Cerebral hemorrhage Etiology and pathogenesis

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