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Diabetic ketoacidosis in a patient undergoing distal pancreatectomy

To the Editor:

Although diabetic ketoacidosis (DKA) occurs in totally pancreatectomized patients,[1]it has never been reported after partial pancreatectomy. We describe the development of DKA in a patient who underwent distal pancreatectomy. A 60-year-old man with gastric cancer was treated with D2 gastrectomy along with splenectomy and distal pancreatectomy followed by Roux-en-Y reconstruction in July, 2009. He had not been previously diagnosed as having diabetes. He received chemotherapy with TS-1 (100 mg/d) from October, 2009 to February, 2010. At the beginning of February, 2010, he complained of appetite loss and general fatigue. Gastro-endoscopy showed no abnormality, and contrast-enhanced computed tomography of the abdomen also did not show any abnormality other than the absence of stomach, spleen, and pancreatic body and tail (Fig.). However, he still could not eat food except for candy and a nutritional supplementary high-calorie drink. He was admitted to the emergency department in a coma with Kussmaul breathing in the middle of February, 2010. Blood gas analysis revealed severe metabolic acidosis (pH, 7.13; pCO2, 15.6 mmHg; HCO3-, 5.2 mEq/L; anion gap, 37.7). Plasma glucose (1179 mg/dl) and hemoglobin A1c levels (13.2%; normal range, 4.3%-5.8%) were significantly elevated; however, the serum insulin level was very low (0.84 μIU/ml; normal range, 1.7-10.4 μIU/ml). Serum levels of total ketones (14 063 μmol/L; normal range, <130 μmol/L), acetoacetate (2981 μmol/L; normal range, <55 μmol/L) and beta-hydroxybutyrate (11082 μmol/L; normal range, <85 μmol/L) were greatly increased. These data suggested DKA. Hydration and continuous insulin infusion promptly ameliorated his consciousness and blood glucose levels. Intensive insulin therapy following insulin infusion further reduced the glucose toxicity, and his insulin secretion recovered (C-peptide level, 30.8 μg/d) at 5 days after admission. Finally, his blood glucose level before each meal became <150 mg/dl with metformin (750 mg/d), mitiglinide (30 mg/d) and insulin glargine (3 units/d) treatment, and he left hospital.

Fig. Contrast-enhanced computed tomography of the abdomen.

This is the first report of the development of DKA in a patient who underwent distal pancreatectomy. We usually pay attention to the development of diabetes in totally pancreatectomized patients; however, we are not likely to be attentive to glucose metabolism in patients who undergo distal pancreatectomy. Although D2 gastrectomy, splenectomy, and chemotherapy with TS-1 have not been reported to be associated with the development of DKA, total gastrectomy has been reported to be involved in the development of diabetes.[2]In this case, over-intake of simple sugar, total gastrectomy, and distal pancreatectomy may lead to the development of DKA. We should presume that distal pancreatectomy is a risk for the development of DKA.

Hidekatsu Yanai

Department of Internal Medicine

Kohnodai Hospital

National Center for Global Health and Medicine

Chiba 272-8516, Japan

Tel: +81-47-373-3501

Fax: +81-47-372-1858

Email: dyanai@hospk.ncgm.go.jp

1 Barnes AJ, Bloom SR, Goerge K, Alberti GM, Smythe P, Alford FP, et al. Ketoacidosis in pancreatectomized man. N Engl J Med 1977;296:1250-1253.

2 Yamamoto H, Tsuchihashi H, Akabori H, Naitoh H, Maegawa H, Tani T. Postprandial hyperglycemia after a gastrectomy and the prediabetic state: a comparison between a distal and total gastrectomy. Surg Today 2008;38:685-690.