Case Presentation: TS is a 58 year-old male with a past medical history of prediabetes, pulmonary embolism, and stage II colon cancer treated via hemicolectomy in 2016 who presented to the hospital with dyspnea and altered mental status. On exam, he was febrile to 38.6 degrees Celsius. His abdomen was distended and diffusely tender to palpation. He was hypoxic and severely tachypneic with Kussmaul respirations. The patient was started on BiPAP and admitted to the ICU. His labs revealed a blood glucose of 755, anion gap of 26, bicarbonate of 6, beta-hydroxybutyrate of 8.5, and a lactate of 7.1. The lipase level was greater than 1800, and the triglyceride level was 528. He was anuric with acute renal failure on admission. The patient underwent a CT of his abdomen and pelvis that revealed severe pancreatitis. Of note, his most recent hemoglobin A1c (HbA1c) 5 years ago was 6.1%. Repeat HbA1c upon admission was 12.0%. He was diagnosed with diabetic ketoacidosis (DKA) in the setting of severe pancreatitis. The patient was started on IV insulin and fluids. Throughout the night, he showed further signs of distributive shock as he became hypotensive with worsening mentation. He was intubated for airway protection, initiated on CRRT, and started on vasopressors as well as empiric antibiotics. The infectious work-up was unrevealing, and antibiotics were discontinued. He eventually improved on IV insulin with significant fluid repletion and was subsequently extubated.
Discussion: This is a fascinating case, as it is unclear whether the acute pancreatitis led to DM complicated by DKA, or whether his prediabetes progressed to poorly-controlled DM, leading to DKA and hypertriglyceridemia with development of acute pancreatitis. Recent literature studies show an association between new diagnoses of DM and acute pancreatitis. A meta-analysis from 2014 revealed that 15% of patients were diagnosed with DM within 12 months of acute pancreatitis. This risk increased by more than twofold over 5 years. Another meta-analysis from 2019 found heterogeneity between the incidence of DM following cases of severe pancreatitis and cases of mild pancreatitis. The incidence was found to be 39% in severe cases and 14% in mild cases. These studies support the idea that this patient may have developed DM in the setting of acute pancreatitis. There are also reports of rare cases of DKA causing acute pancreatitis due to hypertriglyceridemia. According to a recent case series, this triad of hypertriglyceridemia, DKA, and acute pancreatitis occurs in approximately 4% of cases. The pathophysiology is well-understood, as DKA is an insulin-deficient state that leads to conversion of free fatty acids into VLDL. However, low levels of lipoprotein lipase lead to poor clearance of VLDL and consequent elevation of triglycerides. The same study notes that this triad is associated with a worse prognosis than simple acute pancreatitis. It is more likely to present with multi-organ failure and has a higher inpatient mortality rate. Thus, it is also possible that the patient’s DKA led to a severe case of pancreatitis.
Conclusions: This case represents a rare, severe manifestation of DKA. It is unclear whether the acute pancreatitis led to new-onset DM with DKA or vice versa. It also reinforced medical management of DKA in the setting of multi-organ system dysfunction. The patient’s anion gap eventually closed, and he was transitioned to basal-bolus insulin. As he continued to improve, he was weaned off vasopressors, extubated, and transferred to the medicine floor for further management.