Cerebral hemorrhage Etiology and pathogenesis



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Cerebral hemorrhage


Etiology and pathogenesis

  • Hypertension and arteriosclerosis

  • Atherosclerosis, bleeding tendency (hemophilia, leukemia, aplastic anemia, thrombocytopenia), congenital angiomatous malformation, arteritis, tumor

  • lenticulostriate arteries vertical to MCA

  • Microaneurysms → rupture



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



Clinical feature

  • Age: 50-70

  • Male > female

  • Occur at physical exertion or excitement

  • Sudden onset of focal signs

  • Usually accompanied by headache and vomiting

  • May have consciousness disturbance



Clinical feature

  • 1. Putamen hemorrhage

  • contralateral hemiplegia, hemianesthesia, and hemianopia

  • Eyes are frequently deviated toward the side of the affected hemisphere

  • Aphasia if dominant hemisphere is affected



Clinical feature

  • 2. Thalamus hemorrhage

  • contralateral hemiplegia, hemianesthesia, and hemianopia

  • Deep sensation disturbance

  • Ocular signs

  • Disturbance of consciousness



Clinical feature

  • 3. Pontine hemorrhage

  • Mild: crossed paralysis

  • Severe (>5ml)

  • coma

  • pinpoint pupils

  • hyperpyrexia

  • tetraplegia

  • die in 48 hours



Clinical feature

  • 4. Cerebellar hemorrhage

  • Occipital headache, intense vertigo and repeated vomiting, ataxia, nystagmus

  • Severe cerebellar hemorrhage : coma, compression of brain stem, tonsillar herniation



Clinical feature

  • 5. Lobar hemorrhage

  • Seen in AVM, Moyamoya disease,

  • Headache, vomiting, neck stiffness

  • Seizure

  • Focal signs



Investigation

  • 1. CT

  • First choice

  • High density blood

  • Mass effect and edema

  • High density → isodensity → low density



Investigation

  • 2. MRI

  • Brain stem hemorrhage

  • <24h, not distinguishable with thrombosis

  • 3. DSA

  • Young and with normal blood pressure

  • 4. CSF

  • Bloody

  • Done only when the CT is not available and without increased ICP



Diagnosis

  • Age >50, with hypertension

  • Sudden onset of headache, vomiting, focal sign

  • Occur at physical exertion or excitement

  • CT: high density blood



Differential diagnosis

  • Coma: poisoning, hypoglycemia, hepatic or diabetic coma

  • Focal signs: cerebral infarction, brain tumor, subdural hematoma, SAH



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 day

  • Furosemide, albumin, dexamathasone



Treatment

  • 4. Control hypertension: <180/105mmHg in acute stage, ACEI, beta-blocker

  • 5. Prevent complications:

  • Infection:antibiotics

  • gastric hemorrhage: Cimetidine, Losec

  • Venous thrombosis: heparin



Treatment

  • 6. Surgical therapy:

  • Putamen, lobar: >40-50 ml, deteriorating

  • Cerebellum: >15ml, diameter>3cm

  • Thalamus: obstructive hydrocephalus →ventricular drainage

  • 7. Rehabilitation



Subarachnoid hemorrhage SAH



SAH

  • Cranial bone → dura mater → arachnoid → pia mater → brain lobe

  • Primary spontaneous SAH

  • Traumatic SAH

  • Secondary to cerebral hemorrhage



Etiology

  • 1. Intracranial saccular aneurysm

  • 2. AVM (arteriovenous malformation)

  • 3. Hypertension and atherosclerosis

  • 4. Moyamoya disease

  • 5. Mycotic aneurysm, tumor, polyarteritis nodasa, bleeding disease



Pathology

  • Anterior cerebral and anterior communicating

  • Internal carotid

  • Middle cerebral

  • Basilar



Clinical 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



Clinical feature

  • 3. Acute SAH

  • Sudden onset of severe headache: “explode, burst, the worst of my life”

  • Vomiting

  • Associated with physical exertion, excitement

  • Transient loss of consciousness or coma

  • Pain of neck, back, leg

  • Mental symptoms: apathy, lethargy, delirium



Clinical feature

  • 3. Acute SAH

  • Signs of meningeal irritation: neck stiffness, positive Kernig’s sign

  • Fundus examination: papilloedema, sub-hyaloid hemorrhage

  • Cranial nerve palsy



Clinical feature

  • 4. Delayed neurologic deficits

  • Rerupture: 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



Investigation

  • 1. CT

  • Subarachnoid clot in 75% of cases



Investigation

  • 2. CSF

  • Uniformly blood-stained

  • Xanthochromia: 12 hours to 2-3 weeks

  • ICP ↑

  • 3. DSA: etiologic diagnosis, important to surgery

  • 4. MRA, CTA



Diagnosis

  • Sudden onset of severe headache, vomiting

  • Neck stiffness, positive Kernig’s sign

  • Uniformly blood stained CSF

  • CT shows subarachnoid clot



Differential diagnosis

  • Cerebral hemorrhage

  • Meningitis

  • Tumor

  • Psychosis



Treatment

  • 1. General management

  • Absolute bed rest for 4-6 weeks

  • Prevent constipation, excitement

  • Sedatives and analgesics

  • 2. Reduce ICP

  • Mannitol, Furosemide, albumin



Treatment

  • 3. Prevent rerupture

  • Antifibrinolytic drugs: EACA for 3 weeks

  • 4. Prevent cerebrovascular spasm

  • Nimodipine, flunarizine

  • 5. Lumbar puncture to replace CSF

  • 6. Surgery: within 24-72 hours




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