For ICH patients, an elevated troponin level >0.4 ng/mL was found in 15% within 24 hours of admission and was associated with increased in-hospital mortality.21 In another study of 49 patients with supratentorial ICH, exclud- ing those who died within 12 hours or were moribund, 20% had elevated troponin levels, although this was not associated Heart failure can occur as the result of myocardial isch- emia, infarction, stress-induced cardiomyopathy, or uncon- trolled hypertension in the setting of acute ICH. Neurogenic pulmonary edema is an increase in interstitial and alveolar fluid in the setting of an acute central nervous system injury well documented in subarachnoid hemorrhage but prevalent in ICH as well.178 Neurogenic pulmonary edema presents abruptly and progresses quickly after the neurological insult. Radiographically, it is indistinguishable from cardiogenic pulmonary edema. Resolution usually occurs within several days. Intubation with mechanical ventilator support is often required for airway protection and maximum oxygen delivery. ICH patients may be at risk for acute respiratory distress syn- drome from multiple different origins179 ; however, at present, ways to prevent this have not been studied. When ICH patients develop acute respiratory distress syndrome, it is reasonable to use ventilation strategies used in non-neurological patients (such as low-tidal-volume ventilation)180 ; however, attention should be paid to avoid ICP elevations or inadequate cerebral oxygen delivery. Other medical complications in ICH patients include acute kidney injury, hyponatremia, gastrointestinal bleeding, impaired nutritional status, urinary tract infections, and post- stroke depression. 