9326 A Case Of Diabetic Ketoacidosis Obscured By Metabolic Alkalosis In An Individual With End-stage Renal Disease

Abstract Disclosure: A.L. Messersmith: None. K. Bayrakdar: None. D. Killeen: None. Diabetic ketoalkalosis (DKALK) is a term coined in the literature by Bleicher in 1967, characterized by diabetic ketoacidosis (DKA) with concomitant metabolic alkalosis. Patients with DKALK may present with normal to elevated bicarbonate and an alkalotic pH secondary to recurrent vomiting, ingestion of alkali, contraction alkalosis from hyperglycemia-induced osmotic diuresis, or diuretics. Here we discuss a 33-year-old female who presented to the hospital with non-bloody, nonbilious vomiting for two days and unremitting abdominal pain that started the day of arrival to the emergency department (ED) along with two ulcers localized to the lateral aspect of her foot with purulent discharge. Her past medical history was significant for insulin dependent diabetes mellitus complicated by recurrent DKA, diabetic peripheral neuropathy and retinopathy, amputation of the left fifth toe at the mid metatarsal secondary to osteomyelitis, hypertension, and end-stage renal disease (ESRD) on hemodialysis (HD). Blood glucose was 302 mg/dL, bicarbonate 30 mmol/L, chloride 96 mmol/L without an anion gap, lactic acid 3.6 mmol/L, and urinalysis positive for glucose and ketones. Blood cultures grew Staphylococcus hominis and epidermidis, and Actinetobacter lwoffii. Magnetic resonance imaging was compatible with chronic osteomyelitis of the fifth metatarsal stump. On the third day of hospitalization, after worsening abdominal pain, nausea, and vomiting, repeat laboratory results showed a blood glucose 580 mg/dL, chloride 95 mmol/L, beta-hydroxybutyrate 4.23 mmol/L; and a pH of 7.609 and bicarbonate of 23 mmol/L on ABG with an anion gap of 23 mmol/L. The patient was treated with insulin, intravenous fluids, potassium, and antibiotics with resolution of symptoms. Diabetic ketoalkalosis is a condition rarely reported in the literature. Case reports have included association with type I diabetes in patients with underlying gastroparesis presenting for abdominal discomfort and vomiting. Loss of hydrochloric acid from vomiting increases bicarbonate in the body. Volume contraction activates the renin-angiotensin-aldosterone system (RAAS), which acts on the kidneys to reabsorb sodium and bicarbonate, generate new bicarbonate, and excrete hydrogen ions into the urine. The delta ratio can be used to identify DKALK, along with the presence of serum or urine ketones, and an elevated anion gap. In DKALK the de