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