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16 Cards in this Set
- Front
- Back
ICH cause and risk
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HTN --> medial lipohyalinosis, microaneurysm, microdissections.
CAA --> amyloid depositions, vessel inflammation, microaneurysm, microhemorrhages risk factors: increased age, maleness, HTN, binge EtOH, hemorrhagic diathesis, vascular malformations, antithrombotic meds, sympathomimetic drugs, reperfusion syndrome, aneurysm, abscess, tumor |
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ICH sxs
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occurs during exertion
head pain, N/V, altered consciousness focal deficits (100%) depending on location increased systemic BP, seizures, deep hemorrhage comps: hydrocephalus --> increased ICP |
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ICH treatment
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manage severe HTN (sys < 120 then < 100)
hyperosmolar tx (mannitol, hypothermia, sedation) to decrease edema coagulation facotrs control hematoma expansion but no better outcome surgery: hemicrniectomy, craniectomy with drainage, sterotactic craniotomy, suboccipital crniectomy for posterior fossa |
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ICH dx modality
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cerebral CT
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SAH cause and risk
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berry aneurysms (hypoplasic vessel without muscularis or internal lamina at the bifurcation) (80%), AV malformations
risk: age, femalehood, HTN, tobacco |
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SAH sxs
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mental status change, focal deficits, WHOL, N/V, nuchal rigidity, CN palsies (esp CN VI), seizures, coma, decerebrate
comps: vasospasm --> delayed cerebral ischemia, rehemorrhage, cardiac arrythmias, increased troponin, cardiogenic myopathy (takotsubo), hydrocephalus, seizures |
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SAH dx modality
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cerbral CT catches 95% on day 1 but 50% on second day
missed in 25% LP at least 6 hours after symptoms to find blood or xanthochromia (connected to subarachnoid space) angiography is gold standard for detecting aneurysms also look for IVH transcranial doppler for vasospasm (look for increased blood velocity) |
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SAH treatment
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surgical clipping/coiling of aneurysm
decrease pressure (nicardipine, labetolol) cardiac: may need inotropes salt tablets, seizure meds PRN vasospasm: hypervolemia, hypertension, hemodilution. nimodipine (CCB) can improve outcome, though no knows effect on vasospasm. angioplasty and intra-arterial nicardiepine (CCB) if severe |
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SDH cause and risk
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head trauma: MVA, falls, assaults --> torn bridging veins
arterial rupture (minority) low CSF (eg after LP) --> traction on bridging veins --> rupture risk: cerebral atrophy (aging, chronic EtOH, previous head trauma), coagulopahty, intracranial hoTN, vascular anomalies |
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SDH sxs
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acute: coma (50%) (lucid interval followed by deterioration). post fossa: like increased ICP (headaches, anisocoria, dysphagia, vomiting) with CN palsies, nuchal rigidity.
chronic: insidious headache, light-headedness, cognitive decline, apathy, somnolence, maybe seizures. usually more global than focal. |
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SDH dx modalities
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head CT: high-density crescentic collection if acute, isodense/hypodense crescent-shaped deformation if chronic.
MRI is more sensitive |
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SDH mgmt
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surgical if SDH is more than 10 mm thick or midline shifts > 5 mm.
if chrnoic, also surgical for moderate/severe cognitive impairment |
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EDH cause and risk
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head trauma, especially with lateral skull fracture. usually due to torn middle-meningeal artery
risk: teenage boys (probably) |
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EDH sxs
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spectrum: coma, momentary loss of consciousness. have a lucid interval and then deterioration.
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EDH dx modalities
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head CT: 8% not apparent due to severe anemia, severe hoTN, slow venous bleeding
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EDH mgmt
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surgical for acute, symptomatic EDH to prevent hematoma expansion
non-operable managment is possible if small |