What is more likely to cause diabetic ketoacidosis (DKA), pancreatitis or pyelonephritis?

From the Guidelines

Pancreatitis is more likely to cause diabetic ketoacidosis (DKA) than pyelonephritis. This is because pancreatitis directly affects insulin production and metabolism, creating a higher risk for DKA development, as noted in a study on hyperglycemic crises in diabetes 1. When the pancreas becomes inflamed, insulin secretion can be significantly impaired, leading to severe insulin deficiency. Without adequate insulin, cells cannot use glucose for energy, causing the body to break down fat for fuel instead, producing ketones and leading to acidosis. Additionally, the metabolic stress from pancreatitis increases counter-regulatory hormones like glucagon, cortisol, and catecholamines, which further elevate blood glucose and ketone production. While pyelonephritis (kidney infection) can potentially trigger DKA through general inflammatory stress responses and dehydration, it doesn't directly impair insulin production like pancreatitis does, as discussed in the context of precipitating factors for DKA or HHS 1. Some key points to consider include:

• Infection is a common precipitating factor for DKA or HHS, but pancreatitis has a more direct impact on insulin production and metabolism.
• Other precipitating factors for DKA or HHS include cerebrovascular accident, alcohol abuse, myocardial infarction, trauma, and certain drugs, as outlined in the study on hyperglycemic crises in diabetes 1.
• Patients with pancreatitis should be closely monitored for signs of DKA, including excessive thirst, frequent urination, nausea, vomiting, abdominal pain, and fruity-smelling breath, especially if they have diabetes or are at risk for it.

From the Research

Comparison of DKA Causes

• Pancreatitis is more likely to cause DKA than pyelonephritis, as several studies have shown a strong association between acute pancreatitis and DKA 2, 3, 4.
• A study of 100 consecutive episodes of DKA found that 11% of patients had acute pancreatitis, with the etiology of AP being hypertriglyceridemia, alcohol, drug-induced, or idiopathic 2.
• Another study found that 28% of acute pancreatitis patients with type 2 diabetes developed DKA within 48 hours of admission, with risk factors including age, BMI, poor previous blood glucose control, and uric acid concentration 3.
• In contrast, there is limited evidence to suggest a direct link between pyelonephritis and DKA, although it is possible that pyelonephritis could trigger DKA in patients with underlying diabetes or other risk factors.
• A case report highlighted the rare occurrence of DKA as a complication of acute pancreatitis in a nondiabetic patient, suggesting that pancreatitis can cause DKA even in the absence of pre-existing diabetes 4.

Pathophysiology

• The destruction of pancreatic tissue in acute pancreatitis can lead to the release of glucagon and other hormones, contributing to the development of DKA 5, 2.
• Stress hyperglycemia and post-pancreatitis diabetes mellitus are also potential underlying mechanisms for the development of DKA in patients with acute pancreatitis 4.
• The association between pancreatitis and DKA is supported by studies showing that patients with acute pancreatitis are at increased risk of developing DKA, particularly if they have underlying diabetes or other risk factors 2, 3.