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Discussion of Spontaneous Cerebral Hemorrhages
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CEREBROVASCULAR ACCIDENT OR “BRAIN ATTACK”
Third leading cause of death750, 000 cases/yearLeading cause of significant disabilityCost: $40 billion/year
Types of Stroke
Ischemic, 80%
- thrombosis, 50% (small & large-vessel)
- embolism, 30%Hemorrhagic, 20%
- intracerebral (HTN as risk)
- subarachnoid (aneurysm)
CEREBRAL HEMORRHAGE
HEMORRHAGIC STROKEPRIMARY INTRACEREBRAL
HEMORRHAGESUBARACHNOID HEMORRHAGEHEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY
CEREBRAL HEMORRHAGE
HEMORRHAGIC STROKEPRIMARY INTRACEREBRAL
HEMORRHAGESUBARACHNOID HEMORRHAGEHEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY
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”
Right Middle Cerebral Artery Territory Infarct
Risk Factors For Hemorrhagic Transformation of a Bland Infarct
Advanced ageEmbolization as etiologyHigh systolic BPCT shows mass effectLarger territory strokesAnticoagulationHistory of coagulopathy
HEMORRHAGIC INFARCT
CEREBRAL HEMORRHAGE
HEMORRHAGIC STROKEPRIMARY INTRACEREBRAL
HEMORRHAGESUBARACHNOID HEMORRHAGEHEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY
RISK FACTORS FOR ICH
Advancing ageHTN (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 smokingalcoholism
PRIMARY INTRACEREBRAL HEMORRHAGE
Five most common sites:
putamen: 35 % - 50%
subcortical white matter 30%
thalamus: 10%-15%
pons 5%-12%
cerebellar white matter <5%
THE ANTERIOR CIRCULATION
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)
Massive Right Putaminal Hemorrhage
Subcortical White Matter ICH
Pontine Hemorrhage
Thalamic Hemorrhage
Right Cerebellar Hemorrhage
CEREBRAL HEMORRHAGE
HEMORRHAGIC STROKEPRIMARY INTRACEREBRAL
HEMORRHAGESUBARACHNOID HEMORRHAGEHEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY
SUBARACHNOID HEMORRHAGE
Accounts for 5-10% of all strokes Incidence has not declined in 30 years80% due to rupture of intracranial saccular
aneurysm30-day mortality rate 50%Most deaths occur within one week
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%
CAUSES OF SUDDEN DEATH IN SAH
Large intraparenchymal hematomaDestruction of brain tissueAcute hydrocephalus Increased intracranial pressureCardiac arrhythmias, MI, PE and
respiratory failure
LEADING CAUSES OF DEATH ON HOSPITALIZED PATIENTS
Sequelae of initial hemorrhageRecurrent aneurysmal Vasospasm leading to ischemic strokeSevere medical complications
CEREBRAL HEMORRHAGE
HEMORRHAGIC STROKEPRIMARY INTRACEREBRAL
HEMORRHAGESUBARACHNOID HEMORRHAGEHEMORRHAGE FROM CEREBRAL
AMYLOID ANGIOPATHY
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
HEMORRHAGE SECONDARY TO CEREBRAL AMYLOID ANGIOPATHY (CAA)
Most common cause of lobar hemorrhages in non-hypertensive individuals
Elderly patientsEvidence of small microbleeds in MRILong-term recurrence increased
RISK FACTORS FOR CAA LOBAR HEMORRHAGE
Advanced ageAPOE epsilon2 or epsilon4Alzheimer’s disease
RISK FACTORS FOR NON-CAA ICH
Family history of ICHFrequent use of alcoholPrevious ischemic strokeLow serum cholesterol level
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)
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
SUBACUTE INTRACEREBRAL HEMORRHAGE
Under special circumstances, the following tests may be required:
Cervical spine x-rayArterial blood gasLumbar punctureElectroencephalogram (EEG)
Glasgow Coma Scale
1 2 3 4 5 6
Eyes Does not open eyes
Opens eyes in response to painful stimuli
Opens eyes in response to voice
Opens eyes spontaneously N/A N/A
Verbal Makes no sounds
Incomprehensible sounds
Utters inappropriate words
Confused, disoriented
Oriented, converses normally
N/A
Motor Makes no movements
Extension to painful stimuli
Abnormal flexion to painful stimuli
Flexion / Withdrawal to painful stimuli
Localizes painful stimuli
Obeys Commands
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)
CASE SPECIFIC MANAGEMENT
Correctible/controllable causes of hemorrhage (e.g. warfarin)
Clipping of aneurysm
Herniation
Early clinical signs: mental status change, pupillary dilatation, vomiting
Late clinical signs: ocular paresis, decerebrate rigidity, coma and death
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
Before Intraven-
tricular TPA
After
INTRAVENTRICULAR HEMORRHAGE
Intracerebral hemorrhage has frequent early, ongoing
bleeding and progressive deterioration, severe clinical deficits and subsequent high mortality and morbidity rates.
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