Endocrine Abstracts

Case history: A 39 year old male patient presented via ambulance to our unit with a deliberate mixed overdose. He had a past medical history of type 2 diabetes mellitus, depression and hypertension. He had ingested an uknown amount of atenolol, dapagliflozin, ramipril, co-codamol with both cocaine and benzodiazepines detected in urine toxicology. On arrival to hospital, the patient had fluid refractory hypotension, with a systolic blood pressure of 70mmHg and HR 45BPM. Given the concern of beta blocker toxicity he received an IV glucagon bolus with a good, although transient, haemodynamic effect. He was therefore commenced on a continuous glucagon infusion with a satisfactory and sustained haemodynamic response. Overnight, he began vomitng and became increasingly acidotic (H+70), despite BP 100/60 and passing good volumes of urine. U+ES, LFTs and lactate were all improving. Bedside ketone monitoring was not available on site. Laboratory ketones showed ‘positive+++’.

Investigations: On admission biochemistry revealed:

1. AKI (serum creatinine was 236 from baseline of 85) K+4.2

2. acidosis with H+50.4

3. paracetamol level was below the treatment line

4. salicylate and alcohol were undetectable

5. Lactate 4.0 mmol/l

Overnight bloods were repeated that showed a worsening acidosis, H+70, improving renal function (creatinine 120), normal liver function tests and a lactate of 1.0 mmol/l.

Results and treatment: This patient developed ketoacidosis without significant hyperglycaemia. At this point, the glucagon infusion was stopped, and patient was started on the National DKA protocol, with fixed rate insulin infusion and IV fluids. The patient remained haemodynamically stable on cessation of glucagon, the acidosis resolved rapidly with the commencement of IV insulin. The patient was fit for discharge two days later.

Conclusions and points for discussion: There is a lack of information and guidance available on the toxicology of the relatively novel SGLT2 inhibitors. In this situation, the overdose was confounded by acute renal failure (likely ACEi related) and refractory hypotension (secondary to beta-blockade). The euglycaemic DKA that ensued was likely secondary to both dapaglifolozin overdose and the concomitant administration of glucagon. Interestingly, insulin can be a therapeutic option in beta blocker overdose. In this case, routine glucose monitoring was not sufficient to ensure no adverse effect, in a diabetic patient receiving glucagon following beta-blocker and SGLTi overdose. The authors postulate bedside blood ketone monitoring could have prevented the development of euglycaemic DKA.