Cerebrovascular accidents, or strokes, are a major cause of death and disability worldwide. There are two main types of strokes - ischemic strokes, which account for 80% of cases and are caused by blockage of blood flow to the brain, and hemorrhagic strokes, which make up the remaining 20% and result from bleeding in or around the brain. Hemorrhagic strokes can be further divided into primary intracerebral hemorrhages caused by bleeding within the brain tissue itself, subarachnoid hemorrhages caused by bleeding on the surface of the brain, and hemorrhages due to cerebral amyloid angiopathy. Risk factors, evaluation, management, and complications of hemorrhagic

2. CEREBROVASCULAR ACCIDENT
OR ―BRAIN ATTACK‖
 Third leading cause of death
 750, 000 cases/year
 Leading cause of significant disability
 Cost: $40 billion/year

3. Types of Stroke
 Ischemic, 80%
- thrombosis, 50% (small & large-vessel)
- embolism, 30%
 Hemorrhagic, 20%
- intracerebral (HTN as risk)
- subarachnoid (aneurysm)

4. CEREBRAL HEMORRHAGE
 HEMORRHAGIC STROKE
 PRIMARY INTRACEREBRAL
HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY

5. CEREBRAL HEMORRHAGE
 HEMORRHAGIC STROKE
 PRIMARY INTRACEREBRAL
HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY

6. HEMORRHAGIC STROKE
 The transformation of a bland infarct into a
hemorrhagic infarct is a common
occurrence (highest in autopsy studies)
 ―The concept of migratory embolus‖

7. Right Middle Cerebral Artery Territory Infarct

9. Risk Factors For Hemorrhagic
Transformation of a Bland Infarct
 Advanced age
 Embolization as etiology
 High systolic BP
 CT shows mass effect
 Larger territory strokes
 Anticoagulation
 History of coagulopathy

10. HEMORRHAGIC INFARCT

13. CEREBRAL HEMORRHAGE
 HEMORRHAGIC STROKE
 PRIMARY INTRACEREBRAL
HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY

14. RISK FACTORS FOR ICH
 Advancing age
 HTN (autopsy studies on patients with ICH
showed high incidence of LVH;
PROGRESS – Perindopril Protection
Against Recurrent Stroke Study:76%
relative risk reduction of ICH in
comparison to placebo
 Cigarette smoking
 alcoholism

15. PRIMARY INTRACEREBRAL
HEMORRHAGE
 Five most common sites:
putamen: 35 % - 50%
subcortical white matter 30%
thalamus: 10%-15%
pons 5%-12%
cerebellar white matter <5%

18. THE ANTERIOR CIRCULATION

19.  Most ICH originate from the rupture of
small deep penetrating arteries (50 to 200
um); most common: lenticulostriates
 Same arteries are recognized to be
occluded in lacunar infarcts (process:
fibrinoid necrosis or lipohyalinosis)

21. Massive Right Putaminal Hemorrhage

22. Subcortical White Matter ICH

23. Pontine Hemorrhage

24. Thalamic Hemorrhage

26. Right Cerebellar Hemorrhage

27. CEREBRAL HEMORRHAGE
 HEMORRHAGIC STROKE
 PRIMARY INTRACEREBRAL
HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY

28. SUBARACHNOID HEMORRHAGE
 Accounts for 5-10% of all strokes
 Incidence has not declined in 30 years
 80% due to rupture of intracranial saccular
aneurysm
 30-day mortality rate 50%
 Most deaths occur within one week

29. RUPTURED ANEURYSM SITES: International
Cooperative Study On The Timing Of Aneurysm Study
 Anterior communicating artery (ACom)
34%
 ICA 30%
 MCA 22%
 Basilar tip, PICA, basilar trunk branches—
7.6%

32. CAUSES OF SUDDEN DEATH IN SAH
 Large intraparenchymal hematoma
 Destruction of brain tissue
 Acute hydrocephalus
 Increased intracranial pressure
 Cardiac arrhythmias, MI, PE and
respiratory failure

33. LEADING CAUSES OF DEATH ON
HOSPITALIZED PATIENTS
 Sequelae of initial hemorrhage
 Recurrent aneurysmal
 Vasospasm leading to ischemic stroke
 Severe medical complications

35. CEREBRAL HEMORRHAGE
 HEMORRHAGIC STROKE
 PRIMARY INTRACEREBRAL
HEMORRHAGE
 SUBARACHNOID HEMORRHAGE
 HEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY

36. CEREBRAL AMYLOID ANGIOPATHY
 Amyloid deposition in the cerebral vessels
sufficient to cause symptomatic vascular
dysfunction
 Vessel rupture and spontaneous ICH
untreatable and unpreventable
 Prevalence of CAA: 2.3% age 65-74; 8%
age 75-84 ;12.1% 85 and older

37. HEMORRHAGE SECONDARY TO CEREBRAL
AMYLOID ANGIOPATHY (CAA)
 Most common cause of lobar
hemorrhages in non-hypertensive
individuals
 Elderly patients
 Evidence of small microbleeds in MRI
 Long-term recurrence increased

38. RISK FACTORS FOR CAA LOBAR
HEMORRHAGE
 Advanced age
 APOE epsilon2 or epsilon4
 Alzheimer’s disease

39. RISK FACTORS FOR NON-CAA ICH
 Family history of ICH
 Frequent use of alcohol
 Previous ischemic stroke
 Low serum cholesterol level

40. ICH: EVALUATION AND WORK-UP:
 History and PE
 Computed Tomography (CT) scan of the head
 12-lead EKG, chest X-ray
 Complete blood count, PT, PTT
 Chemistries (sodium, phosphate, glucose
abnormalities may mimic stroke)
 Urine and serum toxicology (drugs and alcohol)

41. Other Neuroimaging Techniques &
Ancillary Tests
 Magnetic Resonance Imaging (MRI)
Diffusion Weighted Imaging (DWI),
Magnetic Resonance Angiography (MRA)
 Ultrasound (Carotid Duplex, Transcranial
Doppler, 2-D echo)
 Conventional Angiography

43. SUBACUTE INTRACEREBRAL HEMORRHAGE

44. Under special circumstances, the
following tests may be required:
 Cervical spine x-ray
 Arterial blood gas
 Lumbar puncture
 Electroencephalogram (EEG)

45. Glasgow Coma Scale
1 2 3 4 5 6
Opens eyes in Opens eyes in
Does not open Opens eyes
Eyes response to response to N/A N/A
eyes spontaneously
painful stimuli voice
Utters Oriented,
Makes no Incomprehensibl Confused,
Verbal inappropriate converses N/A
sounds e sounds disoriented
words normally
Abnormal Flexion /
Makes no Extension to Localizes Obeys
Motor flexion to painful Withdrawal to
movements painful stimuli painful stimuli Commands
stimuli painful stimuli

46. Overview of ICH Management
ICH has frequent early, ongoing bleeding and
progressive deterioration, severe clinical deficits
and subsequent high mortality and morbidity
rates
 Good general supportive management (airways,
oxygenation, circulation, glucose level, fever, DVT
prophylaxis)
 Slowing or stopping initial bleeding
 Blood removal from parenchyma or ventricles
 Management of complications of blood in the rain
(increased ICP, decreased CPP)

47. CASE SPECIFIC MANAGEMENT
 Correctible/controllable causes of
hemorrhage (e.g. warfarin)
 Clipping of aneurysm

48. Herniation
 Early clinical signs: mental status change,
pupillary dilatation, vomiting
 Late clinical signs: ocular paresis,
decerebrate rigidity, coma and death

49. TREATMENT OF BRAIN
SWELLING
Cerebral perfusion pressure =MAP-ICP
 Fluid Restriction (1200 ml /day/m2)
 Controlled hyperventilation: 25 mm Hg
 Mannitol, 0.25 mg/kg IV over 20 minutes; repeat PRN,
serum osmolality maintained in the range of 300-
320mOsm/l
 Barbiturate coma, with ICP monitoring (subrachnoid bolt,
IV catheter or Camino catheter): maintain CPP greate
than 50 mmHg; pentobarbtial serum level of 2-4 mg/dl
 Drainage of CSF (ventriculostomy)
 Lobectomy

50. Before Intraven-
tricular TPA
After

57.  INTRAVENTRICULAR HEMORRHAGE

58. Intracerebral hemorrhage has
frequent early, ongoing
bleeding and progressive
deterioration, severe clinical
deficits and subsequent high
mortality and morbidity rates.

59. THANK YOU!