Endocrine Abstracts

Case history: 41-year-old lady with background of T1DM (1993), previous DKA (2017), and treated thyrotoxicosis (2017-2019) presented with 3 day history of vomiting, diarrhoea, poor oral intake, and shortness of breath. She was anxious, though not agitated. She denied palpitation though remained tachycardic. She denies abdominal pain, jaundice, or oedema legs. Her only medication was basal-bolus regimen to which she was compliant. She does not smoke, drink or use illicit drugs. O/E: PR 140/min, BP 121/55 mmHg, Temperature 38.2⁰C, RR 24/min, Saturation 96% (air). She was severely dehydrated with hand tremors and a nontender diffuse goitre without bruit, thyroid eye disease or heart failure signs. Systemic examination was otherwise unremarkable.

Investigations: VBG: pH 7.176, HCO3^-8.9, base excess -17.8, glucose 23.2, lactate 5.8. Ketones 6.4. Bloods showed Na⁺ 135, K⁺ 2.9, Urea 8.4, Creatinine 53, eGFR >90, Mg²⁺ 0.54, Ca²⁺ 2.45, CRP 3.7, FBC mild neutrophilic leucocytosis, β-hCG negative. ECG showed sinus tachycardia, Chest X-ray was normal, and urine dip ruled out infection. TSH <0.01, Free T4 >100, Free T3 47.7, TRab positive, NT-pro-BNP 4390, and bedside ECHO mild LVSD.

Results and treatment: DKA protocol initiated on arrival. As sinus tachycardia persisted despite adequate hydration, and no other specific trigger for DKA found, in view of previous thyrotoxicosis, a relapse was considered. Bloods confirmed thyrotoxicosis and Burch-Wartofsky Point Scale (BWPS) score of 55 was highly suggestive of thyroid storm. Urgent endocrine review was sought and patient put on PTU [500 mg stat, 200 mg Q4H], hydrocortisone [200 mg stat, 100 mg TDS], propranolol [40 mg TDS], and cholestyramine [4 gram TDS]. Patient was managed in ITU for 48 hours with endocrinology and cardiology inputs. Electrolyte imbalance were corrected.

Conclusion and points for discussion: When common triggers for DKA including infection, infarction, ‘infant-on-board’, indiscretion, and insulin deficiency are excluded, we should look for rare triggers like drugs, thyrotoxicosis, Cushing’s or acromegaly. Vomiting and shortness of breath are so common with DKA that, we may fail to consider possibility of thyroid storm. Renal loss of Mg²⁺ from DKA and GI loss from thyrotoxicosis could explain the hypomagnesemia and resultant hypokalaemia. Fever, acute confusion, and deranged LFTs could all be misleading, as they may point towards sepsis, whereas they might have originated from thyroid storm. Both DKA and thyroid storm are procoagulant states. Diagnosis of thyroid storm is clinical, and is not proportionate to the severity of thyroid dysfunction. Early diagnosis which requires a high index of suspicion would improve the outcome.