Acute metonitazene poisoning reversed by naloxone

saturation of 62% on room air, a respiratory rate 44 breaths per min and a heart rate 144 beats per min. On arrival at hospital the patient was sweating and in respiratory distress; respiratory rate 30 breaths per min, oxygen saturations 89–91% on 15L O2, heart rate 143 beats per min, BP 176/109, GCS 15. Arterial blood gas analysis at 2h post-exposure showed pH 7.2, PCO2 8.8 kPa (66 mmHg), PO2 5.2 kPa (39 mmHg), HCO3 26mmol/L, BE 3.2. Subsequent arterial blood gas analysis showed worsening mixed acidosis with type 2 respiratory failure. The patient was intubated and ventilated 4h post-exposure. Vasopressor support was required and continuous venovenous haemodiafiltration was started for hyperkalaemia (K 7.8mmol/L) resistant to insulin/dextrose treatment. He received a single dose of intravenous hydrocortisone. Serial chest X-rays demonstrated worsening patchy consolidation throughout the lungs with the exception of the left lower zone. Due to worsening hypoxaemia and rising PCO2, despite proning, the patient was established on venovenous ECMO the same day as admission which was continued for 7 days. Veno-venous ECMO was used as opposed to veno-arterio ECMO as the patient did not have myocardial failure. A CT pulmonary angiography one day post-exposure showed multiple small volume bilateral non-occlusive pulmonary emboli and evidence of a chemical bronchopneumonia with extensive bilateral patchy consolidation, tree-in-bud opacity, and centrilobular ground-glass opacities (Figure 1). No pre-existing risk was established for pulmonary emboli. The patient was treated with low-molecular weight heparin, switched to argatroban due to sub-therapeutic anti-Xa concentrations and subsequently re-established on dalteparin. Clotrimazole and co-trimoxazole were given empirically due to respiratory secretions. Sputum cultures subsequently grew Haemophilus influenzae, Staphylococcus aureus, and Group B Strep. The patient was extubated on day 19. He self-discharged on day 34 before follow up chest imaging was conducted. Benzalkonium chloride is a quaternary ammonium compound which likely reacted with sodium hypochlorite in the patient’s respiratory tract to form chloramine compounds which caused the profound and widespread chemical pneumonia seen in this case. This case describes the early use of ECMO for a severe chemical pneumonitis adding to its previously described use for the management of acute respiratory distress syndrome (ARDS) following toxic gas exposures [3,4]. Disclosure statement