cerebral hemorrhage. etiology and pathogenesis hypertension and arteriosclerosis atherosclerosis,...
TRANSCRIPT
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Cerebral hemorrhageCerebral hemorrhage
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Etiology and pathogenesis Etiology and pathogenesis
Hypertension and arteriosclerosisAtherosclerosis, bleeding tendency
(hemophilia, leukemia, aplastic anemia, thrombocytopenia), congenital angiomatous malformation, arteritis, tumor
lenticulostriate arteries vertical to MCAMicroaneurysms → rupture
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Pathology Pathology
Site: basal ganglia (70%), brain lobe, brain stem, cerebellum
Lateral hemorrhage: the bleeding is confined lateral to the internal capsule (lenticular nucleus, external capsule)
Medial hemorrhage: thalamus hematoma →edema →herniation hematoma →stroke capsule
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Clinical featureClinical feature
Age: 50-70Male > femaleOccur at physical exertion or excitementSudden onset of focal signsUsually accompanied by headache and
vomiting May have consciousness disturbance
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1. Putamen hemorrhagecontralateral hemiplegia, hemianesthesia,
and hemianopiaEyes are frequently deviated toward the
side of the affected hemisphereAphasia if dominant hemisphere is affected
Clinical featureClinical feature
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2. Thalamus hemorrhage contralateral hemiplegia, hemianesthesia,
and hemianopiaDeep sensation disturbanceOcular signsDisturbance of consciousness
Clinical featureClinical feature
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3. Pontine hemorrhageMild: crossed paralysisSevere (>5ml) coma pinpoint pupils hyperpyrexia tetraplegia die in 48 hours
Clinical featureClinical feature
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4. Cerebellar hemorrhageOccipital headache, intense vertigo and
repeated vomiting, ataxia, nystagmusSevere cerebellar hemorrhage : coma,
compression of brain stem, tonsillar herniation
Clinical featureClinical feature
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5. Lobar hemorrhageSeen in AVM, Moyamoya disease, Headache, vomiting, neck stiffnessSeizureFocal signs
Clinical featureClinical feature
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Investigation Investigation
1. CT First choice High density blood Mass effect and edema High density →
isodensity → low density
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2. MRIBrain stem hemorrhage<24h, not distinguishable with thrombosis3. DSAYoung and with normal blood pressure4. CSFBloodyDone only when the CT is not available and
without increased ICP
Investigation Investigation
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Diagnosis Diagnosis
Age >50, with hypertensionSudden onset of headache, vomiting, focal
signOccur at physical exertion or excitementCT: high density blood
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Differential diagnosisDifferential diagnosis
Coma: poisoning, hypoglycemia, hepatic or diabetic coma
Focal signs: cerebral infarction, brain tumor, subdural hematoma, SAH
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Treatment Treatment
1.Keep rest, monitoring, air way, good nursing
2. Keep electrolytes and fluid balance.
3. Reduce ICP: 20% Mannitol 125-250ml, 3 to 4 times per
dayFurosemide, albumin, dexamathasone
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4. Control hypertension: <180/105mmHg in acute stage, ACEI, beta-blocker
5. Prevent complications:Infection:antibioticsgastric hemorrhage: Cimetidine, LosecVenous thrombosis: heparin
Treatment Treatment
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6. Surgical therapy: Putamen, lobar: >40-50 ml, deterioratingCerebellum: >15ml, diameter>3cmThalamus: obstructive hydrocephalus
→ventricular drainage
7. Rehabilitation
Treatment Treatment
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Subarachnoid hemorrhageSubarachnoid hemorrhageSAHSAH
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SAH SAH
Cranial bone → dura mater → arachnoid → pia mater → brain lobe
Primary spontaneous SAH
Traumatic SAHSecondary to cerebral
hemorrhage
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Etiology Etiology
1. Intracranial saccular aneurysm 2. AVM (arteriovenous malformation) 3. Hypertension and atherosclerosis4. Moyamoya disease5. Mycotic aneurysm, tumor, polyarteritis
nodasa, bleeding disease
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Pathology Pathology
Anterior cerebral and anterior communicating
Internal carotid Middle cerebralBasilar
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Clinical featureClinical feature
1. Age of onset: Saccular aneurysm: adult 30-60 AVM: juvenile Hypertension: more than 60
2. Prodromal symptoms Warning leaks: headache, vomiting Cranial nerve paralysis: oculomotor
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3. Acute SAHSudden onset of severe headache: “explode,
burst, the worst of my life”VomitingAssociated with physical exertion, excitementTransient loss of consciousness or comaPain of neck, back, legMental symptoms: apathy, lethargy, delirium
Clinical featureClinical feature
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3. Acute SAHSigns of meningeal irritation: neck stiffness,
positive Kernig’s signFundus examination: papilloedema,
sub-hyaloid hemorrhageCranial nerve palsy
Clinical featureClinical feature
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4. Delayed neurologic deficitsRerupture: in first 4 weeks, again has severe
headache, vomiting, unconsciousness, with poor outcome. Due to fibrinolysis
Cerebrovascular spasm: 4-15 days after initial SAH, → cerebral infarction →disturbance of consciousness and focal signs
Hydrocephalus: 2-3 weeks after SAH, → gait difficulty, incontinence, dementia
Clinical featureClinical feature
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InvestigationInvestigation
1. CTSubarachnoid clot in
75% of cases
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2. CSFUniformly blood-stainedXanthochromia: 12 hours to 2-3 weeks ICP ↑
3. DSA: etiologic diagnosis, important to surgery
4. MRA, CTA
InvestigationInvestigation
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Diagnosis Diagnosis
Sudden onset of severe headache, vomitingNeck stiffness, positive Kernig’s signUniformly blood stained CSFCT shows subarachnoid clot
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Differential diagnosisDifferential diagnosis
Cerebral hemorrhageMeningitisTumorPsychosis
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TreatmentTreatment
1. General management Absolute bed rest for 4-6 weeksPrevent constipation, excitementSedatives and analgesics
2. Reduce ICPMannitol, Furosemide, albumin
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3. Prevent reruptureAntifibrinolytic drugs: EACA for 3 weeks
4. Prevent cerebrovascular spasmNimodipine, flunarizine
5. Lumbar puncture to replace CSF
6. Surgery: within 24-72 hours
TreatmentTreatment