|
| |
Intracerebral
haemorrhage
Aetiology
Primary: approximately half result from long standing hypertension
Secondary: neoplasm, vasculitis, bleeding disorder, prior embolic
infarction, aneurysm, vascular malformation, trauma
Pathophysiology
- thought to be due to extravasation of blood from ruptured micro-aneurysms
along walls of small intracerebral arterioles. These develop at sites of
vascular branching where mechanical stress is maximal
- processes which result in aneurysm formation include lipohyalinosis and
fibrinoid necrosis which weaken the walls of arterioles. Aneurysm formation
enhanced by chronic hypertension
- alternative explanation for ICH that has been suggested is arteriole
microdissection
- continued extravasation of blood results in formation of a haematoma with
secondary development of cerebral oedema. May be resultant mass effect. PET
data suggests that development of perihaematoma oedema may not be due to
secondary brain ischaemia but may be due to reperfusion injury but other
data (eg microdialysis data) suggests that it is due to ischaemia
- ± extension to ventricles
- early expansion of haematoma appears to occur from multiple small vessels
in low blood flow area around the haematoma. Continued bleeding/re-bleeding
is common
Clinical features
- onset usually during waking hours when patient is active
- abrupt onset
- progressive development of neurological deficit over minutes to hours. (cf.
fluctuating or stepwise progression of deficit commonly seen in
atherosclerotic infarcts, maximal deficit at onset in embolic strokes)
- prior TIA rare
- average age at onset 50-70 years (younger than in other types of stroke)
- ± lateralized headache
- vomiting common
- ± nuchal rigidity
- fits at onset in 17%. More common than in ischaemic stroke. More likely to
occur if bleeding involves cerebral cortex
- 44-72% comatose by the time of presentation
Investigations
Specific symptoms
Tends to occur in certain locations: putamen (30-50%), subcortical white
matter (15%), thalamus (10%), cerebellum (10%)
Putamenal
- due to bleeding from lenticulostriate vessel
- abrupt development of flaccid hemiplegia, hemisensory loss, homonymous
hemianopia, paralysis of conjugate gaze to the side opposite the lesion and
early alteration in level of consciousness. ± subcortical aphasia (dominant
hemisphere) or hemineglect (non-dominant)
Lobar (subcortical white matter)
- less commonly related to BP than ICH in other
locations
- signs and symptoms depend on anatomical site
- associated with higher incidence of seizures and headache at onset
- most common in parietal and occipital lobes
- lowest mortality and best prognosis for good functional recovery
Thalamic
- unilateral sensorimotor deficit
- sensory signs predominate
- ± downward deviation of eyes with impairment of vertical gaze and small
sluggish or unreactive pupils (Parinaud’s syndrome): due to downward
pressure on vertical gaze centre in midbrain tectum
- aphasia or apraxia depending on side of ICH
- ± forced conjugate deviation of eyes
Pontine
- rapid onset of coma, quadriplegia, brainstem dysfunction and small
unreactive pupils
- almost always extends into 4th ventricle
- high mortality
- almost always arises from paramedian branch of basilar artery. Cases of
unilateral pontine ICH have a less dismal outcome
Cerebellar
(CT
scan)
- alteration of consciousness is unusual at onset but progressive
deterioration is typical
- majority of patients will initially have 2 of following: gait, truncal or
limb ataxia; LMN VII lesion, ipsilateral gaze palsy
- other common presenting signs and symptoms: nausea, vomiting, vertigo,
nystagmus
Treatment
Medical
- control hypertension to minimize risk of further bleeding but risk of
causing cerebral ischaemia as autoregulation is impaired. Some recommend aiming
for systolic BP of 110-160 mmHg while others suggest that treatment should
only be instituted if systolic BP in acute phase of ICH is >200 mmHg.
Decrease BP slowly. b blockers are agents of choice
with diuretics being second choice. Ca blockers, nitroprusside and hydralazine
should be avoided as vasodilatation may lead to increased cerebral oedema and
intracranial pressure
- management of intracranial hypertension
- anticonvulsants not routinely required. Haemorrhage into cortex predisposes
to fits. Fits have been seen following haemorrhage into caudate but not
putamenal or thalamic bleeds
- recombinant factor VII currently being studied as a means of reducing
rebleeding but there is a risk that it may increase secondary damage if the
perihaematoma oedema is due to ischaemia
Surgery
- cerebellar ICH >3 cm or in smaller lesions with clinical progression
because cerebellar haemorrhage causes death in up to 60%. Surgical mortality
is greatly reduced if the patient is still awake before operation: therefore
early intervention is indicated
- ± lobar haemorrhage in patients who continue to deteriorate
- surgery for putamenal haemorrhage is controversial
- inappropriate for thalamic and pontine haemorrhages
- shunt for acute hydrocephalus
Prognosis
- increased size of haematoma (>30 ml associated with poor prognosis), decreased GCS, increased pulse pressure all
associated with worse prognosis
- pontine ICH has highest mortality followed by cerebellar, basal ganglia.
Lobar lowest
Further reading
Fischer M, Weaver JP. Cerebrovascular disease. In Rippe JM, Irwin RS, Fink
MP, Cerra FB (eds), Intensive Care Medicine, 3rd ed. Little Brown & Co.,
Boston, 1996, pp 2010-19
|
