Download SDL 10 Intracranial Hemorrhage HYPERTENSIVE CEREBROVASCULAR

SDL 10
Intracranial Hemorrhage
HYPERTENSIVE CEREBROVASCULAR
DISEASE/HYPERTENSIVE HEMORRHAGE
DEFINITION
 Common clinical malady that can lead to lacunar
infarcts, slit hemorrhages, HTN encephalopathy, as
well as massive intracerebral hemorrhages
 MAJOR RISK FACTOR FOR STROKE w/ risk increasing
w/ elevated systolic BP
 10-20% of strokes
ETIOLOGY/PATHOGENESIS
 Elevated serum lipids (high low density lipoproteins,
diabetes mellitus, tobacco smoking, illicit drug use)
o Latter are risk factors for development of
atherosclerosis in cerebral vasculature
 Hypertensive cerebrovascular disease  leads to
spontaneous intracranial hemorrhage and lacunar
infarcts
CLINICAL MANIFESTATIONS
 Headaches (pounding), dizziness
 Hypertensive intracranial hemorrhages – pts may
undergo rapid demise w/ internal capsule and basal
ganglia stroke symptoms
 Hypertensive encephalopathy – acute neurologic
syndrome char. by diffuse cerebral dysfunction,
severe headache, confusion, and vomiting precipitated
by severe and sudden elevation of systemic BP
o If not treated, progress to coma or fatal
hemorrhage
MORPHOLOGY
 HTN = risk factor for developing arteriosclerosis
 Vessels at most risk = end arteries (penetrating
vessels) where there is little collateral flow
o Blood vessel morphologic change can include:
arteriosclerosis, lipohyalinosis (fibrinoid
necrosis), and Charcot-Bouchard aneuryms
o Predisposes patient to lacunar infarction and
hemorrhage
o Lacune = infarct that results from lipohyalinosis of
small penetrating end arteries
 Hypertensive intraparenchymal hemorrhages
originate in putamen up to 50-60% of time
 HTN hemorrhage assoc. w/ extravasation of blood w/
compression of surrounding brain tissue
 Microscopically eval – early lesions w/ central clotted
blood surrounded by rim of brain tissue showing
anoxic neuronal, glial changes, and edema
Intracerebral hemorrhage caused by hypertensive
cerebrovascular disease located w/in area of left basal
ganglia
LABORATORY AND RADIOLOGICAL STUDIES
 Hyperlipoproteinemia
 Elevated serum glucose and hemoglobin A1-C
(findings for diabetes mellitus)
 Use CT or MRI
 On CT, small vessel changes are seen on white matter
for pts w/ hypertensive cerebrovascular disease
TREATMENT/PROGNOSIS
 Medical control of HTN and atherosclerosis is
centerpiece of preventive therapy
 Antihypertensive treatments for all pts w/ ischemic
stroke and transient ischemic attacks
 Lifestyle modifications – weight loss, diet rich in
veggies, fruits, low fat dairy products, regular
exercise, limited alcohol/salt consumption/tobacco
use
 Discontinue illicit drugs is required
 Calcium channel blockers, ACE inhibitors, diuretics
can help
CEREBRAL AMYLOID ANGIOPATHY RELATED
CEREBRAL HEMORRHAGE
DEFINITION
Cerebreal amyloid angiopathy (CAA) – deposition of
beta-amyloid protein in walls of cortical and
leptomeningeal arteries
~predisposes pts to spontaneous cerebral hemorrhage
 Deep cerebral hemorrhages assoc w/ chronic HTN,
hemorrhages assoc w/ CAA are more peripheral and
involve cerebral cortex and adjacent structures
 15% of all cerebral hemorrhages in elderly
 CAA can mimic CNS vasculitis (could even coexist)
ETIOLOGY/PATHOGENESIS
 Beta-amyloid protein deposition – cleavage product of
beta amyloid precursor protein on chromosome 21
 Amyloid protein forms HIGHLY INSOLUBLE FIBRILS
measuring 8-10 nanometers in diameter
 Deposition occurs in walls of arteries and arterioles of
cerebral cortex and meninges
o Capillaries and veins less often affected by CAA
o Blood vessels of deep white matter are typically
spared
 Arterial and arteriolar amyloid deposition initially
appears in the basement membrane around smooth
muscle cells at peripheral aspect of tunica media and
tunica adventitia
 PROGRESSIVE DESTRUCTION OF SMOOTH MUSCLE
 Endothelium is generally spared until late stages
 Vessels become rigid and fragile – some undergo
fibrinoid necrosis and ruptures w/ hemorrhage
Histologic section showing thick-walled arterioles in
patients with CAA
CLINICAL MANIFESTATIONS
 Strokes due to CAA-assoc hemorrhage FREQUENTLY
OCCUR in the frontal and frontoparietal regions
 Symptoms range from massive cerebral lobar stroke
to progressive dementia
 Parietal lobe involvement by CAA may result in
CONTRALATERAL NEGLECT SYNDROME
 CAA commonly identified in demented patients w/
Alzheimer’s-like neurofibrillary pathology
MORPHOLOGY
 Acute massive lobar hemorrhage
 Multiple cortical and subcortical hemorrhages may be
seen at different stages of development
 Microscopically, involved blood vessels show
leptomeningeal and cortical arteries w/
effacement of normal morphology w/ amorphous
eosinophilic material
 Loss of smooth muscle tissue w/ preservation of
endothelium leads to double-barrel contour of
affected blood vessels
 CONGO RED is histo stain that gives amyloid a
“cotton-candy” pink appearance
 Ultrastructural findings show 8-10 nanometer
amyloid fibrils in extracellular spaces of arteries and
arterioles
Left – large cerebral lobar hemorrhage in 67 yo pt w/
CAA
Right – thick appearing blood vessels w/ prominent
eosinophilic (red) ring. These blood vessels are fragile,
rupture, and lead to formation of hemorrhages
LABORATORY/RADIOLOGICAL STUDIES
 No clinical lab studes are useful in dx of CAA
 Tissue sections show amyloid deposition w/in blood
vessel wall
 Congo red stains used to show amorphous pink
material
 Polarizing microscopy of Congo red stained tissue
shows “apple green birefringence”
 Thioflavin T staining highlights amyloid w/ yellow
fluorescence
Congo red stained histo section from patient w/ CAA.
Polarizing microscopy shows “apple green
birefringence”
TREATMENT/PROGNOSIS
 Acute cerebral lobar hemorrhages result in death of
patient due to mass effect and herniation
 Smaller hemorrhages aren’t lethal, can be treated
symptomatically
 No helpful medications at the moment
SUBARACHNOID HEMORRHAGE RELATED TO
RUPTURED SACCULAR ANEURYSMS INVOLVING
CIRCLE OF WILLIS
DEFINITION
 4 categories: intraparenchymal, subdural,
subarachnoid, epidural
o intracranial – occur anywhere w/in CNS
o epidural & subdural – assoc w/ trauma
o Hemorrhages assoc w/ brain parenchyma &
subarachnoid space – likely due to HTN
vasculopathy
 2 types of spontaneous (non-traumatic) recognized
o Intraparenchymal (intracerebral)
o Subarachnoid
o Cause: hypertension (>50%), vascular
malformations, aneurysms, amyloid angiopathy,
vasculitis, hemorrhage related to neoplasm
(metastatic), drugs leading to HTN, coagulopathy
 Causes of spontaneous SUBARACHNOID hemorrhage
include:
o Ruptured saccular (berry) aneurysm
o Ruptured vascular malformations
o Ruptured mycotic aneuryms
o Coagulopathy
o Vasculitis
o Sinus/Vein thrombosis
 Sites prone to developing intracerebral hemorrhages
and lacunar infarcts
o Lobar subcortical area, putamen, caudate nucleus,
thalamus, pons, cerebellum
 Underlying vascular pathology related to
intracerebral hemorrhage development is
LIPOHYALINOSIS
Saccular (berry) aneurysm – most common type
~ 2x common in women than men
~ 25% of deaths from ruptured aneurysms leading to
SAH
~ located at Circle of Willis
~ Atherosclerotic (fusiform) aneurysms involve
BASILAR ARTERY – large ecstatic vessels that compress
brainstem
Mycotic aneurysms – result from infectious
endocarditis
~ Emboli break off from heart valve tissue and lodge
w/in peripheral vessels near surface of brain 
inflammation/weakening of vessel wall  aneurysm
ETIOLOGY/PATHOGENESIS
 Conditions genetically related: polycystic kidney
disease, Ehler-Danlos, Marfan syndrome,
neurofibromatosis type 1, etc
 Non-genetic: fibromuscular dysplasia and coarctation
of aorta
 Risk factors: chronic HTN, smoking, female, AfricanAmerican
CLINICAL MANIFESTATIONS
 Most saccular (berry) aneurysms are asymptomatic
until they rupture
 50% of patients experience initial small bleed
(sentinel hemorrhage)
 “WORST HEADACHE OF MY ENTIRE LIFE”
 vomiting, nuchal rigidity, speech impairment, possible
loss of consciousness
 25-50% of patients die at time of 1st rupture
 Lethargy, photophobia, fever
 Focal deficit possible
MORPHOLOGY
 Grossly – thin-walled sacs attached to arterial branch
point via narrow neck
o Aneurysm rupture assoc w/ extensive basal SAH
 Dissection of blood thru CNS parenchyma occurs if
rupture site is oriented towards brain. Hemorrhage
may extend into ventricles
 Organization of basal SAH may obstruct CSF flow and
cause hydrocephalus
 Microscopically – aneurysm sac has fibrocollagenous
wall and may contain thrombotic or fibrocalfic
material
 Junction btwn aneurysm neck and adjacent artery
shows loss of elastin fibers and smooth muscle
Left – Circle of Willis w/ 3 saccular (berry) aneurysms)
Right – ruptured saccular aneurysm due to massive
basal subarachnoid hemorrhage. Extensive blood clot
at base of brain
LABORATORY/RADIOLOGICAL STUDIES
 CEREBRAL ANGIOGRAPHY – most sensitive/specific
for localization of saccular (berry) aneurysm
 CT can detect hemorrhage in 95% cases w/in 3 days
 If CT scan is negative and suspicion is high for
intracranial hemorrhage, LUMBAR PUNCTURE CAN
HELP
 Blood IDed in spinal fluid
o Be careful to exclude possibility that blood present
in CSF is not due to trauma assoc w/ performance
of lumbar puncture
 Older hemorrhages  CSF xanthochromia (yellow
discoloration of CSF – normally clear)
CSF fluid from 47 yo pt w/ subarachnoid hemorrhage
showing xanthochromia compared to clear CSF
TREATMENT/PROGNOSIS
 25% of patients who experience ruptured saccular
aneurysm and SAH die w/in 24 hours of acute
aneurysm rupture
 25% more die w/in 3 months of rupture
 Emergency therapy – stabilize cardiorespiratory
function and prevent further hemorrhage
 Aneurysm >10mm diameter = candidate for
neurosurgical clipping
 Endovascular embolization is alternative treatment
option