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Background Calcium channel blocker (CCB) overdose carries substantial mortality without advanced organ support. Ingestion of a fixed-dose antihypertensive combination with a non-steroidal anti-inflammatory drug (NSAID) is an uncommon polypharmacy toxidrome. The role of intravenous lipid emulsion (ILE) and methylene blue in refractory cases remains poorly defined. Case report A 64-year-old man (135 kg) ingested approximately 300 mg amlodipine, 300 mg perindopril, 75 mg indapamide and 15,000 mg naproxen with ethanol. Despite apparent stability on arrival he deteriorated to 77/47 mmHg, pH 7.20 and lactate 10.5 mmol/L. Seven hours of escalating treatment — noradrenaline (peak 58 mcg/min), vasopressin, calcium and high-dose insulin euglycaemic therapy (HIET) — failed to restore haemodynamic targets. Intralipid 20% was given (total approximately 8.9 mL/kg), followed 35 minutes later by methylene blue 140 mg (1.0 mg/kg). Lactate fell from 10.5 to 6.1 mmol/L over the subsequent 55 minutes with the noradrenaline dose unchanged. All vasopressors were stopped within 14 hours. HIET was accompanied by concurrent glucose, potassium and phosphate nadirs (1.7, 1.7 and 0.27 mmol/L). KDIGO stage 2 acute kidney injury (peak creatinine 303 µmol/L) required no renal replacement therapy and resolved completely (creatinine 81 µmol/L at 3.5 months). The patient was discharged on day 9. Conclusion Sequential ILE and methylene blue were temporally associated with rapid metabolic recovery in refractory circulatory shock following polypharmacy antihypertensive overdose. Individual contributions cannot be determined from a single case, and a delayed effect of concurrent HIET cannot be excluded. These agents may represent rescue options when conventional therapy is insufficient.
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Danial et al. (2026) studied this question.
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