**3. Delayed cerebral ischemia**

Rebleeding after SAH remains one of the most serious early complications; the reported incidence is up to 15% in the first 24 hours, and the mortality rate is approximately 70% [26–28]. Prognosis is closely related to initial bleeding, rebleeding, and DCI. The presence of intraventricular and intracerebral hemorrhage also adversely affects prognosis. Cardiac symptoms and neurogenic pulmonary edema are considered indicative of SAH severity. Hypernatremia after SAH is considered as a poor neurological marker. DCI generally begins approximately 3 days after bleeding, and its most severe presence is 1 week after bleeding. Smoking is considered as a risk factor for the development of DCI. The mechanism of DCI is not completely known, but the degree of initial bleeding is likely to be multifactorial with the severity of a function. It is also known that DCI occurs in cerebral regions without signs of angiographic vasospasm. The general recommendation is that angiographic vasospasm should not be treated in the absence of DCI.

DCI is usually treated by administration of nimodipine, via effect of maintenance of normal circulating blood volume and induced hypertension. Nimodipine is a calcium antagonist, and its oral administration is useful in the treatment of vasospasm and DCI. IV application of nimodipine is not recommended. High-dose IV nicardipine (0.15 mg/kg/hr for 14d) has been shown to reduce symptomatic vasospasm but not positively affect the 3-month neurological outcome in a prospective double-blind randomized controlled trial [4, 29–35].

The clinical goal is to prevent rebleeding and DCI, because, in patients with SAH, DCI is considered the most important preventable cause of death and poor neurological prognosis. Delayed cerebral ischemia affects up to 30% of patients and leaves the majority of survivors with motor deficits, cognitive dysfunction, and reduced quality of life. The risk of developing DCI is associated with the severity of initial bleeding [36].

In patients with GCS 8 or less with intracranial hemorrhage, endotracheal intubation should be considered to protect the airway or to clear tracheal secretions. Intubation should be performed with a rapid induction with minimal effect on hemodynamics and not increasing intracranial pressure. Drugs used in induction should be preferred accordingly (e.g., propofol). It should be remembered that propofol may cause a drop in blood pressure. Preventive isotonic liquid bolus should be applied if necessary. Post-expiratory positive pressure (PEEP) up to 12 mmHg is considered safe as long as the mean arterial pressure is maintained [37].
