Retrospective derivation of a causal pathway for diabetic ketoacidosis in adult patients with type 2 diabetes mellitus.

Background: Type 2 ketone-prone diabetes mellitus (T2KPDM) is thought to occur in men of African descent, with obesity who experienced prolonged hyperglycemia; the role of medication non-adherence as a contributing cause remains unstudied.

Research design and methods: This was a retrospective study of unique adults (>18 years) who sought emergency care one of four hospitals in the greater Detroit area. Patients were identified on the basis of a laboratory order for a ß-hydroxybutyrate concentration. Two research coordinators abstracted 119 data fields. Patients were divided into four phenotypes: (1) no prior DM, (2) type 2 DM without prior ketosis, (3) type 2 with prior ketosis and (4) type 1 DM. A ß-hydroxybutyrate >20 mg/dL defined diabetic ketoacidosis (DKA). A directed acyclic graph was constructed to diagram a causal pathway.

Results: Of 450 patients, 326 were non-type I and 37% of these had DKA. Concentrations of ß-hydroxybutyrate, glucose, bicarbonate were not different between non-type1 versus type 1 DM patients. Admission rates to the ICU and hospital lengths of stay were similar between the four phenotypes with DKA. We found no association with sex, race or body mass index. Unadjusted odds for DKA were significant for non-adherence (odds=1.74, 95% CI 1.08 to 2.21) arrival by Emergency Medical Services (odds=0.54, 95% CI 0.33 to 0.86) and private or Medicare insurance (odds=6.80, 95% CI 4.00 to 11.60). The median HbA1C was statistically higher in patients with DKA (median 11.3%) versus those without DKA (median 9.5%, Mann-Whitney U p<0.001) and was also higher in patients with a history of non-adherence. In multivariable analysis, non-adherence was found to be a mediator of DKA with T2KPDM.

Conclusions: in Detroit, MI, prior ketosis and private or Medicare health insurance were significantly associated with new or recurrent DKA in T2KPDM. Medication non-adherence had a mediating role.