Extreme bradycardia in BRASH syndrome unmasked by severe amiodarone-induced hypothyroidism

Introduction: BRASH syndrome – bradycardia, renal failure, AV nodal blockade, shock and hyperkalaemia – is a self-amplifying pathophysiological loop. Its association with severe amiodarone-induced hypothyroidism is rarely described in detail. Case description: A 79-year-old woman with permanent atrial fibrillation on long-term amiodarone and bisoprolol presented after prolonged unwitnessed floor immobilisation with extreme bradycardia (24–30 bpm), haemodynamic instability, KDIGO stage 3 acute kidney injury, hyperkalaemia (5.5 mmol/l), metabolic acidosis, rhabdomyolysis and profound hypothyroidism (TSH 68.5 mUI/l; free T4 4.62 pmol/l) against a normal thyroid baseline 13 months prior. The Popoveniuc myxoedema coma score was 45 (high-risk zone). High-sensitivity troponin T showed flat kinetics consistent with type 2 myocardial injury. Isoproterenol was required for bradycardia refractory to initial metabolic correction, achieving a ventricular rate of 62–68 bpm with QTc shortening from 0.62 s to 0.38 s. The patient was discharged on day 8 with renal recovery and improving thyroid function. Thyroid antibody negativity at 30-day follow-up was consistent with an amiodarone-induced rather than autoimmune aetiology. Conclusion: This case illustrates BRASH syndrome presenting with only mild hyperkalaemia in the context of severe amiodarone-induced hypothyroidism, which may have potentiated the pathophysiological loop. Systematic thyroid monitoring during long-term amiodarone therapy and multi-target metabolic correction, including isoproterenol as a pharmacological bridge, may avert invasive pacing.