2. • 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).
• Sudden onset of a neurologic deficit from a vascular mechanism are
85% ischemic and 15% are primary hemorrhages [subarachnoid and
intraparenchymal].
3. ETIOLOGY
• Hypertension
• Cerebral amyloid angiopathy (CAA)
• Chronic Liver Disease
• Cigarette smoking
• Old age and more common in males than females
• Sympathomimetic drugs like cocaine, heroin, amphetamine,
ephedrine.
4. PATHOLOGY
• Explosive entry of blood into the brain parenchyma causes
immediate cessation of function in that area as neurons are
structurally disrupted and white-matter fibre tracts are split apart.
• The haemorrhage itself may expand over minutes or hours, or it may
be associated with a rim of cerebral oedema,which, along with the
haematoma, acts like a mass lesion to cause progression of the
neurological deficit.
5. MANAGEMENT
CLINICAL EXAMINATION AND HISTORY
Common clinical manifestations of hemorrhagic stroke are Acute onset headache, vomiting, neck
stiffness, increases in blood pressure, and the rapidly developing neurological signs
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.
Contralateral sensorimotor deficits are the features in hemorrhage of the basal ganglia and
thalamus.
Extension of thalamic hematoma into the midbrain can cause vertical gaze palsy, ptosis, and
unreactive pupil.
Cranial nerve dysfunction with contralateral weakness indicates brainstem hematoma.
6.
7. INVESTIGATIONS
Investigation of acute stroke aims
to confirm the vascular nature of
the lesion, distinguish cerebral
infarction from haemorrhage and
identify the underlying vascular
disease and risk factors
8. CT SCAN
• Computerized tomography (CT) is
usually the initial investigation.
• The hemorrhage increases in
attenuation from 30-60 Hounsfield
units (HU) in the hyperacute phase
to 80 to 100 HU over hours.
• CT is considered the “gold standard”
in detecting acute hemorrhage due
to its sensitivity.
Small Cortical hemorrhage
9. MRI
• T2 susceptibility-weighted magnetic
resonance imaging (MRI) has the same
sensitivity as CT to detect acute
hemorrhage.
• These sequences are more sensitive than
CT for identification of prior hemorrhage.
• MRI can distinguish between the
hemorrhagic transformation of infarct
and primary hemorrhage. MRI can detect
underlying causes of secondary
hemorrhages, such as vascular
malformations
• The paramagnetic properties of
deoxyhemoglobin allow early detection
of hemorrhage in MRI.
10. VASCULAR IMAGING
TECHNIQUES
• Doppler or duplex Ultrasound
scan
• CT angiogram
• MR angiogram
• Intra-arterial angiography
MR Angiogram showing giant aneurysm
at the middle cerebral artery bifurcation
11. OTHER INVESTIGATIONS
• Blood investigations such as bleeding time, clotting time, platelet count,
peripheral smear, prothrombin time (PT) 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.
• investigations to rule out vasculitis are the quantitative evaluation of
immunoglobulins, thyroid antibodies, rheumatoid factor
12. TREATMENT
• Treatment is aimed at minimising the volume of brain that is
irreversibly damaged, preventing complications , reducing the
patient’s disability and handicap through rehabilitation, and reducing
the risk of recurrent stroke
13.
14.
15. 1. Blood pressure Management
• BP should be reduced gradually to 150/90 mmHg using beta-blockers (labetalol,
esmolol), ACE inhibitor (enalapril), calcium channel blocker (nicardipine), or
hydralazine
• 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 outcomes. For patients presenting
with SBP >220 mmHg, an aggressive reduction of BP with a continuous
intravenous infusion is needed.
MANAGEMENT OF HEMORRAGHIC STROKE
16. 2. MANAGEMENT OF ICP
• Treatment for raised ICP is elevating the head of the bed to 30
degrees and using osmotic agents (mannitol, hypertonic saline).
• Mannitol 20% is given at a dose of 1.0 to 1.5 g/kg
17. Hemostatic Therapy
• Hemostatic therapy is given to reduce the progression of
hematoma.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) are used.
18. Antiepileptic Therapy
• Lobar hematoma and the enlargement of hematoma produce
seizures, which are associated with neurological worsening
• 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.Those with clinical seizures or electrographic seizures
should be treated with antiepileptic drugs.
19. Surgical Interventions
Surgery through the skull might be required to remove the blood and
relieve pressure on the brain if the area of bleeding is large enough.
• Surgical clipping:-a tiny clamp at the base of the aneurysm, to stop
blood flow to it. This clamp can keep the aneurysm from bursting, or
it can keep an aneurysm that has recently hemorrhaged from
bleeding again.
• Angioplasty and stents.
20. General Care
• Good medical care, nursing care, and rehabilitation are paramount.
• Percutaneous endoscopic gastrostomy may be needed to prevent
aspiration.
• Screening for myocardial ischemia with electrocardiogram and cardiac
enzyme testing is recommended in hemorrhagic stroke.
• Lifestyle modifications like Smoking cessation,Lower salt intake,Lower
fat intake, Lower the excess intake of alcohol and Lose excess weight