Sepsis as a Precipitating Factor for Diabetic Ketoacidosis (DKA)

Pathophysiological Mechanism

Sepsis triggers a stress response that increases counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone) which oppose insulin action 1
This hormonal imbalance leads to increased hepatic glucose production, impaired peripheral glucose utilization, and enhanced lipolysis with subsequent ketogenesis 1
The inflammatory response in sepsis further exacerbates insulin resistance, contributing to hyperglycemia and ketone production 3
Sepsis can cause a significant increase in plasma triglycerides and free fatty acids (up to four-fold), potentially overwhelming the body's ability to utilize them properly 3

According to the American Diabetes Association guidelines, infection is the most common precipitating factor in the development of DKA 2
The American College of Cardiology is not mentioned in this context, however, the American Diabetes Association recommends considering infection as a precipitant in DKA development 2

When sepsis is identified as the precipitating factor for DKA, treatment must address both conditions simultaneously 4
Management includes aggressive fluid resuscitation to restore circulatory volume and tissue perfusion 4
Insulin therapy to correct hyperglycemia and resolve ketoacidosis 4
Appropriate antibiotic therapy based on suspected source of infection 4
Close monitoring of electrolytes, particularly potassium 4
Identification and treatment of the underlying infection source 4

DKA patients may be normothermic or even hypothermic despite having infection, primarily due to peripheral vasodilation 1
Hypothermia, if present, is a poor prognostic sign in DKA patients with infection 1
Abdominal pain in DKA patients may be either a result of the metabolic derangement or a sign of intra-abdominal infection requiring further evaluation 1