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Intracerebral hemorrhage (ICH) accounts for more than 10% of all strokes with approximately 79,000 cases in the United States per year.1 These patients have a high mortality (>25%), and survivors often have profound neurologic deficits, with only the minority of patients regaining functional independence at 6 months.2,3

The incidence of ICH increases exponentially with age and is higher in men than in women. Independent risk factors for ICH include hypertension (the most significant risk factor, present in >75%), alcohol abuse, thrombolytic therapy, cocaine or amphetamine use, cigarette smoking, and diabetes mellitus.4,5

Anticoagulant therapy and daily aspirin use are also independent risk factors for ICH. In a meta-analysis of the literature, for every 1,000 patients treated with aspirin for 5 years, there will be one excess ICH caused by this therapeutic intervention. On the other hand, 14 acute myocardial infarctions will be avoided in this same population, so benefits of therapy far outweigh risk.6 Patients on anticoagulant therapy have a 7- to 10-fold higher incidence of ICH.7 The mortality in this population is approximately 60%—almost double that of the general population.8,9 ICH occurs in 2–9 per 100,000 patients receiving anticoagulant therapy per year.10 A strong association between over-anticoagulation and ICH exists; however, the majority of bleeds occur in patients with a therapeutic international normalized ratio (INR).8,9

This chapter will discuss the diagnosis and management of spontaneous ICH and will then separately address diagnostic and management strategies for subarachnoid hemorrhage (SAH).

Presentation and Diagnosis

Patients with an ICH generally present with sudden onset of neurologic deficits (Figure 34-1). These are often rapidly progressive. A full neurologic examination including mental status, cranial nerves, motor strength, sensory, reflexes, and cerebellar coordination should be documented on presentation to the emergency room and followed sequentially (hourly neuro checks). Exam findings can help localize the lesion, but more importantly, form the baseline to evaluate for signs of deterioration. Cerebral hemispheric subcortical white matter or putamenal hemorrhages can present with gaze deviation (involvement of eye fields—gaze toward the lesion) and/or contralateral hemiparesis/plegia, aphasia (dominant side—perisylvian subcortical white matter), neglect or agnosias (parietal subcortical white matter), and contralateral hemianopsia (occipital lobe subcortical white matter). Thalamic hemorrhages can present with aphasia (dominant side), neglect (nondominant side), contralateral sensory or motor deficits (if adjacent internal capsule motor fibers are involved), oculomotor derangements, visual field cuts, and/or small reactive pupils. Brainstem lesions can present with coma, quadriparesis, locked-in syndrome, horizontal gaze paresis, ocular bobbing, pinpoint pupils, nystagmus, hyperthermia, and abnormal breathing patterns. Fixed midposition pupils and hippus are suggestive of midbrain involvement. Cerebellar hemorrhages can present with limb or truncal ataxia, nystagmus, skewed gaze, brainstem findings secondary to mass effect on the brainstem, and signs of elevated intracranial pressure (ICP)/hydrocephalus from complete effacement of the fourth ...

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