Delayed Cerebral Ischemia (DCI)

Delayed Cerebral Ischemia (DCI)

Delayed Cerebral Ischemia is defined as any neurologic deterioration (focal or global) presumed secondary to cerebral ischemia that persists >1 hour and cannot be explained by any other neurologic or systemic condition such as significant hydrocephalus, sedation, hypoxemia, seizures, electrolyte imbalances, renal injury, or hepatic impairment.

Thus, Delayed Cerebral Ischemia is a diagnosis of exclusion.

Delayed Cerebral Ischemia occurs in 30% of patients at any time within the first 21 days after symptom onset.

However, the peak incidence of Delayed Cerebral Ischemia is between 4 and 12 days after symptom onset.

How can Delayed Cerebral Ischemia be prevented? 

Oral nimodipine should be administered to all patients with an SAH.

Oral nimodipine 60 mg q4h has a neuroprotective effect as it improves neurologic outcomes but does not reduce cerebral vasospasm.

Avoidance of hypovolemia is the mainstay of preventive therapy for delayed cerebral ischemia.

Patients with hyper- or hypovolemia have a significantly higher mortality.

Maintenance of euvolemia and normal circulating blood volume is recommended to prevent DCI.

How is Delayed Cerebral Ischemia treated? 

The primary goal of treating DCI is prevention of ischemic strokes. Induced hypertension has become the major component of hemodynamic augmentation therapy.

Patients clinically suspected of DCI should undergo a trial of induced hypertension, which should be maintained for at least 72 hours or until stability is achieved and is slowly weaned off after that.

Blood pressure augmentation should progress in a stepwise fashion with assessment of neurologic function at each MAP level to determine if a higher blood pressure target is appropriate.


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