Euglycemic diabetic ketoacidosis in type 2-diabetes mellitus treated with SGLT2 inhibitors - a report on two cases

Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new second-line medication in the management of hyperglycemia in type 2 diabetes. These drugs can be associated with the development of diabetic ketoacidosis (DKA) with normal or moderately increased blood glucose levels. This is a life-threatening clinical condition termed euglycemic DKA, of which the diagnosis can be delayed due to the relative euglycemia. We report on two patients with type 2 diabetes who presented to the Emergency Department with malaise, nausea and vomiting. Both patients had been taking dapagliflozin for at least six months. A risk factor for the development of ketoacidosis, namely heavy alcohol consumption, was found in one of the patients. Arterial blood gas analysis showed severe metabolic acidosis with increased anion gap, positive serum and urine ketones and normal arterial lactate. The patients were treated in Internal Medicine with intravenous fluids, insulin, sodium bicarbonate and potassium. Dapagliflozin was stopped. Both patients recovered uneventfully. Even in the absence of significant hyperglycemia, accurate interpretation of arterial blood gas analysis and serum ketones should lead to correct diagnosis of euDKA

Hypokalemic rhabdomyolysis in a patient with a laparoscopic adjustable gastric banding

Rhabdomyolysis is an acute skeletal muscle disorder characterized by altered integrity of the cell membranes of muscle fiber cells. It can be related to a variety of factors: muscular trauma, muscle enzyme deficiencies, infections, drugs, toxins, alcohol ingestion, endocrinopathies and electrolyte imbalances such as hypokalemia. We report the case of a 46-year-old woman admitted to the Emergency Department for frequent episodes of vomiting associated with food intake in the last two weeks, general muscular weakness and myalgia. Physical examination on admission was unremarkable, except for a symmetrical and dominantly proximal muscular weakness of all four extremities. Blood pressure was 116/70 mmHg with a sinus bradycardia (53 beats/min) on the electrocardiogram. Laboratory tests showed a metabolic alkalosis with marked hypokalemia (K+= 1.9 mEq/l) and elevation of muscular enzymes (myglobin= 993 ng/ml, troponin T= 0,10 ng/ml e CK= 1113 U/l). No symptoms of recurrent rhabdomyolysis were reported, patient denied alcohol consumption and there was not clinical evidence of hyperthyroidism. A iatrogenic etiology could not be excluded for certain because patient was in therapy with lansoprazole (Naranjo algorithm 3/13) but, revealing medical history that she underwent a laparoscopic adjustable gastric banding for the treatment of a severe obesity, we focused our attention on hypokalemia, due to persistent vomiting. Fasting, administration of metoclopramide and infusion of potassium chloride resulted in steady improvement of clinical conditions and normalization of electrolyte imbalance. At the clinical follow-up of three months, after partial deflation of the gastric banding, the patient was asymptomatic with muscular enzymes and potassium levels in the normal range. Authors discuss the pathophysiologic mechanisms of these alterations

Metformin-induced lactic acidosis in a type 2 diabetic patient with acute renal failure

Metformin is a biguanide commonly used in type 2 diabetes mellitus (DM). Lactic acidosis, a potentially life-threatening metabolic disorder, may be due to a number of different causes, including metformin therapy. We present a case of a severe metformin-induced lactic acidosis in a patient with type 2 DM, admitted to the emergency department with a history of dehydration due to diarrhoea and complicated by acute renal failure. Patient complained malaise and severe weakness and was tachypneic (Kussmaul's respiration), agitated and confused, with a Glasgow Coma Scale score of 13/15. Heart rate was 75 b/min and blood pressure 110/80 mmHg. The pH was 6.87, HCO3-15 mmol/l, potassium 6.9 mEq/l. The renal function was markedly impaired with a creatinine of 9.75 mg/dl, and pancreatic enzymes, amylase and lipase, were also increased in absence of abdominal pain. Patient was treated with intravenous fluids, bicarbonate infusion and haemodialysis with bicarbonate buffered replacement fluid. Clinical conditions improved rapidly, with a progressive normalization of the acid-base balance and the other laboratory data. Authors discuss the pathophysiologic mechanisms of these alterations with particular regard to the role played by metformin as potential cause of lactic acidosis