Intracranial complications of hypervolemic therapy in patients with a delayed ischemic deficit attributed to vasospasm
- 1 March 1993
- journal article
- Published by Journal of Neurosurgery Publishing Group (JNSPG) in Journal of Neurosurgery
- Vol. 78 (3) , 423-429
- https://doi.org/10.3171/jns.1993.78.3.0423
Abstract
✓ This investigation has revealed the frequency of various intracranial complications that may result from hypervolemic therapy for a delayed ischemic deficit following subarachnoid hemorrhage (SAH). Among 323 patients with SAH, 112 patients developed a delayed ischemic deficit, 94 of whom underwent hypervolemic therapy. Infarction due to vasospasm was found ultimately in 43 of these 94 patients. Twenty-six patients (28%) developed an intracranial complication during hypervolemic therapy: cerebral edema was aggravated in 18, and a hemorrhagic infarction developed in eight. In 13 of 18 patients with aggravation of edema, delayed ischemic deficit developed within 6 days after the SAH; at that time, a massive new infarction was found in four and edema in 10 patients. After hypervolemic therapy, the 18 patients with aggravation of edema deteriorated rapidly, and 14 of them died. In every case in which hemorrhagic infarction followed hypervolemic therapy, a new infarct was found on computerized tomography (CT) when the delayed ischemic deficit became apparent. Hemorrhagic infarction developed as the delayed ischemic deficit resolved, with one exception. In patients who sustained no complication from hypervolemia, the incidence of both massive new infarction and edema at the time when the delayed ischemic deficit was manifested was only 1%. In 44 of 68 patients who sustained no complication from hypervolemia, the delayed ischemic deficit was manifested on or after the 7th day following the SAH. This study suggests that hypervolemic therapy is contraindicated in a patient who is found to have a massive abnormality on CT at the time when a delayed ischemic deficit is manifested, especially when it occurs within 6 days after the SAH. To avoid hemorrhagic infarction, it is important to discontinue hypervolemic therapy as soon as the delayed ischemic deficit resolves.Keywords
This publication has 23 references indexed in Scilit:
- Prophylactic Hypervolemia without Calcium Channel Blockers in Early Aneurysm SurgeryNeurosurgery, 1992
- Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulationJournal of Neurosurgery, 1990
- Effects of Intravascular Volume Expansion on Cerebral Blood Flow in Patients with Ruptured Cerebral AneurysmsNeurosurgery, 1987
- Hemorrhagic Infarction following Vasospasm due to Ruptured Cerebral AneurysmsNeurologia medico-chirurgica, 1987
- Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.Stroke, 1985
- Depression of Circulating Blood Volume in Patients after Subarachnoid Hemorrhage: Implications for the Management of Symptomatic VasospasmNeurosurgery, 1984
- Hemorrhagic Infarction following Vasospasm due to Ruptured Intracranial AneurysmsNeurologia medico-chirurgica, 1982
- Relationship of cerebral blood flow to cardiac output, mean arterial pressure, blood volume, and alpha and beta blockade in catsJournal of Neurosurgery, 1980
- Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humansJournal of Neurosurgery, 1977
- Postoperative hypertension in the management of patients with intracranial arterial aneurysmsJournal of Neurosurgery, 1976