traumatic brain injury 1.6 million head injuries in us annually 250,000 hospital admissions 60,000...

Traumatic Brain Injury

• 1.6 million head injuries in US annually

• 250,000 hospital admissions• 60,000 deaths• 70,000 - 90,000 permanent

neurologic disabilities• Causes

– Motor vehicle accidents– Falls

Primary Survey

1. Stabilize the spine2. Establish adequate airway3. Ensure adequate ventilation4. IV access to initiate volume resuscitation Avoid secondary insults to brain

HypoxiaHypotension

Determine level of consciousness examine pupils

Secondary Survey

• Once relatively stable• Includes a complete neurologic examination• Severity of the head injury is classified clinically by

GCS– 13 to 15 mild – 9 to 12 moderate– 8 or less severe

• Assess strength, sensation

Overall goal with neurologic injury

• Presume injury until proven otherwise• Identify early• Allow injured tissue the best chance to repair itself– Adequate delivery of oxygen and glucose– Avoid infection

• Preserve residual nervous tissue

Primary Brain Injury

• Trauma: concussion, contusion,diffuse axonal injury

• Ischemia: global, regional• Inflammation• Direct Injury: hemorrhage,

penetrating injury• Compression: tumor, edema,

Hematoma• Metabolic insults• Excitatory toxicity: seizures, illicit

drugs, severe hyperthermia

Secondary Brain Injury

• Hypoperfusion: hypotension, high intracranial pressure, vasospasm– Single episode SBP <90 mm Hg increases morbidity & doubles mortality*

• Hypoxemia* **– pO2 ≤ 60 mm Hg increases poor outcome from 28% to 71% *– Increases mortality

50% from 14.3% **

• Harmful mediators: reperfusion, inflammation• Electrolyte changes

*Chestnut RM, et al. J Trauma 1993;34:216-222**Jones PA, J Neurosurg Anesth 1994;6:4-14

Basic Premises:

1. Monro-Kellie hypothesis 3 compartments: brain, blood, & CSF Increase in one must be compensated

by decrease in others or the ICP will increase2. Compliance volume to pressure relationship

Basic Premises:

1. Monro-Kellie hypothesis2. Compliance3. Cerebral autoregulation

Intact autoregulation

Lang et al JNNP 2003;74:1053-1059

Intact autoregulation

Intact autoregulation

Lang et al JNNP 2003;74:1053-1059

Defective autoregulation

Basic Premises:

Monro-Kellie hypothesis2. Compliance3. Cerebral autoregulation4. CPP = MAP – ICP

Optimal cerebral perfusion pressure (CPP) in patients with acute traumatic brain injury by current guidelines

is:A. Maintaining a mean arterial pressure of greater than 90 mm Hg.B. 50-70 mm Hg.C. greater than 70 mm Hg.D. determined without an ICP monitor.E. not important, ICP is the parameter to follow

Cerebral perfusion pressure

CPP = MAP - ICPNormal is 70-100 mm HgAdequate 50-60 mm HgIschemia 30-40 mm Hg

High MAP

• WARNING ! ↑ in BP may be a sign of ↑ICPDO NOT TREAT/OVERTREAT BP alone

CPP = MAP - ICP70 = 75 - 5

70 mm Hg = ↑ ← ↑70 = 110 - 4035 = 75 - 40

Cerebral perfusion pressure

CPP=MAP-ICP Current AANS guidelines specify ICP

<20 & CPP of 50-70 mmHg• Lower CPP : poorer outcome

(ischemic)• Higher CPP: more ARDS

J Neurotrauma. 2007; 24:S59-64

Initial Management – Pre-hospital

• A B C D• Intubate early if GCS <8• Systolic BP of < 110 requires fluid resuscitation • Rapid transport to trauma center• Avoid sedation if possible to preserve neuro exam

Early Hospital Management

• Intubate if GCS <8• Rapid sequence preferred – Avoid increased ICP with placement of ETT

• Preferred drugs– Etomidate – rapid acting, short duration, min BP effect– Rocuronium- short duration, no BP effect, no increased ICP

• 100% O2 until transferred to ICU• Initial target PCO2 should be 35 to 40 mm Hg• MAP goal 90• Use only LR or NS – NO HYPOTONIC FLUID

Maintain Oxygenation!

Hypoxemia ≤ 60 mm

Hg increases poor outcome from 28% to 71% (trauma)

• CT head – non contrast– All patients at risk

• GCS <15• Depressed skull or evidence of basilar skull fracture• Focal neuro deficits

– GCS 15, +LOC

• Neurosurgical consultation– Surgical evacuation

• all acute traumatic extra-axial hematoma >1 cm • subdural or epidural hematoma > 5 mm with an equivalent midline shift and GCS<8• depressed, open, and compound skull fractures• recommended if hematoma > 20 ml with mass effect

ICU Management

• Serial neurologic exams• ICP monitor recommended in patients with a GCS

score < 8– intracranial HTN > 60%

• No RCT’s to support improved outcomes with ICP monitor

• Studies demonstrate outcome is inversely proportional to max ICP reading and time spent >20

ICP MonitoringDifferent sites1) Intraventricular- Gold standard

2) Intraparenchymal3) Subarachnoid4) Subdural5) EpiduralDifferent modalities1) Fiberoptic2) Fluid-coupled

Jugular Venous Oximetry

Continuous SjVO2 Blood Draws for

CvO2

Value Normal IschemiaSjVO2 > 60% <50% (10 min.)

Tissue PO2 Monitoring:Pbto2 Licox- Integra• Direct measurement of tissue

oxygen tension (?)• Local measurement• Part of ICP-bolt system• Experimental use in Europe since 1992• Approved for use in Europe,

Canada, and US

Management of Intracranial HTN

• 3 targets– Intracranial blood volume reduction– CSF drainage– Brain parenchyma reduction

Cerebral blood volume

• Decrease– Elevate head to 30

degrees– Midline position of

head– Sedation– Muscle relaxation– Decrease airway

pressure

• Increase– Ischemia– Acidosis– Hypercapnia– Increased

venous pressure– Hyperthermia

Hyperventilation

Begins almost immediatelyPeak effect in 30 minutesLowers ICP by 25-30% in most

patientsMay decrease cerebral blood flow:

No lower than pCO2 of 30mm HgNormalize within hours

Ventilation: Hyperventilation

PaCO2 of 25-30 mm Hg can causesignificant vasoconstriction andreduction in cerebral blood flow

Coles JP, Crit Care Med 2002;30:1950-1959Diringer MN. J Neurosurg 2002;96:103-108Imberti R. J Neurosurg 2002;96:97-102Muizelaar J Neurosurg 1991;75:731-739Cold. Acta Neurochir 1989;96:100-106Raichle, et al. Stroke 1972;3:566-575

Hyperventilation

Hyperventilation lowers CBF, and therefore ICP, by raising the extracellular pH in the CNS

• CO2 is not the direct mediator of this response Hyperventilation does not ‘stop working;’

however, The choroid plexus exports bicarbonate to lower the pH 6 hour time course• The cause of the ICP elevation is usually

progressive• Further attempts at hyperventilation will raise

intrathoracic pressure, decreasing jugular venous return and thereby raising ICP

• CBF is independent of MAP between 50-150– Autoregulation– With injury 50% pts lose autoregulation ability– GOAL – Normal MAP or MAP >90– Treat hypotension with thoughts of cause– Treat HTN with B-blockers, nicardipine– Use vasodilators with caution

Hemodynamic

Marik, P. E. et al. Chest 2002;122:699-711

Cerebral autoregulation in normal subjects and patients with chronic hypertension

Osmotic Agents: Mannitol

Acts within 20-30 minutes Dosage: 0.25-1 g/kg bolus Filtered needles! Actions:1) osmotic gradient2) may increase cardiac preload, output and elevate MAP3) improves rheology of red blood cells4) decreases CSF production5) free radical scavenger

Osmotic Agents: Mannitol

• Serum osmolality <320 mOsm/L vs osmolar gap <10

• Measured osmoles – (2Na +glu/18+BUN/2.8)• Watch for osmotic diuresis:

Dehydration and hypotension• MAINTAIN EUVOLEMIA

Hypertonic Saline

3% saline 250cc bolus (run in as fast as possible)

7% saline bolus23.4% saline 30cc bolus

Fever

Each increase in 1degree Celsius increases cerebral metabolic rate by 7%

One study w/ exercise: 1.5º C increased CMRO2 by 23% increase in CMRO2

Vasodilation CBV ICP Increases O2 requirements Increases CO2 production (may need to adjust

ventilator minute ventilation!!!)

Nunnely SA et al. J Appl Physiol 2002;92:846-851.

McIntyre L et al JAMA 2003

Pentobarbital coma may result in:

A. hyperthermia.B. hypertension.C. increased respiratory drive.D. unreactive large pupils.E. increased electrographic activity

Additional methods to decrease ICPfor when conventional management fails

No demonstrated benefit

• Barbiturate coma– Reduce O2 demand– No cellular toxicity– Burst suppression by

continuous EEG

• Hypothermia– Reduce O2 demand – Do not actively rewarm

cold patients

• Decompressive Craniectomy– Last resort

Sedation

• Fentanyl is analgesic of choice– Min BP effect, depresses cough

• Propofol– easily titratable, rapidly reversible– decreases cerebral metabolic rate– Potentiates GABA inhibition– Inhibitions methyl-D-aspartate glutamate receptors – Inhibits voltage-dependent calcium channels– Potent antioxidant– Inhibits lipid peroxidation

• Can paralyze if needed, but keep to minimum

Seizure Prophylaxis

• Anti-seizure medication– 7 days after severe injury– Usually phenytoin

• Avoid abnormal electrolytes• Hyponatremia

– SIADH– Cerebral salt wasting

• Hypomagnesemia

Hemicraniectomy:

Mattiello, J. A. et al. N Engl J Med 2001;344:580

4 types of acute post-traumatic intracranial hemorrhage:

Subdural hematoma

Subarachnoidhemorrhage

Periventricular and frontal lobecontusions with

intraparenchymalhematoma

EPIDURAL HEMATOMA

EPIDURAL HEMATOMA

Acutesubdural

hematoma

Chronicsubdural

hematoma

Subarachnoidhemorrhage

EPIDURAL HEMATOMA

Multipleintraparenchymalhematomas with

surrounding edema

Diffuse Axonal Injury

• May cause immediate and prolonged unconsciousness• High morality, high morbidity, often persistent

vegetative state• Identified by diffusion-weighted MRI• Caused by shearing forces affecting axons leading to

dysfunction of the reticular activating system• Axons are not torn but sequential, focal changes that

lead to swelling and disconnection over multiple hours • Apoptosis may play role in axonal injury

Gilman, S. N Engl J Med 1998;338:889-896

CT in Patients with Craniocerebral Trauma

MultipleIntraparenchymal

hemorrhages

Subarachnoidhemorrhage

Depressed skullfracture

Poor prognosis

• Advanced age• Female <50• Anticoagulation at time of trauma• Low GCS at arrival• Hypotension• Abnormal pupillary widening• Traumatic SAH

Things to keep in mind…

• Spine injury until proven otherwise• Many intraparenchymal hematomas may be delayed,

appearing on the CT scan 24 h after the initial insult• Low threshold to repeat CT scan– Clinical changes– Continued uncontrollable intracranial HTN

Acute Spinal Injury

• 10,000 new cases annually• Males 16-30 make up 80%• Most due to MVA 36%, violence 29%, falls 21%• Quadriplegia is slightly more common than paraplegia• Rare to completely transect cord• 6-8% of head trauma will also have spine injury• Main goal is early identification• Insult is associated with an injury response that results

in neuronal destruction

Secondary injury

• cascade of tissue injury– vascular compromise– inflammatory changes – cellular dysfunction– free radical generation

• hallmark is spinal cord edema• peaks 3 to 6 days after injury• subsides over a period of weeks

Initial Resuscitation

• Regular ABC’s• Immobilize neck until cleared or

stabilized– Head between two sandbags– Placement of cervical collar

• Immobilize entire spine – Transportation on a rigid spine board– Log rolling

• 25-50% of cervical spine injuries also have head injury

Neurologic exam

• Early• Sequential• Include

– Strength– Sensation – pain, position

• Neurologic level: most caudal segment of the spinal cord with normal bilateral motor (strength >3/5) and sensory (light touch and pinprick) function

Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518

The NEXUS Low-Risk Criteria

Stiell, I. G. et al. N Engl J Med 2003;349:2510-2518

The Canadian C-Spine Rule

Imaging• Cervical spine films

– AP, lateral, and odontoid – Additional laterals

• If entire c-spine or C7–T1 space not seen• Abnormal vertebral alignment, bony structure,

intervertebral space, and soft tissue thickening• Flexion and extension films

• SCIWORA (spinal cord injury without radiologic abnormality)• CT scan – best for bones

– If not adequate visualization by X-ray• MRI

– Modality of choice for characterizing acute cord injury – Best for edema, hemorrhage, ligamentous injury

Neuroresuscitative Agents

• High dose steroids– 30mg/kg bolus – 5.4mg/kg/hr x 23H– Give for 48H if not given within 3H

• Effective if given in first 8 hours

Injury classification– Stable– Unstable– Soft tissue or fracture

Surgery• Decompress neural tissue• Prevent cord injury by ensuring stability• Options include– bed rest in traction (rarely done)– external immobilization– open reduction with internal fixation

Order of injury Repair

• Any open fractures first• Then any closed fracture– Tibia– Femur – within 24h– Pelvis– Spine– Upper extremity

Ligamentous injury

Odontoid Fracture

Atlas fracture

C2 Hangman’s Fracture

C6 Fracture with retropulsionto cord

Soft tissue swelling

subluxation of C4-C5 with spinal cord compression

Compression fracture

LumbarBurst

fracture

Cord Injury Syndromes

• Complete cord lesion - all sensory and motor function below the lesion is abolished

• Central cord lesion – motor function lost upper>lowersuspended sensory loss in cervicothoracic dermatomes

• Posterior Cord syndrome – diminished proprioception and fine touch

• Brown-Sequard syndrome - cord hemisection ipsilateral loss of pain and proprioception, contralateral pain and temp loss, suspended ipsilateral loss of all sensation

• Spinal shock – lack of neurologic function after trauma that can last until 4 weeks

Systemic Effects of SCI

• Cardiovascular– Almost solely related to

interruption of sympathetic pathway at T1-L2

– Bradycardia• Resolves with stimulation• Resolves after 2 months• Rare to need pacemaker

– Hypotension• Give volume• Low dose pressors

• Respiratory– Related to level of injury– Thoracic levels eliminates intercostals– Diaphragm alone to inspire – phrenic nerve (C3-5)– Cervical lesions decreases cough and secretion clearance– Decreased tidal volumes– Minimal expiratory help– Status improves with time

Autonomic hyperreflexia

• Loss of central inhibition• hyper-reactive sympathetic

reflexes to cord below level of lesion

• Bladder or bowel distention usual causes – HTN– Arrythmias– Headaches– Vasodilation above lesion

level

In Summary

• Appropriate pre-hospital care is essential• Assume injury until proven otherwise• Evaluate as early as possible to prevent

unnecessary immobilization• Earlier steroids with spinal injury• Follow clinical exam

References

• Czosnyka M. Pickard JD. Monitoring and interpretation of intracranial pressure. Journal of Neurology, Neurosurgery & Psychiatry. 75(6):813-21, 2004 Jun.

• Gunnarsson T. Fehlings MG. Acute neurosurgical management of traumatic brain injury and spinal cord injury. Current Opinion in Neurology. 16(6):717-23, 2003 Dec.

• Hutchinson PJ. Kirkpatrick PJ. Decompressive craniectomy in head injury. Current Opinion in Critical Care. 10(2):101-4, 2004 Apr

• Longhi L. Stocchetti N. Hyperoxia in head injury: therapeutic tool?. Current Opinion in Critical Care. 10(2):105-9, 2004 Apr

• Marik, PE. Varon, J. and Trask, T Managament of Head Trauma*Chest. 2002; 122: 699 - 711.

• Marshall LF. Head injury: recent past, present, and future. Neurosurgery. 47(3):546-61, 2000 Sep

• Patel RV. DeLong W Jr. Vresilovic EJ. Evaluation and treatment of spinal injuries in the patient with polytrauma.Clinical Orthopaedics & Related Research. (422):43-54, 2004 May.