A presentation that will help clinicians attain the basic diagnostic skills required to effectively manage patients.

1. SURGERY
SUB-DURAL HAEMORRHAGE
DR. CHONGO SHAPI (BSc. HB, MBChB)

2. SUB-DURAL HAEMATOMA
A subdural hematoma (SDH) is classified by the amount
of time that has elapsed from the inciting event, if known,
to the diagnosis. When the inciting event is unknown, the
appearance of the hematoma on CT scan or MRI can help
date the hematoma.
1. Acute SDHs are less than 72 hours old and are
hyperdense compared to the brain on CT scan.
2. Subacute SDHs are 3-20 days old and are isodense or
hypodense compared to the brain.
3. Chronic SDHs are older than 20 days and are
hypodense compared to the brain.
An acute SDH commonly is associated with extensive
primary brain injury. This diffuse parenchymal injury
correlates strongly with the outcome of the patient
The presence of brain atrophy or loss of brain tissue due
to any cause, such as old age, alcoholism, or stroke,
provides a potential space between the dura and the brain
surface for a SDH to form
Pathophysiology:
Acute subdural hematoma
The usual mechanism to produce an acute SDH is high-
speed impact to the skull. This causes brain tissue to
accelerate relative to a fixed dural structure, which, in
turn, tears bridging veins. This mechanism also leads to
associated contusions, brain edema, and diffuse axonal
injury.
The ruptured blood vessel often is a vein connecting the
cortical surface to the dural sinuses. Alternatively, a
cortical vessel can be damaged by direct laceration. An
acute SDH due to a ruptured cortical artery may be
associated with only minor head injury, and no cerebral
contusions may be associated.
Chronic subdural hematoma
A higher incidence of chronic SDH exists in men. The
male-to-female ratio is 2:1. Most adults with chronic SDH
are older than 50 years.
25-50% of chronic SDH pts have no identifiable history
of head trauma. If a patient does have a history of head
trauma, it usually is mild.
The average time between head trauma and chronic SDH
diagnosis is 4-5 weeks.
Risk factors for a chronic SDH
1.Chronic alcoholism
2.Epilepsy
3.Coagulopathy
4.Arachnoid cysts
5.Anticoagulant therapy (including aspirin)
Neurologic examination may demonstrate hemiparesis,
papilledema, hemianopsia, or third cranial nerve
dysfunction, such as an unreactive dilated pupil or a
laterally deviated eye of limited movement. In patients
aged 60 years or older, hemiparesis and reflex asymmetry
are common presenting signs. In patients younger than 60
years, headache is a common presenting symptom.
Chronic SDHs are observed bilaterally in 8.7-32% of
cases.
Indications for surgery
Emergent surgical evacuation should occur in patients
with an acute SDH larger than 5 mm in thickness (as
measured by axial CT scan) and causing any neurological
signs, such as lethargy, unresponsiveness (coma), or focal
neurological deterioration.
Surgery for chronic SDH is indicated if SDH is
symptomatic or producing significant mass effect on
imaging studies
Lab Studies:
-To determine whether defective coagulation was
involved in the formation of the acute SDH and to correct
any coagulation abnormalities a prothrombin time (PT),
activated partial thromboplastin time (aPTT), and a
platelet count should be performed. A bleeding time may
detect platelet dysfunction.
-Routine trauma lab studies that aid in the initial
assessment include hemoglobin, electrolytes, and a
drug/alcohol screen. Obviously, the drug and alcohol
screens are important in correlating the neurological
examination with the imaging studies.
Imaging Studies:
a)Computed tomography scan of the head without
contrast
Acute SDH appears on CT scan as a crescent-shaped
hyperdense area between the inner table of the skull and
the surface of the cerebral hemisphere
Medical therapy:
Acute subdural hematoma
Small acute SDHs less than 5 mm thick on axial CT
images, without sufficient mass effect to cause midline
shift or neurological signs, can be followed clinically .
Hematoma resolution should be documented by serial
imaging because an acute SDH that is treated
conservatively can evolve into a chronic hematoma.
Emergent medical treatment of an acute SDH causing
impending transtentorial herniation is the bolus
administration of mannitol (in the patient who is
adequately fluid resuscitated with an adequate blood
pressure). Surgical evacuation of the lesion is the

3. 6.Cardiovascular disease (hypertension, arteriosclerosis),
7.Thrombocytopenia
8.Diabetes
9.Severe dehydration
10.Extremes of ages
Clinical presentation often is insidious, with symptoms of
decreased level of consciousness, balance problems,
cognitive dysfunction and memory loss, motor deficit
(such as a hemiparesis), headache, or aphasia. Acute
presentation also is possible, as in the case of a patient
who presents with a seizure.
Surgical therapy:
Acute subdural hematoma
Surgery for acute SDH consists of a large craniotomy
(centered over the thickest portion of the clot) to
decompress the brain, stop any active subdural bleeding,
and evacuate any intraparenchymal hematomas in the
immediate vicinity of the acute SDH.
The craniotomy exposure should include the sylvian
fissure because this can be a likely source of a ruptured
cortical vessel. If brain injury and edema are associated,
an intracranial pressure (ICP) monitor should be placed.
Chronic subdural hematoma
Liquefied chronic SDHs commonly can be treated with
drainage through 1-2 burr holes. Burr holes are placed so
that conversion to a craniotomy is possible if needed. A
closed drainage system sometimes is left in the subdural
space for 24-72 hours postoperatively. Small catheter
drainage via twist drill craniotomy at the bedside also has
been described as adequate treatment.
A nonliquified chronic SDH cannot be decompressed
adequately by burr holes and must be removed by
craniotomy.
Bilateral chronic hematomas must be drained from both
sides, usually during the same operation through burr
holes placed on each side of the head.
Preoperative details:
Phenytoin (Dilantin) is administered to decrease the risk
of developing early posttraumatic seizures (within the
first 7 d after the injury). Patients have an estimated risk
of greater than 20% for developing posttraumatic epilepsy
after an acute SDH. Phenytoin only should be continued
for 7 days after the injury because it is not effective in
preventing late posttraumatic seizures (beginning 1 wk or
more after the injury).
Acute subdural hematoma
After the evacuation of an acute SDH, medical treatment
is aimed at controlling the ICP below 20 mm Hg and
maintaining the cerebral perfusion pressure above 60-70
mm Hg. These parameters are vital to maintain during the
perioperative period. Within 24 hours of removing an
acute SDH, a follow-up CT scan should be obtained
routinely
definitive treatment and should not be delayed.
Chronic subdural hematoma
Without mass effect on imaging studies and no
neurological symptoms or signs except mild headache, a
chronic SDH can be followed with serial scans and may
resolve.
No medical therapy has been shown to be effective in
expediting rapid resolution of acute or chronic SDHs