Surgical Management of Traumatic Brain Injury

Dhaval ShuklaDepartment of Neurosurgery

NIMHANS

Intracranial Hematomas (ICH)

• ICH is the commonest cause of secondary deterioration after TBI

• ICH constitutes >70% of the causes of death in patients who ‘talk and die’

Intracranial Hematomas (ICH)

• Though technically simple emergency surgery may be among the most frustrating procedures performed by neurosurgeons– Complications: heavy bleeding and brain swelling – Operations frequently occur at night– Less experienced surgeons are delegated to do

surgeries– Decisions regarding removal of contusions may be

difficult

Pathoanatomical Classification

Imaging Parameters

(A/2) - B

Volume Basal Cisterns

Midline Shift

Preoperative surgical checklist

1. Blood to laboratory for:(A) cross matching (2 units of whole blood)(B) coagulation studies

(I) PT(Ii) APTT(Iii) Platelet count

(C) blood gas analysis(D) routine full blood count and electrolytes

Preoperative surgical checklist

2. X-rays of chest and cervical spine3. Consent4. Foley catheter5. Two large bore peripheral i.v. lines6. Arterial catheter7. Protection of both eyes8. Adequately secured endotracheal tube

Properative Medications

• Antibiotics• Mannitol• Anticonvulsants– ICH, Depressed fractures

– Phosphenytoin: Loading 18 mg/ kg iv in 100 ml NS

over 30 min

• No steroids

Extradural Hematoma (EDH)

• Contact injuries resulting from blunt trauma to

the skull and meninges

• 1-2% of all head injuries

• Fractures: 30 to 91 %

EDH - Clinical

• Lower incidence in elderly and young infants

• Unconsciousness– 30 to 60 % mild or no loss of consciousness

– 20 % unconscious from the time of injury

– Lucid interval in only 20 to 50 %

EDH - Clinical

• Rapidly symptomatic– 1/4th enlarge

– Mean time to enlargement • 8 h after injury

– No enlargement later than • 36 h from injury

EDH – Imaging

• Associated intracranial injuries in 24 to 75 %

NIMHANS

EDH - Surgery

Craniotomy with hitch stitchesNIMHANS

EDH - Outcome

• Mortality: 0 to 12 %• Favorable outcome 55 to 89 %• Level of consciousness – Conscious: Favorable outcome in 90 to 100 % Mortality 0 to 5 %– Coma: Favorable outcome in 38 to 73 % Mortality 11 to 41 %

EDH - Outcome

• Pupillary status– Normal reactivity: Favorable outcome in 84 to 100%– Abnormal pupil unilateral: Favorable outcome in 55

to 100 %– Abnormal pupil bilateral: Unfavorable outcome and

mortality

• Presence of associated intracranial injuries– Mortality: Three times

Subdural Hematoma (SDH)

• Incidence: 12 to 29 % of severe TBI• Most lesions over cerebral convexities in the

frontal and temporal regions • Extent of secondary brain injury may be more

important than the subdural clot itself• SDH more likely to develop complications of

cerebral ischemia, cerebral edema, and increased intracranial pressure

SDH - Clinical

• Mean age: 31 to 47 years• Coma (GCS < 8): 37 to 80 %• Lucid interval: 12 to 38 %• Pupillary abnormalities: 30 to 50 %• Unconsciousness out of proportion to external

injury and size of blood clot• Acute SDH can enlarge but also ‘disappear’

SDH - Imaging

NIMHANS

Surgery for acute SDH

Craniotomy with or without bone flap replacement and duraplasty

In comatose patients with small SDH an ICP monitoring can guide a careful conservative management

SDH - Outcome

• Most lethal of all head injuries• Mortality: 30 to 90 %• Favorable outcome: 19 to 30 %• Timing of surgery?• Strongest determinant of outcome: sustained

intracranial pressure • None of the patients above 60 years of age

have good recovery

Chronic SDH (CSDH)

• Acute: < 3 days

• Subacute: 4 -20 days

• Chronic: > 21 days

• CSDH may completely organize and resolve or

calcify

CSDH - Clinical

• Incidence: 7.35 per 100,000 per year seen in the age group 70 to 79 years

• Rare in age < 40• History of head injury: 50 to75 %• Risk factors: Chronic alcoholism, brain atrophy,

CSF shunts, seizure disorders, and impaired coagulation

• Dementia, stroke, transient ischemic attacks, other mass lesions

CSDH - Clinical

• Headache: 80 %• Altered sensorium: 28 to 100 %• Motor deficits: 24 to 62 %• Gait abnormality: 40 %• Memory loss or confusion: 33 %• Papilledema: 25 %

An erroneous admission diagnosis up to 40 %

CSDH - Imaging

• Bilateral: 15 to 20 %• Intravenous administration of contrast to look

for enhancement of the inner membrane particularly for isodense CSDH

CSDH - Treatment

• Twist drill craniostomy– Failure: 5 to 24 %

• Burr holes – Success: 86 to 95 %

• Craniotomy• Subdural shunt• Outcome– All deaths occur in patients in poor clinical grade or

secondary to medical conditions

Cerebral Contusions

• Contusion: Perivascular hemorrhage about small blood vessels and necrotic brain

• Hematoma: Contusions with blood content of at least 2/3rd of the volume of the lesion and appearing more homogeneous

• Cerebral laceration: Pia-arachnoid is torn• Burst lobe: cerebral contusion and hematoma,

with concomitant acute SDH

Delayed Traumatic Intracerebral Hematomas (DTICH)

• 6 hours to 30 days• 0.6 to 7.4 %• Pathogenesis:– Increased vessel fragility– Increased intramural pressure– Increased capillary wall permeability– Fibrinolysis– Rupture of a post-traumatic aneurysm

Contusion – Clinical Features

• 8.2 % of all injuries• 13 – 35 % of severe TBI• Neurological deficits• Restlessness• Seizures• Progressive neurological deterioration– 33 %– 24 to 72 hours (up to 7 to 10 days)

Contusion - Imaging

• Salt and pepper: • Coup and contre coup (remote): Frontal/

Temporal• Multiple

NIMHANS

Surgery for cerebral contusions

Craniotomy with evacuation of lesionDecompressive craniectomy and

bone flap placement in abdominal wall

Contusion - Outcome

• Presence of traumatic subarachnoid hemorrhage on an admission is powerful predictor outcome

• Older age, alcoholism, and coagulation disorders• Posttraumatic epilepsy• Psychiatric disorders• Mortality– Coup: 16.4 %– Contrecoup:44.1%– DTICH: 35 to 40 %

Depressed Fracture

• Incidence: 6 % • Significantly depressed if the outer table of

one or more of the fractured segments lies below the inner table of the surrounding skull

• Compound depressed fracture: 75 to 91 %• Dural tear: 51 to 60 %• Associated parenchymal injuries: 50 – 71%

Depressed Fracture - Clinical

• Focal neurological deficits

• No LOC: 25 %

• Post-traumatic amnesia <1 hour: 25 %

• Seizures

• CSF leak and meningitis

Depressed Fracture - Imaging

• Always assess for fractures on bone windows

NIMHANS

Surgery for depressed fracture

Elevation with debridementDuraplasty Antibiotics

NIMHANS

Surgery for depressed fracture involving venous sinus

• Observation alone

• Debridement and closure of an overlying scalp

laceration without fracture elevation

• Fracture elevation and exposure of the

damaged sinus, followed by sinus repair or by

sinus ligation in presence of hematoma

Depressed Fracture - Outcome

• Infection: 1.9 – 10.6%

• Morbidity: 11 %

• Late epilepsy: 15 %

• Mortality: 1.4 – 19 % (depending on

associated lesions)

Posterior Fossa Lesions

• < 3 % of injuries

• 1.2 – 12.9 % of all EDH

• 0.5 – 2.5 % of all SDH

• 1.7% of all contusions

• Posterior fossa ICH almost always occur in older

children and young adults

Posterior Fossa Lesions - Clinical

• Rapid and life threatening neurological

deterioration

• Patients can have respiratory and cardiac

arrest without clinical signs of progressive

neurological deterioration

• Headache, neck pain, and vomiting

Posterior Fossa Lesions - Imaging

• Fourth ventricular compression• Hydrocephalus• Supratentorial extension of EDH• Associated supratentorial lesion• Cervical spine injuries

NIMHANS

Surgery for posterior fossa lesions

• Neurological dysfunction or deterioration

• Distortion or obliteration of IV ventricle

• Cisternal compression

• Hydrocephalus

Suboccipital craniectomy and evacuation with or without EVD

NIMHANS

Posterior Fossa Lesions - Outcome

• GCS• Associated supratentorial lesions• Location– Parenchymal vs extraparenchymal– Midline vs lateral

• Hydrocephalus• Acuity of presentation

Decompressive Craniectomy

Decompressive craniectomy (DECRA)

DECRA significantly decreases ICP but associated with more unfavorable outcomes

Cooper DJ, et al. NEJM, 2011.

Lobectomy for Brain Swelling

• Swollen and contused temporal pole may cause tentorial herniation and brain-stem compression

• More controversial• > 80 % still have raised ICP postoperatively• Patients under 40 years with higher initial GCS

benefit more

Complications

Diffuse intraoperative bleeding

Diffuse brain swelling

Diffuse Intraoperative Bleeding

1. Check the coagulation studies.2. Transfuse blood and fresh frozen plasma as

appropriate, usually 6–10 units.3. Consider development of an ICH, either on

the same or opposite side4. Optimize cerebral perfusion pressure

Use vasopressor agents if necessary

Diffuse Intraoperative Bleeding

5. Thiopental 250mg–1 g in incremental doses6. More mannitol and lower PaCO2 to ~ 28 mmHg

by increasing ventilation7. Rule out intraoperative pneumothorax

Management• Factor VII and Tranexamic acid do not help

significantly• Complete normalization of the hematological

parameters by replacing the appropriate factors

Diffuse Brain Swelling

• Most commonly seen with acute SDH

• Anticipated when preoperative CT scan shows

brain swelling (midline shift out of proportion

to thickness of SDH)

• Anesthesia causes

– Impaired ventilation

Diffuse Brain Swelling

• Surgical causes:

– Ipsilateral ICH beyond the craniotomy margin

– Contralateral fracture or small hematoma on the

preoperative CT

• Management

– Decompressive craniectomy

– Mortality 50 %

Postoperative Management