medline] 62 Iida H, Tachibana S, Kitahara T, Horiike S, Ohwada T, Fujii K. Association of head trauma with cervical spine injury, spinal cord injury, or both. J Trauma (1999) 46:4502.[ISI][Medline] 63 Ikonomidou C, Turski L. Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury? Lancet Neurol (2002) 1:3836.[CrossRef][ISI][Medline] 64 Injury ESGoNiSH. A multicenter trial of the efficacy of nimodipine on outcome after severe head injury. J Neurosurg (1994) 80:797804.[ISI][Medline] 65 Jennett B. Epidemiology of head injury. J Neurol Neurosurg Psychiatry (1996) 60:3629.[ISI][Medline] 66 Jennett B, Teasdale G, Braakman R, Minderhoud J, Knill-Jones R. Predicting outcome in individual patients after severe head injury. Lancet (1976) 1:10314.[ISI][Medline] 67 Jennett B, Teasdale G, Galbraith S, et al. Severe head injuries in three countries. J Neurol Neurosurg Psychiatry (1977) 40:2918.[Abstract] 68 Jeremitsky E, Omert L, Dunham CM, Protetch J, Rodriguez A. Harbingers of poor outcome the day after severe brain injury: hypothermia, hypoxia, and hypoperfusion. J Trauma (2003) 54:3129.[ISI][Medline] 69 Johnstone AJ, Lohlun JC, Miller JD, et al. A comparison of the Glasgow Coma Scale and the Swedish Reaction Level Scale. Brain Inj (1993) 7:5016.[ISI][Medline] 70 Jones PA, Andrews PJ, Midgley S, et al. Measuring the burden of secondary insults in head-injured patients during intensive care. J Neurosurg Anesthesiol (1994) 6:414.[ISI][Medline] 71 Kakarieka A, Braakman R, Schakel EH. Clinical significance of the finding of subarachnoid blood on CT scan after head injury. Acta Neurochir (Wien) (1994) 129:15.[CrossRef][Medline] 72 Klauber MR, Barrett-Connor E, Marshall LF, Bowers SA. The epidemiology of head injury: a prospective study of an entire community-San Diego County, California, 1978. Am J Epidemiol (1981) 113:5009.[Abstract/Free Full Text] 73 Klauber MR, Marshall LF, Luerssen TG, Frankowski R, Tabaddor K, Eisenberg HM. Determinants of head injury mortality: importance of the low risk patient. Neurosurgery (1989) 24:316.[ISI][Medline] 74 Knoller N, Levi L, Shoshan I, et al. Dexanabinol (HU-211) in the treatment of severe closed head injury: a randomized, placebo-controlled, phase II clinical trial. Crit Care Med (2002) 30:54854.[CrossRef][ISI][Medline] 75 Kobayashi S, Nakazawa S, Otsuka T. Clinical value of serial computed tomography with severe head injury. Surg Neurol (1983) 20:259.[CrossRef][ISI][Medline] 76 Kuday C, Uzan M, Hanci M. Statistical analysis of the factors affecting the outcome of extradural haematomas: 115 cases. Acta Neurochir (Wien) (1994) 131:2036.[CrossRef][Medline] 77 Laird AM, Miller PR, Kilgo PD, Meredith JW, Chang MC. Relationship of early hyperglycemia to mortality in trauma patients. J Trauma (2004) 56:105862.[ISI][Medline] 78 Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg (1991) 75:54551.[ISI][Medline] 79 Langham J, Goldfrad C, Teasdale G, Shaw D, Rowan K. Calcium channel blockers for acute traumatic brain injury. Cochrane Database Syst Rev (2003) [Update of Cochrane Database Syst Rev. 2000;(2):CD000565; PMID: 10796727], CD000565. 80 Larner AJ. False localising signs. J Neurol Neurosurg Psychiatry (2003) 74:4158.[Abstract/Free Full Text] 81 Levi L, Guilburd JN, Linn S, Feinsod M. The association between skull fracture, intracranial pathology and outcome in pediatric head injury. Br J Neurosurg (1991) 5:61725.[ISI][Medline] 82 Link TM, Schuierer G, Hufendiek A, Horch C, Peters PE. Substantial head trauma: value of routine CT examination of the cervicocranium. Radiology (1995) 196:7415.[Abstract] 83 Lobato RD, Rivas JJ, Cordobes F, et al. Acute epidural hematoma: an analysis of factors influencing the outcome of patients undergoing surgery in coma. J Neurosurg (1988) 68:4857.[ISI][Medline] 84 Lokkeberg AR, Grimes RM. Assessing the influence of non-treatment variables in a study of outcome from severe head injuries. J Neurosurg (1984) 61:25462.[ISI][Medline] 85 Lu J, Marmarou A, Choi S, et al. Mortality from traumatic brain injury. Acta Neurochir Suppl (2005) 95:2815.[Medline] 86 Luber SD, Brady WJ, Brand A, Young J, Guertler AT, Kefer M. Acute hypoglycemia masquerading as head trauma: a report of four cases. Am J Emerg Med (1996) 14:5437.[CrossRef][ISI][Medline] 87 Maas AI, Dearden M, Teasdale GM, et al. EBIC-guidelines for management of severe head injury in adults. European Brain Injury Consortium. Acta Neurochir (Wien) (1997) 139:28694.[CrossRef][Medline] 88 Maas AIR, Hukkelhoven CWPM, Marshall LF, Steyerberg EW. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classification and combinations of computed tomographic predictors. Neurosurgery (2005) 57:117382.[ISI][Medline] 89 Maas AIR, Murray G, Henney H III, et al. Efficacy and safety of dexanabinol in severe traumatic brain injury: results of a phase III randomised, placebo-controlled, clinical trial. Lancet Neurol (2006) 5:3845.[CrossRef][ISI][Medline] 90 Manley G, Knudson MM, Morabito D, Damron S, Erickson V, Pitts L. Hypotension, hypoxia, and head injury: frequency, duration, and consequences. Arch Surg (2001) 136:111823.[Abstract/Free Full Text] 91 Marion DW, Carlier PM. Problems with initial Glasgow Coma Scale assessment caused by prehospital treatment of patients with head injuries: results of a national survey. J Trauma (1994) 36:8995.[ISI][Medline] 92 Marion DW, Darby J, Yonas H. Acute regional cerebral blood flow changes caused by severe head injuries. J Neurosurg (1991) 74:40714.[ISI][Medline] 93 Marmarou A, Anderson RL, Ward JD. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg (Suppl) (1991) 75:159166. 94 Marshall LF, Gantille T, Klauber MR. The outcome of severe head injury. J Neurosurg (Suppl) (1991) 75:S2536. 95 Marshall LF, Maas AI, Marshall SB, et al. A multicenter trial on the efficacy of using tirilazad mesylate in cases of head injury. J Neurosurg (1998) 89:51925.[ISI][Medline] 96 Marshall LF, Marshall SB, Klauber MR, Clark MV. A new classification of head injury based on computerised tomography. J Neurosurg (Suppl) (1991) 75:S1420. 97 Massagli TL, Michaud LJ, Rivara FP. Association between injury indices and outcome after severe traumatic brain injury in children. Arch Phys Med Rehabil (1996) 77:12532.[CrossRef][ISI][Medline] 98 Maxwell WL, Bullock R, Landholt H, Fujisawa H. Massive astrocytic swelling in response to extracellular glutamatea possible mechanism for post-traumatic brain swelling? Acta Neurochir Suppl (Wien) (1994) 60:4657.[Medline] 99 Mendelow AD, Gillingham FJ. Extradural haematoma: effect of delayed treatment. Br Med J (1979) 2:134.[ISI][Medline] 100 Menegazzi JJ, Davis EA, Sucov AN, Paris PM. Reliability of the Glasgow Coma Scale when used by emergency physicians and paramedics. J Trauma (1993) 34:468.[ISI][Medline] 101 Miller JD, Sweet RC, Narayan R, Becker DP. Early insults to the injured brain. JAMA (1978) 240:43942.[Abstract] 102 Wilson M, Montgomery H. Impact of genetic factors on outcome from brain injury. Br J Anaesth (2007) 99:4348.[Abstract/Free Full Text] 103 Morris GF, Bullock R, Marshall SB, Marmarou A, Maas A, Marshall LF. Failure of the competitive N-methyl-D-aspartate antagonist Selfotel (CGS 19755) in the treatment of severe head injury: results of two-phase III clinical trials. The Selfotel Investigators. J Neurosurg (1999) 91:73743.[ISI][Medline] 104 Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of prolonged hyperventilation in patients with severe head injury: a randomized clinical trial. J Neurosurg (1991) 75:7319.[ISI][Medline] 105 Murray GD, Teasdale GM, Braakman R, et al. The European Brain Injury Consortium survey of head injuries. Acta Neurochir (Wien) (1999) 141:22336.[CrossRef][Medline] 106 Murray JA, Demetriades D, Berne TV, et al. Prehospital intubation in patients with severe head injury. J Trauma (2000) 49:106570.[ISI][Medline] 107 Nakamura N, Yamaura A, Shigemori M, et al. Final report of the Japan neurotrauma data bank project 19982001: 1,002 cases of traumatic brain injury. Neurol Med Chir (Tokyo) (2006) 46:56774.[CrossRef][Medline] 108 Narayan RK, Greenberg RP, Miller JD, et al. Improved confidence of outcome prediction in severe head injury. A comparative analysis of the clinical examination, multimodality evoked potentials, CT scanning, and intracranial pressure. J Neurosurg (1981) 54:75162.[ISI][Medline] 109 Network, Scottish Intercollegiate Guidelines. Early Management of Patients with a Head Injury (2000) Edinburgh: SIGN. 110 Ng I, Lee KK, Lim JHG, Wong HB, Yan XY. Investigating gender differences in outcome following severe traumatic brain injury in a predominantly Asian population. Br J Neurosurg (2006) 20:738.[CrossRef][ISI][Medline] 111 Obrist WD, Langfitt TW, Jaggi JL, Cruz J, Gennarelli TA. Cerebral blood flow and metabolism in comatose patients with acute head injury. Relationship to intracranial hypertension. J Neurosurg (1984) 61:24153.[ISI][Medline] 112 Patel HC, Menon DK, Tebbs S, Hawker R, Hutchinson PJ, Kirkpatrick PJ. Specialist neurocritical care and outcome from head injury. Intensive Care Med (2002) 28:54753.[CrossRef][ISI][Medline] 113 Peek-Asa C, McArthur D, Hovda D, Kraus J. Early predictors of mortality in penetrating compared with closed brain injury. Brain Inj (2001) 15:80110.[ISI][Medline] 114 Pfenninger E, Ahnefeld FW, Kilian J, Dell U. Behavior of blood gases in patients with craniocerebral trauma at the accident site and at the time of admission to the clinic. Anaesthesist (1987) 36:5706.[ISI][Medline] 115 Phonprasert C, Suwanwela C, Hongsaprabhas C, Prichayudh P, O’Charoen S. Extradural hematoma: analysis of 138 cases. J Trauma (1980) 20:67983.[ISI][Medline] 116 Phuenpathom N, Choomuang M, Ratanalert S. Outcome and outcome prediction in acute subdural hematoma. Surg Neurol (1993) 40:225.[CrossRef][ISI][Medline] 117 Pietropaoli JA, Rogers FB, Shackford SR, Wald SL, Schmoker JD, Zhuang J. The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries. J Trauma (1992) 33:4037.[ISI][Medline] 118 Pigula FA, Wald SL, Shackford SR, Vane DW. The effect of hypotension and hypoxia on children with severe head injuries. J Pediatr Surg (1993) 28:3104.[CrossRef][ISI][Medline] 119 Povlishock JT. Traumatically induced axonal injury: pathogenesis and pathobiological implications. Brain Pathol (1992) 2:112.[ISI][Medline] 120 Ransom GH, Mann FA, Vavilala MS, Haruff R, Rivara FP. Cerebral infarct in head injury: relationship to child abuse. Child Abuse Negl (2003) 27:38192.[CrossRef][ISI][Medline] 121 Reilly PL. Brain injury: the pathophysiology of the first hours. Talk and Die revisited. J Clin Neurosci (2001) 8:398403.[CrossRef][ISI][Medline] 122 Reilly PL, Simpson DA, Sprod R, Thomas L. Assessing the conscious level in infants and young children: a paediatric version of the Glasgow Coma Scale. Childs Nerv Syst (1988) 4:303.[ISI][Medline] 123 Rivas JJ, Lobato RD, Sarabia R, Cordobes F, Cabrera A, Gomez P. Extradural hematoma: analysis of factors influencing the courses of 161 patients. Neurosurgery (1988) 23:4451.[ISI][Medline] 124 Roberts I. Aminosteroids for acute traumatic brain injury. Cochrane Database Syst Rev (1999) 3. doi:10.1002/14651858. CD001527. 125 Roberts I, Smith R, Evans S. Doubts over head injury studies. Br Med J (2007) 334:2924.[Free Full Text] 126 Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet (2004) 364:13218.[CrossRef][ISI][Medline] 127 Rosner MJ, Newsome HH, Becker DP. Mechanical brain injury: the sympathoadrenal response. J Neurosurg (1984) 61:7686.[ISI][Medline] 128 Rutledge R, Lentz CW, Fakhry S, Hunt J. Appropriate use of the Glasgow Coma Scale in intubated patients: a linear regression prediction of the Glasgow verbal score from the Glasgow eye and motor scores. J Trauma (1996) 41:51422.[ISI][Medline] 129 Sakas DE, Bullock MR, Teasdale GM. One-year outcome following craniotomy for traumatic hematoma in patients with fixed dilated pupils. J Neurosurg (1995) 82:9615.[ISI][Medline] 130 Sarrafzadeh AS, Peltonen EE, Kaisers U, Kuchler I, Lanksch WR, Unterberg AW. Secondary insults in severe head injurydo multiply injured patients do worse? Crit Care Med (2001) 29:111623.[CrossRef][ISI][Medline] 131 Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev (2001) 4. doi:10.1002/14651858. CD000173. 132 Seelig JM, Becker DP, Miller JD, Greenberg RP, Ward JD, Choi SC. Traumatic acute subdural hematoma: major mortality reduction in comatose patients treated within four hours. N Engl J Med (1981) 304:15118.[Abstract] 133 Selladurai BM, Jayakumar R, Tan YY, Low HC. Outcome prediction in early management of severe head injury: an experience in Malaysia. Br J Neurosurg (1992) 6:54957.[ISI][Medline] 134 Servadei F, Murray GD, Penny K, et al. The value of the worst computed tomographic scan in clinical studies of moderate and severe head injury. European Brain Injury Consortium. Neurosurgery (2000) 46:705.[CrossRef][ISI][Medline] 135 Servadei F, Nasi MT, Cremonini AM, Giuliani G, Cenni P, Nanni A. Importance of a reliable admission Glasgow Coma Scale score for determining the need for evacuation of posttraumatic subdural hematomas: a prospective study of 65 patients. J Trauma (1998) 44:86873.[ISI][Medline] 136 Sharples PM, Storey A, Aynsley-Green A, Eyre JA. Causes of fatal childhood accidents involving head injury in northern region, 197986. Br Med J (1990) 301:11937.[ISI][Medline] 137 Sheinberg M, Kanter MJ, Robertson CS, Contant CF, Narayan RK, Grossman RG. Continuous monitoring of jugular venous oxygen saturation in head-injured patients. J Neurosurg (1992) 76:2127.[ISI][Medline] 138 Shohami E, Novikov M, Bass R. Long-term effect of HU-211, a novel non-competitive NMDA antagonist, on motor and memory functions after closed head injury in the rat. Brain Res (1995) 674:5562.[CrossRef][ISI][Medline] 139 Simpson DA. Clinical examination and grading. In: Head Injury: Pathophysiology and Management of Severe Closed Head InjuryReilly PL, Bullock MR, eds. (1997) London: Chapman and Hall Medical. 14565. 140 Simpson DA, Cockington RA, Hanieh A, Raftos J, Reilly PL. Head injuries in infants and young children: the value of the Paediatric Coma Scale. Review of literature and report on a study. Childs Nerv Syst (1991) 7:18390.[ISI][Medline] 141 Starmark JE, Stalhammar D, Holmgren E. The Reaction Level Scale (RLS85). Manual and guidelines. Acta Neurochir (Wien) (1988) 91:1220.[CrossRef][Medline] 142 Starmark JE, Stalhammar D, Holmgren E, Rosander B. A comparison of the Glasgow Coma Scale and the Reaction Level Scale (RLS85). J Neurosurg (1988) 69:699706.[ISI][Medline] 143 Stiefel MF, Tomita Y, Marmarou A. Secondary ischemia impairing the restoration of ion homeostasis following traumatic brain injury. J Neurosurg (2005) 103:70714.[ISI][Medline] 144 Stiell IG, Wells GA, Vandemheen K, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet (2001) 357:13916.[CrossRef][ISI][Medline] 145 Stocchetti N, Croci M, Spagnoli D, Gilardoni F, Resta F, Colombo A. Mass volume measurement in severe head injury: accuracy and feasibility of two pragmatic methods. J Neurol Neurosurg Psychiatry (2000) 68:147.[Abstract/Free Full Text] 146 Sultan HY, Boyle A, Pereira M, Antoun N, Maimaris C. Application of the Canadian CT head rules in managing minor head injuries in a UK emergency department: implications for the implementation of the NICE guidelines. Emerg Med J (2004) 21:42025.[Abstract/Free Full Text] 147 Tatman A, Warren A, Williams A, Powell JE, Whitehouse W. Development of a modified paediatric coma scale in intensive care clinical practice. Arch Dis Child (1997) 77:51921.[Abstract/Free Full Text] 148 Teasdale G, Bailey I, Bell A, et al. The effect of nimodipine on outcome after head injury: a prospective randomised control trial. The British/Finnish Co-operative Head Injury Trial Group. Acta Neurochir Suppl (Wien) (1990) 51:3156.[Medline] 149 Teasdale G, Jennett B. Assessment and prognosis of coma after head injury. Acta Neurochir (Wien) (1976) 34:4555.[CrossRef][Medline] 150 Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet (1974) 2:814.[CrossRef][ISI][Medline] 151 Teasdale G, Knill-Jones R, van der Sande J. Observer variability in assessing impaired consciousness and coma. J Neurol Neurosurg Psychiatry (1978) 41:60310.[Abstract] 152 Temkin NR, Dikmen SS, Wilensky AJ, Keihm J, Chabal S, Winn HR. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med (1990) 323:497502.[Abstract] 153 Tennant A. Admission to hospital following head injury in England: incidence and socio-economic associations. BMC Public Health (2005) 5:21.[CrossRef][Medline] 154 Tennant A. The epidemiology of head injury. In: Traumatic Brain Injury Rehabilitation: Services, Treatments and OutcomesChamberlain MA, Neumann V, Tennant A, eds. (1996) London: Chapman Hall. 155 The Association of Anaesthetists of Great Britain and Ireland. Recommendations for the Safe Transfer of Patients with Brain Injury (2006) London: The Association of Anaesthetists of Great Britain and Ireland. 156 Thornhill S, Teasdale GM, Murray GD, McEwen J, Roy CW, Penny KI. Disability in young people and adults one year after head injury: prospective cohort study. Br Med J (2000) 320:16315.[Abstract/Free Full Text] 157 Tolias CM, Bullock MR. Critical appraisal of neuroprotection trials in head injury: what have we learned? NeuroRx (2004) 1:719.[CrossRef][Medline] 158 Trauma Committee of the American College of Surgeons. Advanced Trauma Life Support Program for Physicians (2004) 7th Edn. Chicago: American College of Surgeons. 159 Udekwu P, Kromhout-Schiro S, Vaslef S, Baker C, Oller D. Glasgow Coma Scale score, mortality, and functional outcome in head-injured patients. J Trauma (2004) 56:10849.[ISI][Medline] 160 Van den Berghe G, Schoonheydt K, Becx P, Bruyninckx F, Wouters PJ. Insulin therapy protects the central and peripheral nervous system of intensive care patients. Neurology (2005) 64:134853.[Abstract/Free Full Text] 161 Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med (2001) 345:135967.[Abstract/Free Full Text] 162 Van der Naalt J, Van Zomeren AH, Sluiter WJ, Minderhoud JM. One year outcome in mild to moderate head injury: the predictive value of acute injury characteristics related to complaints and return to work. J Neurol Neurosurg Psychiatry (1999) 66:20713.[Abstract/Free Full Text] 163 Van Dongen KJ, Braakman R, Gelpke GJ. The prognostic value of computerized tomography in comatose head-injured patients. J Neurosurg (1983) 59:9517.[ISI][Medline] 164 Van Putten HP, Bouwhuis MG, Muizelaar JP, Lyeth BG, Berman RF. Diffusion-weighted imaging of edema following traumatic brain injury in rats: effects of secondary hypoxia. J Neurotrauma (2005) 22:85772.[CrossRef][ISI][Medline] 165 Vassar MJ, Fischer RP, O’Brien PE, et al. A multicenter trial for resuscitation of injured patients with 7.5% sodium chloride. The effect of added dextran 70. The multicenter group for the study of hypertonic saline in trauma patients. Arch Surg (1993) 128:100311.[Abstract] 166 Vassar MJ, Perry CA, Gannaway WL, Holcroft JW. 7.5% sodium chloride/dextran for resuscitation of trauma patients undergoing helicopter transport. Arch Surg (1991) 126:106572.[Abstract] 167 Vassar MJ, Perry CA, Holcroft JW. Analysis of potential risks associated with 7.5% sodium chloride resuscitation of traumatic shock. Arch Surg (1990) 125:130915.[Abstract] 168 Vassar MJ, Perry CA, Holcroft JW. Prehospital resuscitation of hypotensive trauma patients with 7.5% NaCl versus 7.5% NaCl with added dextran: a controlled trial. J Trauma (1993) 34:62232.[ISI][Medline] 169 Vespa P, Boonyaputthikul R, McArthur DL, et al. Intensive insulin therapy reduces microdialysis glucose values without altering glucose utilization or improving the lactate/pyruvate ratio after traumatic brain injury. Crit Care Med (2006) 34:8506.[CrossRef][ISI][Medline] 170 Vollmer DG, Torner JC, Jane JA. Age and outcome following traumatic coma: why do older patients fare worse? J Neurosurg (Suppl) (1991) 75:S3749. 171 Vos PE, Battistin L, Birbamer G, et al. EFNS guideline on mild traumatic brain injury: report of an EFNS task force. Eur J Neurol (2002) 9:20719.[CrossRef][ISI][Medline] 172 Vos PE, van Voskuilen AC, Beems T, Krabbe PF, Vogels OJ. Evaluation of the traumatic coma data bank computed tomography classification for severe head injury. J Neurotrauma (2001) 18:64955.[CrossRef][ISI][Medline] 173 Wakai A, Roberts I, Schierhout G. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev (2007) 1. doi:10.1002/14651858. CD001049.pub4. 174 Wardlaw JM, Easton VJ, Statham P. Which CT features help predict outcome after head injury? J Neurol Neurosurg Psychiatry (2002) 72:18892.[Abstract/Free Full Text] 175 Waters RJ, Nicoll JAR. Genetic influences on outcome following acute neurological insults. Curr Opin Crit Care (2005) 11:10510.[CrossRef][ISI][Medline] 176 Werner C, Engelhard K. Pathophysiology of traumatic brain injury. Br J Anaesth (2007) 99:49.[Abstract/Free Full Text] 177 Winchell RJ, Hoyt DB. Endotracheal intubation in the field improves survival in patients with severe head injury. Trauma Research and Education Foundation of San Diego. Arch Surg (1997) 132:5927.[Abstract] 178 Yates PJ, Williams WH, Harris A, Round A, Jenkins R. An epidemiological study of head injuries in a UK population attending an emergency department. J Neurol Neurosurg Psychiatry (2006) 77:699701.[Abstract/Free Full Text] 179 Young B, Ott L, Dempsey R, Haack D, Tibbs P. Relationship between admission hyperglycemia and neurologic outcome of severely brain-injured patients. Ann Surg (1989) 210:46672.[ISI][Medline]
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.Back to top
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.Back to top
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.
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 patients 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)Back to top
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. 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). 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).Back to top
Delayed Injuries / DASH
especially in coumadin folks
even worse in plavix patients (Ann Emerg Med 2012;59:460)
CT and observe if minor trauma s LOC or amnesia
if LOC, most likely need repeat CT and 24 hours observation
One mans 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.)Back to top
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;192:743745.
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;65:785788. 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;53:668672. 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;58:518522. Ovid Full Text Mount Sinai Serials Request Permissions Bibliographic Links [Context Link]Back to top
Reversal of Anti-Plt Drugs
plt transfusions associated with worse outcome in pts with GCS >12 and ICH (J Trauma. 2011;71: 358363). Not a causation study.Back to top
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.
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.
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.Back to top
35 seems to be as good as 33 in a before and after trial (J Trauma 66(1), January 2009, pp 166-173)
This trial demonstrates no benefit of hypothermia over TTM management (no fever) Journal of Neurotrauma. April 1, 2015, 32(7): 422-429. doi:10.1089/neu.2013.3197.Back to top
Where to put the transducer
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)Back to top
Sympathetic HyperactivityBack to top
Nimodipine for Traumatic SAH
doesn’t help in SR (Lancet Neurol 2006;5:1029) and Cochrane (Calcium Channel Blockers for Acute Traumatic Brain Injury)Back to top
The Lancet Neurology, Very early hypothermia induction in patients with severe brain injury (the National Acute Brain Injury Study: Hypothermia II): a randomised trial
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 0·761·53; p=0·67). 12 patients in the hypothermia group died compared with eight in the normothermia group (RR 1·30, 95% CI 0·582·52; p=0·52).
This trial did not confirm the utility of hypothermia as a primary neuroprotective strategy in patients with severe traumatic brain injury.Back to top
Probably shoot for 180 mg/dl.
Tight plasma control leads to hypoglycemia in the injuryed areas of the brain (Neurocrit Care 2010;12:317) and (Crit Care Medicine 2012;40(6):1923)
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)Back to top
transpyloric nutritition reduces incidence of overall and late pneumonia
and improves nutriitional efficacy (Inten Care Med 2010;36:1532)Back to top
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
Predicting survival after acute civilian penetrating brain injuries
The SPIN score
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)Back to top
Jugular Bulb Oximetry
<50-55% or >80% are bad, shoot for 65-75%Back to top
Isolated Traumatic SAH
no need for repeat CT or ICU
( Journal of Trauma and Acute Care Surgery Issue: Volume 74(2), February 2013, p 581–584) and (Journal of Trauma and Acute Care Surgery Issue: Volume 74(6), June 2013, p 1504–1509)Back to top
Dilated and Fixed in EDH and SDH
Prognosis of patients with bilateral fixed dilated pupils secondary to traumatic extradural or subdural haematoma who undergo surgery: a systematic review and meta-analysis
Primary objective To review the prognosis of patients with bilateral fixed and dilated pupils secondary to traumatic extradural (epidural) or subdural haematoma who undergo surgery.
Methods A systematic review and meta-analysis was performed using random effects models. The Cochrane Central Register of Controlled Trials and PubMed databases were searched to identify relevant publications. Eligible studies were publications that featured patients with bilateral fixed and dilated pupils who underwent surgical evacuation of traumatic extra-axial haematoma, and reported on the rate of favourable outcome (Glasgow Outcome Score 4 or 5).
Results Five cohort studies met the inclusion criteria, collectively reporting the outcome of 82 patients. In patients with extradural haematoma, the mortality rate was 29.7% (95% CI 14.7% to 47.2%) with a favourable outcome seen in 54.3% (95% CI 36.3% to 71.8%). In patients with acute subdural haematoma, the mortality rate was 66.4% (95% CI 50.5% to 81.9%) with a favourable outcome seen in 6.6% (95% CI 1.8% to 14.1%).
Conclusions and implications of key findings Despite the poor overall prognosis of patients with closed head injury and bilateral fixed and dilated pupils, our findings suggest that a good recovery is possible if an aggressive surgical approach is taken in selected cases, particularly those with extradural haematoma.