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By
definition, it excludes traumatic and aneurismal hematomas.
25%
of all the strokes present with intracerebral haematoma (ICH) and
account for 2-4% of all deaths. They are twice as common as SAH.
Over two thirds are known to be fatal. The patients are usually
middle aged or over, with a male preponderance. The incidence is
about 1 per 10,000 with a 30day mortality of 44%.
Etiology:
There
are two categories, primary and secondary.
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Primary
ICH:
It
is associated with hypertension and distinct from
haemorrhagic infarcts. It has been suggested that
hypertensive changes in the arterial wall, such as, hyaline
degeneration, and microaneurysms are at fault. Another
suggestion is the thin walled vessels (such as
lenticulostriates), originating directly from the main
vessel are subjected to higher intravascular pressure than
the cortical vessels and tend to rupture.80% of them are
supratentorial.
Mostly,
the location is central and deep.
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Putamen
-55%
Thalamus
-10%
Subcortical whitemater
-15%
Cerebellar hemisphere
-10%
Pons
-10%
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Secondary
ICH :
It
is associated with a medical condition other than hypertension,
representing about 20% of all ICHs.
They
may be due to:
Coagulopathies
(10-15%)-Among these, platelet disorders are important. About 5%
of those receiving heparin, irrespective of the dosage, develop
thrombocytopenia. The platelet defects may be hereditary (Von
Willebrand’s disease) or acquired through drugs (Aspirin,
penicillin, or new cephalosporins) or through disease (myeloproliferative
and dysplastic disorders, uraemia, cirrhosis, SLE, multiple myeloma).
AVMs
(7%) represent a heterogenous group with different histological
types (cavernoma, AVMs, venous angioma and capillary telangiectosis).
Vasculopathies
(5%), such as cerebral amyloid angiopathy, polyarterites nodosa and
necrotizing vasculopathy in drug abusers, tend to produce multiple
subcortical haematomas.
Tumors
(2%) such as glioblastoma and metastatic tumors such as, melanoma,
choriocarcinoma, renal cell carcinoma and bronchogenic carcinoma,
are the most frequent tumors in producing ICH.
Pathophysiology:
The
hematomas may be massive (>5cm ) with extension into the
ventricles or may be small (<1.5 cm ).
The
extravasated blood forms a roughly circular or oval mass which grows
in volume for a brief period. Adjacent brain tissue is displaced and
compressed resulting in extensive edema and ischemia. Ischemic area
may be much larger than the area of clot.
Cerebellar
and brainstem ICH may produce obstructive hydrocephalus which may
add to the problems. In large hemorrhage, there is midline shift and
the vital centers are compromised.
Rebleeding
is rare.
Resolving
haematomas may develop into a cyst over a period of months, with a
gliotic wall which may be orange colored due to haemosiderin laden
macrophages.
Clinical
features:
It
depends on the site and size of the hematoma.
Sudden
headache, vomiting with depressed level of consciousness and focal
signs is the usual mode of presentation.
Absence
of neck stiffness may help to exclude SAH .
The
large ones are usually associated with LOC.
In
putaminal ICH, the patient develops sudden hemiplegia with
conjugate horizontal gaze deviation towards the clot. Speech may be
involved if the dominant hemisphere is involved.
In
thalamic ICH, the findings are as in putaminal ICH; in
addition, there may be neck retraction, paralysis of vertical gaze
with upward gaze palsy, inequality of pupils, and skew deviation
with the contra lateral eye being displaced downward and medially.
Cerebellar
ICH presents with severe headache, nausea and vomiting and imbalance
and depressed level of consciousness.
Pontine
ICH present with coma, pin point pupils and decerebrate rigidity.
Cortical
ICH may present with headache and seizures.
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Investigations:
CT
scan will reveal the clot and other associated features such
as midline shift and hydrocephalus. A contrast CT may
suggest a vascular problem, which may necessitate an
angiography.
MRI
gives a better delineation of the above; in addition
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the
age of the haematoma can be guessed. MRI may suggest an
associated AOVM.
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Thalamic hge.
with intraventricular extension
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Cerebellar
hge
due
to Cavernoma
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Ext.capsule Hge
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Angiography
should be carried out whenever there is a suggestion of
vascular malformation, in the absence of previous
hypertension or coagulopathies before a life saving clot
evacuation. When surgery is not planned, the angiography can
wait for few weeks to avoid a false negative angiography.
Coagulation
studies must be done as a routine in addition to ECG, chest
X-ray and other general investigations.
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Management:
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intratumoral
bleed ---- plain and contrast CT
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Supportive
care control of hypertension, reduction of
ICP without compromising the CPP and prevention of complications are the
mainstay. Fluid and electrolytes and tissue oxygenation must be
closely monitored. The aim is to avoid secondary events.
An
aggressive decrease of high BP may lead to cerebral ischaemia. Ideally,
it should not be lowered below 150mm Hg systolic and 100 mm of Hg
diastolic.
Should
general measures to control the raising ICP fail, hyperventilation may
help; but must be employed with careful watch on pCo2, arterial blood
pressure and preferably with ICP monitoring as well. The CPP should not
be compromised.
Osmotherapy
with mannitol may help only when the serum osmolality is lower
than 300 mosm/kg.
Prophylactic
anti convulsant therapy is advised by most physicians with no supporting
evidence.
The
role of Surgical intervention is controversial.
Neurosurgeons
and neurologists advocate that large cerebellar hemorrhages
with compression of the brain stem or obstruction of the
fourth ventricle should be surgically removed as soon as
possible. Surgical removal of large lobar hemorrhages in
young patients who are clinically deteriorating has also been
recommended based on anecdotal experience.
On the other hand, the results of such surgery in hematomas within the
basal ganglia and other deep structures are unacceptable.
Standard
craniotomy for surgical removal of primary brain stem or
thalamic hemorrhages has been all but abandoned because of
the extremely poor outcomes in almost all patients.
Craniotomy:
Craniotomy
and evacuation of the clot has been the standard approach for removal of
intraparenchymal hemorrhage. In addition a decompressive
craniectomy with a duraplasty is prefered by some. Its
major advantage is adequate exposure to remove the clot. It is not
difficult or time-consuming. The major disadvantage of a more
extensive surgical approach is that it may lead to further
brain damage, particularly in patients with deep-seated hemorrhages.
In addition, the effectiveness of clot removal by craniotomy is
far from ideal.
There have been
numerous nonrandomized series comparing craniotomy and best medical
treatment of ICH. Recently Morgenstern and colleagues reported a
single-center, randomized trial (STICH Trial) of standard
craniotomy versus best medical therapy in patients with
supratentorial ICH; the goal was to perform surgery 12
hours after symptom onset. Patients had to have a
supratentorial ICH with a volume 10 cm3 and a GCS
score of 5 to 15. Of the 34 patients in the randomized trial,
17 were randomized to removal of the ICH by standard
craniotomy. The median time to surgery for the 17 patients was
8.3 hours (minimum 3.75 hours and maximum 26.1 hours). The 6-month
mortality for the surgical group was 17.6% compared with
23.5% for the medical group. The median 6-month Barthel index
score for survivors in the surgical group was also similar to
the median Barthel index score for the medical group.
However, the groups were not balanced with regard to ICH location.
Only 1 of the 17 patients (6%) in the surgical group had a
lobar hemorrhage compared with 7 of 17 patients (41%) of the
medical group.
Nonrandomized
treatment series of patients with cerebellar hemorrhage report
good outcomes for surgically treated patients who have large
(>3 cm) cerebellar hemorrhages or cerebellar
hemorrhages with brain stem compression or hydrocephalus. In
these patients, medical management alone often results in bad
outcomes. Smaller cerebellar hemorrhages without brain stem compression
that are managed medically do reasonably well.
Newer
techniques: The
grim results of conventional craniotomy have stimulated a search for
more tolerable, less traumatic, and safer methods of clot removal.
Technical advances in removal of ICH include improved localization of
the hemorrhage by stereotactic devices or intraoperative ultrasound
and better surgical techniques.
Innovations
in devices to break up and remove the blood clot include
modifications of an Archimedes screw inside a cannula, a specially
designed ultrasonic aspirator, a modified nucleotome, a double track
aspiration, and intraoperative CT monitoring.
Intraoperative ultrasound has also been used to identify the hemorrhage
and monitor its removal in real time..
Stereotactically
controlled endoscopic evacuation
is gaining popularity. It permits localization of the lesion, and
removal of the clot is performed under optic control, which may be
important in cases of cryptic arteriovenous malformations. This
high-tech method may be simple, fast, safe, and effective and provides
for continuous intraoperative volume removal.
Fibrinolysis
aids rapid
dissolution of the remaining blood. The aim is to achieve a mass
reduction as well as to reduce the extension of perifocal edema and
minimize the amount of tissue damage. The most commonly used
thrombolytic protocol has been administration of 6000 U of
urokinase once or twice daily via a catheter into the bed of
the hematoma with subsequent drainage and aspiration. A
urokinase washout can be performed for up to 7 days after the
bleeding.This procedure is often repeated over several days until the
majority of the hematoma has been aspirated.
Hematoma
puncture and catheter placement for fibrinolytic therapy could be
achieved with high accuracy and safety using frameless stereotaxy. This
method, reportedly, allows unrestricted trajectory selection with
catheter positioning along the main hematoma axis. Further studies are
required to investigate if frameless stereotactic puncture and clot
lysis could contribute to improve the outcome of patients with ICH.
Outcome:
The
natural course of spontaneous ICH leads to a 30-day mortality rate of
45%. The
patient's initial level of consciousness, hemorrhage size, and
intraventricular extension of blood has proven to be accurate predictors
of outcome. Less commonly, age, sex, hypertension, and mass effect may
indicate harmful effects on outcome in patients with ICH.
The
author recommends that patients with smaller hematomas who are alert,
stable, or improving should be treated medically and the patients with
larger hematomas who show progressive neurological deficit, prolonged
functional impairment, and intracranial hypertension should be treated
surgically. Patients with a GCS score <4 should also be
treated medically because they uniformly die or have
extremely poor functional outcome that cannot be improved by
surgery. Easily accessible supratentorial hematomas with mass effect,
especially in the young and in those with a GCS score >5, must be
evacuated. The aim of surgery should be the removal of as much of the
clot as possible, with minimal disruption of surrounding brain tissue.
If possible, surgery should also remove the underlying cause
of hemorrhage, such as an arteriovenous malformation, and
prevent complications of ICH such as hydrocephalus and mass
effect of the blood clot. More complete clot removal may
decrease elevated ICP and local pressure effects of the blood
clot on the surrounding brain. Stereotactic aspiration may be
associated with better outcomes than standard craniotomy; but
this hypothesis has yet to be tested in a randomized study.
Ultra-early removal of ICH by localized, minimally invasive
surgical procedures is promising but untested. Further study
of the dynamics of hemorrhage and additional results are needed prior to
making a decision on how to divide patient management into the two
categories of surgical and nonsurgical treatment.
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