Head Injury Overview
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HEAD INJURY
DR. DHAVAL SHUKLA, MChASSOCIATE PROFESSOR
DEPARTMENT OF NEUROSURGERYNIMHANS, BANGALORE.
NIMHANS
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NIMHANS
Epidemiology
• Incidence 150/ 100000
• Prevalence 97/ 100000
• Mortality 20/ 100000
• Case fatality 10%
• Burden of casualty 40%
NIMHANS
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NIMHANS
Pathophysiology
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NIMHANS
Intracranial Pressure ICP
• Normal values < 10 - 15mmHg for adults and older children
• 3 to 7 mm Hg for young children• 1.5 to 6 mm Hg for term infants• ICP can be subatmospheric in newborns• ICP values > 20 - 25 mm Hg require treatment• Sustained ICP > 40 mm Hg indicate severe, life-
threatening intracranial hypertension.
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NIMHANS
Cerebral Perfusion Pressure (CPP)
• CPP = MAP - ICP• Normal cerebral blood flow (CBF) with a CPP
ranging from 50 to 150 mm Hg• CPP < 50 mm Hg CBF falls passively with CPP • After injury the ability of the brain to pressure
autoregulate may be absent or impaired and, even with a normal CPP, CBF can passively follow changes in CPP
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NIMHANS
Raised ICP in TBI
• Intracranial hematoma: EDH, SDH, Contusions• Cerebral edema• Hyperemia• Hypoventilation • Increased intrathoracic or intra-abdominal
pressure • Hydrocephalus
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NIMHANS
Secondary raised ICP
• 30% of patients• 3 to 10 days after trauma• Delayed hematoma • Hypoxia • Hypotension • Vasospasm• Hypoventilation• Hyponatremia
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NIMHANS
ICP WAVES
• Lundberg A waves: Plateau waves– Amplitude > 50 mm Hg lasting 5 to 20 min.– Accompanied by increase in MAP
• Lundberg B waves: Pressure pulses– Amplitude 50 mm Hg and lasting 30 sec. to 2 min.
• Lundberg C waves: – Amplitude 20 mm Hg and frequency of 4 – 8/ min.
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NIMHANS
ICP WAVES
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NIMHANS
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NIMHANS
Age distribution
Age groups (years)
Perc
enta
ge
NIMHANS
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NIMHANS
Cause
Etiology
Perc
enta
ge
NIMHANS
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NIMHANS
Alcohol
• 24% regular consumers
• 15% under influence of alcohol
• More severe injuries
• Multiple intracranial hematomas
• Delirium and withdrawal
• Liver dysfunctionNIMHANS
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NIMHANS
Concussion
• Transient loss of brain function due to blow on head
• Orientation, Immediate memory, Concentration
• Grade 1: __ Transient Confusion
__ No Loss of Consciousness
__ Concussion Symptoms < 15 min.
• Grade 2: __ Transient Confusion
__ No Loss of Consciousness
__ Concussion Symptoms > 15 min.
• Grade 3: __ Any Loss of Consciousness, Brief or Prolonged
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NIMHANS
Unconsciousness
• Concussion
• At time of impact
– Worsening
– Improving
• Delayed
• Lucid interval
• Amnesia
NIMHANS
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NIMHANS
Seizures
• Generalized tonic clonic or focal
• Status epilepticus in 10 – 15%
• Postictal unconsciousness
• Immediate
– No significance
• Early
– Severe injury
NIMHANS
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NIMHANS
Other symptoms
• Vomiting
– Raised ICP
• ENT bleeding
– Skull base #
NIMHANS
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NIMHANS
Examination
• A – Airway Wounds • B – Breathing ENT bleeding• C – Circulation CSF leak• D – Disability• E – Exposure • F – Foley/ family• G – Gastric tube
NIMHANS
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NIMHANS
Breathing
Cheyne-Stokes
Apneusis
Ataxic breathing
Neurogenic hyperventilation
Apnea
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NIMHANS
Associated injuriesPe
rcen
tage
Sites NIMHANS
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NIMHANS
Glasgow coma score (GCS)
• Post resuscitation
• Best response
• Swollen eye
• Aphasia
• Endotracheal intubation
• Quadriplegia NIMHANS
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NIMHANS
Pain response
DO NOT PINCH
NIMHANS
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NIMHANS
(GCS)
Eye Response
• 4 - eyes open spontaneously
• 3 - eye opening to verbal command
• 2 - eye opening to pain
• 1 - no eye opening
• ES - eye swollenNIMHANS
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NIMHANS
(GCS)
Motor Response
• 6 - obeys commands
• 5 - localizing pain
• 4 - withdrawal from pain
• 3 - flexion response to pain
• 2 - extension response to pain
• 1 - no motor responseNIMHANS
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NIMHANS
Motor response
NIMHANS
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NIMHANS
(GCS)
Verbal Response
• 5 - oriented
• 4 - confused
• 3 - inappropriate words
• 2 - incomprehensible sounds
• 1 - no verbal response
• VT - endotracheal tube
NIMHANS
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NIMHANS
Severity
Severity
Perc
enta
ge
NIMHANS
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NIMHANS
Pupils
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NIMHANS
Ocular movements
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NIMHANS
Neurological deficits
• Optic nerve
– With local injury
• Facial nerve
– UMN / LMN
– Ear bleed
• Limb movements
– Hemiplegia contralateral to pupillay dilatation
– Hemiplegia ipsilateral to pupillay dilatation
• Kernohan’s notch
NIMHANS
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NIMHANS
Treatment - Airway
• Hypoxia doubles mortality
• pO2 > 60 mm Hg or SaO2 >90%
• Endotracheal intubation
– GCS < 8
– Maxillofacial injuries
– Restless patient requiring heavy sedation
– Status epilepticus
NIMHANS
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NIMHANS
Treatment - Breathing
• No prophylactic hyperventilation
• Mechanical ventilation
– Coma GCS < 8
– Severe raised ICP
– Uncontrolled status epilepticus
– Awaiting surgery
NIMHANS
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NIMHANS
Treatment - Circulation
• 16 or 18G iv cannula
• 500 ml NS
• Maintain SBP > 90 mm Hg
• Hypotension doubles mortality
• Do not give dextrose containing fluids
• Foley’s catheterizationNIMHANS
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NIMHANS
CT scan
• Bradycardia
• Vomiting
• Severe headache
• Neuro. deficits
• Early seizures
• Skull fracture
• CSF leak
• Extremes of age
• Alcohol consumption
• Loss of consciousness
NIMHANS
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NIMHANS
CT scan classification Focal Diffuse
Normal Minor Swelling Shift
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NIMHANS
MRI
• After clinical stabilization
• If CT scan is normal and patient is uncosncious
• 25 days after injury for prognostication
• Limited use only for research
• T1, T2, FLAIR and T2*
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NIMHANS
Lab investigations
• CBC with platelet count
• RBS
• Urea/ creatinine
• Na+/ K+
• PT/ APTT
• Blood group/ cross matchNIMHANS
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NIMHANS
Monitoring
Hourly
• Pulse rate < 60 bpm
• BP < 90 mm Hg
• GCS > 2 score deterioration
• Pupils Asymmetry
• Limb movement PaucityNIMHANS
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NIMHANS
Treatment
• Head of bed elevation
• Normal blood pressure
• Normal oxygenation
• Normal temperature
• Normal blood glucose
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NIMHANS
Indications for ICP monitoring
GCS: 3–8 (after resuscitation)1. Abnormal admission head CT scan2. Normal admission head CT scan plus two or
more of the followinga. Age > 40 yrs.b. Motor posturingc. Systolic blood pressure < 90 mm Hg
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NIMHANS
Complications of ICP monitoring
• Infection: 5% to 14%– Antibiotic-coated catheters has been shown to
reduce the risk for infection from 9.4% to 1.3%.• Hemorrhage: 1.4%• Malfunction, obstruction, and malposition
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NIMHANS
Goals of ICP treatment
1. Maintain ICP at less than 20 to 25 mm Hg.2. Maintain CPP at greater than 60 mm Hg by
maintaining adequate MAP.3. Avoid factors that aggravate or precipitate
elevated ICP.
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NIMHANS
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NIMHANS
Mannitol
• Available as 20%
• Max. dose 5 ml/ kg
• BP should be normal
• Decorticate or decerebrate posturing
• Rapid deterioration of GCS
NIMHANS
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NIMHANS
Hypertonic saline (HS)
• 3% to 23.4% HS as effective as mannitol• Advantage over mannitol
– Hypovolemic and Hypotensive patients
• Adverse effects – Hematologic
• bleeding secondary to decreased platelet aggregation and prolonged coagulation time
– Electrolyte abnormalities• Hypokalemia and hyperchloremic acidosis
Hyponatremia should be excluded before administering hypertonic saline, to reduce the risk for central
pontine myelinolysis
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NIMHANS
Barbiturates
• Pentobarbital– Loading dose 10 mg/kg – 5 mg/kg every hour for 3 doses– Maintenance 1 to 2 mg/kg/h
• Titrated to a serum level of 30 to 50 mg/mL or until EEG shows a burst suppression pattern
• Barbiturate coma in patients with refractory intracranial hypertension increases twofold greater chance of controlling the ICP
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NIMHANS
Barbiturates
• Mechanism: – Coupled reduction in CBF and CMRO2, with an immediate
effect on ICP– Retention of CO2 reactivity by brain
• Complications:– Hypotension 58%– Hypokalemia 82%– Respiratory 76%– Infections 55%– Hepatic 87%– Renal dysfunction 47%
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NIMHANS
Hypothermia
• Cerebral metabolism reduced by 5-7% for each oC reduction– Decreased glucose & O2 consumption
• Prevents cell injury leading to apoptosis– Inhibition of caspase activation– Prevents mitochondrial dysfunction– Decreased excitatory neurotransmitters– Modification of intracellular ion concentration– Modification of intracellular acidosis
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NIMHANS
Hypothermia
• Suppresses inflammatory processes• Decreases free radical production• Reduces vascular permeability
– Reduced brain oedema• Helps maintain cell membrane integrity• Prevents hyperthermia
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NIMHANS
Hypothermia
• 13 studies involving 1321 patients in last 15 years– All reported a reduction in ICP– Most observed improved neurological outcome especially
in patients with low GCS (4-7) on admission– Results however not significant
• Adverse effects– Hypotensive episodes and bradycardia more common– Low magnesium– Insulin resistance
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NIMHANS
Decompressive Craniectomy (DECRA)
• Less time with raised ICP• Fewer interventions for increased ICP • Fewer days in ICU• Worse scores on the GOS• Greater risk of unfavorable outcome • Rates of death at 6 months similar
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NIMHANS
Antibiotics
• Not routinely required
• For contaminated depressed fracture
• Endotracheal intubation
• Cefotaxime 1 gm tid
NIMHANS
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NIMHANS
Risk of seizures
NIMHANS
Perc
enta
ge
Severity
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NIMHANS
Anticonvulsants
• Phenytoin
– Loading 18 mg/ kg iv in 100 ml NS over 30 min
– Maintenance 5 mg/ kg/ day
• 10 – 14 days for prophylaxis
• Continue as case of epilepsy in early PTS
NIMHANS
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NIMHANS
Pharmacological Neuroprotection
• Pre-clinical and clinical data are disconnected• Need adequate pre-clinical TBI models• Virtually no early phase trials in TBI
• Dosing• Duration of treatment• Time of treatment initiation
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NIMHANS
Design Problems
• Weaknesses in study design • Insufficient power/sample size• Inadequate outcome measures or lack of
sensitivity of the outcomes measure • Too small effect sizes• Too variable population
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NIMHANS
Facts• No single measure can capture the multidimensional
nature of TBI outcome
• Combination of drugs are needed for the treatment of TBI
• Current Trials– Progesterone (SYNAPSE)– Citicoline (COBRIT)– Erythropoetin
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NIMHANS
Perioperative management
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NIMHANS
Operative management
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NIMHANS
Surgery for EDH
Surgery
Any GCS
• Volume > 30 cc
• Volume > 20 cc
– Basitemporal
– Posterior fossa
Conservative
• Volume <20 cc
• Thickness < 15 mm
• Midline shift< 5 mm
• GCS > 8
• No deficits
Craniotomy with hitch stitchesNIMHANS
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NIMHANS
Surgery for acute SDH
Any GCS
• Thickness > 10 mm
• Midline shift > 5 mm
Thickness < 10 mm
Midline shift < 5 mm
• GCS < 9
• Deteriorated by 2 GCS
• Pupillary asymetry
Craniotomy with or without bone flap replacement and duraplasty
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NIMHANS
Surgery for cerebral contusions
Volume > 50 cc
• Any GCS
Volume > 20 cc
• GCS 6 – 8
• Progressive deterioration
• Failure of medical treatment
• Midline shift > 5 mm
• Cisternal compression
Craniotomy with evacuation of lesionDecompressive craniectomy and
bone flap placement in abdominal wall
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NIMHANS
Surgery for posterior fossa lesions
• Neurological dysfunction or deterioration• Distortion or obliteration of IV ventricle• Cisternal compression• Hydrocephalus
Suboccipital craniectomy and evacuationNIMHANS
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NIMHANS
Surgery for depressed fracture
Surgery
• Compound (open)
• Thickness > cranium
Nonoperative
• No dural breach
• No significant hematoma
• < 1 cm
• No infection
• No cosmetic deformity
• No pneumocephalus
Elevation with debridementDuraplasty Antibiotics
NIMHANS
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NIMHANS
Glasgow outcome scale (GOS)
GOSGOS
FavorableFavorable UnfavorableUnfavorable
Good
Recovery
Good
Recovery
Upper
Lower
Upper
Lower
Moderate
Disability
Moderate
DisabilitySevere
Disability
Severe
DisabilityVegetative
State
Vegetative
StateDeathDeath
Upper
Lower
Upper
LowerUpper
Lower
Upper
Lower
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NIMHANS
Outcome assessment
Periods of improvement
• 3 months - 66%
• 6 months - 90%
• 12 months - 95%
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NIMHANS
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NIMHANS
Prevention If treatment is duty then prevention is responsibility
Helmet
• Not compulsory for pillion riders
• 60% compliance
• <5% at time of injury
• 6 times increase in mortality without helmet
• Myths – baldness, headache, neck injury, decreased vision
etc.
NIMHANS
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NIMHANS
No head injury is so trivial
that it can be ignored
Nor so serious
that life can be despaired off
NIMHANS