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intracerebral hemorrhage (ICH)
hemorrhage directly into the cerebral parenchyma
see intraparenchymal hemorrhagic stroke for
- cerebellar hemorrhage
- pontine hemorrhage
Etiology:
1) hypertension (most common)
- putamen, thalamus, basal ganglia [12]
2) amyloid angiopathy (common in elderly)
- suspect in patient with hemorrhage outside distribution common for hypertensive hemorrhage (supratentorial lobar hemorrhages) [12]
3) arteriovenous malformations (AVM)
4) bleeding diatheses
5) pharmacologic anticoagulation
6) antiplatelet agents
- combination of NSAIDs & antidepressants (NNH=244) [8]
- low dose aspirin 75-300 mg QD does not increase risk [10]
7) CNS infections
8) brain tumor with hemorrhage
9) cocaine may be precipitating factor
10) tobacco abuse, alcohol abuse
11) decreased LDL cholesterol increases risk [2]
12) increased HDL cholesterol increases risk [2]
13) SSRI use [2]
Epidemiology:
- intraparenchymal hemorrhagic strokes account for 15% of all strokes
Pathology:
- most commonly small penetrating vessels in the putamen, thalamus bleed into the brain parenchyma
- basal ganglia, pons, cerebellum also affected
- hypertension is a risk factor for hematoma expansion [2]
- blood pressure > 140/80 mm Hg after intracerebral hemorrhage is associated with poor prognosis [2]
Clinical manifestations:
1) 1/3 of non-comatose patients deteriorate rapidly
- 50% mortality
3) hematomas > 50 mL are most likely to cause deterioration
4) patients with amyloid-related hemorrhages
a) frequently normotensive
b) generally have prior cognitive deficits
Laboratory: urine toxicology for cocaine
Special laboratory:
- cerebral angiography with catheter intra-arterial digital subtraction
a) patients < 45 years of age
b) intraparenchymal hemorrhage related to cocaine (high incidence of vascular anomalies)
c) spontaneous intraventricular hemorrhage without parenchymal hemorrhage [14]
- continuous EEG monitoring
- probably indicated for patients with mental status changes disproportional to the extent of brain injury [7]
Radiology:
- non-contrast computed tomography (CT) of the brain
- repeat neuroimaging may be required if changes in neurological status occur due to
- expansion of hematoma
- cerebral edema
- computed tomography angiography (CTA)
- venography [14]
- exclude central venous thrombosis
- lobar spontaneous intracranial hemorrhage (ICH) in patients < 70 years
- deep/posterior fossa hemorrhage in patients < 45 years or < 70 years without hypertension
- magnetic resonance angiography
- spontaneous ICH & negative CTA/venography [14]
Complications:
- much higher mortality than ischemic stroke [2]
- 15-40% 90 day mortality [14]
Differential diagnosis:
- ischemic stroke can not be distinguished from intracranial hemorrhage on the basis of clinical manifestations
- head CT without contrast distinguishes
Management:
1) see general measures under stroke (CVA)
2) neurosurgery consultation
a) craniotomy for arteriovenous malformation (AVM)
b) benefits of surgery uncertain for supratentorial ICH [7]
c) also see intracranial hemorrhage
3) treatment of systolic hypertension > 180 mm Hg [2]
- avoid IV nitroprusside & nitroglycerin [2]
- nitroprusside & nitroglycerin may raise intracranial pressure [2]
- nicardipine or labetolol to maintain systolic blood pressure between 140-160 mm Hg [2,5]; target systolic BP is 140 mm Hg [2]
- assumption is that excessively high systolic blood pressure will increase hematoma size
- lowering of systolic BP to 140 mm Hg may not be harmful [4]; may be helpful (no lower limit cited) [7]; may be harmful [2]
- target systolic blood pressure of 110-139 mm Hg does not improve outcomes relative to standard treatment of 140-179 mm Hg [9]
- maintain systolic BP 130-150 mm Hg, target systolic BP 140 mm Hg [14]
- avoid goals of systolic BP < 140 mm Hg [2]
4) mannitol, hypertonic saline, barbiturate coma, hyperventilation to reduce intracranial pressure
5) do not use glucocorticoids to lower intracranial hypertension [7]
6) correct elevated INR
- vitamin K IV for warfarin-associated intracranial hemorrhage
- add 4-factor prothrombin complex concentrate [2]
- for patients taking direct oral factor Xa inhibitor (rivaroxaban, apixaban) stop the anticoagulant & treat with 4-factor prothrombin complex concentrate or andexanet alfa
- for dabigatran reverse anticoagulation with idarucizumab
- 4-factor prothrombin complex concentrate may have fewer complications & correct the INR more rapidly than fresh frozen plasma [7]
- 4-factor prothrombin complex preferable to fresh frozen plasma [14]
- recombinant factor VIIa of no benefit [6]
7) routine platelet transfusion not indicated [2]
8) statin use is controversial [3] (not addressed in [7])
9) prophylaxis for venous thromboembolism in non-ambulatory patients
- pneumatic compression from hospital day 1 [7]
- low dose LMW heparin [14]
10) postpone do not resuscitate order until at least the 2nd day of hospitalization [7]
11) for patients with spontaneous ICH, inpatient stroke unit indicated [14]
12) followup
- neurorehabilitation
- long-term goal of BP <130/80 is reasonable for prevention of recurrent ICH [7]
- avoid anticoagulants for 4 weeks
- with or without mechanical heart valve
- may decrease recurrence of ICH [7]
- pharmacologic prophylaxis for venous thromboembolism safe after 24 hours if no evidence of expanding hematoma [2]
- safe to restart antiplatelet agent after 11 weeks [11,13]
General
hemorrhagic stroke
References
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