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• W2020390010 abstract "Hoorn et al1Hoorn E.J. Carlotti A.P. Costa L.A. MacMohan B. Bohn G. Zietse R. et al.Preventing a drop in effective plasma osmolality to minimize the likelihood of cerebral edema during treatment of children with diabetic ketoacidosis.J Pediatr. 2007; 150: 467-473Abstract Full Text Full Text PDF PubMed Scopus (95) Google Scholar have compared a group of patients with diabetic ketoacidosis (DKA) and cerebral edema (CE) with 2 control groups without CE, 1 group with and the other group without hypernatremia. Their findings suggest that a gradual decrease in plasma glucose level and a concomitant increase in serum sodium level decrease the likelihood of CE. This finding brings us a little closer to understanding the mechanisms of CE in DKA. However, our analysis of the authors’ data reveals a characteristic of the CE group that the authors did not highlight but that may be crucial. The CE group had significantly lower levels of serum sodium at the start of therapy than even the low-sodium control group (LSCG). Their 95% confidence interval (CI) was below the normal serum sodium threshold (135 mEqL), whereas that of the LSCG was above this threshold. We have previously shown that patients with DKA have elevated osmolality (measured osmolality evaluated by depression of the freezing point) and a large osmolar gap (osmolar gap = measured osmolality − calculated osmolality; calculated osmolality = 2 × PNa + PGlucose (in mmol/l).2Puliyel J. Puliyel M. Hincliff R. Hypertonicity in diabetic ketoacidosis: unexpected biochemical correlates and clinical implications.1997Google Scholar Unmeasured substances like ketoacids are responsible for the osmolar gap. Using a modified red blood cell saline fragility test, we previously showed that ketoacids are osmotonic in nature and cause fluid shifts across cell membranes.3Puliyel J.M. Osmotonicity of acetoacetate: possible implications for cerebral edema in diabetic ketoacidosis.Med Sci Monit. 2003; 9: BR130-BR133PubMed Google Scholar Like glucose, ketoacids also are responsible for effective osmolality in DKA. Hooran et al’s finding of significant hyponatremia before the onset of treatment in patients with CE concurs with our findings. Patients with DKA and high serum osmolality (due to high levels of glucose [a measured substance] and ketoacids [unmeasured]) will respond with reduced serum sodium levels in an effort to maintain serum osmolality as close to normal as possible. Treatment of DKA produces a drop in glucose and ketoacid levels. Physicians know to use care to decrease glucose levels gradually, but they are not aware of how quickly ketoacid levels can change. We believe that Hoorn et al have demonstrated that a serum sodium level <135 mEq/L before treatment is a risk factor for the development of CE and may indicate high levels of unmeasured osmotic substances in the blood. Moreover, we reiterate that patients with DKA should have serum osmolality measured objectively by such techniques as the depression of the freezing point, because this provides a clearer index of the changes occurring during the treatment of DKA.4Puliyel J.M. Bhambhani V. Ketoacid levels may alter osmotonicity in diabetic ketoacidosis and precipitate cerebral edema.Arch Dis Child. 2003; 88 ([letter]): 366Crossref PubMed Google Scholar ReplyThe Journal of PediatricsVol. 152Issue 1PreviewWe are pleased to respond to the comments on our article expressed in the foregoing three letters. Two of the letters raise concerns regarding the case-control design of our study, one letter claims to have found an error in the reported fluid retention, and finally, one letter suggests a role for unmeasured osmolytes. Here we respond to each letter individually, although several of our comments also refer to the other two letters and to diabetic ketoacidosis (DKA) and cerebral edema (CE) in general. Full-Text PDF DKA-related cerebral edema and intravenous fluid therapy: Potential pitfalls of uncontrolled retrospective studiesThe Journal of PediatricsVol. 152Issue 1PreviewThe retrospective analysis of children with diabetic ketoacidosis (DKA) by Hoorn et al1 compared 12 children with cerebral edema (CE) with 2 control groups without CE. The authors found that the CE group had a decline in effective osmolality during treatment but the control groups did not, and that the CE group received and retained more fluid. They concluded that the drop in effective osmolality may play a causal role in the development of CE. Full-Text PDF Treatment of diabetic ketoacidosis and the risk of cerebral edemaThe Journal of PediatricsVol. 152Issue 1Preview“For every complex problem there is an answer that is clear, simple, and wrong.” — H.I. Mencken Full-Text PDF" @default.
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• W2020390010 title "Cerebral edema in diabetic ketoacidosis with serum sodium <135 mEq/L" @default.
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