Pathogenesis of cerebral edema after treatment of diabetic ketoacidosis

Silver, Solomon; Clark, Edward C.; Schroeder, Barbara M.; Sterns, Richard H.

doi:10.1038/ki.1997.169

Cited by 70 publications

(26 citation statements)

References 24 publications

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“…In this sense, the use of hypo-osmolar fluids, such as 0.45% NaCl, could be a factor in worsening the condition, whereas the use of normal saline could play a protective role (23,24). In support of this idea, our patients' Na (corrected by Katz formula) (14) was maintained in the normal range during the whole period of treatment in both groups and we did not have to administer hypotonic fluid at any time.…”

Section: Subcutaneous Fast-acting Insulin Analogmentioning

confidence: 53%

“…It affects mainly children and adolescents (0.46 -4.6%) and has a high mortality rate (up to 25%), and sequellae occur in 10 -25% of survivors (1). Many factors have been implicated in cerebral edema, such as the degree of acidosis and hyperglycemia, changes in serum osmolality and oncotic pressure, hypernatremia at admission, low pCO 2 , use of bicarbonate, and vigorous fluid infusion, especially in the first hours of treatment, leading to a sharp fall in glycemic levels (21)(22)(23)(24). However, there is no consensus that hypotonic fluids predispose a patient to cerebral edema.…”

Section: Subcutaneous Fast-acting Insulin Analogmentioning

confidence: 99%

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Subcutaneous Use of a Fast-Acting Insulin Analog

et al. 2005

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OBJECTIVE—To look for technical simplification and economic efficiency in the treatment of pediatric diabetic ketoacidosis (DKA) with subcutaneous use of the fast-acting insulin analog (lispro) and compare its use with regular intravenous insulin treatment. RESEARCH DESIGN AND METHODS—In this controlled clinical trial from June 2001 to June 2003, we randomized 60 episodes of DKA with a blood glucose level ≥16.6 mmol/l (300 mg/dl), venous pH <7.3 and/or bicarbonate <15 mmol/l, or ketonuria greater than ++. Of the 60 episodes, 30 were treated with subcutaneous lispro (0.15 units/kg) given every 2 h (lispro group) and the other 30 cases received continuous intravenous regular insulin (0.1 unit · kg−1 · h−1; CIRI group). Volume deficit was repaired with 10-ml/kg aliquots of 0.9% sodium chloride. Laboratory monitoring included hourly bedside capillary glucose, venous blood gas, β-hydroxybutyrate, and electrolytes. Plasma blood glucose levels were measured on admission, 2 h after admission, when capillary blood glucose reached ≤13.8 mmol/l (250 mg/dl), and 6, 12, and 24 h thereafter. RESULTS—Capillary glucose levels decreased by 2.9 and 2.6 mmol · l−1 · h−1 in the lispro and CIRI groups, respectively, but blood glucose fluctuated at different time intervals. In the CIRI group, metabolic acidosis and ketosis resolved in the first 6-h period after capillary glucose reached 13.8 mmol/l, whereas in the lispro group, they resolved in the next 6-h interval; however, both groups met DKA recovery criteria without complications. CONCLUSIONS—DKA treatment with a subcutaneous fast-acting insulin analog represents a cost-effective and technically simplified procedure that precludes intensive care unit admission.

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Section: Subcutaneous Fast-acting Insulin Analogmentioning

confidence: 53%

Section: Subcutaneous Fast-acting Insulin Analogmentioning

confidence: 99%

Subcutaneous Use of a Fast-Acting Insulin Analog

et al. 2005

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“…Published DKA models use adult animals and vary considerably depending on the species, the pancreatic toxin used, the route of drug administration, and the dosage (10). The prevalent DKA model uses adult rats injected with STZ (45-200 mg/kg) (14,19,20). DKA was also observed in adult rats 48 h after injection with ALX (21), and in adult rabbits and dogs injected with STZ/ALX (22,23).…”

Section: Discussionmentioning

confidence: 99%

“…injection allowing for slow systemic adsorption. The concentration of insulin (1.0 U R, 1 U NPH) administered to mice is exaggerated to account for reduced human insulin responsiveness in rodents (14). All mice were killed 2 h posttreatment for analysis of serum biochemistry and DKA-CE.…”

Section: Methodsmentioning

confidence: 99%

Combined Insulin and Bicarbonate Therapy Elicits Cerebral Edema in a Juvenile Mouse Model of Diabetic Ketoacidosis

Rose

Wang

et al. 2007

Pediatr Res

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Cerebral edema in diabetic ketoacidosis (DKA-CE) occurs primarily in children and can develop during DKA therapy. The treatment factors contributing to DKA-CE remain elusive. Our objectives were to characterize an age-appropriate DKA mouse model and to determine which DKA therapies contribute to DKA-CE. Juvenile mice were briefly fed a high-fat diet and injected with two pancreatic ␤-cell toxins: streptozocin and alloxan. Severe insulin and leptin deficiencies associated with hyperosmolar ketoacidosis rapidly developed, indicating DKA. DKA mice were treated with re-hydration Ϯ insulin and brain water content (BWC) measured as an indicator of DKA-CE. As expected, glucose and ␤-OH-butyrate corrected in DKA mice that received rehydration and insulin. BWC significantly increased above control levels only in DKA mice that received combined insulin and bicarbonate therapy, indicating the development of DKA-CE. Microscopically, DKA-CE brains had perineuronal and perivascular edema, with microvacuolation in the white matter tracts. These results indicate that insulin-deficient juvenile mice develop biochemical changes that are similar to those of DKA in children. Increased BWC was observed only in DKA mice that received combined insulin and bicarbonate therapy, suggesting that rapid systemic alkalinization in the presence of insulin may contribute to DKA-CE. (Pediatr Res 61: 301-306, 2007)

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“…It is most common in children with newly diagnosed diabetes, but it has been reported in children with known diabetes and in young people in their twenties (72)(73)(74). Fatal cases of cerebral edema have also been reported with HHS.…”

Section: Phosphatementioning

confidence: 99%