Intracranial Pressure/Cerebral Perfusion Pressure-Targeted Management of Life-Threatening Intracranial Hypertension Complicating Diabetic Ketoacidosis-Associated Cerebral Edema A Case Report
ABSTRACT Symptomatic cerebral edema from diabetic ketoacidosis occurs infrequently but carries a high rate of mortality and morbidity owing to complications from intracranial hypertension. Treatment options are limited but include hyperosmolar therapy with mannitol or hypertonic saline, tracheal intubation for airway protection, and hyperventilation via mechanical ventilation. We describe here the successful use of an intracranial pressure/cerebral perfusion pressure-targeted management strategy through ventriculostomy catheter placement with intracranial pressure monitoring and cerebrospinal fluid drainage, hyperosmolar therapy with hypertonic saline, and controlled hyperventilation to treat life-threatening complications of cerebral edema in a pediatric patient with severe diabetic ketoacidosis.
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ABSTRACT: * Based on some research evidence, DKA is a significant contributor to morbidity and mortality in children who have type 1 diabetes, and cerebral edema is responsible for most of the deaths during DKA in children. (Dunger, 2004). * Based on strong research evidence, treatment of DKA requires replacement of water and electrolytes and correction of the insulin deficiency. (Dunger, 2004). * Based on some research data and consensus opinion, after providing initial volume expansion (if needed), fluid resuscitation of children who have DKA should be calculated to rehydrate evenly over at least 48 hours. Initial fluid resuscitation should be with an isotonic solution; subsequent fluid management should be with a solution that has a tonicity of at least 0.45% saline. (Dunger, 2004). * Based on strong research evidence, insulin treatment for DKA should begin at a dose of 0.1 units/kg per hour and generally should remain at or above this level until the ketoacidosis is resolved. (Dunger, 2004). * Based on some research evidence, risk factors for the development of cerebral edema during treatment of DKA include the severity of acidosis, greater hypocapnia (after adjusting for the degree of acidosis), higher blood urea nitrogen concentration at presentation, and treatment with bicarbonate. (Dunger, 2004; Glaser, 2002).Pediatrics in Review 01/2009; 29(12):431-5; quiz 436. DOI:10.1542/pir.29-12-431 · 0.82 Impact Factor
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ABSTRACT: To explore whether the carbon dioxide-bicarbonate (P(CO(2))-HCO(3)) buffering system in blood and cerebrospinal fluid (CSF) in diabetic ketoacidosis should influence the approach to ventilation in patients at risk of cerebral edema. Medline search, manual search of references in articles found in Medline search, and use of historical literature from 1933 to 1967. A clinical vignette is used--a child with severe diabetic ketoacidosis who presented with profound hypocapnia and then deteriorated--as a basis for discussion of integrative metabolic and vascular physiology. Studies included reports in diabetic ketoacidosis where arterial and CSF acid-base data have been presented. Studies where simultaneous acid-base, ventilation, respiratory quotient, and cerebral blood flow data are available. We revisit a hypothesis and, by reassessing data, put forward an argument based on the significance of low [HCO(3)](CSF) and rising Pa(CO(2))- hyperventilation in diabetic ketoacidosis and the limit in biology of survival; repair of severe diabetic ketoacidosis and Pa(CO(2))-and mechanical ventilation. The review highlights a potential problem with mechanical ventilation in severe diabetic ketoacidosis and suggests that the P(CO(2))--HCO(3) hypothesis is consistent with data on cerebral edema in diabetic ketoacidosis. It also indicates that the recommendation to avoid induced hyperventilation early in the course of intensive care may be counter to the logic of adaptive physiology.Pediatric Critical Care Medicine 08/2005; 6(4):405-11. DOI:10.1097/01.PCC.0000164343.20418.37 · 2.33 Impact Factor
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ABSTRACT: A 6-y retrospective case note review was performed to determine the causes of ketoacidosis. 135 patients and 463 diabetic years were involved. Fifty-two ketoacidosis episodes occurred: 19 episodes in new patients and 33 episodes in 19 patients with established diabetes. 27% of newly diagnosed patients presented in ketoacidosis. They were similar in terms of age, sex and proportion living in single parent families to those presenting without ketoacidosis. The 33 ketoacidosis episodes occurring in established patients included 12 episodes in 3 children who were transferred to our care because of uncontrolled diabetes. Insulin omission was the cause of ketoacidosis in 9/19 (47%) patients, and was suspected in a further 5/19 (26%). Family and school problems were common and 14/19 patients came from single parent families. Established patients aged > or = 11 y were predominantly female (10F, 2M), whereas patients aged < or = 10 y were predominantly male (6M, 1F). 7 patients with multiple ketoacidosis episodes were all > or = 11 y and 6 were female. Families with > or = 2 diabetic children appeared vulnerable, 4 cases coming from 3/7 such families.Acta Paediatrica 06/1998; 87(5):537-41. DOI:10.1080/08035259850158245 · 1.84 Impact Factor