Traumatic brain injury

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Presentation Transcript

Management of Traumatic Head Injury: 

Management of Traumatic Head Injury Dalhousie Critical Care Teaching Rounds

Objectives: 

Objectives Know how to calculate CPP and the normal CPP range. Discuss the management principles for raised ICP. Discuss the issues for prevention of secondary injury in SAH including control of temperature, glucose control, prevention and treatment of vasospasm with nimodipine and HHH therapy. Know how to work up and treat different Na disorders including SIADH, cerebral salt wasting and DI

Neurophysiology: 

Neurophysiology CPP = MAP – CIP N= 50-70 Trauma Increase volume of intracranial components Loss of autoregulation Increased CSF production Hypercapnia and hypoxic insults

Management of Head Injury: 

Emergency Diagnostic or Therapeutic Procedures Tracheal Intubation Fluid Resuscitation Ventilation/Oxygenation Sedation Management of Head Injury Severe Head Injury GCS≤8 ATLS Trauma Evaluation Deterioration Herniation CT Scan ICU ± Hyperventilate ± Mannitol Surgical Drainage

Management of Raised ICP: 

Raised ICP>25mm Hg Management of Raised ICP First Line Rx Measure ICP Maintain CPP>70 mm Hg Ventricular Drain Elevate HOB Normal Vent/Oxygenation Mannitol Sedation Raised ICP>25mm Hg CT

Management of Raised ICP: 

Raised ICP>25mm Hg Management of Raised ICP Second Line Rx Maintain CPP>70 mm Hg Furosemide Chemical Paralysis CSF Removal Vasopressor Barbiturates Hyperventilation Monitor SjO2 Raised ICP>25mm Hg

Head Injury: 

Head Injury Primary Head Injury Result of energy absorption Difficult to prevent Results from neuronal or axonal disruption shear laceration vascular disruption Secondary Head Injury Result of insults that occur after primary injury Easier to prevent Causes ischemia hypoxia cerebral edema intracranial hypertension abnormalities of cerebral blood flow metabolic derangements

Role of ICP Monitoring: 

Role of ICP Monitoring May help in earlier detection of intracranial mass lesions Rationalizes therapy (ICP vs CPP) CSF drainage Helps in determining prognosis May or may not improve outcome CPP=MAP-ICP

ICP Monitors: 

ICP Monitors Intraventricular Catheter “Gold standard” Pros: Allows drainage of CSF (to dec ICP), allows “re-zeroing” Cons: Invasive, difficult to insert, infection risk Interparenchymal Probe Pros: Low infection rate Cons: Local pressure, “drift of zero”

ICP Monitors: 

ICP Monitors Subarachnoid Probe Pros: Low infection rate, no brain penetration Cons: Limited accuracy, high failure, requires flushing Epidural Probe Pros: Easy to insert, extra cranial Cons: Limited accuracy, relatively delicate Others: Transcranial doppler Tympanic membrane displacement Lumbar CSF pressure

Management of Traumatic Brain Injury: 

Management of Traumatic Brain Injury

AANS & BTFHead Injury Guidelines (2000): 

AANS & BTF Head Injury Guidelines (2000) Past Reliance on expert opinion Documented variability of practice Rely on scientific evidence and not expert opinion Task force of experts with each Expert assigned a topic Medline search Review and grading of papers on topic Multiple iterations Involvement of national and international organizations

Hyperventilation: 

Hyperventilation CBF is the lowest in the first 24 hrs after injury Hyperventilation decreases CBF (3%/torr) Hypervent to a PCO2 26 CBF by 31% and CBV by 7% Can CBF and A-VdO2 to ischemic levels Effect of hyperventilation transient (4 hours) CBF 90% of control at 4 hours of hyperventilation

Hyperventilation: 

Hyperventilation Muizelaar et al 1991 RCT Obrist et al 1984 Cohort study Hyperventilation had a greater effect on CBF than ICP Schnieder et al 1995 Cohort study Hyperventilation second leading cause of jugular desaturation Sioutos et al 1995 Cohort study 1/3 of patients had CBF < 18 ml/100g/min Hypervent decreased CBF further N= 77

Use of Hyperventilation: 

Use of Hyperventilation Standards In absence of increased ICP chronic hyperventilation should be avoided (PCO2 < 25) Guidelines Use of prophylactic hyperventilation (PaCO2 < 35) should be avoided during the first 24 hrs after head injury because it may compromise CBF Options Hyperventilation may be necessary for brief periods when there is neurologic deterioration or for raised ICP refractory to standard therapy

Glucocorticoids: 

Glucocorticoids Useful in patients with brain tumor Experimental evidence Restoration of altered permeability in the lab Reduced CSF production Attenuation of free radical production Meta analysis has showed no benefit Alderson et al 1997 No benefit in clinical trial of Tirilazad 17 amino steroid N=1170 North America N=1128 Europe

CRASH Study: 

CRASH Study Head injury with GCS ≤ 14 Primary outcome Death at 2 weeks Disability at 6 months (not yet reported) 10,008 subjects Multicentre RCT Randomization groups Placebo Methylprednisolone Load 2 gms Maintenance 0.4 gm/hr for 47 hours Mortality Placebo 18% Steroids 21% Lancet 2004; 364: 1321-38

Glucocorticoids in Severe Head Injury: 

Glucocorticoids in Severe Head Injury Standards Not recommended for reducing ICP or improving outcome

Blood Pressure and Oxygenation: 

Blood Pressure and Oxygenation TCDB study Large prospectively collected data set N=717 Anesthesia Study Observational study of patients with severe head injury requiring surgery with in 72 hours of admission N=53 Death Chesnut et al 1997 Pietropaoli et al 1992 Outcome %

Blood Pressure and Oxygenation: 

Blood Pressure and Oxygenation No class I evidence Randomization probably not ethical Standards nil Guidelines Hypotension (SBP<90) and hypoxia (PO2<60)must be avoided and if present corrected immediately Options Mean arterial pressure > 90 CPP >70

Rational for ICP Monitoring: 

Rational for ICP Monitoring Correlation between high ICP and poor outcome Intracranial hypertension more likely in those with CT abnormalities or adverse features Age >40 Motor posturing SBP<90 Narayan et al 1982

Intracranial Pressure Monitoring: 

Intracranial Pressure Monitoring Standards nil Guidelines Indicated for severe head injury with abnormal CT Indicated for severe head injury with normal CT with 2 or more of age greater than 40 motor posturing Systolic BP less than 90 mm Hg Not indicated for mild or moderate head injury

Does ICP Monitoring Improve Outcome: 

Does ICP Monitoring Improve Outcome No randomized controlled trial Improved outcome with ICP monitoring over historical data Saul and Ducker 1982 (Class II) Rx ICP 20-25  mortality 46% Rx ICP >15  mortality 28% Eisenberg et al 1988 (Class I) Better outcome if ICP responded to Pentobarb Colohan et al 1989 (Class II) 2 centers with lower mortality in center with ICP monitoring Groups managed at different time periods Other confounding factors

Does ICP Monitoring Improve Outcome: 

Does ICP Monitoring Improve Outcome No randomized controlled trial Ghajar et al 1995 (Class III) Meta analysis demonstrating decreased mortality with CSF drainage Lane et al 2000 (Class II) Retrospective study of trauma database 5507 head injured patients Used AIS scores to define injury Results multivariate analyses controlling for AIS head, ISS and injury mechanism indicated that ICP monitoring was associated with significantly improved survival (p < 0.015)

Cerebral Perfusion Pressure: 

Cerebral Perfusion Pressure CBF low following head injury Compression of cerebral vessels Reduced cerebral metabolism Vasospasm CBF lowest first 24 hrs after injury Ischemia common at autopsy Correlation with CBF, GCS and outcome Failure to maintain adequate CPP may lead to increased ICP and poor outcome

Physiology: 

Physiology ICP, CPP, CBF and CMRO2 CPP = MAP – ICP (or CVP)‏ Monroe-Kellie Doctrine

Cerebral Perfusion Pressure: 

Cerebral Perfusion Pressure Fortune et al 1994 (Class II) N=14 CPP maintained above 70 mm Hg Mortality 14% Rosner et al 1990 (Class II) N= 34 CPP kept above 70 mm Hg Mortality 21%, good outcome 68% Bruce et al 1973 (Class II) N=14 Study of the effect of increasing the blood pressure on ICP When BP increased by 30 mm Hg, ICP increased by 5 mm Hg Robertson et al 1999 (Class I) N=189 Comparison of ICP vs CPP targeted therapy Fewer SVO2 episodes in CPP targeted group No difference in GOS, ICP, Higher ARDS in CPP targeted group

Guidelines for Cerebral Perfusion Pressure: 

Guidelines for Cerebral Perfusion Pressure Standards nil Guidelines CPP maintained at a minimum of 60 mm Hg

Mannitol: 

Mannitol No controlled trials with placebo Mechanism of action (Early vs Late) Plasma volume expansion reduces blood viscosity increases CBF increases cerebral oxygen delivery Osmotic gradient Circulating mannitol may cross BBB avoid continuous administration contraindicated in renal failure

Mannitol: 

Mannitol Schwartz et al 1984 (Class I) N=59 Mannitol group had lower outcome mortality in DAI 41% vs 77% Better CPP in mannitol group Fortune et al 1995 (Class II) N=22 Studied effect of mannitol and hyperventilation on SJVO2 196 interventions on 22 patients SJVO2 increased with mannitol and decreased with hyperventilation

Mannitol Use in Severe Head Injury: 

Mannitol Use in Severe Head Injury Standards nil Guidelines Mannitol effective for control of ICP after severe head injury 20 percent solution 0.25 to 1 g/kg IV bolus Repeat doses can be administered every six to eight hours Options indications transtentorial herniation and neurologic deterioration not attributable to systemic pathology Serum osmolarity kept < 320 Maintain euvolemia Intermittent boluses may be more effective than continuous infusion

Barbiturates: 

Barbiturates Lower ICP Mechanisms alterations of vascular tone suppression of metabolism inhibition of free radical lipid peroxidation coupling of CBF to metabolic demands Assumptions Can effect long term ICP control when other treatments have failed Absolute ICP control improve outcome

Barbiturates: 

Barbiturates 3 randomized control trials 2 prophylactic trials showed no benefit 1 raised intracranial pressure therapeutic trial showed improved survival if ICP responded to barbiturates

Schwartz et al (1984): 

Schwartz et al (1984) Barbiturates with mannitol for initial therapy for increased ICP Randomized when ICP>25 mm Hg for more than 15 minutes N=59 Mortality

Eisenberg et al (1988): 

Eisenberg et al (1988) Control of ICP primary outcome Randomized to barbiturates or control n=73 Treatment failure in control arm resulted in barbiturates Survival 92% if ICP responded to barbiturates vs 17% if no ICP response ICP Control %

Barbiturate Use in Severe Head Injury: 

Barbiturate Use in Severe Head Injury Standards nil Guidelines Barbiturates may be considered hemodynamically stable salvageable head injury refractory intracranial hypertension

Hypothermia: 

Hypothermia Use supported by; Animal data Single centre trials Success in related conditions global cerebral hypoxia One Multi-centre RCT (NABISH) NEJM 2001; 344: 556-63 N=368 Target temp 33 Hypothermia for 48 hours

Temperature Control and Induced Hypothermia: 

Temperature Control and Induced Hypothermia Most effective method for brain protection decreases both basal and electrical metabolic requirements CMR decreases by 6% to 7%/°C metabolic requirements continue to decrease even after electrical silence

NABISH Results NEJM 2001; 344: 556-63: 

NABISH Results NEJM 2001; 344: 556-63 Hypothermia More hospital days with complications Lower ICP Criticisms Accepted MAP of 50 Slow cooling Rapid and active rewarming

But Food for Thought…: 

But Food for Thought… JAMA 2003 Jun 11;289(22):2992-9. Prolonged therapeutic hypothermia after traumatic brain injury in adults: a systematic review. Meta-analysis of 12 rct Decreased risk of death RR0.81 and poor neurologic outcome RR0.78 Prolonged duration of hypothermia seemed better

Hypertonic Saline: 

Hypertonic Saline Potential advantages Quicker management of hypotension Osmotic dehydration lower ICP WBC immunomodulation May decrease glutamate Earlier studies suggested a mortality benefit and lower ICP Meta-analysis demonstrated improved survival rates, especially in head trauma (38% versus 27%) Wade CE, Kramer GC, Grady JJ, et al. Efficacy of hypertonic 7.5% saline and6%dextran-70 in treating trauma: a meta-analysis of controlled clinical studies. Surgery 1997;122:609–16. Cooper et al JAMA 2004 Prehospital admin of 250 ml 7.5% HS vs RL RCT 229 subjects 6 mos GOS main outcome No difference in GOS or survival Trend to lower ICP with HS

SAFE trial: 

SAFE trial Subgroup analysis of trauma patients with severe brain injury 460 patients Mortality higher in albumin group 33.2% vs. 20.4 saline group Saline or Albumin for Fluid Resuscitation in Patients with Traumatic Brain InjuryN Engl J Med 2007;357:874-84.

Other stuff to consider: 

Other stuff to consider Decompressive craniectomy Antieplileptic therapy Management of fever Position Treatment of hypertension ICP >20 and CPP>160 Fluid/electrolyte Osmolarity should be 280-305 Avoid hyponatremia Hypertonic saline in mannitol resistant ICP

Summary: 

Summary Avoid hypotension and hypoxia Maintain CPP Hyperventilation should only be undertaken with herniation or appropriate monitoring of CPP and cerebral oxygenation