Malignant cerebral edema in patients with hypertensive intracerebral hemorrhage associated with hypertonic saline infusion: A rebound phenomenon?

Adnan I. Qureshi, Jose I. Suarez, Anish Bhardwaj

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Hypertonic saline was recently introduced as a new hyperosmolar agent for treatment of intracranial hypertension and cerebral edema. It has the potential to cause a rebound phenomenon similar to other osmotic agents. The authors report on two patients with cerebral edema caused by hypertensive intracerebral hemorrhage who were treated with hypertonic saline infusion. Both patients improved clinically after 24 hours of hypertonic saline administration. However, both patients deteriorated clinically, 48 and 96 hours after initiation of therapy, despite continued hypertonic saline administration. Compared with pre-treatment computed tomographic scans, edema volume on repeat scans increased from 131 cc to 262 cc, and from 171 cc to 239 cc in the first and second patients, respectively, despite the lack of change in hematoma volume. Malignant edema formation late in the course of intracerebral hemorrhage after prolonged administration of hypertonic saline may represent a rebound phenomenon of hyperosmolar therapy. Further studies are warranted to identify the occurrence of this phenomenon and the subset of patients susceptible to it.

Original languageEnglish (US)
Pages (from-to)188-192
Number of pages5
JournalJournal of Neurosurgical Anesthesiology
Volume10
Issue number3
StatePublished - Jul 1998
Externally publishedYes

Fingerprint

Hypertensive Intracranial Hemorrhage
Brain Edema
Edema
Intracranial Hypertension
Cerebral Hemorrhage
Therapeutics
Hematoma

Keywords

  • Cerebral edema
  • Hypertonic saline
  • Intracranial pressure

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine
  • Clinical Neurology

Cite this

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AU - Suarez, Jose I.

AU - Bhardwaj, Anish

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N2 - Hypertonic saline was recently introduced as a new hyperosmolar agent for treatment of intracranial hypertension and cerebral edema. It has the potential to cause a rebound phenomenon similar to other osmotic agents. The authors report on two patients with cerebral edema caused by hypertensive intracerebral hemorrhage who were treated with hypertonic saline infusion. Both patients improved clinically after 24 hours of hypertonic saline administration. However, both patients deteriorated clinically, 48 and 96 hours after initiation of therapy, despite continued hypertonic saline administration. Compared with pre-treatment computed tomographic scans, edema volume on repeat scans increased from 131 cc to 262 cc, and from 171 cc to 239 cc in the first and second patients, respectively, despite the lack of change in hematoma volume. Malignant edema formation late in the course of intracerebral hemorrhage after prolonged administration of hypertonic saline may represent a rebound phenomenon of hyperosmolar therapy. Further studies are warranted to identify the occurrence of this phenomenon and the subset of patients susceptible to it.

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