Endocrine Abstracts

Introduction: Diabetic ketoacidosis (DKA) is characterized by the triad – ketonemia, metabolic acidosis and hyperglycemia. It is typically associated with type 1 Diabetes Mellitus (T1D) and the most common culprits are infections and poor therapeutic compliance.

Clinical Case Description

The present case deals with a 25–year–old female patient, with T1D diagnosed in 2008, without microvascular or macrovascular complications. She presented with poor metabolic control (Haemoglobin A1c (HbA1c) = 11.7%) under functional insulin therapy with insulin glargine and aspart, guided exclusively by reading of the Flash Glucose Monitoring (CGM) system, which recorded values within glycemic goals.

The patient was admitted to the Emergency Room (ER) with DKA, exhibiting hyperglycemia of 578 mg/dl, severe metabolic acidemia (pH 6.9 and HCO3– not measurable – low) and ketonemia of 4.4 mmol/l. Other triggering factors were excluded.

This DKA was treated with fluid therapy and IV infusion of rapid acting insulin. Clinical and analytical resolution of DKA was achieved, progressing with oral tolerance and resuming subcutaneous insulin regimen. However, due to phlebitis of the left forearm in a site of arterial puncture and acute cystitis, DKA recurred. Standard treatment of DKA was reimposed, along with amoxicillin/clavulanic acid. After this recurrence, the patient exhibited flexion of the 4th and 5th fingers of the left hand, decreased strength in the ipsilateral hand and absence of distal pulses, consistent with left brachial artery and upper–extremity deep vein thrombosis which was treated with thromboembolectomy. At discharge, she presented good glycemic control under insulin pump therapy.

Five months later, the patient developed paracentral acute middle maculopathy, with hypovision of the left eye. For this reason, a genetic study was conducted, compatible with high prothrombotic risk (heterozygous Factor V Leiden mutation; homozygous methylenetetrahydrofolate reductase (MTHFR) mutation; Plasminogen Activator Inhibitor–1 (PAI–1) 4G/5G promoter polymorphism). Treatment with hyperbaric oxygen therapy was performed, with complete visual recovery along with rivaroxaban. Currently, under insulin perfusion pump, she presents sustained metabolic control (HbA1c = 6.2%).

Conclusion: This particular case alerts us to several risks: self–monitoring of DM1 exclusively based on a flash system, failure in the self–awareness of symptoms, possibility of recurrent DKA and, finally, thrombotic events as a serious and rare complication of DKA, in genetically predisposed patients.