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Cerebral Hemorrhage By Arlyn M. Valencia, M.D. Associate Professor, University Of Nevada School Of Medicine
1.
2. CEREBROVASCULAR ACCIDENT
OR ―BRAIN ATTACK‖
Third leading cause of death
750, 000 cases/year
Leading cause of significant disability
Cost: $40 billion/year
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‖
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
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%
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)
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%
30.
31.
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
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)
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
58. Intracerebral hemorrhage has
frequent early, ongoing
bleeding and progressive
deterioration, severe clinical
deficits and subsequent high
mortality and morbidity rates.