DEATH CAUSED BY HYPERGLYCEMIC HYPEROSMOLAR STATE AT THE ONSET OF TYPE 2 DIABETES ALBA E. MORALES, MD, AND ARLAN L. ROSENBLOOM, MD Seven obese African American youth were considered to have died from diabetic ketoacidosis (DKA) due to type 1 diabetes, despite meeting the criteria for hyperglycemic hyperosmolar state and not for DKA. All had previously unrecognized type 2 diabetes, and death may have been prevented with earlier diagnosis or treatment. (J Pediatr 2004;144:270-3) T ype 2 diabetes mellitus (T2DM), associated with increased rates and severity of obesity, now accounts for as much as one half of newly diagnosed diabetes in children age 10 to 21 years, depending on the socioeconomic and ethnic composition of the population. 1 Acute decompensation with diabetic ketoacidosis (DKA) has been recognized to occur at the time of diagnosis in as many as 25% of children with T2DM. 1 Hyperglycemic hyperosmolar state (HHS), considered a complication in elderly patients with T2DM, has not been appreciated in young patients with T2DM. 2 We report seven obese African American youths who died with HHS at the onset of T2DM. CASE REPORTS Patient 1 was seen in the emergency department after 5 days of dizziness, lethargy, headaches, and vomiting, and was given oral ibuprofen for migraine. Later the same day, his pediatrician prescribed a combination of aspirin, butalbital, codeine, and caffeine (Fiorinal; Novartis Pharmaceutical Corp, East Hanover, NJ). The next day, the pediatrician saw him again and told him to continue taking this medication and to eat a soft diet. One day later, the patient became extremely lethargic and weak and was taken to a different emergency department, where diabetes was diagnosed and treated with appropriate doses of insulin and intravenous saline. Ten minutes after rapid intravenous injection of 100 mEq sodium bicarbonate, his serum potassium concentration was 1.8 mmol/L. An electrocardiogram showed multiple rhythm disturbances. He died 3 hours later, after a transvenous pacemaker failed to restore cardiac rhythm. Postmortem findings included mild fatty changes of the liver and no inflammatory changes in the pancreatic islets (Table). Patient 2 had been diagnosed 2 years earlier with hypercholesterolemia. His father and older brother had T2DM. When his primary care physician saw him for a routine sports examination, the urine analysis showed a large glucose concentration. The next day, he began persistent emesis, abdominal pain, and malaise, and 3 days later, he saw his physician again. His weight had dropped 3.2 kg during the 4 days between the visits, and he had a diffusely tender abdomen. He was prescribed promethazine suppositories and told to increase his oral intake of fluids. Three days later, he was found unresponsive, asystolic, and apneic, with fixed, dilated pupils. At postmortem examination, vitreous glucose concentration was 34 mmol/L (619 mg/dL); there was acute purulent bronchiolitis and cerebral edema. Microscopic examination of the pancreas showed no inflammatory changes in the islets. Patient 3 was seen by his primary care physician for nausea, vomiting, diarrhea, increased thirst, and increased urination for 1 day. He was told to refrain from eating for 6 to 8 hours. After numerous episodes of vomiting and diarrhea, he went to an emergency department, where he was given 2 L lactated Ringer solution intravenously; no laboratory studies were performed. The electrocardiogram monitor was noted just before discharge to From the Division of Pediatric Endo- crinology, University of Florida Col- lege of Medicine, Gainesville, Florida. Presented in part at the annual meeting of the Pediatric Academic Societies, Baltimore, Maryland, May 4-7, 2002. Submitted for publication June 25, 2003; revision received Sept 4, 2003; accepted Oct 28, 2003. Reprint requests: Arlan L. Rosen- bloom, MD, Children’s Medical Ser- vices Center, 1701 SW 16th Ave, Building B, Gainesville, FL 32608-1153. E-mail: rosenal@peds.ufl.edu. 0022-3476/$ - see front matter Copyright ª 2004 Elsevier Inc. All rights reserved. 10.1016/j.jpeds.2003.10.061 DKA Diabetic ketoacidosis HHS Hyperglycemic hyperosmolar state T1DM Type 1 diabetes mellitus T2DM Type 2 diabetes mellitus 270