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Head Injury and Anesthesia

Tod Sloan, MD, MBA, PhD University of Colorado at Denver and Health Science Center

CRASH 2007

SLOAN, TOD, MD,PHD

Head Injury 1897


The manner of treatment is of importance in only a minority of cases since many subjects of intracranial injury are fated to die whatever measures may be adopted Questions: Should we place greater emphasis on mildly injured patients? Do we really understand severe head injury?
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Head Injury
Most common cause of death and disability in young people and children 1.6 million head injuries per year (US) [150,000 pediatric HI] 16% 250,000 admitted to hospital 70,000-90,000 left with permanent neurologic disabilities [ 29,000 children] 32% 52,000-80,000 deaths per year 26% [7,000 children] Severe Approximate mortality 25% Mild Cost of care $1 billion annually
Marik Chest 122:699, 2002
Moderate

Traffic accidents, assaults (firearms), falls, (esp ETOH, drugs)


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Glascow Coma Scale


Motor Function 1 None 2 Abn. Extension 3 Abn. Flexion 4 Withdraws 5 Localizes 6 Obeys Verbal Response 1 None 2 Incomprehensible 3 Inappropriate 4 Confused 5 Oriented Eye Opening 1 None 2 To Pain 3 To Speech 4 Spontaneous

The neurologic exam is the best guide to the severity of injury

Score: 3 - 15 Severe Head Injury < 8 Moderate Head Injury 9-12 Mild Head Injury 13-15
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Outcome: Glascow Coma Score

Jaggi J Neurosurg 72:176, 1990


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Head Trauma - Injury


Primary Injury Damage from actual trauma Secondary Injury Damage from deranged Physiology -Hypotension, Hypoxemia, ICP, etc. Biochemical Injury Processes
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Secondary Insults
Hypotension Hyperthermia Hypercapnea Hypocapnea Inflammation Cascade of biomedical events mediated by free radicals, free iron, excitatory neurotransmitters Hypoxia Anemia Hyperglycemia Hypoglycemia Electrolyte Abn. Acid-Base Abn.

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SLOAN, TOD, MD,PHD

Head Trauma - Resuscitation


Airway Ventilation Cardiovascular Stability Lower ICP Cerebral Perfusion Pressure CPP = MAP ICP Complications

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SLOAN, TOD, MD,PHD

Head Trauma - Cervical Spine Injury


Commonly seen with Head Trauma 9% (60% Cervical) Sevitt, 1968 5% Maloney, 1969 Clinical Correlates Neck Pain, Neurologic Injury Lateral Cervical Spine Film May be missed on lateral x-rays 15-26% unstable patients missed

Clearing the neck is next to impossible!


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Head Trauma - Basilar Skull Fracture


Requires Mechanical Blow to Head Mastoid, Occiput, Supra Orbital Facial Bones Or Mandible Clinical Correlates CSF Leak, Battle Sign, Raccoon Eyes Cranial Nerve Injuries Vestibulocochlear, Olfactory Intracranial Air Increases Risk with Nasal Passage Avoid Nasal Endotracheal Tubes Increased Risk Cerebral Infection
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Head Injury - Airway


Awake controlled intubation most desirable Surgical airway may be required with facial trauma Asleep intubation with direct laryngoscopy can be done using midline stabilization Cricoid pressure is probably best done using bi-manual technique Succinylcholine remains the fastest onset muscle relaxant Hyperkalemia with SCI or Head Injury - 24 hr to 1 year post injury Increase in ICP appears related to gamma motor neuron stimulation associated with fasiculations -can be blunted by other means to lower ICP
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Airway- Breathing
Provide adequate oxygenation avoid hypoxemia inc CBF/ICP Provide adequate ventilation avoid inc PaCO2/CBF/ICP Maintain ETCO2 35-40 mmHg

Prophylactic hyperventilation worsens outcome


The Brain Trauma Foundation J Neurotrauma, 17:513, 2000

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Predictors of Outcome
Age CT scan diagnosis Admission GCS score Pupillary reactivity Hypotension

Hypotension is the only factor amenable to therapy


National Traumatic Coma Databank
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AB-Circulation
Hypotension is the primary risk factor for poor outcome Most hypotension is due to hemorrhage Systolic BP < 110 mmHg probably need volume resuscitation Systolic < 90 mmHg needs aggressive management. Strategy: euvolemia, normotension, hyperosmolarity Older management strategy of dehydration
No decrease cerebral edema Possibility of hypotension
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Normal Physiological Effects on Cerebral Blood Flow


Autoregulation Local Cerebral Blood Flow is adjusted across a wide blood pressure to maintain relatively constant blood flow (MAP 2/3 - 1 1/2 normal) Vasodilatation at low pressure Vasoconstriction at high pressures Pressure dependent above and below limits of vasoconstriction Dilation Constriction and dilation
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Hypotension and Hypoxia


100% 80% 60% 40% 20% 0% None GR/MD SD/PVS Dead

Hypoxia

Hypotension

+ Hypoxia
Chestnut J Trauma 34:216, 1993
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Reducing ICP: The Brain


Fluid Management
Use Normo-natremic Fluids (e.g. normal saline, Normosol, Isolyte not lactated ringers, D5W) Maintain osmolarity of blood (recall controversy of colloid in trauma) Avoid glucose administration Appears to increase extent of ischemic injury Use glucose as needed with endocrine problems
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Pathophysiology of Brain Injury


Disrupted autoregulation
Loss - Allows pathologic vasodilation Raise lower limit of autoregulation Decreased metabolism
Loss of metabolic-vascular coupling

Vascular Pathology
Hyperemia leading to increased cerebral blood volume and increased ICP without inducing ischemia Decreased CBF in early hours (loss autoregulation) Vasospasm

Disrupted BBB
68% fatal injuries had ischemia, hyperemia common in non-fatal injuries Fessler, Annals Int Med, 22:998, 1993
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Triphasic CBF response to injury

*
1. Reduction global CBF (often to ischemic levels *) autoregulation disrupted, lost at ischemia 2. Supranormal levels 12-24 hours hyperemia metabolism and flow may remain coupled 3. Eventual fall to normal levels and/or vasospasm
Menon Br Med Bull 55:226, 1999
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Injury and Autoregulation


Injury

Low CBF
Vasospasm, Raise lower limit of autoregulation, Direct injury

High CBF Normal CBF


Normal autoregulation Loss autoregulation, ischemia

Hyperventilation may aggravate ischemia! Low BP a problem

Hyperventilation may lower ICP

Hyperventilation may help prevent edema! High BP a Problem


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CBF
Cerebral ischemia dominates HI as the single most important event determining outcome Hyperventilation could cause further ischemia
Lewelt J Neurosurg 53:500, 1980

In some HI, low CBF is normal (i.e. associated with normal oxygen extraction (matched metabolism)
Obrist J Neurosurg 61:241, 1984

In some HI, increases in flow are associated with luxury perfusion with a propensity for edema correctable with hyperventilation Hyperventilation could improve outcome
Cruz Crit Care Med 21:1225, 1993

CBF tends to increase in children with HI

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Acute Head Injury


ICP with altered consciousness 44% > 20 mmHg 38% > 10 mmHg 18% < 10 mmHg

55% with GCS < 7 (Coma)

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Physiological Effects of Raised ICP


Hypertension Bradycardia
Cushings Triad

Ventilatory Dysrhythmias
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Elevated ICP
Most significant cause of morbidity and mortality with head trauma Miller J Neurosurg 47:503, 1977 Acute elevations may be associated with seizures ICP > 25 mmHg use barbiturates (may control up to 25% of patients Ingvar, Cerebral Function and Metabolism, Copenhagen 1977, p 156

Cerebral Perfusion Pressure


CPP = MAP - ICP
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Craniotomy
30-50% of HI patients benefit from craniotomy Acute subdural 90% mortality if evacuated > 4 hours 30% mortality if evacuated < 4 hours
Seeling NEJM 304:1511, 1981

70% decrease mortality if < 2 hours


Haselsberger Acta Neurochir 90:111, 1988

Underlying brain injury determines outcome in 80%


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ICP Management
Lower Brain Bulk: 800-1000 cc
Mannitol, lasix, hypertonic saline steroids (tumors)

Lower Venous Volume: 60-70 cc


Head elevated, neck neutral, lower CVP

Lower CSF Volume: 120-150 cc


Drainage ?

Lower Arterial Volume: 30-40 cc


Sedation, Treat pain, fever, seizures Hyperventilation, Barbiturates, Hypothermia
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Mannitol
Osmotic dehydration of the Brain Reduces blood viscosity and expands vascular volume - increasing CBF resulting in vasoconstriction and dec CBV/ICP May cause dehydration, hypotension and pre-renal azotemia Opens blood-brain barrier cause reverse osmotic shift

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Hypertonic Saline
Increase blood pressure
Bring volume from tissues into circulation

Lower ICP
Cause osmotic cerebral dehydration

Small volume resuscitation (250 cc) appears promising, but controversial


Simma Crit Care Med 26:1265, 1998

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Hypothermia
Shown to be protective during ischemia in numerous animal studies In man, no improvement with HI and worsens infarct during ischemia
Clifton NEJM 344:556, 2001, Dietrich J Neurotrauma, 9 Suppl:475, 1992

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Management Alternatives
Reduce ICP
Lower ICP < 20 mm Hg

Improve CPP
Raise CPP (60-70 mmHg)to improve CBF

Optimize Vascular Congestion


Lower ICP, raise MAP Optimized ventilation to reduce hyperemia, CBV and ICP Optimize regional metabolism and CBF

Reduce Cerebral Edema


Increase plasma oncotic pressure, relative hypovolemia, lower MAP
Eker Crit Care Med 26:1881, 1998
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Cerebral Management I
Traditional Therapy ICP focused Pathophysiology: Control ICP
Barbiturate Coma Hyperventilation Osmotherapy Neuromuscular Block CSF Drainage

CPP ignored, goal is ICP < 20 mmHg


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Cerebral Management II
Rosner - Adjust CPP Pathophysiology vasodilatory cascade lowered CPP because dec BP or inc ICP cause vasodilation Rx raise BP break cycle CPP - > 70-80 mmHg, above lower limit autoregulation to keep CBF normal
Rosner J Neurosurg 83:949, 1995
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Cerebral Management III


Lund Therapy Pathophysiology: poor control of microvascular pressures results in brain edema Rx 1. preserve colloid osmotic pressure
(albumin and RBC) 2. Reduce capillary hydrostatic pressures by reducing BP (metoprolol, clonidine) 3. Reduce cerebral blood volume by vasoconstriction (low dose barbitruates and dihydroergotamine) CPP - > 50-60 mmHg depending on adequate perfusion (minimum level not producing ischemia), High level promotes edema.
Eker Crit Care Med 26:1881, 1998, Grande J Trauma 42:S23, 1997
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Cerebral Management IV
Individualized Therapy Management is directed at the specific pathophysiology Vascular causes hypnotic-sedative agents Edema osmotic agents CPP- treat as necessary
Miller Acta Neurochir Suppl (Wien) 57:152, 1993
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Anesthesia and HI
Inhalational Agents
Decrease metabolism Change metabolic coupling

Minimal Impact at Low Dose


Increase CBF/ICP at higher Doses Generally desirable to keep below 1 MAC Use other methods to lower CBF/ICP N2O is at least as bad as potent inhalational agents
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Anesthesia and HI
Intravenous Agents Decrease metabolism Maintain metabolic coupling Desirable Impact Decrease CBF/ICP Effect limited at full synaptic depression May have hemodynamic impact at higher doses Opioid effect appears related to vasodilation from decreased BP and autoregulation
Ketamine is an exception as it increases CBF/ICP and is undesirable
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Summary: Head Injury


Initial Management: ABCs Acquire airway (C-spine, Basilar skull fracture) Ventilation (Hyperventilate if necessary) Blood pressure (Maintain adequate CPP) Reduce ICP Anesthesia using intravenous based agents for severe ICP elevations Postoperative care for complications
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Evolution of Head Injury


1960s HI Data Bank: Jennett et. al. in Glascow began collecting data on large numbers of HI patients 1972 Introduction of CT assess hemorrhagic lesions 1974 Glascow Coma Scale Teasdale and Jennett assess unconsciousness 1979 National Traumatic Coma Data Bank 1970s 1980s Concept secondary injury ICP centered treatment: role surgery, hyperventilation, barbiturates, osmotic agents, steroids 1990s CPP centered treatment (70 mmHg) 1995 Brain trauma foundation guidelines (revised 2000)

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Field Guidelines
All reasonable efforts should be made to avoid hypoxemia and hypotension

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Brain Trauma Recommendations


Initial Management O: ABCs Physiologic Resuscitation O: Sedation and neuromuscular blockade G: Avoid BP <90 mmHg G: Avoid O2 saturation <90% ICP Monitoring G: appropriate with severe HI and CT abnormalities G: Treat ICP >20-25 mmHg O: CPP maintained >70 mmHg Hyperventilation S: Avoid prolonged PaCO2 <25 mmHg R: Avoid prophylactic PaCO2 <25 mmHg O: Brief PaCO2 <25 mmHg top control ICP
Standards, Guidelines, Options
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Brain Trauma Recommendations


Mannitol G: Effective for control ICP 0.25-1 gm/Kg if volume resuscitated O: Boluses better than infusion, Keep serum Osm <320 mosm Barbiturates G: High dose may be considered in salvageable severe HI with refractory inc ICP Steroids S: Not Recommended Nutrition G: replace metabolism with enteral or parenteral feedings with 15% protein. Antiseizure Prophylaxis S: Prophylaxis of late seizures not recommended O: Recommended prevention early seizures with phenytoin and carbamizine
Standards, Guidelines, Options
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Head Injury and Anesthesia


Tod Sloan, MD, MBA, PhD University of Colorado at Denver and Health Science Center Tod.Sloan@uchsc.edu

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