YTM- Neuro week 2

Acute epidural hemorrhage

Epidural hematoma arises with a temporal / parietal fracture and laceration of

middle meningeal artery/ vein. Less often tear in dural venous sinus.
Lateral skull fracture that lacerates middle meningeal artery / vein Patient
may or may not lose consciousness initially, but a lucid interval lasting 1-2
days is followed by rapid evolution, over hours of headache, progressive
obtundation, hemiparesis, finally ipsilateral papillary dilatation from uncal

herniation. Death may followed if treatment is delayed

A fews hours later headache of increasing severity develops, with vomiting,
drowsiness, confusion, aphasia, seizure (may be one sided), hemiparesis with

slightly increase tendon reflexes, and a babinski sign.

As coma develops, the hemiparesis may give a way to bilateral spasticity of

the limbs and babinski sign.

HR often slow ( <60 beats/m) and bounding, with concomitant rise in Systolic

BP (Cushing effect), Pupil may dilate on the side of hematoma.

LUMBAR PUNCTURE is contracindicated in this setting.
Death , if an expanding clot is not removed surgically comes at the end of a

comatose period is a result of respiratory arrest.

Visual of a fracture line across the groove of medial meningeal arterty and
knowledge of side of the head was struck aid in diagnosis and

lateralizations of the lesions.

Meningeal vessels may occasionally be torn without fracture. CT scan is

definitive and revealed lens shaped clot with smooth inner margin.
Treatment : surgical procedure consists of placement of burr holes in an
emergency situation, preferably a craniotomy,drainage of the hematoma,

identification and ligation of the bleeding vessel.

Operative results often excellent except in extended fractures and laceration

of dural venous sinuses, bilateral hematoma.

If coma bilateral babinski signs, spaciticity, decerebrate rigidity supervene
before operation means displacement of central structures & compression of

midbrain have oocured ; prognosis is poor.

Small epidural hemorrhage can be followed by serial CT scanning and will be
seen to enlarge gradually for a week or two and then be absorbed. There is
controversy about the benefit of removing these smaller clots in patient who
has no symptomps, with careful clinical and imaging surveillance , most can
be left alone.

YTM- Neuro week 2

Acute Subdural Hematoma

Can be acute, subacute, or chronic. Headache and altered consciousness are

the principal manifestations. In contrast to epidural hematoma time between

trauma and the onset of symptoms is typically longer.

The hemorrhage tends to be located over the cerebral convexities and

associated skull fracture is uncommon.

Found in severe head trauma, it carries poor prognosis, not because of
subdural blood itself but because it is often associated with underlying

parenchymal injury, mortality as high as 50 %

May be unilateral or bilateral, there may be a brief lucid interval between the
blow of the head and advent of coma. More often patient is comatose from
time of the injury and coma deepens progressively. May be combined with

epidural hemorrhage, cerebral contusion, laceration

Subdural clots more than a few millimeter in thickness can be accurately
visualized by the CT scan more than 90 percent cases, but the window
settings must be appropriate to avoid obscuring of the clot by adjacent bone
as well as marked compression of one lateral ventricle, but if there are

YTM- Neuro week 2

bilateral clots there may be no shift and the ventricles may appear

symmetrically compressed.
Rapidly evolving subdural hematomas are usually result of tearing the
bridging veins and symptoms are caused by compression of adjacent brain

and deep structures.

Unlike epidural arterial hemorrhage, which is steadily progressive, the rising

of ICP usually arrest venous bleeding.

Subdural hematoma on prosterior fossa gives rise to headache, vomiting,
pupilary inequality, dysphagia, cranial nerve palsies, rarely stiff neck and
ataxia of trunk and gait if the patient is well enough to be tested for these

functions.
Treatment : both hematoma itself and at the associated parenchymal injury.
Neurosurgical removal of the hematoma is necessary, contused brain tissue
must be often resected as well. At surgery duraplasty may be performed,
bone plate may be left out, rather than put back in order to provide room for

the swollen brain and prevent potentially lethal intracranial hypertension.

Place Burr holes and evacuate the clot before coma has developed : most

common
Larger hematoma particularly after several hours have passed and the blood
has clotted consists of craniotomy to permit control of bleeding and removal

of the clot
Interval between loss of consciousness and surgical drainage is most
important determinant of outcome in serious cases

YTM- Neuro week 2

Subdural
Chronic
Subdural Hematoma
hematoma
Etiology is incompletely understood. There are one or more minor traumatic
episodes. Fluid collection lies between the inner dural membrane and the arachnoid
and is probably derived from an initial hemorrhage of the bridging veins.
Granulation tissue is found in the wall of the hematoma. This tissue is thought to be
the source of repeated. Secondary bleeding into the fluid collection so it slowly
expands rather than being resorbed.
Manifestation : produced on underlying brain tissue and depend on the side of
hematoma. Chronic subdural hematoma overlying the central region may be
clinically indistinguishable from an infarct.
Treatment consists operative removal or percutaneous drainage . Relatively high
recurrence rate. The presence of a subdural hematoma contraindicates theurapeutic
anticoagulation, which may cause additional bleeding into the hematoma cavity
producing mass effect.