Introduction: Cocaine use has been reported as a precipitating factor for diabetic ketoacidosis (DKA) in patients with diabetes. The development of DKA in the setting of cocaine use is contributed by the stimulatory effect of cocaine on counter-regulatory hormone release, leading to increased ketoacid production. We report a case of DKA associated with cocaine ingestion.
Case: A 46-year-old man presented with a 1-day history of abdominal pain, nausea and polyuria. He had type 2 diabetes mellitus of 8 years duration and was on metformin monotherapy. There was no personal or family history of autoimmunity. Examination revealed tachycardia and mild epigastric tenderness. Investigations demonstrated: serum glucose 23.6mmol/L (range: 3.5-5.4), pH 7.02 (range: 7.30-7.40) and point-of-care ketone 4.6mmol/L (range: <0.6), consistent with severe diabetic ketoacidosis. Inflammatory markers were raised, likely due to acute inflammatory response to DKA as there was no evidence of an infection. An abdominal CT excluded acute intra-abdominal pathology including pancreatitis. The cause of his DKA was initially unclear and investigations for autoimmune diabetes were under way. Upon further questioning, it was revealed that he had ingested 1 gram of cocaine approximately 16 hours prior to presentation and was hospitalised 2 years ago with DKA associated with cocaine use. Due to the plausible temporal relationship between cocaine use and symptom onset, cocaine ingestion was implicated as the cause of his ketoacidosis. Intravenous insulin infusion was commenced. He was transitioned to subcutaneous insulin following resolution of ketoacidosis. HbA1c was 7.8%. Islet autoantibodies returned negative. He was counselled to avoid cocaine use in the future due to the risk of recurrent DKA.
Conclusion: Cocaine use is a known precipitating factor in the development of DKA. Our case illustrates the importance of considering recreational drug use as a trigger of DKA when the precipitant is not apparent after excluding common causes.