SUBDURAL

HAEMATOMA
GOURI G
Roll No : 58
 CLINICAL SCENARIO 1
While playing football, a 22 year old male student
was struck on his head by another player’s knee.
Immediately after the trauma he became drowsy
and 5 min later he developed coma. He did not have
convulsions or vomiting. On neurological examination
he was in coma, and dense hemiparesis to the left side.
CT scan revealed concavo convex lesion in the right
side of hemisphere.
 CLINICAL SCENARIO 2

A 73 year old male presented with headache which

increased gradually with periods of acute worsening.
It was associated with nausea and vomiting. patient
also complained of memory loss, difficulty with gait
and balance. He is on anticoagulants. No history of
trauma.
 CRANIUM

Highest placed cavity

Contains brain, meninges ; outer duramater , middle
arachnoid , inner pia mater
Dura mater is the thickest
It encloses the cranial venous sinuses and has a
distinct blood supply and nerve supply
Dura is separated from the arachnoid by a potential
subdural space
 CEREBRAL DURAMATER

Two layers ; outer endosteal and inner meningeal

Meningeal layer is folded on itself to form partitions
– divide cranial cavity into compartments
Folds are : falx cerebri , tentorium cerebelli , falx
cerebelli , diphragma sellae
BLOOD SUPPLY
 VENOUS SINUSES

Walls are formed by dura mater

No muscles in their walls
No valves
Communicate with veins outside the skull
through emissary veins
 BRIDGING VEINS
Drain the underlying neural tissue and puncture
dura mater to, empty into venous sinuses
Rupture of bridging veins cause subdural
hematoma
 CEREBRAL BLOOD FLOW
Brain is dependent on continuous cerebral
bloodflow for oxygen and glucose
Normal – 55ml / min for 100g of brain tissue
Ischemia results when rate falls below 20ml /
min
CPP = MAP - ICP
ICP AND MONRO KELLIE DOCTRINE
Cranium is a “rigid box” – incompressible brain
Any expansion in contents maybe initially
accomodated by exclusion of fluid
components ,venous blood and CSF
Further expansion associated with exponential
rise in ICP
Cerebral herniation
Herniation of uncus of temporal lobe over the
tentorium – pupil abnormalities
Cerebellar tonsillar herniation – foramen
magnum – compresses medullary vasomotor &
resp centres – cushing’s triad (htn, bradycardia
and irregular resp)
Patient is then said to be coning
 SUBDURAL HAEMATOMA
Collection of blood b/w brain and dura

 ACUTE
 CHRONIC
ACUTE SUBDURAL HAEMATOMA
Collection of blood in subdural space
Most commonly traumatic in origin
Injury to cortical veins & often due to laceration
of cortex of brain which bleeds and blood gets
collected in the subdural space.
 MECHANISM OF INJURY

Encountered in two broadly distinct contexts

 Firstly high energy injury mechanisms – rupture

of cortical surface vessels with sig associated
primary brain injury. Results in expanding
hematoma with rapid deterioration and
developing signs of raised ICP.
 Second group, older and often anticoagulated –
lower energy injury leads to venous bleeding
around the brain.
Depending upon the total vol of bleeding – acute,
chronic or may even remain clinically silent.
Latter group may present much later with a further
‘acute-on-chronic’ presentation.
 CLINICAL FEATURES
Loss of consciousness occur immediately after
trauma and is progressive.
Convulsion is common
Features of raised intracranial pressure – high bp
, bradycardia , vomiting
Focal neurological deficit or hemiparesis can
occur
CT scan shows concavo-convex lesion
 MANAGEMENT

 History

Pre injury states- fits, alcohol, chest pain

Speed of vehicles, height fallen
Conscious state and hemodynamic stability of
patient after accident
Medication-antiplatelets and anticoagulants.
 PRIMARY SURVEY

• Adequate oxygenation and circulation

• Check blood glucose levels
• Check pupil size and response
• Glasgow coma scale score – eyes open, verbal,
motor components.
• Check focal neurological deficits before
intubation
 TREATMENT

Antibiotics
Anticonvulsants
Surgical decompression by craniotomy
CHRONIC SUBDURAL HEMATOMA

Common cause of a/c neurological deterioration

in the elderly
Gradual collection of blood in subdural space
Patients who have received antiplatelet or
anticoagulants, who are thrombocytopenic, are
at increased risk
 MECHANISM

Cerebral atrophy in old age

Stretching of cortical dural bridging veins

Hematoma expand over days /weeks by osmosis

Symptoms of raised ICP or focal deficits

 CLINICAL FEATURES

Common in old age

History of minor trauma
Presents with headache,confusion,
disorientation, gradually with altered level of
consciousness ,drowsiness
Later convulsions ,features of intracranial
hypertension ,coning
Extensor plantar response, pupillary changes
develop eventually
 INVESTIGATIONS
 CT scan shows concavo-convex lesion
o diffuse hypodensity overlying the brain surface
o recent bleeding may be hyperdense or isodense
o mixed density indicate acute-on-chronic SDH
 Serum electrolytes
 Blood grouping and cross matching
 TREATMENT

Anticoagulants reversed by giving vit K or by

transfusion of recombinant clotting factors
Conservative- corticosteroids for small bleeds
Antibiotics
Anticonvulsants for 3 years
Craniotomy
For majority drainage is done using burr holes
Urgency dictated by the clinical condition of the
patient
If clinically stable – a delay of 7-10 days to allow
platelet function to normalize after withdrawal of
aspirin/clopidogrel
 SUMMARY
A subdural hematoma is a bleed ocuring b/w
brain and dura
Most common cause is trauma resulting in
injury to bridging veins
CT is best imaging modality to assess SDH –
diffuse concave appearance
a/c SDH – urgent evacuation by craniotomy /
craniectomy
c/c SDH – burr hole drainage is usually
preferred
THANK YOU !