ICH consists of three distinct phases: (1) initial hemor
-
rhage, (2) hematoma expansion, and (3) peri-hematoma ede
-
ma.
19
The initial hemorrhage is caused by rupture of cerebral
arteries influenced by the aforementioned risk factors. The dis
-
ease outcome depends primarily on the latter two phases of
progression. Hematoma expansion, occurring hours after ini
-
tial symptom onset, involves an increase in intracranial pres
-
sure (ICP) that disrupts the integrity of the local tissue and the
blood-brain barrier. Additionally, obstructed venous outflow
induces the release of tissue thromboplastin, resulting in local
coagulopathy
2
. In over a third of patients, hematoma expan
-
sion is associated with hyperglycemia,
20, 21,22
hypertension,
23
and anticoagulation.
24-26
The initial size of the hemorrhage
and the rate of hematoma expansion are important prognos
-
tic variables in predicting neurologic deterioration. Hematoma
size >30 ml is associated with greatly increased mortality.
27
Following the expansion, cerebral edema forms around the
hematoma, secondary to inflammation and disruption of the
blood-brain barrier. This peri-hematoma edema is the primary
etiology for neurological deterioration and develops over days
following the initial insult.
In
up to 40% of ICH cases, the hemorrhage extends into
the cerebral ventricles causing intraventricular hemorrhage
(IVH).
28
This is associated with
acute obstructive hydro
-
cephalus
and substantially worsened prognosis.
2,28
ICH and
accompanying edema may also disrupt or compress adjacent MUMJ
Clinical Review
17