{"id":5405,"date":"2011-09-06T15:55:35","date_gmt":"2011-09-06T15:55:35","guid":{"rendered":"http:\/\/crashtext.org\/misc\/severe-traumatic-brain-injury.htm\/"},"modified":"2018-02-24T17:43:22","modified_gmt":"2018-02-24T22:43:22","slug":"severe-traumatic-brain-injury","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/trauma\/system\/severe-traumatic-brain-injury.htm\/","title":{"rendered":"Severe Traumatic Brain Injury"},"content":{"rendered":"
Neglected phases of TBI-apneic and catecholamine surge<\/a><\/p>\n Severe injury=GCS<8<\/span><\/p>\n Suspect elevated ICP if:<\/p>\n GCS<8 or<\/p>\n GCS \u2264 10 and:<\/p>\n Hematoma volume > 30 ml (A,B,C,\/2)<\/p>\n Midline Shift > 1 cm<\/p>\n Pineal shift > 5 mm<\/p>\n Compression of the Lateral Ventricles<\/p>\n B. Level II<\/p>\n Blood pressure should be monitored and hypotension (systolic blood pressure 90 mm Hg) avoided.<\/p>\n C. Level III<\/p>\n Oxygenation should be monitored and hypoxia (PaO<\/p>\n 2 60 mm Hg or O2 saturation 90%) avoided.<\/p>\n B. Level II<\/p>\n 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.<\/p>\n C. Level III<\/p>\n Restrict mannitol use prior to ICP monitoring to patients with signs of transtentorial herniation or progressive neurological deterioration not attributable to extracranial causes.<\/p>\n C. Level III<\/p>\n 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.<\/p>\n B. Level II<\/p>\n Periprocedural antibiotics for intubation should be administered to reduce the incidence of pneumonia. However,<\/p>\n 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.<\/p>\n C. Level III<\/p>\n Routine ventricular catheter exchange or prophylactic antibiotic use for ventricular catheter placement is not<\/p>\n recommended to reduce infection. Early extubation in qualified patients can be done without increased risk of pneumonia.<\/p>\n C. Level III<\/p>\n Graduated compression stockings or intermittent pneumatic compression (IPC) stockings are recommended,<\/p>\n 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.<\/p>\n B. Level II<\/p>\n Intracranial pressure (ICP) should be monitored in all salvageable patients with a severe traumatic brain injury (TBI; Glasgow Coma Scale [GCS] score of 3\u00968 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals<\/p>\n hematomas, contusions, swelling, herniation, or compressed basal cisterns.<\/p>\n C. Level III<\/p>\n 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:<\/p>\n age over 40 years,<\/p>\n unilateral or bilateral motor posturing, or<\/p>\n systolic blood pressure (BP) 90 mm Hg.<\/p>\n B. Level II<\/p>\n Treatment should be initiated with intracranial pressure (ICP) thresholds above 20 mm Hg.<\/p>\n C. Level III<\/p>\n A combination of ICP values, and clinical and brain CT findings, should be used to determine the need for treatment.<\/p>\n B. Level II<\/p>\n 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).<\/p>\n C. Level III<\/p>\n CPP of <50 mm Hg should be avoided.<\/p>\n C. Level III<\/p>\n 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.<\/p>\n B. Level II<\/p>\n Prophylactic administration of barbiturates to induce burst suppression EEG is not recommended.<\/p>\n 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.<\/p>\n 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.<\/p>\n B. Level II<\/p>\n Patients should be fed to attain full caloric replacement by day 7 post-injury.<\/p>\n B. Level II<\/p>\n Prophylactic use of phenytoin or valproate is not recommended for preventing late posttraumatic seizures (PTS).<\/p>\n Anticonvulsants are indicated to decrease the incidence of early PTS (within 7 days of injury). However, early PTS is not associated with worse outcomes.<\/p>\n B. Level II<\/p>\n Prophylactic hyperventilation (PaCO2 of 25 mm Hg or less) is not recommended.<\/p>\n C. Level III<\/p>\n Hyperventilation is recommended as a temporizing measure for the reduction of elevated intracranial pressure (ICP).<\/p>\n Hyperventilation should be avoided during the first 24 hours after injury when cerebral blood flow (CBF) is often<\/p>\n critically reduced.<\/p>\n If hyperventilation is used, jugular venous oxygen saturation (SjO<\/p>\n 2) or brain tissue oxygen tension (PbrO2) measurements are recommended to monitor oxygen delivery.<\/p>\n A. Level I<\/p>\n 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.<\/p>\n Guidelines for Management of TBI (Brain Trauma Taskforce, braintrauma.org)<\/p>\n Not following these guidelines led to poorer outcome (Acta Neurochir 1999;141(11):1203-8)<\/p>\n 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<\/p>\n Any episode of hypotension or hypoxia dramatically increases head injury mortaility (Archives of Surg 2001:136;1118-1123)<\/p>\n 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.<\/p>\n New study shows that hypotensive increases the mortality dramatically, but not more than non-head injured trauma patients (J Trauma 2005;59:830-835)<\/p>\n brain hits opposite wall first. Air bubble in soda bottle (Neurocritical Care 2004;1:384)<\/p>\n Widespread structural failure of axons<\/p>\n <\/a><\/p>\n A Simple Tool To Predict The Need To Operate On A Subdural Hematoma<\/p>\n Single center experience: Injury 46(1):76-79, 2015.<\/i><\/p>\n<\/div>\n Crash Prognosis Calculator<\/a><\/p>\n motor component of GCS is most important as well as the ability to obey simple one-step commands<\/p>\n 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<\/p>\n Somatosensory evoked potentials are best predictors (Inten Care Med 2005;31:765)<\/p>\n Predictive ability of the GCS score (J Neurosci Nursing 2007;39(2):68) Age, GCS, and pupillary reaction are the most predictive Motor Score is most important part of the gcs<\/p>\n ICP Monitor, either ventriculostomy or bolt (parenchymal strain gauge) if abnormal CT or normal CT c 2 of 3:\u00a0 SBP<90, Age>40, posturing<\/p>\n (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)<\/p>\n CPP=MAP-ICP<\/p>\n 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<\/p>\n Norepinephrine but not dopamine was able to increase CBF in patients with head injury (Crit Care Med 2004;32(4):1049)<\/p>\n 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.<\/p>\n 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)\u00a0 and ( Intensive Care Med. 2004 Jan;30(1):45-50.Pharmacokinetics and pharmacodynamics of dopamine and norepinephrine in critically ill head-injured patients.)<\/p>\n Review of Vasopressors for Neurologic Injuries (Neurocrit Care 2009;11:112)<\/p>\n CPP and Hypoxia (Crit Care 2005;9:R670)<\/p>\n risk of hypoxia high at CPP<60. If >70, then it is much less<\/p>\n Article 1<\/a><\/p>\n Article 2<\/a><\/p>\n <\/a><\/p>\n Review (Crit Care Med 2005;33(6):1392)<\/p>\n <\/a>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<\/p>\n ICP>20<\/p>\n 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)<\/p>\n <\/a><\/a><\/a><\/a><\/p>\n keep head 30 to 45 degrees<\/p>\n Treat any fever aggressively<\/p>\n Ensure CO2 35-40<\/p>\n Review of hyperventilation (Chest 2005;127(5):1812)<\/p>\n hypervent more than 24 hours is almost certainly not helpful and most likely deleterious<\/p>\n Hyperventilation stops working after 12-24 hours and brain resets at new CO2 (Chest 2005;127(5):1812)<\/p>\n 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)<\/p>\n A recent review demonstrated that perhaps we should consider hypertonic, not mannitol the gold standard for ICP measurement (Crit Care 2012;16:113<\/a>)<\/p>\n Another great review (Neurocrit Care. 2012 Aug;17(1):117-30. Hyperosmolar therapy for intracranial hypertension.)<\/p>\n And a meta-analysis of Hypertonic Saline (J Neurosurg 2012;116:210<\/a>)<\/p>\n 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)<\/p>\n 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)<\/p>\n 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<\/p>\n But the osmotic diuresis can lead to hypotension and accumulation of mannitol in CNS can lead to a rebound effect<\/p>\n 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<\/p>\n Up to Osm of 320-330<\/p>\n 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)<\/p>\n plasma volume expander duration of 90 minutes to ~6 hours<\/p>\n also may be free radical scavenger and may inhibit apoptosis<\/p>\n Mass General Mannitol Protocol<\/a><\/p>\n Meta-Anal of Hypertonic vs. Mannitol shows hypertonic is better (Crit Care Med 2011;39:554)<\/p>\n 3% 250 cc bolus over 10-15 minutes (~4 cc\/kg)<\/p>\n Can get hyperchloremic acidosis (add amp of bicarb to bag). Keep Na<160 and Osm<330 (Some would say 360 for hypertonic saline)<\/p>\n 7.5% in dextran is half NaCl and half NaAcetate (~2 cc\/kg)<\/p>\n 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\u00a0 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.<\/p>\n 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)<\/p>\n Give over 10 minutes into a central line<\/p>\n Stephan Mayer’s Protocol<\/a><\/p>\n In one protocol, 3% half acetate and half chloride was effective for TBI (Crit Care Med 1998;26(3):440)<\/p>\n 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 \u0096 a randomized clinical trial<\/p>\n 9. Vialet R, Albanese J, Thomachot L, et al: Isovolume hypertonic solutes (sodium chloride or mannitol) in the treatment of refractory posttraumatic intracranial hypertension: 2 mL\/kg 7.5% saline is more effective than 2 mL\/kg 20% mannitol. Crit Care Med 2003; 31:1683\u00961687<\/p>\n 12. Francony G, Fauvage B, Falcon D, et al: Equimolar doses of mannitol and hypertonic saline in the treatment of increased intracranial pressure. Crit Care Med 2008; 36:795\u0096800<\/p>\n 13. Battison C, Andrews PJ, Graham C, et al: Randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline\/6% dextran solution on increased intracranial pressure after brain injury. Crit Care Med 2005; 33:196\u0096202, discussion 257\u0096198<\/p>\n 14. Berger S, Schurer L, Hartl R, et al: 7.2% NaCl\/10% dextran 60 versus 20% mannitol for treatment of intracranial hypertension. Acta Neurochir Suppl (Wien) 1994; 60:494\u0096498<\/p>\n 15. Freshman SP, Battistella FD, Matteucci M, et al: Hypertonic saline (7.5%) versus mannitol: A comparison for treatment of acute head injuries. J Trauma 1993; 35:344\u0096348<\/p>\n 16. Harutjunyan L, Holz C, Rieger A, et al: Efficiency of 7.2% hypertonic saline hydroxyethyl starch 200\/0.5 versus mannitol 15% in the treatment of increased intracranial pressure in neurosurgical patients: A randomized clinical trial [ISRCTN62699180]. Crit Care 2005; 9:R530\u0096R540<\/p>\n 17. Mirski AM, Denchev ID, Schnitzer SM, et al: Comparison between hypertonic saline and mannitol in the reduction of elevated intracranial pressure in a rodent model of acute cerebral injury. J Neurosurg Anesthesiol 2000; 12:334\u0096344<\/p>\n 18. Zornow MH, Oh YS, Scheller MS: A comparison of the cerebral and haemodynamic effects of mannitol and hypertonic saline in an animal model of brain injury. Acta Neurochir Suppl (Wien) 1990; 51:324\u0096325<\/p>\n onset 15-30 minutes, lasts 1-3 hours<\/p>\n 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.<\/p>\n Review article (Anesth Analg 2006;102:1836)<\/p>\n when calculating osmal for brain effects, include glucose, but not the BUN<\/p>\n Excellent Editorial (Crit Care Med 2006;34(12):3037)<\/p>\n Study vs. placebo in SAH with ICP (Crit Care Med 2006;34(12):2912)<\/p>\n 2cc\/kg over 30 min of 7.5% in 6% hydroxyethyl starch 200\/0.5 solution<\/p>\n 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.)<\/p>\n Use of 3% vs. mannitol for brain relaxation in cranis; same effectiveness, less diuresis with 3% (Anesth 2007;107:697)<\/p>\n Hypertonic sodium lactate (inten care med 2009;35:471) more effective than mannitol in rct<\/p>\n two articles show the saftey of 3% and 7.5% administered peripherally (J Trauma 36(3):323) and (JAMA. 2010;304(13):1455-1464)<\/p>\n Hypertonic vs. Mannitol Comparison<\/a>–Hypertonic is better<\/p>\n 23.4% will reduce intracranial hypertension even when serum and CSF osmolality is high (Neurocrit Care 2012;17:204)<\/p>\n Neurocrit Care 2010;13:24<\/p>\n 85 ml of 8.4% sodium bicarb infused over 30 minutes<\/p>\n effective without hyperchloremic acidosis<\/p>\n RCT comparing the two: 100 ml of 5% vs. 85 ml of NaBicarb 8.4% (Neurocrit Care 2011;15:42)<\/p>\n <\/a>Normal<\/p>\n <\/a>P2 Elevations<\/p>\n <\/a>Rounding\/Monotonous<\/p>\n <\/a>Lundberg A,B, & C waves<\/p>\n Normal<\/p>\n P1=percussion wave, pulsation of choroid plexus, sharp consistent in amplitude<\/p>\n P2=tidal wave, rebound after arterial percussion. Variance in amplitude<\/p>\n P3=dichrotic wave, immediately follows the notch after P2 (which corresponds to the dichrotic notch arterially)<\/p>\n P2 predominance occurs prior to all discernability disappearing<\/p>\n P2:P1 > 0.8 has been thought to be associate with disproportionate increase in ICP, especially when the ICP is > 10<\/p>\n this study shows not necessarily true after a waveform analysis (Am J of Crit Care 2008;17:54<\/p>\n IVC if not already placed<\/p>\n 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<\/p>\n Causes hypokalemia (Intensive Care Med. 2002 Sep;28(9):1357-60.)<\/p>\n 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.<\/p>\n 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<\/p>\n 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”<\/p>\n 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)<\/p>\n ICP and IAP are correlated (Inten Care Med 2005;31:1577)<\/p>\n THAM may lower ICP as well<\/p>\n GHB may be better than barbs<\/p>\n scans obtained within 3-6 hours of injury may not indicate final lesion size a scheduled scan 12-24 hours post-injury in severe tbi seems warranted ICP monitors do not require proph abx other than one dose 30 minutes prior to placement pts need 1 week of dilantin ICP treatment treat normal patients at 20, treat s\/p crani pts at 15<\/p>\n <\/a><\/a><\/a><\/p>\n Ways it\u0092s been described:<\/p>\n Antihypertensive and intracranial volume-targeted therapy<\/p>\n Physiological volume regulation of the intracranial compartments<\/p>\n Central premise:<\/p>\n Impaired autoregulation and blood brain barrier occur in the injured brain<\/p>\n This makes MAP and cerebral capillary hydrostatic pressure driving force behind cerebral edema, and therefore ICP<\/p>\n Furthermore, supporting the CPP with pressors can promote more cerebral edema<\/p>\n Therefore, a good CO with normotension and mild vasoconstriction of precapillary cerebral vessels decreases ICP<\/p>\n The volume-targeted \u0093Lund Strategy\u0094 has several components<\/p>\n Reduction of stress response and cerebral energy metabolism (low dose pentothal, sedation)<\/p>\n Reduction of capillary hydrostatic pressure with systemic antihypertensives (metoprolol and clonidine)<\/p>\n Reduction of capillary hydrostatic pressure with precapillary vasoconstrictors (low-dose pentathol & ergotamine)<\/p>\n Maintenance of colloid osmotic pressure and control of fluid balance<\/p>\n Reduction of cerebral blood volume<\/p>\n What it looks like<\/p>\n Euvolemia to Hypervolemia<\/p>\n Normotension using beta-blockers (metoprolol) and alpha-agonists (clonidine)<\/p>\n Low dose pentothal and dihydroergotamine<\/p>\n CPP typically near traditional limits, but lower CPP tolerated in preference of antihypertensive therapy<\/p>\n ICP effectively kept <20 most of the time<\/p>\n Outcomes<\/p>\n Efficacy of the protocol has been evaluated in experimental and clinical studies<\/p>\n Surrogate physiological\/biochemical improvements (lactate\/pyruvate ratio in the penumbra zone by microdialysis)<\/p>\n Non-randomized\/non-controlled studies suggest significant mortality benefit<\/p>\n Subjective clinical experiences favorable<\/p>\n full description and review (Inten Care Med 2006;32:1475)<\/p>\n 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.)<\/p>\n should be pvO2 > 15-20 mm Hg<\/p>\n Licox will give readings 5 mm Hg lower than Neurotrend (anecdotal)<\/p>\n <\/a><\/p>\n Immediate Surgery<\/p>\n Midline shift>5mm or mass effect<\/p>\n Large or enlarging hematoma<\/p>\n Depressed skull fracture<\/p>\n Posterior fossa mass lesion<\/p>\n Open wound<\/p>\n LICOX<\/p>\n Review Article (Neurocritical Care 2004;1:392)<\/p>\n Hyperventilation adversely affects PbtO2 (Br J Neurosurg 2003;17(4):340-346)<\/p>\n needs 60-90 minutes run in time to equilibrate<\/p>\n Better Review(Curr Opin Crit Care 2002;8:115-120<\/p>\n Hyperoxia causes cerebral vasoconstriction (Curr Opin Crit Care 2004;10:105<\/p>\n In dogs, better neuro outcome when 21% O2 used in brain injury than 100% (Stroke 1998;29:1679)<\/p>\n Review article summarizing some weak human studies showing that cerebral blood flow decreases with hyperoxia (>133 mmHg) (Br J Anaeth 2003;90:774)<\/p>\n Increased fiO2 changed PbO2 but also jug venous saturation (Anesth Analg 2003;97:851)<\/p>\n 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)<\/p>\n Licox waveform tracks CPP regardless of autoregulation (Anesth Analg 2010;110:165)<\/p>\n Excellent Review Article (Crit Care Med 2009; 37:2057\u20132063<\/a>)<\/p>\n Lactate\/Pyruvate Ratio should be >40<\/p>\n <\/p>\n transcranial dopplers PET Xenon CT Scanning If TCD has been calibrated to a quantitative measure of CBF, it can relaibly track changes in CBF can pick up low flow in the initial 24 horus and vasospasm several days post-injury<\/p>\n 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<\/p>\n Hypocapnia is actually a really bad idea (crit care med 2010;38:1348)<\/p>\n keep crit between 30-35 to maximize oxygen delivery but minimize decreased blood flow due to viscosity<\/p>\n for 1st week.\u00a0 Dilantin may cause drug fever.<\/p>\n Dilantin<\/p>\n Keep on for the first week<\/p>\n Free dilantin should be 1-2<\/p>\n feed glutamine containing immune diet for 5-10 days if GCS<8<\/p>\n Temperature<\/p>\n Must manage aggressively any increased temp<\/p>\n 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)<\/p>\n Lovenox<\/p>\n Hold for 72 hours post-injury, post change in status, or post procedure<\/p>\n Uncal-uncus of temporal lobe forced against tentorium cerebelli.\u00a0 CN III compressed, ipsilateral dilated pupil<\/p>\n Central Transtentorial-from above<\/p>\n Cerebellotonsilar-tonsils through foramen magnum, bilat pinpoint<\/p>\n Upwards transtentorial-pontine compression, Bilat pinpoint<\/p>\n usually seen in Subarachnoid Hemorrhage (Inten Care Med 2002;28:1012)<\/p>\n Electric Disturbances<\/p>\n due to stimulation of posterior hypothalamus<\/p>\n problems are tachyarrhythmias and signs of ischemia<\/p>\n t-wave abnormalities are usually benign<\/p>\n ventricular hypokinesis is more rare but can be fatal<\/p>\n Neurogenic Pulmonary Edema<\/p>\n believed to be due to catecholamine hypersecretion<\/p>\n <\/a><\/a><\/a><\/p>\n Article of Systemic Complications after Head Inj (Anaesthesia 2007;62:474)<\/p>\n any severe tbi (not just aSAH) can cause sympathetic surge which can cause direct injury of the myocardium<\/p>\n Neurogenic pulmonary edema can occur up to 14 days after the original TBI. catecholamine storm is implicated.<\/p>\n intense pulmonary vasoconstriction; increased intravascular hydrostatic pressure; and transudation of plasma fluid into extravascular space<\/p>\n these cause direct endothelial injuries<\/p>\n 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.<\/p>\n 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)<\/p>\n 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<\/p>\n <\/a><\/p>\n Consider Diabetes Insipidus<\/p>\n vasopressin drip<\/p>\n Brain Trauma can be the source of hypotension (J Trauma 2003;55:1065)<\/p>\n 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).\u00a0 If the patient is getting tube feeding, then you can add salt to the feeds as an alternative to hypertonic saline.\u00a0 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.\u00a0 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<\/p>\n csw most often from lesions to the hypothalamus or forebrain<\/p>\n loss of weight is suggestive as pt is fluid depleted<\/p>\n – 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<\/p>\n – urine Na+ markedly elevated (variable in SIADH) & urine volume increased in CSW<\/p>\n – high BUN and Hematocrit supports CSW (prerenal azotemia and hemoconcentration)<\/p>\n – elevated serum K+ not usually seen in SIADH and implies CSW<\/p>\n – serum uric acid often increased in volume depletion (CSW) while low in SIADH<\/p>\n – may add oral salt or hypertonic saline to ensure positive sodium balance<\/p>\n – 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)<\/p>\n – 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)<\/p>\n – very effective in preventing hyponatremia from SAH (ARR of 25%, NNT 4) and reduced need for dobutamine to augment cerebral perfusion<\/p>\n in post hoc analysis of SAFE, albumin was assoc. with higher mortality (NEJM 2007;357:874)<\/p>\n prospective study shows it’s there more than we think (Crit Care Med 2005;33:2358)<\/p>\n 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<\/p>\n THE RELATIONSHIP OF INTRAOCULAR PRESSURE TO INTRACRANIAL PRESSURE Ann Emerg Med 43(5):585, May 2004 METHODS: In this prospective study, from Ohio State University, the correlation between IOP and ICP was evaluated in 27 ICU patients without known glaucoma who were undergoing invasive monitoring of ICP due to a variety of conditions that included intracranial hemorrhage, ischemic stroke, trauma, tumor or shunt malfunction. A total of 76 measurements of IOP with a handheld Tono-Pen XL applanation tonometer were performed simultaneously with invasive ICP measurement. RESULTS: At a cut-off of 20 mmHg as an indicator of pressure elevation, the sensitivity and specificity of IOP measurement for elevated ICP were each 100%. All patients with elevated ICP had increased IOP, and all with normal IOP had normal ICP. Although there was a high overall correlation between IOP and ICP (r=0.83), differences between the two parameters were increased with increasing pressure levels and the potential difference between the two techniques at higher ICP ranges could be as great as 40cm H2O. CONCLUSIONS: Results from this pilot study require verification, but suggest that noninvasive measurement of IOP might prove to be a useful indicator of elevated ICP. 19 references (hiestand-1@medctr.osu.edu<\/a>)<\/p>\n Unilateral or bilateral unreactive, dilated pupil Extensor posturing (decerebrate) A sharp decline in GCS<\/p>\n decerebrate posturing=brainstem dysfunction<\/p>\n decorticate posturing=brainstem functioning<\/p>\n Cochrane Database Syst Rev. 2005 Oct 19;(4):CD001049. Related Articles, Links Mannitol for acute traumatic brain injury. Wakai A, Roberts I, Schierhout G. St Vincent’s Hospital, Department of Emergency Medicine, Dublin 4, Ireland. wakai@indigo.ie BACKGROUND: Mannitol is sometimes effective in reversing acute brain swelling, but its effectiveness in the ongoing management of severe head injury remains unclear. There is evidence that, in prolonged dosage, mannitol may pass from the blood into the brain, where it might cause increased intracranial pressure. OBJECTIVES: To assess the effects of different mannitol therapy regimens, of mannitol compared to other intracranial pressure (ICP) lowering agents, and to quantify the effectiveness of mannitol administration given at other stages following acute traumatic brain injury. SEARCH STRATEGY: The review drew on the search strategy for the Injuries Group as a whole. We checked reference lists of trials and review articles, and contacted authors of trials. The searches were last updated in April 2005. SELECTION CRITERIA: Randomised trials of mannitol, in patients with acute traumatic brain injury of any severity. The comparison group could be placebo-controlled, no drug, different dose, or different drug. We excluded cross-over trials, and trials where the intervention was started more than eight weeks after injury. DATA COLLECTION AND ANALYSIS: The reviewers independently rated quality of allocation concealment and extracted the data. Relative risks (RR) and 95% confidence intervals (CI) were calculated for each trial on an intention to treat basis. MAIN RESULTS: In the acute management of comatose patients with severe head injury, the administration of high-dose mannitol resulted in reduced mortality (RR= 0.56; 95% CI 0.39 to 0.79) and reduced death and severe disability (RR= 0.58; 95% CI 0.47 to 0.72) when compared with conventional-dose mannitol. One trial compared ICP-directed therapy to ‘standard care’ (RR for death= 0.83; 95% CI 0.47 to 1.46). One trial compared mannitol to pentobarbital (RR for death= 0.85; 95% CI 0.52 to 1.38). One trial compared mannitol to hypertonic saline (RR for death= 1.25; 95% CI 0.47 to 3.33). One trial tested the effectiveness of pre-hospital administration of mannitol against placebo (RR for death= 1.75; 95% CI 0.48 to 6.38). AUTHORS’ CONCLUSIONS: High-dose mannitol may be preferable to conventional-dose mannitol in the acute management of comatose patients with severe head injury. Mannitol therapy for raised ICP may have a beneficial effect on mortality when compared to pentobarbital treatment, but may have a detrimental effect on mortality when compared to hypertonic saline. ICP-directed treatment shows a small beneficial effect compared to treatment directed by neurological signs and physiological indicators. There are insufficient data on the effectiveness of pre-hospital administration of mannitol.<\/p>\n 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:<\/p>\n 2 ml\/kg body weight in 20 minutes. The aim was to decrease ICP<\/p>\n to .25 mm Hg or to increase CPP to .70 mm Hg. In case the<\/p>\n rst infusion failed, the patient received a second infusion within<\/p>\n ten minutes after the end of the rst infusion. Treatment failure<\/p>\n was de ned as the inability to decrease ICP to .35 mm Hg or to<\/p>\n increase CPP to .70mmHg with two consecutive infusions of the<\/p>\n selected osmotic solution. In that case, the protocol was stopped,<\/p>\n and patients were followed up for mortality or 90-day neurologic<\/p>\n status. Because 20% mannitol can crystallize at ambient temperature,<\/p>\n injections could not be performed in a blinded manner.<\/p>\n Twenty patients were randomised, ten to each group. Outcome<\/p>\n was assessed at 90 days using the Glasgow Outcome Scale administered<\/p>\n by a practitioner who was blind to acute patient care.<\/p>\n One trial compared mannitol to hypertonic saline (Vialet 2003).<\/p>\n This trial was randomised and single blind. Only patients with<\/p>\n head injury and persistent coma who required osmotherapy to treat<\/p>\n episodes of intracranial hypertension resistant to standard therapy<\/p>\n were included. For mannitol compared to hypertonic saline in<\/p>\n the treatment of refractory intracranial hypertension episodes in<\/p>\n comatose patients with severe head injury, the RR for death was<\/p>\n 1.25 (95% CI 0.47 to 3.33).<\/p>\n Brain oedema peaks at 3\u00965 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<\/a> Patients requiring intervention usually have large multilobar infarctions.194<\/a>, 195<\/a>, 196<\/a> and 197<\/a> Cerebellar infarctions with oedema can obstruct flow of cerebrospinal fluid, leading to acute hydrocephalus and increased intracranial pressure.192<\/a><\/p>\n Hypertonic Saline Reduced Intracranial Pressure From Brain Trauma<\/strong><\/p>\n Article content is available to ACEP members only<\/strong>; if you are an ACEP member, but do not have a Web account, please take a moment to create one now. <\/a><\/p>\n<\/span>CT Interpretation<\/a><\/span><\/h2>\n
<\/span>New BTF Recs<\/span><\/h2>\n
<\/span>Guidelines<\/span><\/h2>\n
<\/span>ED Goals<\/span><\/h2>\n
<\/span>Injuries<\/span><\/h2>\n
<\/span>Coup Contracoup<\/span><\/h3>\n
<\/span>Diffuse Axonal Injury<\/span><\/h3>\n
<\/span>Who Needs Surgery?<\/span><\/h2>\n
\n
<\/span>Prognosis<\/span><\/h2>\n
<\/a><\/h2>\n
<\/span>ICP Monitoring<\/span><\/h2>\n
<\/span>Cerebral Perfusion Pressure<\/span><\/h2>\n
<\/span>Herniation<\/span><\/h2>\n
<\/span>Elevated ICP<\/span><\/h2>\n
<\/a><\/h3>\n
<\/span>Eucapnia<\/span><\/h3>\n
<\/span>Rx ICP or Augment CPP???<\/span><\/h2>\n
<\/span>Osmotic Therapy<\/span><\/h2>\n
<\/span>Mannitol<\/span><\/h3>\n
<\/span>Hypertonic saline<\/span><\/h3>\n
<\/span>Sodium Bicarb as Omostic Therapy<\/span><\/h3>\n
<\/span>ICP Monitoring Waves<\/span><\/h2>\n
<\/span>CSF Drainage<\/span><\/h3>\n
<\/span>Barb Coma<\/span><\/h3>\n
<\/span>Decompressive Craniectomy<\/span><\/h3>\n
<\/span>Decompressive Laparotomy<\/span><\/h3>\n
<\/span>Repeat CTs<\/span><\/h2>\n
<\/span>Intracranial Volume Targeted (\u0093Lund Concept\u0094)<\/strong><\/span><\/h2>\n
<\/span>Brain Tissue Oxygen Monitoring (PbtO2)<\/span><\/h2>\n
<\/span>Brain Micro-Dialysis<\/span><\/h2>\n
<\/span>Cerebral Blood Flow<\/span><\/h2>\n
<\/span>Vents in Heads<\/span><\/h2>\n
<\/span>Transfusion in Head Injury<\/span><\/h2>\n
<\/span>Seizure prophylaxis<\/span><\/h2>\n
<\/span>Nutrition<\/span><\/h2>\n
<\/span>Anticoagulation<\/span><\/h2>\n
<\/span>Herniation<\/span><\/h2>\n
<\/span>Pulmonary and Cardiac Sequelae<\/span><\/h2>\n
<\/span>EAST Guidelines<\/span><\/h2>\n
<\/span>Factor VII<\/span><\/h2>\n
<\/span>Sodium Abnormalities<\/span><\/h2>\n
Cerebral Salt Wasting<\/h4>\n
<\/span>Fluids<\/span><\/h2>\n
<\/span>Adrenal Insufficiency<\/span><\/h2>\n
<\/span>Signs of Herniation<\/span><\/h2>\n
<\/span>Reversal of Antiocogaulation and Antiplatelet Drugs<\/a><\/span><\/h2>\n