Postmortem Diagnosis of Diabetic Ketoacidosis Presenting as the “Dead-in-Bed Syndrome”

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 758-785-Diabetes Case Reports: Type 1, Type 2, MODY & Complications
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-768
Jennie Luna*1, M.G.F. Gilliland2, Colin Hebert3 and Robert J Tanenberg1
1Brody School of Medicine, East Carolina University, Greenville, NC, 2Brody School of Medicine, Greenville, 3Vidant Medical Center, Greenville, NC
Introduction:  Death at home from severe hypoglycemia is not uncommon in young patients with type 1 diabetes (the so called “Dead in Bed Syndrome”).  Recent literature has documented both the hypoglycemia and potentially fatal arrhythmias that are hypothesized to result in death.  On the other hand, death from diabetic ketoacidosis (DKA) almost invariably occurs in the hospital setting (e.g., emergency room or intensive care unit).

Clinical case:  We report a case of a 25-year-old male with a history of poorly controlled type 1 diabetes mellitus despite use of an insulin pump (continuous subcutaneous insulin infusion therapy), who was found deceased in his own undisturbed bed.  There was vomitus noted on the pillow but no obvious cause of death.  The insulin pump and tubing were intact and attached to the left lower quadrant abdominal wall.  As part of the autopsy, the insulin pump and his glucometer were downloaded.  The insulin pump was empty but working correctly with the last reported activity 3 days prior to his demise.  Vitreous humor fluid was obtained and analyzed demonstrating: glucose 755 mg/dl (n=70-105 mg/dl), sodium 131 mEq/L (n=135-145 mEq/L), chloride 90 mEq/L (n=96-108 mEq/L), carbon dioxide <5 mEq/L (n=22-33 mEq/L) and an anion gap >36 mEq/L (n=4-12 mEq/L).  Toxicology was negative for drugs and revealed elevated levels of acetone and Isopropanol.  This biochemical evaluation was consistent with diabetic ketoacidosis (DKA) as the cause of death.  Microscopic examination of the kidneys showed marked subnuclear vacuolization in the proximal tubules, consistent with the diagnosis of Armanni-Ebstein lesion.  First described in 1877, these lesions are strongly associated with diabetic ketoacidosis and reflect accumulation of lipid in the setting of excessive glucose reabsorption seen preceding death from diabetic coma. 

Conclusion:  The most likely cause of death at home in young patients with type 1 diabetes is severe hypoglycemia.  However in this case, autopsy confirmed DKA based on vitreous humor biochemistry and microscopic examination of the kidneys demonstrating the Armanni-Ebstein phenomenon.  We conclude analysis of the vitreous fluid and microscopic examination of the kidneys for the presence of Armanni-Ebstein lesion are useful to help determine the cause of death in patients with type 1 diabetes mellitus.

Nothing to Disclose: JL, MGFG, CH, RJT

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