Emergency management of

diabetic ketoacidosis I read with great interest the paper by Hardern and Quinn.1 However, it seems that there is some misinterpretation of the quoted papers. In the introduction, the authors write ‘‘DKA is a potentially fatal metabolic dis-order’’. It would be useful to point out that it is only life threatening in its most severe stage: coma.2 They summarise the pathogen-esis of coma in DKA on page 212: ‘‘Severe acidosis has adverse effects on many organs, espcially the brain...’’. Indeed, according to Alberti,3 very low blood pH is the immediate cause of coma: the glycolytic enzyme phos-phofructokinase is inactivated by decreasing pH and, thus, the glucose utilisation in brain cells is impaired. On page 212, the authors write ‘‘It may, therefore, seem appealing to give bicarbonate as treatment for the metabolic acidosis that occurs in DKA. There is no evidence to support this’ ’ with quotations of Lutterman, Lever, Morris and Viallon. Morris and Viallon did not observe comatose patients. Lutterman has given sodium bicarbonate to four coma-tose patients, all recovered to full alertness. The same result has been observed by Lever in 27 patients with ‘‘deep coma’ ’ and he did not observe adverse reactions to this treat-ment. Where is there a published report on a similar number of comatose patients with DKA, with zero lethality, without sodium bicarbonate, and without increase of the low blood pH? On the same page, they quote the paper of Hale: ‘‘no metabolic benefits from bicarbo-nate administration’’. However, in the group with bicarbonate administration, the blood pH increased within 120 minutes to 7.23, whereas in the group without bicarbonate it only increased to 7.12. In a comatose patient, such a difference can be life saving