Endocrine Abstracts

Purpose: To present a rare case of diabetic ketoacidosis due to thyrotoxicosis and massive pulmonary embolism.

Case presentation: A 40-year-old man from Cameroun, with history of type 2 diabetes treated with gliclazide and metformin, presented with vomiting and abdominal pain. His vital signs were: blood pressure 140/80 mmHg, heart rate 184 beats per minute and temperature 38.2 °C. On admission, laboratory investigation revealed hyperglycemia, hyperosmolality and metabolic acidosis with ketonouria. On examination, the thyroid gland was tender at palpation. Thyroid function tests showed thyrotoxicosis whereas the thyroid ultrasound scan diminished vascularity. Thyroid autoantibodies were negative. The patient was treated with iv fluids, continuous iv infusion of insulin and enoxaparin in prophylactic dose. Alongside, ibuprofen 1800mg daily, propranolol 80mg daily and prednisolone 30mg daily were given as acute thyroiditis treatment. Other causes of ketoacidosis were excluded (negative antibodies for latent autoimmume diadetes of the adult, c peptide: 3.3ng/ml, absent biochemical or clinical signs of infection) which lead to the deduction that the main cause of diabetic ketoacidosis was indeed thyrotoxicosis. During his hospitalization, the patient presented a prefainting episode with hypoxemia and hypotension. The ABGs revealed respiratory alkalosis while the laboratory results showed high levels of d-dimmers and thrombocytopenia. CTPA identified multiple deficits in main and sub-main arterial branches, confirming the diagnosis of massive pulmonary embolism. Since the patient was on prophylactic enoxaparin treatment, heparin induced thrombocytopenia (HIT) was suspected, nevertheless antibody testing was negative. Due to low platelets, thrombolysis was considered unsafe and the patient underwent successful thromboaspiration, with subsequent clinical and hemodynamic improvement. Although the antibodies for HIT were negative the patient was treated with γ-globulin which resulted in gradual platelet increase. All other inherited and acquired coagulation disorders were excluded and no deep vein thrombosis was found. Insulin dose requirements were reduced along with tapering of prednisolone dose. On long term follow up he maintained normal thyroid function and good glycaemic control solely on metformin 1700mg daily and sitagliptin 100mg daily.

Conclusion: Diabetic ketoacidosis is a rare complication in type 2 diabetes patients during acute illness. Thyrotoxicosis due to acute thyroiditis is a rare precipitating factor that should be considered in tachycardic febrile patients with diabetic ketoacidosis. Thyrotoxicosis induced diabetic ketoacidosis can be a highly challenging condition to treat and intensive monitoring is required.