Sunday 22 January 2012
CERIBRAL HEMMORAGE
A cerebral hemorrhage or haemorrhage (or intracerebral hemorrhage , ICH ) is a subtype of intracranial hemorrhage that occurs within the brain tissue itself. Intracerebral
hemorrhage can be caused by brain trauma, or it can occur spontaneously in hemorrhagic stroke . Non-traumatic intracerebral hemorrhage is a
spontaneous bleeding into the brain tissue.[1] A cerebral hemorrhage is an intra-axial hemorrhage ; that is, it occurs within the
brain tissue rather than
outside of it. The other
category of intracranial
hemorrhage is extra-axial
hemorrhage, such as epidural, subdural, and subarachnoid hematomas, which all occur within the skull but outside of
the brain tissue. There are two
main kinds of intra-axial
hemorrhages: intraparenchymal hemorrhage and intraventricular hemorrhages. As with other types of hemorrhages within
the skull, intraparenchymal
bleeds are a serious medical emergency because they can increase intracranial pressure, which if left untreated can
lead to coma and death. The mortality rate for intraparenchymal bleeds is over 40%. [2] Signs and symptoms Patients with
intraparenchymal bleeds have
symptoms that correspond to
the functions controlled by
the area of the brain that is damaged by the bleed. [3] Other symptoms include those
that indicate a rise in intracranial pressure due to a large mass putting pressure on the brain.[3] Intracerebral hemorrhages are often
misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and
signs. A severe headache
followed by vomiting is one
of the more common
symptoms of intracerebral
hemorrhage. Some patients may also go into a coma
before the bleed is noticed. Causes CT scan showing hemorrhage in the posterior fossa[1] Intracerebral bleeds are the
second most common cause of stroke , accounting for 30–60% of hospital admissions for stroke. [1]High blood pressure raises the risks of spontaneous
intracerebral hemorrhage by two to six times. [1] More common in adults than in
children, intraparenchymal
bleeds due to trauma are
usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration- deceleration trauma,[4][5][6] rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is a not
uncommon cause of
intracerebral hemorrhage in
patients over the age of 55. A
very small proportion is due
to cerebral venous sinus thrombosis. Infection with the k serotype of Streptococcus mutans may also be a risk factor, due to its
prevalence in stroke patients
and production of collagen- binding protein.[7] Risk factors for ICH include: [8] Hypertension Diabetes Menopause Current cigarette smoking Alcoholic drinks (≥2/day) Tramautic intracerebral
Hematomas are divided into
acute and delayed. Acute
intracerebral Hematomas
occur at the time of the injury
while delayed intracerebral Hematomas have been
reported from as early as 6
hours post injury to as long as
several weeks. It is important
to keep in mind that
intracerebral Hematomas can be delayed because if
symptoms begin to appear
several weeks after the
injury, concussion is no longer
considered and the symptoms
may not be connected to the injury. Diagnosis Spontaneous ICH with hydrocephalus on CT scan[1] Intraparenchymal
hemorrhage can be recognized
on CT scans because blood appears brighter than other
tissue and is separated from
the inner table of the skull by
brain tissue. The tissue
surrounding a bleed is often
less dense than the rest of the brain due to edema, and therefore shows up darker on
the CT scan. Treatment Treatment depends
substantially of the type of
ICH. Rapid CT scan and other diagnostic measures are used
to determine proper
treatment, which may include
both medication and surgery. Medication Antihypertensive therapy
in acute phases. The AHA/
ASA and EUSI guidelines
(American Heart
Association/American
Stroke Association guidelines and the European
Stroke Initiative guidelines)
have recommended
antihypertensive therapy
to stabilize the mean arterial pressure at 110 mmHg. One paper showed
the efficacy of this
antihypertensive therapy
without worsening
outcome in patients of
hypertensive intracerebral hemorrhage within 3 hours onset.[9] Giving Factor VIIa within 4 hours limits the bleeding
and formation of a hematoma. However, it also increases the risk of thromboembolism.[10] Mannitol is effective in acutely reducing raised
intracranial pressure. Acetaminophen may be needed to avoid hyperthermia , and to relieve headache. [10] Frozen plasma, vitamin K , protamine, or platelet transfusions are given in case of a coagulopathy.[10] Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage.[10] H2 antagonists or proton
pump inhibitors are
commonly given for stress
ulcer prophylaxis, a
condition somehow linked with ICH. [10] Corticosteroids, in concert with antihypertensives, reduces swelling. [11] Surgery Surgery is required if the hematoma is greater than 3 cm (1 in), if there is a
structural vascular lesion or lobar hemorrhage in a young patient.[10] A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.[12] Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.[10] Other treatment Tracheal intubation is indicated in patients with
decreased level of
consciousness or other risk of airway obstruction. [10] IV fluids are given to maintain fluid balance, using normotonic rather than hypotonic fluids. [10] Prognosis The risk of death from an
intraparenchymal bleed in
traumatic brain injury is
especially high when the
injury occurs in the brain stem.[2] Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause
damage to cranial nerve X, the vagus nerve , which plays an important role in blood circulation and breathing.[4] This kind of hemorrhage can
also occur in the cortex or subcortical areas, usually in
the frontal or temporal lobes when due to head injury, and
sometimes in the cerebellum. [4][13] For spontaneous ICH seen on
CT scan, the death rate
(mortality ) is 34–50% by 30 days after the insult, [1] and half of the deaths occur in the first 2 days. [14] The inflammatory response
triggered by stroke has been
viewed as harmful, focusing
on the influx and migration of
blood-borne leukocytes,
neutrophils, and macrophages. New area of interest are the Mast Cells.[15] Epidemiology It accounts for 20% of all cases
of cerebrovascular disease in the US, behind cerebral thrombosis (40%) and cerebral embolism (30%).[16] It is two or more times more
prevalent in black American patients than it is in white.
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