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16 Cards in this Set

  • Front
  • Back
ICH cause and risk
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
ICH sxs
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
ICH treatment
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
ICH dx modality
cerebral CT
SAH cause and risk
berry aneurysms (hypoplasic vessel without muscularis or internal lamina at the bifurcation) (80%), AV malformations

risk: age, femalehood, HTN, tobacco
SAH sxs
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
SAH dx modality
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)
SAH treatment
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
SDH cause and risk
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
SDH sxs
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.
SDH dx modalities
head CT: high-density crescentic collection if acute, isodense/hypodense crescent-shaped deformation if chronic.

MRI is more sensitive
SDH mgmt
surgical if SDH is more than 10 mm thick or midline shifts > 5 mm.

if chrnoic, also surgical for moderate/severe cognitive impairment
EDH cause and risk
head trauma, especially with lateral skull fracture. usually due to torn middle-meningeal artery

risk: teenage boys (probably)
EDH sxs
spectrum: coma, momentary loss of consciousness. have a lucid interval and then deterioration.
EDH dx modalities
head CT: 8% not apparent due to severe anemia, severe hoTN, slow venous bleeding
EDH mgmt
surgical for acute, symptomatic EDH to prevent hematoma expansion

non-operable managment is possible if small