Elsevier

Pediatric Neurology

Volume 21, Issue 4, October 1999, Pages 721-727
Pediatric Neurology

Original Articles
Risk factors for developing brain herniation during diabetic ketoacidosis

https://doi.org/10.1016/S0887-8994(99)00079-XGet rights and content

Abstract

The charts were reviewed of children admitted in diabetic ketoacidosis (DKA) to one hospital within 12 years. The frequency of brain herniation after admission was nine of 153 children admitted for one or more episodes of DKA. The severity of acidosis and hypercapnea were the most reliable risk factors. None of the children who maintained a blood pH greater than 7.1 and a capillary blood partial pressure of carbon dioxide (Pco2) greater than 20 mm Hg manifested brain herniation. The rate of initial fluid administration in severe DKA was also a risk factor. Of 119 patients having a blood pH less than 7.1 or Pco2 less than 20 mm Hg, none of 32 receiving less than 25 mL/kg, one of 42 receiving 25-50 mL/kg, and eight of 40 receiving more than 50 mL/kg of intravenous fluid during the first (in Patient 9, the second) 4 hours of therapy sustained brain herniation. Equally dehydrated unaffected patients initially receiving 25-50 mL/kg/4 hours of intravenous fluid did not develop signs of hypovolemia or worsening DKA. In this series, hydrating at a rate greater than 50 mL/kg during the first 4 hours offered no advantage and was associated with an increased risk of brain herniation.

Introduction

Death during diabetic ketoacidosis (DKA) in children is usually the result of acute cerebral complications [1]. Although cerebral vessel thrombosis or hemorrhage accounts for some fatalities, the single most common cause of death is acute cerebral edema progressing to brain herniation. Cranial computed tomography (CT) scans indicate that asymptomatic brain swelling is often present in DKA before treatment, but progression to brain herniation usually does not occur until several hours after beginning intensive therapy [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21].

Between 1977 and 1989, the frequency of cerebral edema progressing to brain herniation after coming to the hospital was nine of 153 children admitted to the Children’s Hospital and Medical Center in Seattle, Washington for one or more episodes of DKA. The high rate of brain herniation prompted a study of all the children admitted with DKA during that 12-year period to determine whether the clinical presentation, laboratory measurements, or treatment variables were significantly different in affected vs unaffected children.

Section snippets

Subject selection

DKA in this study is defined as hyperglycemia, ketonuria, and acidosis (serum bicarbonate less than 15 mEq/L and blood pH less than 7.3) in addition to the usual clinical findings. The diagnosis of brain herniation was based on clinical signs (coma, unresponsive pupils, loss of doll’s eye movement, respiratory arrest, and decorticate or decerebrate posturing) and postmortem examination or cranial CT findings.

The charts were reviewed of all children aged 19 years or younger who were admitted to

Profile of affected children

A total of 195 episodes of DKA were studied in 153 children. Before the development of DKA, five of the nine affected children and 66 of the 144 unaffected children had not been diagnosed as having diabetes mellitus. One affected patient was only 12 months old; the other patients were 5-16 years of age. The mean age of the affected and unaffected patients was not significantly different (9 vs 11 years). All but one of the affected children had severe DKA on admission (Table 1). In the one

Discussion

The affected children in this series exhibited the syndrome of acute cerebral edema progressing to brain herniation [4], [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21]. Although acutely ill, they were considered to be mentally alert and neurologically intact on presentation. Two to 17 hours after beginning fluid resuscitation and insulin therapy, they demonstrated an abrupt change in the level of consciousness, followed by the appearance of

Acknowledgements

The authors greatly appreciated the help of Gloria A. Bailey, PhD in the preparation of the manuscript.

References (40)

  • M.G. Fitzgerald et al.

    Fatal diabetic ketosis

    BMJ

    (1961)
  • E. Young et al.

    Cerebral edema with irreversible coma in severe diabetic ketoacidosis

    N Engl J Med

    (1967)
  • S.C. Duck et al.

    Cerebral edema complicating therapy for diabetic ketoacidosis

    Diabetes

    (1976)
  • I.A. Fein et al.

    Relation of colloid osmotic pressure to arterial hypoxemia and cerebral edema during crystalloid volume loading of patients with diabetic ketoacidosis

    Ann Intern Med

    (1982)
  • E.J. Krane et al.

    Subclinical brain swelling in childhood during treatment of diabetic ketoacidosis

    N Engl J Med

    (1985)
  • A.I. Winegard et al.

    Cerebral edema in diabetic ketoacidosis

    N Engl J Med

    (1985)
  • W.H. Hoffman et al.

    Cranial CT in children and adolescents with diabetic ketoacidosis

    Am J Neuroradiol

    (1988)
  • G.D. Harris et al.

    Safe management of diabetic ketoacidemia

    J Pediatr

    (1988)
  • E.J. Krane

    Cerebral edema in diabetic ketoacidosis

    J Pediatr

    (1989)
  • A.L. Rosenbloom

    Intracerebral crises during treatment of diabetic ketoacidosis

    Diabetes Care

    (1992)

    • Cited by (0)

    View full text
    Copyright © 1999 Elsevier Science Inc. All rights reserved.