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QJM 2007 100(11):721-735; doi:10.1093/qjmed/hcm096
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© The Author 2007. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Uncovering the basis of a severe degree of acidemia in a patient with diabetic ketoacidosis

M. Gowrishankar1, A.P.C.P. Carlotti2, C. St George-Hyslop3, D. Bohn3, K.S. Kamel4, M.R. Davids5 and M.L. Halperin4

From the 1Division of Pediatric Nephrology, Stollery Children's Hospital, University of Alberta, Edmonton, Canada, 2Hospital das Clinicas, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil, 3Department of Critical Care Medicine, Hospital for Sick Children and Departments of Anaesthesia and Medicine, University of Toronto, Toronto, Canada, 4Division of Nephrology, St Michael's Hospital, University of Toronto, Toronto, Canada, and 5Division of Nephrology and Department of Medicine, Stellenbosch University, Cape Town, South Africa

Address correspondence to Professor M.L. Halperin, Emeritus Professor of Medicine, University of Toronto, St Michael's Hospital Annex, Room 5078, 30 Bond Street Toronto, Ontario, M5B 1W8, Canada. email: mitchell.halperin{at}utoronto.ca


   Abstract

In this teaching exercise, the goal is to demonstrate how an application of principles of physiology can reveal the basis for a severe degree of acidaemia (pH 6.81, bicarbonate <3 mmol/l (PHCO3), PCO2 8 mmHg), why it was tolerated for a long period of time, and the issues for its therapy in an 8-year-old female with diabetic ketoacidosis. The relatively low value for the anion gap in plasma (19 mEq/l) suggested that its cause was both a direct and an indirect loss of NaHCO3. Professor McCance suggested that ileus due to hypokalaemia might cause this direct loss of NaHCO3, and that an excessive excretion of ketoacid anions without Formula in the urine accounted for the indirect loss of NaHCO3. In addition, he suspected that another factor also contributing to the severity of the acidaemia was a low input of alkali. He was also able to explain why there was a 16-h delay before there was a rise in the PHCO3 once therapy began. The missing links in this interesting story, including a possible basis for the hypokalaemia, emerge during the discussion between the medical team and Professor McCance.


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P. Lee and L. V. Campbell
Diabetic Ketoacidosis: the Usual Villain or a Scapegoat?: A novel cause of severe metabolic acidosis in type 1 diabetes
Diabetes Care, March 1, 2008; 31(3): e13 - e13.
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