Spontaneous intracerebral hemorrhage

second most common cause of stroke after ischemic stroke in frequency / hypertension,
amyloid angiopathy, ruptured saccular aneurysm, and vascular malformation
Etiologies Hypertension Cerebral amyloid angiopathy Vascular
malformationsHemorrhagic infarction (including venous sinus thrombosis) Septic
embolism, mycotic aneurysm Brain tumor Bleeding disorders, liver disease,
anticoagulants, thrombolytic therapyCentral nervous system (CNS) infection (eg,
herpes simplex encephalitis)MoyamoyaVasculitisDrugs (cocaine, amphetamines)].
Phenylpropanolamine in appetite suppressants, and possibly cold remedies

Hypertensive vasculopathy is the most common etiology of spontaneous ICH. Cerebral

amyloid angiopathy is the most common cause of nontraumatic lobar ICH in the elderly,
while vascular malformations are the most common cause of ICH in children
Hypertensive hemorrhages occur in the territory of penetrator arteries that branch off
major intracerebral arteries, often at 90 angles with the parent vessel. These small
penetrating arteries may be particularly susceptible to the effects of hypertension .The
blood vessels that give rise to hypertensive hemorrhage generally are the same as those
affected by hypertensive occlusive disease and diabetic vasculopathy, which cause
lacunar strokes. These vessels supply the pons and midbrain (off the basilar artery),
thalamus (off the P1 and P2 segments of the posterior cerebral arteries), and putamen
and caudate (lenticulostriate off the M1 segment of the middle cerebral artery

pseudoaneurysm formation with subclinical leaks of blood is relatively common in

patients with spontaneous ICH. These microbleeds may be a marker of bleeding-prone
microangiopathy due to hyalinosis (chronic hypertension) or amyloid deposition.
Associations between the incidence of microbleeds and lacunar stroke and white matter
hyperintensities have also been reported

Mechanisms of brain injury primary direct mechanical injury to brain parenchyma

by the expanding clot and cytotoxic perilesional edema. Both clot volume and
perilesional edema contribute to the mass effect and increased intracranial pressure
(ICP), which in turn can cause reduced cerebral perfusion and ischemic injury, and in
very large ICH, cerebral herniation .Secondary brain injury after the initial hemorrhage
is an important contributing process. Perihematomal edema is present on CT or MRI in
at least half of patients when the patient is first imaged and progresses, reaching
maximum volume 7 to 12 days after onset; the most rapid expansion occurs in the first
48 hours. The perihematomal region exhibits delayed perfusion and vasogenic and
cytotoxic edema Decreased blood flow to the area surrounding the clot causes local
neuronal ischemia, which leads to further cytotoxic edema and the toxic release of
excitatory amino acids and inflammatory mediators . The edema and ischemia persist
after removal of the hematoma, emphasizing the major contribution of secondary
ischemic injury in ICH and explaining in part why surgical evacuation of the hematoma
often produces disappointing results. Disruption in cerebral autoregulation may
contribute to perihematomal ischemic injury .Increased intracranial pressure and
resulting reduction in cerebral perfusion pressure may play a role; this phenomenon may
be exacerbated by blood pressure lowering. Also , the hemorrhage enlarges in the first
six hours after presentation in a subset of patients ,as the clot expands, surrounding
vessels are stretched, causing new sites of vessel rupture. Risk factors for hematoma
expansion include antithrombotic therapy, sustained elevated blood pressure, large
hematoma size, and evidence of contrast extravasation on initial CT imaging .
Elevated or maximal systolic blood pressure (SBP) after admission may be a more
important measure . A significant hematoma expansion was found associated with
treatment target SBPs of 160 mmHg or greater compared with target SBPs of 150 or
140 mmHg. Contrast extravasation within the hematoma on CT angiography (CTA
spot sign) has been linked to hematoma expansion and poor outcomes in several
studies .A "spot sign" score which grades the number of spot signs, their maximum
dimension has been found to be the strongest predictor of hematoma expansion ,
accumulation of contrast extravasation within the hematoma on postcontrast CT also
predicts subsequent hematoma expansion .

Expansion of ICH into the intraventricular space occurs in 40 to 60 %. Anticoagulant

and antiplatelet therapy are a risk factor

Risk factors Hypertension is the most important risk factor .Other include Older
ageHigh alcohol intakeBlack ethnicityLower cholesterol and lower LDL
cholesterolLower triglycerides Anticoagulation with warfarin increases the risk of ICH
two- to fivefold, depending upon the intensity of anticoagulation. , (INR) >3 is a risk
factor for larger initial hemorrhage volume . aspirin plus clopidogrel increases the risk
of ICH twofold compared with aspirin

CLINICAL PRESENTATION . The neurologic symptoms usually increase gradually

over minutes or a few hours , do not begin abruptly and are not maximal at onset.
Headache, vomiting, and a decreased level of consciousness develop if the hematoma
becomes sufficiently large. Headache and vomiting occur in 50% cases, headache is
most common with cerebellar and lobar hemorrhages. These symptoms are absent with
small hemorrhages that present as gradually progressing stroke.

Seizures in the first days after ICH occur in 4 to 29 %, more common in lobar
hemorrhages (affecting cortical tissue) , often nonconvulsive , may casue midline brain
shift and neurologic deterioration.

Stupor or coma in ICH is an ominous sign except with thalamic hemorrhage, in whom
involvement of the reticular activating system is the cause of stupor rather than diffuse
brain injury; these patients may recover after blood is reabsorbed.

Electrocardiogram changes including a prolonged QT interval, depressed ST segment,

flat or inverted T waves, U waves, and tall peaked T waves refelcting ischemia in the
subendocardium of the left ventricle, likely due to a centrally mediated release of
catecholamines induced by hypoperfusion of the posterior hypothalamus. Ventricular
arrhythmias may occur with brainstem compression

Neurologic signs Putamenal hemorrhage 35 % cases ,hemiplegia, hemisensory loss,

homonymous hemianopsia, gaze palsy, stupor,

Cerebellar hemorrhage 16% usually originate in the dentate nucleus, extend into the
hemisphere and fourth ventricle, and possibly into the pontine tegmentum. Inability to
walk due to imbalance, vomiting, headache (referred to the neck or shoulder, usually
occipital), neck stiffness, gaze palsy, and facial weakness. There is notably no
hemiparesis. Stupor due to brainstem compression Cerebellar hemorrhage is a crucial
diagnosis as frequently deteriorate and require surgery.

Thalamic hemorrhage may extend in a transverse direction to the posterior limb of

the internal capsule, downward to put pressure on the tectum of the midbrain, or may
rupture into the third ventricle. Symptoms include hemiparesis, hemisensory loss, and
occasionally transient homonymous hemianopsia. There may also be an upgaze palsy
with miotic pupils that are unreactive, peering at the tip of the nose, skewed, or "wrong
way eyes" toward the weak side (in contrast to hemispheric cortical injury in which the
eyes are deviated away from the hemiparesis). Aphasia may occur if the bleed affects
the dominant hemisphere or neglect in the nondominant hemisphere.

Lobar hemorrhage neurologic signs depending upon location. most often affect the
parietal and occipital lobes, higher incidence of seizures. Occipital hemorrhages
frequently present with a very dense contralateral homonymous hemianopsia.
Hemorrhages in the frontal region will bring about a contralateral plegia or paresis of
the leg with relative sparing of the arm.

Pontine hemorrhage medial hematoma that extends into the base of the pons. These
often lead to deep coma over the first few minutes following the hemorrhage, probably
due to disruption of the reticular activating system. The motor examination is marked by
total paralysis. The pupils are pinpoint and react to a strong light source. Horizontal eye
movements are absent, and there may be ocular bobbing, facial palsy, deafness, and
dysarthria when the patient is awake.

Noncontrast cranial : define the size and location , extension into the ventricular
system, the presence of surrounding edema, and herniation . Primary ICH needs to be
distinguished from hemorrhagic transformation of a cerebral infarction. A patchy
appearance of the hyperdensity within a larger area of low attenuation is an important
feature, as is a wedge-shaped abnormality that extends to the cortex. A delay from
stroke onset to CT examination can be problematic becasue when an ICH clot retracts
and surrounding edema develops, the appearance of a primary ICH can resemble that of
a hemorrhagic cerebral infarction.. An estimate of ICH volume is useful for severity
and early assessments of prognosis. ABC/2 gives the ICH volume in cubic centimeters.

Contrast-enhanced CT and/or CT angiography (CTA) may reveal a focus of contrast

extravasation (spot sign) suggesting risk for hematoma expansion

Brain MRI hyperacute parenchymal hemorrhage can be accurately detected using

MRI ,also useful in subacute or chronic hematoma and microbleeds .The location of
microbleeds is suggestive of the underlying pathology.Microbleeds in deep gray and
infratentorial brain regions such as the pons, thalamus, and basal ganglia, are
characteristic of hypertensive bleeding prone microangiopathy.Microbleeds in the
cortical-subcortical junction (gray-white junction) are characteristic of cerebral amyloid
angiopathy . A contrast enhanced magnetic resonance imaging (MRI) study is useful to
detect underlying causative lesions such as a vascular malformation, tumor, and cerebral
amyloid angiopathy and should be performed when these are suspected or the cause of
ICH otherwise remains obscure.
No further diagnostic tests are necessary in the severely hypertensive patient with a
well-circumscribed and homogeneous hematoma that is located in a typical location for
hypertensive ICH (eg, putamen/internal capsule, caudate nucleus, thalamus, pons, or
cerebellum) or recent trauma and lesions in the location and with the appearance of
contusion and traumatic hemorrhages (eg, anterior and/or orbital frontal lobes and
temporal lobes at the surface).

Evaluation for a bleeding disorder should be performed in every patient with an ICH,
Anticogulation related bleeds are most often lobar or cerebellar.,develp gradually and
may become progressively larger over hours or even a few days.

Amyloid angiopathy, bleeding into a tumor, and vascular malformations are likely
etiologies of hemorrhages that are lobar or atypical in appearance. Hemorrhages
related to amyloid angiopathy are usually lobar, occasionally cerebellar. predominantly
involve the posterior portions of the brain, including the parietal and occipital lobes.
usually multiple; pt over the age of 65. Other bleeding lesions should be excluded in
patients under the age of 60 if the blood pressure is not sufficiently elevated to make a
firm diagnosis of hypertensive lobar hemorrhage. A repeat MRI after the blood has been
reabsorbed (four to eight weeks) may show residual vascular malformations or tumor.

contrast CT angiography (CTA) or magnetic resonance angiography (MRA) are useful

screening tests for vascular malformations and aneurysms ICH after cocaine use (but
not amphetamines) have a relatively high incidence of underlying aneurysms and
vascular malformations. They require CTA, MRA, and/or angiography).

Spontaneous intracerebral hemorrhage: Treatment and prognosis

Admisson intensive care unit with ideally neurosurgical care available / Early DNR
orders or limitations to care are not always inappropriate after ICH; consider careful
consideration of aggressive, full care during the first 24 hours after ICH onset and
postponement of new DNR orders during that time /Sources of fever should be treated,
goal is normothermia /avoid hyperglycemia , target serum glucose level between 140 to
180 mg/dL (>7.8 to 10 mmol/L) /Intermittent pneumatic compression/Normal saline for
maintenance and replacement fluids; hypotonic fluids are contraindicated
/Hypervolemia should be avoided as it may worsen cerebral edema /Dysphagia is
common /swallowing function evaluation/stop anticoagulant and antiplatelet drugs and
reversed, vitamin K, unactivated prothrombin complex concentrate ,FFP . Protamine
sulfate if heparin-associated ICH

Blood pressure . An increased MAP may be necessary to maintain cerebral perfusion in

some patients, and lowering the arterial pressure below 130 mmHg) may cause ischemia
and worsen neurologic injury For patients with SBP >200 mmHg or MAP >150
mmHg, aggressive reduction with continuous intravenous infusion of medication and
frequent (every five minutes) monitoring. For patients with SBP >180 mmHg or MAP
>130 mmHg and evidence or suspicion of elevated ICP, consider monitoring ICP and
reducing blood pressure to keep CPP in the range of 61 to 80 mmHg For patients with
SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP,
modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood
pressure of 160/90 mmHg) and reexamine every 15 minutes. In SBP of 150 to 200 mm
Hg, acute lowering of SBP to 140 mm Hg is probably safe Labetalol, nicardipine,
esmolol, enalapril, hydralazine, nitroprusside, and nitroglycerin are useful iv meds

If a seizure occurs, appropriate treatment should be administered to prevent recurrent

seizures . Iv fosphenytoin or phenytoin are safe .

Intracranial pressure Elevate the head of the bed to 30 degrees, .Analgesia and
sedation propofol, etomidate, or midazolam. morphine or alfentanil. Mild
hypernatremia should be tolerated. Glucocorticoids should NOT be used to lower the
ICP - Invasive monitoring and treatment of ICP should be considered for patients with
GCS <8, those with clinical evidence of transtentorial herniation, or those with
significant IVH or hydrocephalus - goal of maintaining a cerebral perfusion pressure
(CPP) of 50 to 70 mmHg. Intravenous mannitol is the treatment of choice as an initial
bolus of 1 g/kg, followed by infusions of 0.25 to 0.5 g/kg every six hours. to achieve
plasma hyperosmolality (300 to 310 mosmol/kg) while maintaining an adequate plasma
volume; major side effects include hypovolemia and a hyperosmotic state Barbiturate
coma if mannitol fails .Continuous electroencephalogram monitoring is suggested
during high-dose barbiturate treatment, with the dose titrated to a burst-suppression
pattern of electrical activity Hyperventilation to a PaCO2 of 25 to 30 mmHg causes
dramatic and rapid lowering of ICP but only lasts for minutes to a few hours.
Neuromuscular blockade is sometimes employed Cerebrospinal fluid drainage by
intraventricular catheter placement (ventriculostomy) is an effective means of lowering
ICP . Ventriculostomy also allows direct monitoring of ICP. Ventriculostomy is often
used in the setting of obstructive hydrocephalus, which is a common complication of
thalamic hemorrhage with third ventricle compression, and of cerebellar hemorrhage
with fourth ventricle compression. Ventriculostomy is also frequently used in the setting
of intraventricular hemorrhage with hydrocephalus.

Surgery Cerebellar hemorrhage Surgical removal if cerebellar hemorrhages

greater than 3 cm in diameter who are deteriorating, or who have brainstem
compression and/or hydrocephalus due to ventricular obstruction. External drainage
alone, without posterior fossa decompression, may create the theoretical opportunity for
upward herniation of the cerebellar mass and is not recommended.

Supratentorial hemorrhage Surgical hematoma evacuation is controversial; some

patients may benefit .Consider if life-threatening mass effect from supratentorial ICH,
individualizing treatment decisions based on assessments of prognosis with and without
surgical therapy. Current guidelines suggest consideration of standard craniotomy only
for those who have lobar clots >30 mL within 1 cm of the surface [1,3]. No other patient
group is recommended for surgery, and no surgical method other than standard
craniotomy is supported. The routine evacuation of supratentorial ICH in the first 96
hours is not recommended. Open craniotomy is the most widely studied surgical
techniques in patients with supratentorial ICH [1]. Other methods include endoscopic
hemorrhage aspiration, use of fibrinolytic therapy to dissolve the clot followed by
aspiration, and CT-guided stereotactic aspiration.

A survival benefit for surgery was suggested for subgroups of patients, including those
with poorer prognosis on presentation, those who deteriorated after presentation, and
those with superficial ICH and no intraventricular extension .Because of the
questionable efficacy of surgery, it should only be considered as a life saving procedure
to treat refractory increases in ICP;

Surgery should not be considered for patients who are either fully alert or deeply
comatose. Patients with intermediate levels of arousal (obtundation-stupor) are more
appropriate candidates. Features that support performing surgery include a recent onset
of hemorrhage, ongoing clinical deterioration, involvement of the nondominant
hemisphere, and location of the hematoma near the cortical surface. Features in favor
of less aggressive therapy include serious concomitant medical problems, advanced age,
stable clinical condition, remote onset of hemorrhage, involvement of the dominant
hemisphere, and inaccessibility of the hemorrhage

Intraventricular hemorrhage risk for hydrocephalus, especially if the third and fourth
ventricles are involved. Such patients should be closely monitored. When neurologic
deterioration occurs, an emergent CT scan should be done to exclude the development
of hydrocephalus. Neurologic deterioration in the setting of ventricular enlargement
may be candidates for ventriculostomy and external ventricular drainage.

Early mobilization and rehabilitation -use of of aspirin after the acute phase of ICH
provided that blood pressure is well controlled and that the indication for antiplatelet
treatment is sufficiently strong .In the setting of cerebral amyloid angiopathy, aspirin
use may be associated with a greater risk of recurrent ICH .Do not recommend aspirin
or antiplatelets for those patients with only an "average" risk of recurrent ischemic
stroke. Some experts consider hypertension, diabetes, hypercholesterolemia, and the
absence of heart disease to be markers of average risk. Atrial fibrillation,
cardiomyopathy, large vessel extracranial and intracranial stenoses, and malignancy can
be considered as markers for those with "above average" risk who may benefit . Do not
resume aspirin or antiplatelet therapy for primary prevention of cardiovascular disease.
Antiplatelets should be discontinued for at least 7 to 14 d at low dose 60-100 mg

Resumption of anticoagulation oral anticoagulants may be resumed three to four

weeks after onset of the hemorrhage - INRs in the lower end of the therapeutic range

PROGNOSIS

The 30-day mortality from ICH ranges from 35 to 52 %, 50 % of them occur within the
first two days - 12 and 39 percent of patients achieve independent function

The prognosis after ICH depends upon the location of hemorrhage (supra versus
infratentorial location), size of the hematoma, level of consciousness, patient age, and
overall medical health and condition ,oral anticoagulation therapy, and possibly
antiplatelet therapy, appears to be associated with worse outcomes after ICH , vascular
malformations is associated with lower mortality than other causes of ICH [96,97].

Long-term survival after primary ICH also appears to be decreased ,major causes of
mortality appear to be stroke and ischemic heart disease

The ICH volume on initial head CT scan and level of consciousness on admission may
be particularly important prognostic indicators An ICH volume of 60 cm3 or greater
on initial CT and a Glasgow coma scale score (table 1) of eight or less predicted a 30-
day mortality of 91 percent. An ICH volume less than 30 cm3 and a Glasgow coma
scale score of nine or more predicted a 30-day mortality of 19 percent.

Hematoma growth, particularly within the first 24 hours, is also an independent

predictor of mortality and poor outcome .For each 10 % increase in hematoma volume,
patients were 5 % more likely to die and 16 % more likely to increase the disability
Intraventricular and subarachnoid extension of ICH may be present on initial
evaluation or occur subsequently. Early neurologic deterioration within 48 hours.
Factors measured at 48 hours that were associated with early neurologic deterioration
included ICH growth on repeat head CT, intraventricular bleeding, and high systolic
blood pressure..Pt with with preceding use of anticoagulants or antiplatelet agents
appear to have larger initial hematoma volumes or greater hemorrhage enlargement
leading to worse outcomes Oral anticoagulants mortality rate of 52 to 73 % after
ICH . This increased risk may be mitigated, but not eliminated by rapid reversal of
anticoagulation

ICH score A simple six-point clinical grading scale called the ICH score has been
devised to predict mortality after ICH .The ICH score is determined by adding the score
from each component as follows: Glasgow Coma Scale (GCS) score 3 to 4 (= 2
points); GCS 5 to 12 (= 1 point) and GCS 13 to 15 (= 0 points) ICH volume 30 cm3
(= 1 point), ICH volume <30 cm3 (= 0 points) Intraventricular extension of
hemorrhage present (= 1 point); absent (= 0 points) Infratentorial origin yes (= 1
point); no (= 0 points) Age 80 (= 1 point); <80 (= 0 points)

Thirty-day mortality rates for ICH scores of 1, 2, 3, 4, and 5 were 13, 26, 72, 97, and
100 percent, respectively.

Recurrence ICH , 5%, most common within two years of the first hemorrhage
.Uncontrolled hypertension appears to be the most important risk factor .Others are
Lobar location of initial ICH Olmder ageMale genderOngoing
anticoagulationApolipoprotein E epsilon 2 or epsilon 4 allelesGreater number of
icrobleeds on MRIIschemic stroke history