‘Single presentation, two lifesaving diagnosis’- Simultaneous new presentation of diabetic ketoacidosis and primary adrenal insufficiency
R Maniusyte, S Zaman, D Huntley, T Vakilgilani, St Marys Hospital, Imperial College Healthcare NHS Trust
56-year-old lady visiting from Russia, presented to A&E with a 5-day history of severe vomiting. She was otherwise fit and well and not on any medications. She was not a smoker and drank alcohol only occasionally. Her family history included maternal type 2 diabetes. She had a two-week history of polyuria and polydipsia, but denied any weight loss.
On arrival, she was found to be hypotensive with a BP of 85/60 mmHg and tachycardic, HR:110/min. Her GCS was 15/15 and systemic examination was unremarkable. Investigations showed sodium 101 mmol/L, potassium 5.0 mmol/L, pH 7.26, HCO3 17mmol/L, glucose 23.7 mmol/L, blood ketones 6 mmol/L, serum osmolality 234 mmol/L, urine osmolality 575 mOsm/L, urine sodium 85 mEq/L, random cortisol 129 nmol/L and normal renal, liver and thyroid function tests. The diagnosis of new onset diabetes presenting with diabetic ketoacidosis (DKA) was made. Additionally, the inappropriately low serum cortisol and persistent hypotension raised the possibility of adrenal insufficiency.
She was admitted to medical HDU and treated with IV hydrocortisone 100 mcg four times daily, insulin infusion and careful rehydration with IV fluids in view of severe hyponatraemia. Hypertonic saline was avoided due to the absence of neurological features. Her glucose and sodium were closely monitored and fluids were managed accordingly. DKA resolved and serum sodium increased appropriately to 128 mmol/L within the next 72 hours.
Further investigations were undertaken, including a short Synacthen test, which revealed cortisol 0 min – 208 nmol/L, 30 min – 213 nmol/L and 60 min – 184 nmol/L with significantly elevated ACTH of 1100 pmol/L. Adrenal antibodies were positive and CT pancreas and adrenals was normal. Renin and aldosterone were 22.9 pmol/ml/hr and <60 pmol/L respectively.
With regards to diabetes, C-peptide was 323 nmol/L with paired blood glucose of 15.3 mmol/L, HbA1C was 110 mmol/mol and islet cell and GAD antibodies were positive. Once she was able to eat and drink, her parenteral steroid was switched to oral prednisolone and she was commenced on oral fludrocortisone and subcutaneous insulin injections.
Her results were consistent with primary adrenal insufficiency and type 1 diabetes. She was educated about diabetes, insulin administration, steroid use and sick day rules. DKA and acute adrenal insufficiency have overlapping precipitating factors (eg. infection), clinical presentation (vomiting, general weakness, dehydration, confusion) and biochemical abnormalities (hyponatraemia, metabolic acidosis), therefore, a new diagnosis of acute adrenal insufficiency can be easily masked and missed.