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Hemorrhagic Stroke
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Counselor,
The terms intracerebral hemorrhage (ICH) and
hemorrhagic
stroke are used interchangeably in this discussion and
are
regarded as a separate entity from hemorrhagic
transformation of ischemic stroke. ICH accounts for 10-
15%
of all strokes and is associated with higher mortality
rates
than cerebral infarctions. Patients with hemorrhagic
stroke
present with similar focal neurologic deficits but tend
to be
more ill than patients with ischemic stroke. Patients
with
intracerebral bleeds are more likely to have
headache,
altered mental status, seizures, nausea and vomiting,
and/or
marked hypertension; however, none of these findings
distinguish reliably between hemorrhagic and
ischemic
strokes.
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Pathophysiology:
In ICH, bleeding occurs directly into the brain
parenchyma.
The usual mechanism is thought to be leakage from
small
intracerebral arteries damaged by chronic
hypertension.
Other mechanisms include bleeding diatheses,
iatrogenic
anticoagulation, cerebral amyloidosis, and cocaine
abuse.
ICH has a predilection for certain sites in the brain,
including
the thalamus, putamen, cerebellum, and brain stem. In
addition to the area of the brain injured by the
hemorrhage,
the surrounding brain can be damaged by pressure
produced
by the mass effect of the hematoma. A general
increase in
intracranial pressure may occur.
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Frequency/Mortality/Morbidity:
ICH accounts for 10-15% of all strokes. Recent reports
indicate an incidence exceeding 500,000 new strokes of all
types per year. Stroke is a leading killer and disabler.
Combining all types of stroke, it is the third leading cause of
death and the first leading cause of disability. Morbidity is
more severe and mortality rates are higher for hemorrhagic
stroke than for ischemic stroke. Only 20% of patients regain
functional independence. The 30-day mortality rate for
hemorrhagic stroke is 40-80%. Approximately 50% of all
deaths occur within the first 48 hours.
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History:
Patients' symptoms vary depending on the area of the brain
affected and the extent of the bleeding. Hemorrhagic strokes
are more likely to exhibit symptoms of increased intracranial
pressure than other types of stroke. Headache, often severe
and sudden onset with nausea and/or vomiting occur with
some frequency. Seizures are more common in hemorrhagic
stroke than in ischemic stroke. They occur in up to 28% of
hemorrhagic strokes and generally occur at the onset of the
ICH or within the first 24 hours.
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Physical:
Intracerebral hemorrhage (ICH) may be clinically
indistinguishable from ischemic stroke. Hypertension commonly
is a prominent finding. An altered level of consciousness or
coma is more common with hemorrhagic strokes than with
ischemic strokes. Often, this is due to an increase in
intracranial pressure.
Meningismus may result from blood in the ventricles. Focal
neurologic deficits depends upon the area of brain involved. If
the dominant hemisphere (usually left) is involved, a syndrome
consisting of right hemiparesis, right hemisensory loss, left
gaze preference, right visual field cut, and aphasia may result.
If the nondominant (usually right) hemisphere is involved, a
syndrome of left hemiparesis, left hemisensory loss, right gaze
preference, and left visual field cut may result. Nondominant
hemisphere syndrome also may result in neglect when the
patient has a left-sided hemi-inattention and ignores the left
side.
If the cerebellum is involved, the patient is at high risk of
herniation and brainstem compression. Herniation may cause a
rapid decrease in the level of consciousness, apnea, and death.
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Causes:
Hypertension is the major cause (up to 60% of cases). Other
causes and factors include advanced age (risk factor),
cerebral amyloidosis (affects people who are elderly and
may cause up to 10% of ICHs), coagulopathies (e.g.: due to
underlying systemic disorders), anticoagulant therapy,
thrombolytic therapy for acute myocardial infarction (MI) and
acute ischemic stroke (can cause iatrogenic hemorrhagic
stroke), abuse of cocaine and other sympathomimetic drugs,
arteriovenous malformation, intracranial aneurysm,
vasculitis, intracranial neoplasm, and bleeding due to a brain
tumor.
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Lab and Imaging Studies:
These include: complete blood count, coagulation profile,
electrolytes, serum glucose, blood type and screen. Imaging
studies include: Noncontrast CT of the brain and MRI. MRI,
especially newer techniques such as diffusion-weighted
imaging, has been shown to identify ischemic stroke earlier
and more reliably than CT scanning. MRI is being utilized with
increasing frequency in the evaluation of ischemic stroke.
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Treatment:
Airway, breathing and circulation should always be assessed
first. Heart monitoring should be established and the patient
should have an IV started and oxygen administered. An ECG
should be obtained. Bedside glucose testing should be
performed because hypoglycemia can mimic stroke.
Prophylactic anticonvulsant therapy is often advised. Dilantin
is the drug of choice. Blood pressure should be carefully
monitored. Although BP elevations may risk further
hemorrhage, too rapid or aggressive BP lowering may
compromise cerebral perfusion.
The American Heart Association guidelines recommend
intravenous antihypertensive treatment for patients with mean
arterial pressure (MAP) > 130 mm Hg. MAP should be
maintained above 90 mm Hg to ensure adequate cerebral
perfusion.
Intubation should be performed for patients who demonstrate
potential loss of airway protective mechanisms or signs of
brainstem dysfunction. If intubation is needed, rapid sequence
intubation should be performed with technique and medications
aimed at limiting any increase in intracranial pressure.
Currently, no effective targeted therapy for hemorrhagic
stroke exists. However, some preliminary research indicates
that treatment with hemostatic therapy may be effective. A
recent preliminary study of treatment with recombinant
factor 8 demonstrated reduced mortality and improved
functional outcomes. Further studies are necessary to
determine if this should be accepted as a clinical treatment
option.
A potential treatment of hemorrhagic stroke is surgical
evacuation of the hematoma. The role of surgical treatment
for supratentorial intracranial hemorrhage remains
controversial. Outcomes in published studies are conflicting.
A published meta-analysis of studies suggested some
promise for early surgical intervention. However, a recent
study comparing early surgery versus initial conservative
treatment failed to demonstrate a benefit with surgery.
However, surgical intervention for cerebellar hematoma has
been shown to improve outcome. It can be lifesaving in the
prevention of brainstem compression.
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Complications:
Increased intracranial pressure and herniation are the most
dreaded complications. Worsening cerebral edema is often
implicated in neurologic deterioration in the first 24-48
hours.Expansion of the hematoma is the most common cause
of neurologic deterioration in the first 3 hours. In patients
who are initially alert, 25% will have a decrease in
consciousness within the first 24 hours. Post-stroke seizures
may also develop as a complication.
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Prognosis:
The prognosis varies depending on the severity of stroke and
the location and the size of the hemorrhage. Lower Glasgow
coma scores are associated with poorer prognosis and higher
mortality. A larger volume of blood is associated with a
poorer prognosis. The presence of blood in the ventricles is
associated with a higher mortality rate. Other complicating
medical comorbidities also affect the prognosis.
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Medical/Legal Concerns:
The outcome generally follows the natural progression of the
intracranial hemorrhage. Notwithstanding this, excellent and
timely supportive management can often save the patient.
Failure to act aggressively and a timely manner often results in
an adverse outcome which then might lead to litigation.
Improper management of the patient's blood pressure can also
have a deleterious effect on the patient. Failure to call in a
neurologist and neurosurgeon often leads to a delay in the
proper management of these patients.
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