HEAD INJURY

DR. DHAVAL SHUKLA, MChASSOCIATE PROFESSOR

DEPARTMENT OF NEUROSURGERYNIMHANS, BANGALORE.

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Epidemiology

• Incidence 150/ 100000

• Prevalence 97/ 100000

• Mortality 20/ 100000

• Case fatality 10%

• Burden of casualty 40%

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Pathophysiology

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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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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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Raised ICP in TBI

• Intracranial hematoma: EDH, SDH, Contusions• Cerebral edema• Hyperemia• Hypoventilation • Increased intrathoracic or intra-abdominal

pressure • Hydrocephalus

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Secondary raised ICP

• 30% of patients• 3 to 10 days after trauma• Delayed hematoma • Hypoxia • Hypotension • Vasospasm• Hypoventilation• Hyponatremia

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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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ICP WAVES

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Age distribution

Age groups (years)

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Cause

Etiology

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Alcohol

• 24% regular consumers

• 15% under influence of alcohol

• More severe injuries

• Multiple intracranial hematomas

• Delirium and withdrawal

• Liver dysfunctionNIMHANS

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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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Unconsciousness

• Concussion

• At time of impact

– Worsening

– Improving

• Delayed

• Lucid interval

• Amnesia

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Seizures

• Generalized tonic clonic or focal

• Status epilepticus in 10 – 15%

• Postictal unconsciousness

• Immediate

– No significance

• Early

– Severe injury

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Other symptoms

• Vomiting

– Raised ICP

• ENT bleeding

– Skull base #

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Examination

• A – Airway Wounds • B – Breathing ENT bleeding• C – Circulation CSF leak• D – Disability• E – Exposure • F – Foley/ family• G – Gastric tube

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Breathing

Cheyne-Stokes

Apneusis

Ataxic breathing

Neurogenic hyperventilation

Apnea

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Associated injuriesPe

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tage

Sites NIMHANS

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Glasgow coma score (GCS)

• Post resuscitation

• Best response

• Swollen eye

• Aphasia

• Endotracheal intubation

• Quadriplegia NIMHANS

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Pain response

DO NOT PINCH

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(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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(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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Motor response

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(GCS)

Verbal Response

• 5 - oriented

• 4 - confused

• 3 - inappropriate words

• 2 - incomprehensible sounds

• 1 - no verbal response

• VT - endotracheal tube

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Severity

Severity

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Pupils

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Ocular movements

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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

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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

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Treatment - Breathing

• No prophylactic hyperventilation

• Mechanical ventilation

– Coma GCS < 8

– Severe raised ICP

– Uncontrolled status epilepticus

– Awaiting surgery

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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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CT scan

• Bradycardia

• Vomiting

• Severe headache

• Neuro. deficits

• Early seizures

• Skull fracture

• CSF leak

• Extremes of age

• Alcohol consumption

• Loss of consciousness

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CT scan classification Focal Diffuse

Normal Minor Swelling Shift

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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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Lab investigations

• CBC with platelet count

• RBS

• Urea/ creatinine

• Na+/ K+

• PT/ APTT

• Blood group/ cross matchNIMHANS

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Monitoring

Hourly

• Pulse rate < 60 bpm

• BP < 90 mm Hg

• GCS > 2 score deterioration

• Pupils Asymmetry

• Limb movement PaucityNIMHANS

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Treatment

• Head of bed elevation

• Normal blood pressure

• Normal oxygenation

• Normal temperature

• Normal blood glucose

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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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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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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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Mannitol

• Available as 20%

• Max. dose 5 ml/ kg

• BP should be normal

• Decorticate or decerebrate posturing

• Rapid deterioration of GCS

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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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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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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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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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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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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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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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Antibiotics

• Not routinely required

• For contaminated depressed fracture

• Endotracheal intubation

• Cefotaxime 1 gm tid

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Risk of seizures

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Severity

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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

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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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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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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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Perioperative management

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Operative management

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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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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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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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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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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

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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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Outcome assessment

Periods of improvement

• 3 months - 66%

• 6 months - 90%

• 12 months - 95%

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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.

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No head injury is so trivial

that it can be ignored

Nor so serious

that life can be despaired off

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