This document discusses hemorrhagic stroke, specifically intracerebral hemorrhage. It defines intracerebral hemorrhage as bleeding within the brain tissue itself, accounting for 15% of strokes. Risk factors include hypertension and amyloid angiopathy. Clinical presentation includes sudden onset of focal neurological deficits like weakness or seizures. Diagnostics include CT scans. Prognosis is poor with 50% mortality at 1 year. Management focuses on controlling blood pressure, treating increased intracranial pressure, preventing seizures and infections. Surgical options include removing the hemorrhage via aspiration or craniotomy. Subarachnoid hemorrhage is also discussed as bleeding into the subarachnoid space, often from

1. Presented by: Jeevan Shrestha
Intern
HAEMORRHAGIC STROKE

2.  I have no conflict of interest or disclosure in
relation to this presentation.

3.  Stroke is defined by the World Health
Organization as 'a clinical syndrome consisting of
rapidly developing clinical signs of focal (or global in
case of coma) disturbance of cerebral function
lasting more than 24 hours or leading to death with
no apparent cause other than a vascular origin.‘
 Types:
1. Ischemic stroke : 80 %
2. Hemorrhagic Stroke : 20%

5. Hemorrhagic stroke
 Types:
 Intracerebral Hemorrhage(15%)
- Caused by bleeding within the brain
- tissue itself
 Sub Arachnoid Hemorrhage(5%)
- Caused by extravasation of blood
into the subarachnoid space

6. Risk factors

7. Intracerebral Hemorrhage
 An acute and spontaneous extravasation of blood in
to the brain parenchyma that may extend into
ventricles and subarachnoid space.
- 10-15% of all cases of stroke.
- 6 month mortality is 30-50%
- Classification:
- 1. Primary ICH: Hemorrhage originate from
spontaneous rupture of small arteries or arterioles
damaged by chronic HTN or amyloid angiopathy.
- 2. Secondary ICH: Haemorrhage results from trauma,
rupture of Aneurysm, vascular malformation,
coagulopathy, haemorrhagic transformation of
cerebral infarct, intracranial neoplasm, venous
angioma, dural sinus thrombosis

8. Pathophysiology:
 Early Haematoma growth:
- About 38% had an increase in haematoma
volume
of more than 33% shown by CT within 3
hours of onset.
 Perihaematomal Brain Injury:
- Brain tissue injury and swelling can result in
raised ICP
or herniation.
Plasma released by clotted haematoma seeps
into
the surrounding brain tissue, is the primary
trigger
of inflammatory process.

9. Clinical Presentation
 Onset of a sudden focal neurological deficit while the
patient is active, which progresses over minutes to hours
 Focal neurological deficit:
- Weakness or paresis that may affect a single extremity, one
half of body or all 4 extremities.
- Facial droop
- Monocular or binocular blindness
- Dysarthria
- Ataxia
- Aphasia
- Seizure
- Headache is more common in ICH
- Vomiting
- Increased systolic BP and impaired level of consciousness

10. Brain sites and associated deficits involved in hemorrhagic
stroke include the following:
 Putamen - Contralateral hemiparesis, contralateral
sensory loss, contralateral conjugate gaze paresis,
homonymous hemianopia, aphasia, neglect, or apraxia
 Thalamus - Contralateral sensory loss, contralateral
hemiparesis, gaze paresis, homonymous hemianopia,
miosis, aphasia, or confusion
 Lobar - Contralateral hemiparesis or sensory loss,
contralateral conjugate gaze paresis, homonymous
hemianopia, abulia, aphasia, neglect, or apraxia
 Caudate nucleus - Contralateral hemiparesis, contralateral
conjugate gaze paresis, or confusion
 Brainstem - Quadriparesis, facial weakness, decreased
level of consciousness, gaze paresis, ocular bobbing,
miosis, or autonomic instability
 Cerebellum – Ipsilateral ataxia, facial weakness, sensory
loss; gaze paresis, skew deviation, miosis, or decreased

11. Diagnostics

12. Prognosis
 Mortality ~ 50% at 1 year

13. Management
Blood
Pressure:
IV medications:
Labetalol,
Nicardipine,
Esmolol,
Enalapril,
Hydralazine,
Nitroglycerine

14.  Intracranial Pressure:
-Place ICP monitor or EVD drain in patients with GCS
< 8.
-GOAL: Maintain ICP < 20mmHg ,
Minimal Cerebral Perfusion Pressure >
60mmHg
 Haemostatic therapy: Eptacog alpha
 Anticonvulsant therapy: Lorazepam,Phenytoin,
Fosphenytoin, valproic acid, phenobarbital
 Fever control
 Management of Hypergylcemia:
-Insulin if Blood sugar > 185mg/dl
 Nutrition
 DVT prophylaxis

15. Surgical Management
 Aims:
- Decompression to reduce or prevent elevated ICP
- Removal of acute haematoma to reduce mass effect
- Minimise toxicity from blood breakdown products to
surrounding brain.
- Options:
- Ventriculostomy
- Stereotactic aspiration of haematoma
- Endoscopic haematoma evacuation
- Craniotomy
- Hemicraniectomy for decompression with or without
evacuation of haematoma

16. SUB ARACHNOID
HAEMORRHAGE
-Neurological emergency characterised by
haemorrhage into the subarachnoid space.
-One of the most important cause of sudden, acute
severe headache.
-c/c: ‘the worst headache of my life”
- 85 % of non traumatic cases are due to ruptured
cerebral aneurysm
-30 day mortality of aneurysmal SAH ~
50%
-Incidence: F > M (3:2)
-Risk higher in blacks than in whites
-Incidence increases with age and peaks at 50

17. Causes of subarachnoid
haemorrhage
 Trauma
 Vascular
- Ruptured intracranial aneurysm, AVM, Tumors
with hemorrhage
 Vasculopathy
-Collagen vascular disease, Amyloid angiopathy,
Arterial dissection
 Haematological
- Anticoagulant,leukemia, Hepatic or renal induced
coagulopathy
 Drugs : Cocaine, Amphetamina

19. Clinical Presentation
 Prodormal events:
- Symptoms:Headache, dizziness, orbital pain, diplopia,
visual loss
- Signs: Sensory or motor disturbance, seizure, ptosis,
dysphasia
- Focal neurological findings
- Results due to: Sentinel leaks, Mass effect of
aneurysm
- expansion, Emboli
CLASSIC presentation:
- Sudden onset severe headache(Thunderclap
headache)
- Nausea/vomiting

20. Clinical Grading scales
 The Hunt and Hess grading system
 Grade 0 - Unruptured aneurysm
 Grade I - Asymptomatic or mild headache and slight nuchal
rigidity
 Grade Ia - Fixed neurological deficit without acute
meningeal/brain reaction
 Grade II - Cranial nerve palsy, moderate to severe
headache, nuchal rigidity
 Grade III - Mild focal deficit, lethargy, or confusion
 Grade IV - Stupor, moderate to severe hemiparesis, early
decerebrate rigidity
 Grade V - Deep coma, decerebrate rigidity, moribund
appearance
In the Hunt and Hess system, the lower the grade, the better the
prognosis. Grades 1-3 generally are associated with favorable
outcome; these patients are candidates for early surgery. Grades IV
and V carry a poor prognosis; these patients need stabilization and

21. WFNS Scale
 Grade 1 - Glasgow Coma Score (GCS) of 15,
motor deficit absent
 Grade 2 - GCS of 13-14, motor deficit absent
 Grade 3 - GCS of 13-14, motor deficit present
 Grade 4 - GCS of 7-12, motor deficit absent or
present
 Grade 5 - GCS of 3-6, motor deficit absent or
present

22. Complications
 Hydrocephalus
 Rebleeding
 Vasospasm
 Seizure
 Cardiac dysfunction

23. Investigations
 Serum Chemistry panel, Complete Blood count
 PT, aPTT
 Blood typing/screening
 Cardiac enzymes, ABG, Chest Xray, ECG
 CT without contrast is most sensitive imaging study in
SAH
 CT angiography(Sensitivity= 77-100% ; Specificity=
79-100%)
 MRI

24. Management
 Medical management of SAH focuses on
- Protecting the airway
- Managing the BP
- Preventing rebleeding prior to treatment
- Managing vasospasm(Calcium channel
antagonist Nimodipine)
- Treating Hydrocephalus(EVD or permanent
ventricular shunting)
- Treating Hyponatremia
- Preventing Pulmonary embolus

25.  Bed rest in quiet room and stool softner,if needed,
to prevent straining.
 If headache or neck pain is severe, Mild sedation
and analgesia.
 Adequate Hydration

26. Managing raised ICP
 For stupurous patient, Emergency Ventriculostomy to
measure ICP.
 Medical therapies: Mild hyperventilation, Mannitol
and sedation
 Maintain adequate cerebral perfusion pressure(60-
70mmHg) while avoiding excessive elevation/fall of
arterial pressure

27. Surgical
 Clipping of the aneurysm
 Coiling of the aneurysm

28.  THANK YOU