Traumatic Brain Injury

Report
Traumatic Brain Injury
Katie Clement, MD
PICU Resident Lectures
2011
Objectives
 Understand the mechanisms of Pediatric Traumatic
Brain Injury
 Understand the pathophysiology of TBI
 Understand the management of TBI
Overview
Epidemiology
 Injury is leading cause of death for children
Krug EG et al. Am J Public Health. 2000.
 40% of those are from TBI
Langlois JA et al. Centers for Disease Control & Prevention. 2006.
 Mortality between 17 – 33%
White JR et al. CCM. 2001.
 Most common cause of death & disability in childhood in
developed countries
Krug EG et al.
 3000 children die each year from TBI in the US
Langlois JA et al.
GCS
 Severity of TBI is defined by the GCS Score
 Mild
 GCS 13-15
 Moderate
 GCS 9-12
 Severe
 GCS <9
GCS
Motor Response
Total score ranges from 3 - 15
Verbal Response
Oriented
(age appropriate vocalization,
smiling, cooing, tracks objects)
5
Confused, disoriented
(cries, irritable)
4
Inappropriate words
(cries to pain)
3
6
Localizes pain
5
Withdraws to pain
4
Abnormal flexion to pain
(decorticate posturing)
3
Abnormal extension to pain
(decerebrate posturing)
2
No response
1
Eye Opening
Incomprehensible sounds (moans 2
to pain)
No response
Follows commands
1
Spontaneous
4
To command
3
To pain
2
No eye opening
1
Pathophysiology
Effects of Trauma
 Increase in volume of any or all intracranial
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components
Uncoupling of cerebral blood flow & metabolic activity
(loss of autoregulation) can lead to excessive CBF
Increased CSF production in response to increased
CBF
Hypercapnia or hypoxia (cause vasodilation &
increased CBF)
Herniation, brain swelling, subarachnoid hemorrhage
may obstruct flow of CSF
Hematomas, contusions, edema may increase
intracranial volume
Definition of ICP
 ICP = ICP vascular + ICP CSF
 Used to estimate cerebral perfusion pressure
 CPP = MAP – mean ICP
 CPP: Cerebral Perfusion Pressure
 ICP: Intracranial Pressure
 MAP: Mean Arterial blood Pressure
Normal Values
 ICP is typically ≤ 15 mmHg in adults and lower in
children & newborns
 ICP ≥ 20 mmHg is pathologic in adults
 Physiologic events such as sneezing, coughing, Valsalva
will transiently raise ICP as well
 CPP normals for adults range from 50 – 70 mmHg
 Not well established in children, likely 40 – 60 mmHg
depending on age
 When CPP falls below a critical level, brain receives
inadequate blood flow
Intracranial Pressure
 The intracranial compartment has a fixed internal
volume
 Brain parenchyma – 80%
 CSF – 10%
 Blood – 10%
 ICP is a function of the volume & compliance of each
component
 The Monroe-Kellie Doctrine
Monroe-Kellie Principle
Intracranial compensation for an expanding mass lesion
Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd
ed, Rogers, MC (Ed), Williams and Wilkins 1996. p. 646; figure 18.1.
The relationship between intracranial volume and pressure is nonlinear
An initial increase in volume results in a small increase in pressure because of intracranial compensation (blue line). Once intracranial
compensation is exhausted, additional increases in intracranial volume result in a dramatic rise in intracranial pressure (red line).
Cerebral Edema
 Diffuse swelling more common among infants and
children compared to adults
Lang DA. J Neurosurg 1994
 Infant skull is more compliant, tolerates significant
deformation without fracture
Coats B. J Neurotrauma 2006
 Brain atrophy begins in young adulthood and allows
for more room in the adult skull for brain to expand
Kochanek PM. Dev Neurosci 2006
Cerebral Edema
 Worsened with hypoxia & hypoperfusion
 Types of edema:
 Vasogenic- breakdown of the blood-brain barrier
 Cytotoxic- cellular swelling
 Interstitial- periventricular exudation of cerebrospinal
fluid through the ependymal lining
 Osmotic- movement of water into the interstitial spaces
induced by osmotically active products of tissue injury
and blood clot
Cerebral Autoregulation
 Often impaired in children with TBI
 Impaired autoregulation is associated with worse
outcome
Cerebral autoregulation in hypertension
Kaplan, NM, Lancet 1994
2 Insults
 Primary Injury
 Direct injury to brain parenchyma
 Blunt force: Contusions, hematomas
 Acceleration-deceleration: physical shearing or tearing
of axons
http://www.tbilawyers.com/diffuse-axonal-injury.html
 Secondary Injury:
 Potentially avoidable or treatable
 Hypoxemia
 Hypotension
 Elevated ICP
 Hypercarbia
 Hyper- & Hypoglycemia
 Electrolyte abnormalities
 Enlarging hematomas
 Coagulopathy
 Seizures
 Hyperthermia
 Endogenous cascade of cellular & biochemical events
 Occurs within minutes and continues for months after initial
injury
 Leads to neuronal cell death
Diffuse Axonal Injury
 Widespread damage to axons in the white matter
 Corpus callosum
 Basal ganglia
 Periventricular white matter
 Caused by
 Hypoxic-ischemic injury
 Calcium & ion flux
 Mitochondrial & cytoskeletal dysfunction
 A major cause of morbidity in pediatric TBI
 More extensive DAI associated with worse outcome
Evaluation
Initial Evaluation
 Don’t forget standard trauma protocols:
 Primary Survey
 ABCs!
 Secondary Survey
History
 Mechanism of injury
 Loss of consciousness + duration
 Vomiting
 Headache
 One of the earliest symptoms of increased ICP
 Progression of symptoms
Physical Exam—General
 Hypoxia & hypotension should be immediately
identified and treated
 Respiratory depression, bradycardia, and/or
hypertension may indicate impending herniation and
also requires prompt treatment
 Maintain C-spine immobilization
Neuro exam
 Assign a GCS
 Level of consciousness
 Pupils
 Extraocular movements
 Funduscopic exam
 Brainstem reflexes
 DTRs
 Response to pain
Battle Sign
Raccoon Eyes
CSF Rhinorrhea
Setting-Sun Sign
Late sign of increased
intracranial pressure
Pressure on cranial nerves
III, IV, and VI forces the eyes
downward, revealing a rim of
sclera above the irises.
Funduscopic Exam
www.dontshake.org
http://cloud.med.nyu.edu/modul
es/pub/neurosurgery/cranials.ht
ml
Types of Herniation
a) Subfalcine : uneven, one-sided expansion of a cerebral hemisphere that pushes a
portion of the brain tissue (cingulate gyrus) under the falx cerebri
b) Uncal: medial temporal lobe is pushed against the tentorium. Can compress
brainstem in severe cases
c) Central transtentoral : downward pressure centrally, can cause bilateral uncal
herniation.
d) Extracranial : brain tissue pushes through an opening in the cranial cavity either
surgically or by trauma
e) Tonsillar : swelling or bleeding in the cerebellum pushes the cerebellar tonsils
downward into the foramen magnum. Life threatening b/c can compress the
brainstem
Signs of herniation
 Uncal herniation:
 Third cranial nerve palsy
 Hemiplegia
 Progressive changes in respiratory pattern, pupil size,
vestibuloocular reflexes, posturing
 Cushing’s Triad
 Hypertension
OCCURS LATE!!
 Bradycardia
 Slow, irregular respirations
Mydriasis
 Can be associated with
CN III injury
 Uncal herniation can
cause unilateral
mydriasis & ptosis
Labs
 Depends on type & extent of injury
 Minimum: hct, T&S, UA
 Useful in TBI:
 Glucose
 Hyperglycemia is a poor prognostic indicator
 Electrolytes w/ osmolarity
 Coags
 DIC is associated with poor outcomes
Chiaretti A. Childs Nerv Syst 2002.
Imaging
 CT is preferred initial imaging
 Following initial stabilization
 Focal injuries are readily diagnosed by CT
 Patients with DAI may have normal CT scans
 Most common finding is diffuse cerebral swelling
Subdural
hematoma
www.neurosurgery.com.sg
Epidural
hematoma
http://www.hawaii.edu/medicine/pedi
atrics/pemxray/v5c07.html.
http://uwmedicine.washington.edu/patientcare/our-services/medical-services/strokecenter/pages/articleview.aspx?subid=83
Diffuse Axonal Injury (on MRI)
http://neuroradiologyonthenet.blogspot.com/
2008/05/diffuse-axonal-injury-dai.html
Management
Goals
 Minimize ICP elevation
 Maintain adequate CPP to prevent secondary ischemic
injury
 CPP goal for adults should be 60 – 70 mmHg
 Minimum acceptable for children is not defined, but
recommended 40 – 65 mmHg depending on age.
 Studies show that CPP from 40 – 65 improves outcome
 CPP < 40 associated with poor outcome
 ICP goal typically < 20 mmHg
Adelson PD. PCCM. 2003
Initial Decisions
 Immediate NSGY consultation
 Quickly identify focal injuries that require
neurosurgical intervention
 GCS ≤ 8 or GCS 9-12 and deteriorating/not protecting
airway require intubation
 Recognize signs of herniation & treat if present
 Assure adequate oxygenation, breathing, BP
 Give hyperosmolar therapy
 Provide mild hyperventilation
 Immediate NSGY evaluation
Airway & Breathing
 Advanced airway management necessary if
 Decreasing level of consciousness (GCS ≤ 8)
 Marked respiratory distress
 Hemodynamic instability
 Other considerations
 C-spine immobilization must be maintained
 Nasotracheal intubation contraindicated with midface
trauma or basilar skull fracture
 Cuffed tubes to protect from aspiration
Rapid Sequence Intubation
 Pretreat with lidocaine to minimize increase in ICP
 Preoxygenation
 Etomidate & Thiopental have neuroprotective
properties
 ? Risk of increased ICP with succinylcholine
 Rocuronium may be preferred
Avoid high PEEP and PIP because they will increase
intrathoracic pressure and may impede cerebral venous
drainage.
Monitoring
 Standard VS: HR, BP, Pulse Ox
 Capnography
 To monitor ventilation & avoid excessive
hyperventilation
 ICP monitoring recommended for abnormal head CT &
initial GCS 3 – 8
 Interventions used to decrease ICP require accurate
and continuous ICP monitoring!!
ICP Monitoring
 Indications
 Traumatic brain injury (GCS < 8 with focal findings on CT)
 Obstructive intracranial lesion
 Post operative edema
 Contraindications
 Coagulopathy: i.e. high risk of hemorrhage
 Relative Indications
 Metabolic cerebral edema
ICP Monitoring Options
 External Ventricular
Device (EVD) both
diagnostic and
therapeutic
 Intra-parenchymal
device: Diagnostic guide
to therapy
 Others: diagnostic
Management of ICP
 First tier therapies
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Maintain CPP
Sedation & analgesia
HOB at 30 degrees
Ventriculostomy drain
Neuromuscular blockade
Hyperosmolar therapy (mannitol & hypertonic saline)
Mild hyperventilation
 Second tier therapies
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Hyperventilation
Decompressive craniectomy
High dose barbiturates
Hypothermia (32 – 34 degrees)
Hyperventilation
 Reduces ICP
 May be harmful with routine use
 Results in hypocapnia
Skippen P. CCM 1997.
 Vasoconstriction
 Decreased cerebral blood flow
 Associated with poor outcomes among children with TBI [30]
Adelson PD. Pediatr Neurosurg 1997.
 PCO2 < 30 mmHg associated with increased mortality
Curry R. PCCM 2008.
 Maintain PaCO2 between 35 – 38 mmHg unless signs
of impending herniation
Initial Fluid Management
 Restore volume—Isotonic fluids preferred
 Blood products as indicated
 Outcomes are poor for children who are hypotensive
at initial evaluation
White JR. CCM 2001
Vavilala MS. J Trauma 2003
Luerssen TG. J Neurosurg 1988
Pigula FA. J Pediatr Surg 1993
 Systolic blood pressure should be maintained above
the 5th percentile for age and sex at the minimum
Adelson PD. PCCM. 2003
 Improved outcomes for patients with initially higher
blood pressure
Head Positioning
Maintain head in neutral position to
avoid jugular venous obstruction
As head-up position is increased, ICP may be
reduced, but beyond 30o heads-up CPP is likely
compromised. Second source: Durward, QJ,
Amadner, AL, Del Maestro, RF, et al: Cerebral
and vascular responses to changes in head
elevation in patients with intracranial
hypertension, J Neurosurg 59: 938, 1983.
Sedation and Neuromuscular Blockade
 Maintain adequate analgesia to blunt response to
noxious stimuli
 Maintain sedation to permit controlled ventilation
 Cerebral oxygen consumption may be decreased in
patients receiving neuromuscular blockade
Vernon DD. CCM 2000
Antiseizure Prophylaxis
 Reduces the incidence of early posttraumatic seizures
among children with severe TBI Schierhout G. Cochrane Database Syst Rev 2001
 Seizures increase metabolic demand and increase ICP
 Leads to secondary brain injury
 Retrospective studies demonstrate improved
outcomes among children with TBI treated with
anticonvulsants Tilford JM. CCM 2001
 Recommend anticonvulsants during the first week
following TBI if high risk
 Penetrating skull fractures, hematomas, masses, bleeds
Adelson PD et al. PCCM 2003
Temperature control
 Aggressively prevent & treat hyperthermia
 Raises metabolic demand & ICP
 Hypothermia decreases cerebral metabolism and may
reduce CBF & ICP
(Considered second tier therapy)
 Controversial
 One multicenter trial showed harm
 Control shivering with muscle relaxants
Hyperosmolar Therapy
 Establishes an osmotic gradient between plasma and
parenchymal tissue
 Reduces brain water content
 Extensive research shows that it effectively decreases
ICP in children with TBI
Mannitol
 Decreases ICP effectively based on extensive clinical



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experience
Dose 0.25 – 1 g/kg IV
Adverse effects: hyperosmolarity, hypovolemia,
electrolyte imbalance
Nephrotoxicity can occur, especially if patients are
hypovolemic
Don’t typically use if serum osmolarity >320
Adelson PD et al. PCCM 2003.
Hypertonic Saline
 Can be administered as a bolus or as an infusion
 Optimal dosing not clear
 3% saline commonly used as bolus of 2-6 ml/kg
 Continuous infusion of 0.1 – 1 ml/kg/hr also described
 Effective at reducing ICP in small randomized trials &
Huang SJ. Surg Neurol 2006.
observational reports
 Does not cause profound osmotic diuresis, so
decreased risk of hypovolemia
 Adverse effects:
 Rebound intracranial hypertension
 Central pontine myelinolysis (theoretical, not reported)
Qureshi AI. CCM 2000.
Glucose Control
 Hyperglycemia associated with poor outcomes
 Marker for severity of injury
 Worsens brain tissue lactic acidosis
 Recommend to keep glucose level at least less than
200
Adelson PD. PCCM 2003.
Corticosteroids
 No benefit in trauma
 Large, prospective multicenter trial demonstrated
increased mortality among patients with acute TBI
who received steroids
 Useful only for vasogenic edema from tumors because
they stabilize the BBB
Barbiturate coma—second tier therapy
 Used if ICP refractory to other modalities
 Pentobarbital typically used
 Decreases cerebral metabolic rate and thus cerebral
blood flow
 May have protective effects during periods of hypoxia
and/or hypoperfusion
 Cardiac suppression, hypotension
 Treat with fluids & inotropic support
 No evidence for prophylactic use
Other second tier therapies
 Aggressive hyperventilation (PaCO2 < 30)
 Recommend brain tissue oxygenation monitoring or jugular
venous O2 saturation or CBF monitoring
 Decompressive craniectomy
 Ideal patient has had no episodes of ICP > 40 before surgery,
have had a GCS > 3 at some point
 Evolving herniation syndrome within 48 hrs of injury
 Lumbar CSF drainage
 Not common
 Must have a functioning EVD in place, open basal cisterns, no
mass effect or shift on CT (to avoid herniation)
 Hypothermia
 Core temp 32 – 34 degrees
 More studies needed
Management Algorithm
Adelson PD et al. PCCM 2003
Adelson PD et al. PCCM 2003
Adelson PD et al. PCCM 2003
Second Tier Therapies
Adelson PD et al. PCCM 2003
Summary
 Have Neurosurgery involved EARLY
 For surgical intervention & monitor placement
 Keep ICP <20 mmHg
 Keep CPP appropriate for age (> 40 – 60 mmHg)
References
 Vavilala MS, Waitayawinyu P, Dooney NM. Initial approach to severe traumatic
brain injury in children. www.uptodate.com 2011.
 Huh JW, Raghupathi R. New concepts in treatment of pediatric traumatic brain
injury. Anesthesiology Clin 2009:27;213-240.
 Brasher WK. Elevated intracranial pressure in children. www.uptodate.com
2011.

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