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TEXT BOOK READING

“HEMORRHAGIC STROKE”

Disusun oleh :
Elvani Kostavina Jambormias
Z1C021013
Pembimbing:
dr. Untung Gunarto, Sp.S
 

DEPARTEMEN ILMU PENYAKIT SARAF


FAKULTAS KEDOKTERAN
UNIVERSITAS JENDERAL SOEDIRMAN
RSUD PROF. DR. MARGONO SOEKARJO
PURWOKERTO 
2022
Abstract

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. 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

The etiologies of stroke are varied. The risk of hemorrhagic stroke is increased with the
following factors :

Cerebral amyloid angiopathy (CAA) >


Hypertension > the most common
is an important cause of primary lobar
cause of hemorrhagic stroke
intracerebral hemorrhagic in older
adults
Etiology

Other important Risk Factors


• Cigarette smoking and moderate or heavy alcohol consumption and chronic alcoholism.
• Decreased low-density lipoprotein cholesterol and low triglycerides are also considered to be risk
factors.
• Chronic liver disease also increases the chance of ICH due to coagulopathy and thrombocytopenia.
• Sympathomimetics such as cocaine, heroin, amphetamine, ephedrine, and
phenylpropanolamine carry an increased risk of a cerebral hemorrhage.
• Old age and male sex. The incidence of ICH increases after 55 years of age.

The usual causes of spontaneous subarachnoid hemorrhage (SAH) are ruptured aneurysm,
arteriovenous malformation, vasculitis, cerebral artery dissection, dural sinus thrombosis, and
pituitary apoplexy. 
Images of Hemorrhagic Stroke
Epidemiology

Hemorrhagic stroke contributes to 10% to 20%of strokes annually

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 and the incidence is more
common in men and increases with age
Pathophysiology

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

Secondary injury is contributed by


inflammation, disruption of the blood-brain The Perihematomal edema increases in 24 hours,
The primary injury is due to the compression peaks around 5–6 days, and lasts up to 14 days.
barrier (BBB), edema, overproduction of free
by the hematoma and an increase in the Cerebellar hematoma produces hydrocephalus by
radicals such as reactive oxygen species
intracranial pressure(ICP) compression of the fourth ventricle in the early
(ROS), glutamate-induced excitotoxicity, and
release of hemoglobin and iron from the clot stage.

Physical exertion such as the Valsalva maneuver


Non-aneurysmal spontaneous subarachnoid
producing increased intrathoracic pressure, and
hemorrhage may be either In perimesencephalic SAH, bleeding is mainly
elevated intracranial venous pressure, is a
perimesencephalic or non-perimesencephalic in the interpeduncular cistern
predisposing factor for perimesencephalic
SAH
nonaneurysmal SAH (PM-SAH)
Clinical Manifestation

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.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.
Clincal Manifestation

• 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.
• Usually, pontine hematoma produces coma and quadriparesis .

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.
Treatment/ Management

There are many trails 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)
• 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. 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 .
Treatment/ Management
• 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.
• 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
• Surgery
The different types of surgical treatment for hemorrhagic stroke are craniotomy, decompressive
craniectomy, stereotactic aspiration, endoscopic aspiration, and catheter aspiration.
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
Treatment / Management

• Cerebroprotection
The secondary injury of hemorrhagic stroke comprises 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.
• 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, urinary tract infection, etc. are common problems
Differential 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.
Prognosis

• 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
• 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. 
• ICH score introduced by Hemphill et al. predicts mortality
• The points 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.
Conclusion

• Hemorrhagic stroke is due to bleeding into the brain by the rupture of a blood vessel and
Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage (ICH) and
subarachnoid hemorrhage (SAH). 
• Early diagnosis and treatment are important in view of the usual rapid expansion of hemorrhage,
causing sudden deterioration of consciousness and neurological dysfunction.
• There is a chance of recurrence of Hemorrhagic stroke and hypertension also old age are risk
factors. So, BP should be controlled and Lifestyle modifications should be advised viz. avoidance of
alcohol, tobacco, and illicit drugs.
Thank you

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