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Cerebral edema complicating nonketotic hyperosmolar coma.

A I Arieff

    Mineral and Electrolyte Metabolism
    |January 1, 1986
    PubMed
    Summary

    Cerebral edema is a serious complication during treatment for nonketotic hyperosmolar coma (NKHC). Rapid glucose reduction in NKHC patients can lead to brain swelling, neurological decline, and poor outcomes.

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    Area of Science:

    • Neurology
    • Endocrinology
    • Critical Care Medicine

    Background:

    • Cerebral edema is a known complication of diabetic coma therapy, primarily associated with diabetic ketoacidosis (DKA).
    • Cases in nonketotic hyperosmolar coma (NKHC) are less documented, often lacking robust diagnostic evidence.

    Observation:

    • Five patients with NKHC developed cerebral edema during treatment over nine years.
    • These patients presented with severe hyperglycemia (1,496 ± 296 mg/dl) and hyperosmolality (382 ± 29 mosm/kg), with depressed sensorium.
    • Treatment involved intravenous insulin and saline, leading to a rapid mean plasma glucose fall of 38 mg/dl/h.

    Findings:

    • All patients experienced worsened neurological status, elevated cerebrospinal fluid (CSF) pressure, and brain swelling confirmed by CT scans as glucose levels dropped below 250 mg/dl.
    • Standard treatments including glucose, mannitol, and steroids were ineffective.
    • One patient showed temporary ICP reduction with subdural screw insertion.

    Implications:

    • Aggressive glucose lowering in NKHC may precipitate cerebral edema, a potentially fatal complication.
    • The observed outcomes, including death or persistent vegetative states, highlight the severity and poor prognosis.
    • Further research is needed to refine treatment protocols for NKHC to prevent this devastating complication.

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