Congress report
Intracerebral haemorrhage
Karl Schaller, Philippe Bijlenga
Depar tment of Neurosurger y, University of Geneva Medical Centre, Faculty of Medicine, University of Geneva, Geneva, Switzerland
Funding/potential conflict of interest: No funding. No conflict of interest.
What is the epidemiology of spontaneous intra­
cerebral haemorrhage (ICH)?
The incidence of ICH in the general population is 12–15/
10 000 per year, but reaches its peak of approx. 100/100 000
persons per year in the population >75 years of age. It is
responsible for 8–15% of all strokes in Europe and in North
America, whereas in Japan and in China it accounts for
20–30% of all strokes. The 30-day mortality ranges from
35–50% and is thus 2–6 times that for ischaemic stroke
[1, 3].
The management and prognosis of young patients
presenting with ICH is entirely different as treatable pathologies are usually the underlying cause, e.g., vascular malformations (AVM, cavernomas etc.) or aneurysms, to name
but a few.
Do prognostic criteria exist, and what are
the consequences of spontaneous ICH?
The prognostic criteria associated with outcome are as
follows:
– Initial level of consciousness, e.g., according to the
Glasgow Coma Scale (GCS)
– Localisation of the haematoma
– Haematoma volume
– Additional ventricular haemorrhage
– Presence of midline shift
– Additional hydrocephalus
– Advanced age
– Neurological status on admission
Of these factors, low GCS grade and large haematoma
volume are the most predictive of poor outcome. Mortality
also relates to anatomical localisation of the haemorrhage,
being highest in brainstem ICH.
Only approx. 20% of all affected patients may function
independently six months after the ictus, and the lifetime
cost per case is, according to the recent American literature,
USD 124 000. Chronic diseases of advanced age contribute
Correspondence:
Prof. Dr. med. Karl Schaller
Department of Neurosurgery
University of Geneva Medical Centre
Faculty of Medicine
University of Geneva
Rue Micheli-du-Crest 24
CH-1211 Genève
karl.schaller@hcuge.ch
negatively through increased rates of secondary complications in the course of the disease.
What are the causes and risk factors of intracerebral
haemorrhage (ICH), and how does it occur?
Causes of ICH are as follows (frequent or rare according to the
setting in a tertiary referral centre in Europe):
– Hypertensive haemorrhage (frequent)
– Amyloid angiopathy (frequent)
– Coagulopathy (frequent)
– Vascular malformations (AVM, cavernoma, aneurysm)
(frequent)
– Haemorrhagic transformation of ischaemic infarction
(frequent)
– Drug abuse (cocaine) (rare)
– Tumours (rare)
– Vasculitis / encephalitis (rare)
– Venous occlusion with consecutive haemorrhagic transformation (rare)
Risk factors of ICH:
– Hypertension
– Atherosclerosis
– Hypocholesterolaemia
– Previous brain infarction (increased 5–22 times compared with the normal population)
– Anticoagulants (increased 6–11 times compared with
the normal population)
– Alcohol (increased 5 times compared with the normal
population)
– Amyloid-angiopathy
– Advanced age (>65 years)
There seems to be a genetic disposition for lobar ICH
in the presence of the apoEA2 or apoEA4 alleles. ICH, particularly in elderly patients, is frequently deeply located
or ganglionic, and relates to long-standing arterial hypertension with concomitant atherosclerosis of small and fragile
end-arteries. Even lobar ICH in the elderly may have its
origin in a degenerative process of small arteries, so-called
cerebral amyloidosis.
Once a haematoma has formed, the clot volume may
increase in approx. 30% of patients during the first 24
hours. Morbidity and mortality are caused by the secondary effects exerted by the haematoma, such as neurotoxicity,
neuronal ischaemia, and brain oedema: activation of the coagulation cascade with rupture of the blood brain barrier due
to haemoglobin toxicity, for example, triggers immunologi-
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Congress report
cal reactions such as activation of the complement cascade,
i.e., increased serum MMP3 correlates with mortality. In
parallel, increased intracranial pressure (ICP) leads to reduction of cerebral perfusion pressure (CPP), loss of cerebral
autoregulation and secondary liberation of vasoactive inflammatory metabolites.
What diagnostic measures should be taken in ICH?
After clinical assessment, the most important measure is
cranial computed tomography (CCT). Recent CCT technology allows simultaneous angiography (CTa), and underlying vascular malformations can thereby be excluded. If in
doubt, however, additional 3D digital subtraction angiography (DSA) should be performed if feasible. MRI plays a
minor role in primary diagnostics due to limited access in
ventilated patients. It may however be important during
the further clinical course, e.g., for determination of brain
damage, for perfusion imaging, and for exclusion or visualisation of vascular malformations.
It is of the utmost importance to rule out treatable
pathologies such as cerebral AVMs, cavernomas, aneurysms,
or dural AV fistulas as the underlying cause. Particularly in
young(er) patients, ICH should be regarded as due to rupture of some form of vascular malformation, until proven
otherwise.
What are the therapeutic options, and how should
ICH be managed?
As in the case of supratentorial ICH, unfortunately no ideal
and promising treatment regimen exists. Thus it is immaterial whether these patients are treated surgically (via open
craniotomy, stereotactic aspiration and haematoma lysis,
or endoscopically), or receive intensive care based on a conservative internistic/neurological regimen. Thus it is fully
justified for neurosurgeons to refrain from expensive surgical therapy of whatever type (open craniotomy, stereotactic aspiration and haematoma lysis/drainage, or endoscopic
aspiration). This almost fatalistic attitude has been substantiated by an international multi-centre study (STICH trial) in
more than 1000 patients in whom no difference in outcome
was noted between the groups, who received either intial
surgical treatment or conservative treatment respectively
[5]. However, if patients with additional VEH are excluded
from the surgical group there may be some beneficial effect
from surgery. It is intended to elucidate this further through
the consecutive STICH II trial, which may help to identify a
group which would possibly benefit from surgery. For example, the management of lobar haemorrhage in hypertensive
patients aged between 45 and 70 is still controversial, and
thus it is justifiable to decide according to department policy
and/or on a case-by-case basis. The subgroup analysis of the
STICH trial suggested that this group may benefit from surgical evacuation of the haematoma [6].
A large randomised trial of the use of recombinant factor VIIa (rFVIIa) showed that secondary haematoma growth
could be reduced, but this did not translate into reduced
mortality or a better outcome, due to increased frequency of
thromboembolic events [4].
Management of supratentorial ICH remains, in conclusion,
conservative and supportive. It should focus on reduction
of increased ICP, restoration of cerebral blood flow, and
avoidance of secondary complications [2, 3]:
– Take a precise clinical and patient history!
– Perform a precise neurological exam (including GCS)
– Assessment of respiratory and circulatory situation
– Keep upper part of body at 30°
– Ensure adequate oxygenation
– Sedation in unstable patients (to be maintained on
neurological ICU)
– Reverse anticoagulation (if INR >1.4) (PCC, FFP, vitamin
K)
– MAP <130 mm Hg (180/110 in hypertensives)
– ECG surveillance
– Avoid excessive hypo-/hypertension (ensure physiological CPP!)
– Although the role of hyperosmolar substances is unclear,
they may be administered
– Sensitive temperature management (fever worsens
prognosis)
– Control laboratory values regularly (e.g., creatinine, INR,
PTT, glucose, etc.)
– Perform frequent neurological/circulatory monitoring
(apply cuff, or arterial line, and central venous line)
– (External drainage in case of concomitant hydrocephalus
independently of estimated prognosis)
The position with regard to infratentorial, or cerebellar, ICH
is different: surgical management of these haematomas
improves prognosis and they should be operated upon if
they do not extend into the brainstem [1].
Intense joint efforts are required from clinical and basic neuroscientists of all groups, together with internists
and intensivists, in order to develop preventive measures or
reasonable treatment options for ICH – particularly in our
ageing societies.
Key words: ICH; conservative treatment; surgery; management
References
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