Surgery for Head Injury

11,785 views 51 slides Sep 23, 2014
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About This Presentation

Surgery for Head Injury
Traumatic Intracranial Hematoma
Traumatic Brain Injury


Slide Content

Surgical Management of
Traumatic Brain Injury
Dhaval Shukla
Department 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 spine
3. Consent
4. Foley catheter
5. Two large bore peripheral i.v. lines
6. Arterial catheter
7. Protection of both eyes
8. 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
–1/4
th
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 stitches
NIMHANS

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 2/3
rd
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 lesion
Decompressive 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 debridement
Duraplasty
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 side
4. Optimize cerebral perfusion pressure
Use vasopressor agents if necessary

Diffuse Intraoperative Bleeding
5. Thiopental 250mg–1 g in incremental doses
6. More mannitol and lower PaCO2 to ~ 28 mmHg
by increasing ventilation
7. 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