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Hemorrhagic Stroke

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Hemorrhagic Stroke
Unnithan AKA, Mehta P.

Introduction
Cerebrovascular accident (CVA), otherwise called a stroke, is the third major cause of morbidity and mortality in many developed countries. Stroke
can be either ischemic or hemorrhagic. Ischemic stroke is due to loss of blood supply to an area of the brain. It is a common type of stroke.

Hemorrhagic stroke is due to bleeding into the brain by the rupture of a blood vessel. Hemorrhagic stroke may be further subdivided into
intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH is bleeding into the brain parenchyma, and SAH is bleeding into the
subarachnoid space. Hemorrhagic stroke is associated with severe morbidity and high mortality.[2] Progression of hemorrhagic stroke is associated
with worse outcomes. Early diagnosis and treatment are important in view of the usual rapid expansion of hemorrhage, causing sudden deterioration
of consciousness and neurological dysfunction.

Etiology
Hypertension is the most common cause of hemorrhagic stroke.

Longstanding hypertension produces degeneration of media, breakage of the elastic lamina, and fragmentation of smooth muscles of arteries.
Lipohyalinosis, fibrinoid necrosis of the subendothelium, microaneurysms, and focal dilatations are seen in the arterioles. The
microaneurysms are named as Charcot-Bouchard aneurysms.
The common sites of origin of hypertension-induced intracerebral hemorrhage are the small penetrating arteries that originate from basilar
arteries or the anterior, middle, or posterior cerebral arteries.
Small artery branches of 50 to 700 μm in diameter often have multiple sites of rupture associated with layers of platelet and fibrin
aggregates.
Hypertensive change causes non-lobar intracranial hemorrhage (ICH). Acute hypertension, as seen in eclampsia, also can cause ICH, known
as postpartum ICH.

Cerebral amyloid angiopathy (CAA) is an important cause of primary lobar intracerebral hemorrhage in older adults.

It is characterized by the deposition of the amyloid-β peptide in the capillaries, arterioles, and small- and medium-sized arteries in the
cerebral cortex, leptomeninges, and cerebellum.
This causes ICH in elderly people, commonly associated with variations in the gene encoding apolipoprotein E.
A familial syndrome can occur in young patients, typically associated with mutations in the gene encoding amyloid precursor protein.
The incidence of CAA increases with age to the extent that around 50% of those aged more than 70years have CAA. Recurrent hemorrhages
can occur due to CAA.

Other Important Risk Factors

Cigarette smoking and moderate or heavy alcohol consumption and chronic alcoholism.
Chronic liver disease also increases the chance of ICH due to coagulopathy and thrombocytopenia.
Decreased low-density lipoprotein cholesterol and low triglycerides are also considered to be risk factors.
Dual antiplatelet therapy has an increased risk of ICH than monotherapy.
Sympathomimetics such as cocaine, heroin, amphetamine, ephedrine, and phenylpropanolamine carry an increased risk of a cerebral
hemorrhage.
Cerebral microbleeds (CMBs) associated with hypertension, diabetes mellitus, and cigarette smoking increase the risk of ICH.
Old age and male sex. The incidence of ICH increases after 55 years of age. The relative risk after 70 years is 7.
The tumors which are more prone to bleed are glioblastoma, lymphoma, metastasis, meningioma, pituitary adenoma, and
hemangioblastoma.

The usual causes of spontaneous subarachnoid hemorrhage (SAH) are ruptured aneurysm of a cerebral artery, arteriovenous malformation, vasculitis,
cerebral artery dissection, dural sinus thrombosis, and pituitary apoplexy. The risk factors are hypertension, oral contraceptive pills, substance abuse,
and pregnancy.

Intracranial hemorrhage of pregnancy (ICHOP-intracerebral or subarachnoid hemorrhage) occurs with eclampsia. It is due to the loss of
cerebrovascular autoregulation.

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Epidemiology
Hemorrhagic stroke contributes to 10% to 20%of strokes annually.[1][2][3] The percentage of hemorrhage in stroke is 8-15% in the United States of
America, the United Kingdom, and Australia and 18% to 24% in Japan and Korea. The incidence is around 12% to 15% of cases per 1,00,000 per
year. The incidence is high in low and middle-income countries and Asians. The incidence is more common in men and increases with age. The global
incidence is increasing, predominantly in African and Asian countries. It has been shown in Japan that control of hypertension reduces the incidence
of ICH. The case fatality rate is 25% to 30% in high-income countries, while it is 30% to 48% in low- to middle-income countries. The ICH fatality
rate depends on the efficacy of critical care.

Pathophysiology
The common sites of the bleed are the basal ganglia (50%), cerebral lobes (10% to 20%), the thalamus (15%), pons and the brain stem (10% to 20%),
and the cerebellum(10%)(fig.1,2,3). The hematoma disrupts the neurons and glia. This results in oligaemia, neuro-transmitter release, mitochondrial
dysfunction, and cellular swelling. Thrombin activates microglia, causes inflammation and edema.[2][3]

The primary injury is due to the compression by the hematoma and an increase in the intracranial pressure(ICP).[4]

Secondary injury is contributed by inflammation, disruption of the blood-brain barrier (BBB), edema, overproduction of free radicals such as reactive
oxygen species (ROS), glutamate-induced excitotoxicity, and release of hemoglobin and iron from the clot.

Usually, the hematoma enlarges in 3 hours to 12 hours. The enlargement of hematoma occurs in 3 hours in one-third of cases. The Perihematomal
edema increases in 24 hours, peaks around 5–6 days, and lasts up to 14 days. There is an area of hypoperfusion around the hematoma. The factors
causing deterioration in ICH are an expansion of hematoma, intraventricular hemorrhage, perihematomal edema, and inflammation.[2] Cerebellar
hematoma produces hydrocephalus by compression of the fourth ventricle in the early stage.

Non-aneurysmal spontaneous subarachnoid hemorrhage may be either perimesencephalic or non-perimesencephalic SAH. In perimesencephalic SAH,
bleeding is mainly in the interpeduncular cistern. Physical exertion such as Valsalva maneuver producing increased intrathoracic pressure, and
elevated intracranial venous pressure, is a predisposing factor for perimesencephalic nonaneurysmal SAH (PM-SAH).[5] There is diffuse blood
distribution in non-perimesencephalic SAH (NPM-SAH).[6]

History and Physical

The common presentations of stroke are headache, aphasia, hemiparesis, and facial palsy.[7] The presentation of hemorrhagic stroke is usually acute
and progressing. Acute onset headache, vomiting, neck stiffness increases in blood pressure, and the rapidly developing neurological signs are the
common clinical manifestations of hemorrhagic stroke.[3] Symptoms can lead to the extent and location of hemorrhage.

Headache is more common in a large hematoma.

Vomiting indicates raised intracranial pressure and is common with cerebellar hematoma.
Coma occurs in the involvement of the reticular activating system of the brainstem.
Seizure, aphasia, and hemianopia are seen in lobar hemorrhage. A prodrome consisting of numbness, tingling, and weakness may also occur
in lobar bleed.
Contralateral sensorimotor deficits are the features in hemorrhage of the basal ganglia and thalamus.
Loss of all sensory modalities is the main feature of thalamic hemorrhage.
Extension of thalamic hematoma into midbrain can cause vertical gaze palsy, ptosis, and unreactive pupil.
Cranial nerve dysfunction with contralateral weakness indicates brainstem hematoma.[3]
Usually, pontine hematoma produces coma and quadriparesis.[8]

Cerebellar hemorrhage produces symptoms of raised ICP, such as lethargy, vomiting, bradycardia. Progressive neurological deterioration indicates the
enlargement of hematoma or an increase in edema.

The clinical features of subarachnoid hemorrhage are severe headache described as a thunderclap, vomiting, syncope, photophobia, nuchal rigidity,
seizures, and decreased level of consciousness.[5][6] Signs of meningismus such as Kernig sign (pain on straightening the knee when the thigh is
flexed to 90 degrees) and Brudzinski sign (involuntary hip flexion on flexing the neck of the patient) may be positive.

Evaluation
Computerized tomography (CT) is usually the initial investigation.[9] The hemorrhage increases in attenuation from 30-60 Hounsfield units (HU) in
the hyperacute phase to 80-100 HU over hours.[10] The attenuation may be decreased in anemia and coagulopathy. Vasogenic edema around the
hematoma may increase up to 2 weeks.

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In the subacute phase, the hematoma may be isodense to brain tissue, and magnetic resonance imaging (MRI) may be necessary. The volume of the
hematoma can be measured by the formula AxBxC/2, where A and B are the largest diameter and the diameter perpendicular to that.[11] C is the
vertical height of the hematoma. Intracerebral hemorrhage with a volume of more than 60 cc is associated with high mortality.[12] The other poor
prognostic factors are hematoma expansion, intraventricular hemorrhage, infra-tentorial location, and contrast extravasation on CT scan (spot sign).
[3] The paramagnetic properties of deoxyhemoglobin allow early detection of hemorrhage in MRI.[13] Gradient echo (GRE) imaging is as good as CT
in the detection of acute bleed. MRI can distinguish between the hemorrhagic transformation of infarct and primary hemorrhage. MRI can detect
underlying causes of secondary hemorrhages, such as vascular malformations, including cavernomas, tumors, and cerebral vein thrombosis.

Extravasation of contrast in CT angiogram (CTA) indicates ongoing bleeding and is associated with fatality.[14] Multidetector CT
angiography(MDCTA) is helpful to rule out the causes of secondary hemorrhagic stroke such as arteriovenous malformation (AVM), ruptured
aneurysm, dural venous sinus (or cerebral vein) thrombosis (DVST/CVT), vasculitis, and Moya-Moya disease.[15] (fig.4).

Certain imaging characteristics help in the differentiation of the underlying disease.[16]

Multiple hemorrhages of different ages in parieto-occipital lobes are seen in cerebral amyloid antipathy.
Hemorrhage in an arterial territory indicates hemorrhagic infarction.
Multiple stages of bleed in the same hematoma with a fluid level is seen in anticoagulation induced hemorrhage.
A combination of small ischemic and hemorrhagic lesions indicates vasculitis.
Hemorrhage in the presence of occlusion of arteries is the feature of Moyamoya disease.

Four- vessel digital subtraction angiography (DSA) is necessary in the case of SAH. If the DSA is negative for aneurysm, a repeat study is needed to
confirm. Repeat angiography is advisable at 1-week and 6-weeks intervals.

Blood investigations such a bleeding time, clotting time, platelet count, peripheral smear, prothrombin time (PT) and activated partial thromboplastin
time(aPTT) will detect any abnormality of bleeding or coagulation and any hematological disorder which can cause hemorrhage. Liver function tests
and renal function tests are also needed to exclude any hepatic or renal dysfunction as a cause. The investigations to rule out vasculitis are the
quantitative evaluation of immunoglobulins, thyroid antibodies, rheumatoid factor, antinuclear antibodies (ANA), anti-double-stranded DNA (ds-
DNA antibodies), Histon antibodies, complement, anti-Ro [SS-A] and anti-La [SS-B-] antibodies, cytoplasmic staining and perinuclear staining
antineutrophil cytoplasmic antibodies (c- and pANCA), and anti-endothelial antibodies.[17]

Treatment / Management
There are many different opinions in the treatment of hemorrhagic stroke. There are many trials on the optimal management of hemorrhagic stroke -
Antihypertensive Treatment in Acute Cerebral Hemorrhage(ATACH), Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (
INTERACT ), Factor VIIa for Acute Hemorrhagic Stroke Treatment (FAST ) and Surgical Trial in Intracerebral Haemorrhage (STICH).[18] The role
of surgery in hemorrhagic stroke is a controversial topic.

Blood pressure (BP) Management

BP should be reduced gradually to 150/90mmHg, using beta-blockers (labetalol, esmolol), ACE inhibitor (enalapril), calcium channel blocker
(nicardipine) or hydralazine[2]. BP should be checked every 10-15 minutes. ATACH study observed a nonsignificant relationship between the
magnitude of systolic blood pressure (SBP) reduction and hematoma expansion and 3-month outcome.[19] But the INTERACT study showed that
early intensive BP-lowering treatment attenuated hematoma growth over 72 hours.[20] It has been found that high SBP is associated with neurological
deterioration and death.[21] The recommendation of the American stroke association (ASA) is that for patients presenting with SBP between 150 and
220 mmHg, the acute lowering of SBP to 140 mmHg is safe and can improve functional outcome. For patients presenting with SBP >220 mmHg, an
aggressive reduction of BP with a continuous intravenous infusion is needed.

Management of Raised Intracranial Pressure (ICP)

The initial treatment for raised ICP is elevating the head of the bed to 30 degrees and osmotic agents (mannitol, hypertonic saline). 20 % mannitol is
given at a dose of 1.0 to 1.5 g/kg.[2] Hyperventilation after intubation and sedation, to a pCO of 28 to 32 mmHg will be necessary if ICP increases
further. ASA recommends monitoring of ICP with a parenchymal or ventricular catheter for all patients with Glasgow coma scale (GCS) <8 or those
with evidence of transtentorial herniation or hydrocephalus.[21] The ventricular catheter has the advantage of drainage of cerebrospinal fluid (CSF) in
the case of hydrocephalus. The aim is to keep cerebral perfusion pressure (CPP) between 50 to 70mmHg.

Hemostatic Therapy

Hemostatic therapy is given to reduce the progression of hematoma.[2] This is especially important to reverse the coagulopathy in patients taking
anticoagulants. Vitamin K, prothrombin complex concentrates (PCCs), recombinant activated factor VII (rFVIIa), fresh frozen plasma (FFP), etc. are
used.[2][21] ASA recommends that patients with thrombocytopenia should receive platelet concentrate.[21] Patients with elevated prothrombin time

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INR should receive intravenous vitamin K and FFP or PCCs. FFP has the risk of allergic transfusion reactions. PCCs are plasma-derived factor
concentrates containing factors II, VII, IX, and X. PCCs can be reconstituted and administered rapidly. The FAST trial showed that rFVIIa reduced the
growth of the hematoma but did not improve survival or functional outcome.[22] rFVIIa is not recommended in unselected patients since it does not
replace all clotting factors.[21]

Antiepileptic Therapy

Around 3 to 17% of patients will have a seizure in the first two weeks, and 30% of patients will show electrical seizure activity on EEG monitoring.
[21] Those with clinical seizures or electrographic seizures should be treated with antiepileptic drugs. Lobar hematoma and the enlargement of
hematoma produce seizures, which are associated with neurological worsening. Subclinical seizures and non-convulsive status epileptics also can
occur. Continuous EEG monitoring is indicated in patients with a decreased level of consciousness. Otherwise, prophylactic anticonvulsant
medication is not recommended, according to ASA guidelines.

Surgery

The different types of surgical treatment for hemorrhagic stroke are craniotomy, decompressive craniectomy, stereotactic aspiration, endoscopic
aspiration, and catheter aspiration.[2] STICH trial showed that there is no overall benefit from early surgery for supratentorial intracerebral
hemorrhage when compared with initial conservative treatment.[23] Those who have lobar hemorrhages within 1cm of the surface of the brain and
milder clinical deficits (GCS>9) may benefit from early surgery. Emergency surgical evacuation is indicated in cerebellar hemorrhage with
hydrocephalus or brainstem compression.[21] Patients with cerebellar hemorrhages of >3 cm in diameter will have better outcomes with surgery.
Cerebellar hematoma is evacuated by suboccipital craniectomy. Evacuation of brainstem hemorrhages can be harmful and is not recommended. A
minimally invasive procedure such as stereotactic aspiration is also on trial. Hattori et al. showed in a randomized study that stereotactic evacuation is
of value in patients with spontaneous putaminal hemorrhage, whose eyes will open in response to strong stimuli.[24]

Minimally invasive surgery plus recombinant tissue plasminogen activator(rt-PA) for Intracerebral Hemorrhage Evacuation (MISTIE) was a
randomized, prospective trial that tested image-guided catheter-based removal of the blood clot.[25] It showed a reduction in perihematomal edema
with clot evacuation.

The Clot Lysis: Evaluating Accelerated Resolution of IntraVentricularr Hemorrhage (CLEAR IVH) trial showed that low-dose rt-PA can be safely
administered to stable intraventricular clots and can increase lysis rates.[26] Decompressive craniectomy and hematoma evacuation are now being
done more frequently for hemorrhagic stroke. Moussa and Khedr showed the improvement in outcome gained by adding decompressive craniectomy
with expansive duraplasty to the evacuation of large hypertensive hemispheric ICH in a randomized controlled trial.[27] Decompressive
hemicraniectomy with hematoma evacuation is performed in patients with GCS scores of 8 or less and large hematomas with a volume greater than 60
ml (fig.5).[28] It reduces mortality and may improve the functional outcome.

Cerebroprotection

The secondary injury of hemorrhagic stroke comprises of inflammation, oxidative stress, and toxicity of erythrocyte lysates and thrombin. So,
strategies to reduce these are being tried. Pioglitazone, misoprostol, and celecoxib are tried to reduce inflammatory damage. Edaravone, flavanoid, and
nicotinamide mononucleotide can reduce oxidative stress. The iron chelator deferoxamine is also in the experimental phase. The safety and
neuroprotective efficacy of the cell membrane component citicoline (cytidine-5-diphosphocholine) has been shown in some studies.[29] Rosuvastatin,
a competitive inhibitor of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase, was associated with a better outcome in a trial. The calcium
channel blocker nimodipine improves outcome in SAH by a neuroprotective effect.[30]

General Care

Good medical care, nursing care, and rehabilitation are also of paramount importance.[21] Dysphagia, aspiration, cardiac arrhythmias, stress-induced
cardiomyopathy, cardiac failure, acute kidney injury, gastrointestinal bleeding, and urinary tract infection, etc. are common problems. Percutaneous
endoscopic gastrostomy (PEG) may be needed to prevent aspiration. Screening for myocardial ischemia with electrocardiogram and cardiac enzyme
testing is recommended in hemorrhagic stroke. Intermittent pneumatic compression and elastic stockings reduce the occurrence of deep vein
thrombosis. Multidisciplinary rehabilitation is advised to reduce disability.

Di erential Diagnosis
The differential diagnoses of hemorrhagic stroke are acute hypertensive crisis, pituitary apoplexy, cerebral venous thrombosis, dural sinus thrombosis,
cervical artery dissection, reversible cerebral vasoconstrictive syndrome (RCVS), hemorrhagic neoplasms, arterio-venous malformations, meningitis,
acute subdural hematoma, and hemorrhagic infarct. Imaging studies, such as CT and MRI, can rule out these entities.[31]

Prognosis
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The poor prognostic factors are coma, large hematoma with volume greater than 30cc, intraventricular hemorrhage, posterior fossa hemorrhage, old
age greater than 80 years, hyperglycemia, and chronic kidney disease[3]. Early deterioration and death are the major problems with ICH. Coma, at the
time of the presentation, indicates a grave prognosis. ASA recommends that the monitoring and management of patients with ICH should be in a
dedicated stroke unit. At six months, only 20 percent of patients become independent. The survivors may enter into a state of persistent vegetative
state or locked-in syndrome in case of extensive hemispherical damage or brainstem involvement, respectively.

ICH score introduced by Hemphill et al. predicts mortality.[32] The oints are given as 2 points for GCS 3-4, 1 point for GCS 5-12, 0 points for
GCS13-15, 1 point for>80 years, 0 points for <80 years, 1 point for infratentorial location, 0 points for supratentorial location, 1 point for ICH volume
>30cc, 0 points for volume <30cc. 1 point for intraventricular hemorrhage and 0 points for the absence of intraventricular hemorrhage. The 30-day
mortality of each score is as: 0% for score 0, 13% for score 1, 26% for score 2, 72% for score 3, 97% for score 4, and 100% for scores 5 and 6.

Complications
Complications of ICH include cerebral edema, increased intracranial pressure, hydrocephalus, seizures, venous thrombotic events, hyperglycemia,
increased blood pressure, fever, and infections.[33] Patients with ICH, especially women, have a risk of thromboembolic disease.[21] Almost one-
third of patients with ICH develop pulmonary complications such as pneumonia, aspiration, and pulmonary edema, respiratory failure, and respiratory
distress. About 4% of patients with ICH suffer a cardiac complication such as myocardial infarction, atrial fibrillation, ventricular fibrillation,
ventricular tachycardia, stress-induced cardiomyopathy, and acute heart failure.[34]

Vasospasm, ischemia, rebleeding, seizure, hyponatremia, and hydrocephalus are the complications of SAH. Neurogenic pulmonary edema, an increase
in interstitial and alveolar fluid, commonly occur in subarachnoid hemorrhage.

Deterrence and Patient Education

There is a chance of recurrence of ICH. Hypertension and old age are risk factors. BP should be controlled. Lifestyle modifications should be advised
viz. avoidance of alcohol, tobacco, and illicit drugs. Continued multidisciplinary rehabilitation should be done.

Enhancing Healthcare Team Outcomes

Patients with hemorrhagic stroke should be managed in a dedicated stroke unit with emergency and critical care, neurology and neurosurgery, and
neuroradiology for the best outcome. The intensivists, physicians, and critical care nurses should be well versed in emergency neurological life
support (ENLS). This is especially needed in low- and middle-income countries. The surgical methods should be done and assessed in a standardized
manner. More trials are needed to confirm the role and usefulness of surgical interventions. Cognitive rehabilitation therapy (CRT) also should be
given to the survivors.

Questions
To access free multiple choice questions on this topic, click here.

Figure
Fig.1. CT scan of lobar hemorrhage. Owned by Dr. Ajaya Kumar A.

Figure
Fig.2. CT scan of pontine hemorrhage. Owned by Dr. Ajaya Kumar A.

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Figure
Fig.3. CT scan of cerebellar hemorrhage. Owned by Dr. Ajaya Kumar A.

Figure
Fig.4. CT Angiogram of a patient with ICH. Owned by Dr. Ajaya Kumar A.

Figure
Fig.5. Intraoperative picture of decompressive craniectomy and evacuation of basal ganglia hematoma through corticectomy. Owned by
Dr. Ajaya Kumar A.

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Publication Details

Author Information

Authors

Ajaya Kumar A. Unnithan1; Parth Mehta2.

https://www.ncbi.nlm.nih.gov/books/NBK559173/ 7/8
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8/6/2020 Hemorrhagic Stroke - StatPearls - NCBI Bookshelf

A liations
1
Muthoot Hospital, Kozhencherry
2
University of Illinois, College of Medicine Peoria

Publication History

Last Update: July 6, 2020.

Copyright
Copyright © 2020, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use,
duplication, adaptation, distribution, and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, a link is provided
to the Creative Commons license, and any changes made are indicated.

Publisher

StatPearls Publishing, Treasure Island (FL)

NLM Citation

Unnithan AKA, Mehta P. Hemorrhagic Stroke. [Updated 2020 Jul 6]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-.

https://www.ncbi.nlm.nih.gov/books/NBK559173/ 8/8