Euglycemic Diabetic Ketoacidosis in the ICU: 3 Case Reports and Review of Literature

Abstract

Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus, both type I and type II, as well as other types with diabetes such gestacional diabetes mellitus. It is characterized by blood glucose levels greater than 250 mg/dL and metabolic acidosis (pH < 7.3 and serum bicarbonate < 15 mEq/dL) with an increased anion gap and the presence of ketone bodies in the blood or urine. Within this pathology, there is a subgroup of pathologies which are characterized by being present with no signs of hyperglycemia, posing a diagnostic challenge due to the absence of the main sign of the pathology and the diversity of their pathophysiology. In this article, we will present 3 clinical cases with 3 different forms of clinical presentation: a case of DKA in pregnancy, a case of DKA associated with the use of sodium-glucose cotransporter 2 (SGLT-2) inhibitors, and a third case related to sepsis, together with a narrative review of the literature on the topic.

Sodium-Glucose Linked Transporter Inhibitors as a Cause of Euglycemic Diabetic Ketoacidosis on a Background of Starvation

“…Other causes of euglycemic DKA include pregnancy, cocaine abuse, pancreatitis, cirrhosis, and sepsis; thus, normal plasma glucose levels should not be sufficient to rule out the possibility of DKA in a patient especially if he/she is on sodium-glucose linked transport inhibitors [12,13]. Although the risk of euglycemic DKA in type II DM associated with sodium-glucose linked transport inhibitors is low enough to have an "acceptable frequency" according to the American Diabetes Association, it may be higher in patients with long-standing type II DM during periods of stress such as post-surgery and prolonged starvation [14].…”

Diabetic Ketoacidosis in an Euglycemic Patient

“…Approximately 2.6%-3.2% of DKA admissions are euglycemic [ 8 - 9 ]. DKA-associated with SGLT2 inhibitors has rates ranging from 0.16 to 0.76 events per 1000 patient-years in patients with type 2 diabetes.…”

Euglycemic Diabetic Ketoacidosis in a Young Pregnant Woman Precipitated by Urinary Tract Infection

“…Mechanisms of glycemic control change with each trimester of pregnancy. In the first trimester, placental steroids lead to increased insulin production and decreased fasting glycemia [12]. In later stages of pregnancy, there is an increase in counterregulatory hormones (such as human placental lactogen [HPL]) and decrease in insulin deficiency due to hormonal changes (increase in estrogens, progesterone, HPL, tumor necrosis factor-alpha) both of which lead to hyperglycemia [13,14].…”

“…In later stages of pregnancy, there is an increase in counterregulatory hormones (such as human placental lactogen [HPL]) and decrease in insulin deficiency due to hormonal changes (increase in estrogens, progesterone, HPL, tumor necrosis factor-alpha) both of which lead to hyperglycemia [13,14]. In late pregnancy, the dwindling glucose levels due to increased demand from fetus and placenta, decreased glycogenolysis and gluconeogenesis along with increased renal loss of glucose, causes maternal metabolism to enter a catabolic state and switch to fat as a primary fuel for energy [12]. Increased lipolysis and free fatty acid delivery to the liver causes increased ketogenesis.…”