In May, 2005, a 32-year-old woman lost consciousness soon after drinking a non-alcoholic beverage. She was transported to hospital within 5 min, found to be unresponsive, and intubated. Before intubation, blood gas measurements on room air (possible venous sample), were: pH 7·846, pCO2 24·2 mm Hg, pO2 28·7 mm Hg, HCO3 41·8 mmol/L (base excess [BE] 26 mmol/L); O2 saturation was 79·4%. The beverage had a pH of 9; a working diagnosis of alkaline corrosive injury was made, and she was transferred to our emergency unit. When seen by us, about 1 h after poisoning, her blood pressure was 85/46 mm Hg, despite norepinephrine 8 μg/min; blood gases (on ventilator with 100% oxygen; O2 saturation 100%) pointed to metabolic acidosis: pH 7·096, pCO2 17·2 mm Hg, pO2 385 mm Hg, HCO3 5·4 mmol/L (BE –21·7 mmol/L); blood lactate concentration was 14 mmol/L. The anion gap was 37·6 mmol/L. Cyanide (CN) poisoning was suspected and 2·5 g intravenous hydroxocobalamine was given. Our patient showed signs of improvement 2–3 min after antidote, but a second dose was given 1 h later because of persistent severe metabolic acidosis. She continued to improve, regained consciousness, and was extubated the next morning. Her blood CN concentration on transfer to us was 288·6 μmol/L; her drink had been laced with 1·9% (fi nal concentration in the beverage) potassium cyanide (KCN). The patient was discharged 10 days later; when last seen in 2007, she was well. On May 17, 2005, over ten bottles of a non-alcoholic beverage were spiked with KCN in various convenience stores in Taiwan. Our patient was the fi rst of three people who were poisoned and who collapsed soon after consuming a small amount of the drink. Blood gas data are shown in the fi gure. Even accounting for the change in CO2 as a result of respiratory compensation, and the possible venous sample, the large change in HCO3 from A to B is probably due to huge acid production —typical of CN poisoning. The initial alkalosis seen in our patient could have been due to various factors. The pKa of KCN is 9·21 at 25°C. When it is given orally, the gastric acid environment favours formation of the unionised form of HCN and facilitates HCN absorption across the gastrointestinal mucosa. Initially, the absorbed HCN, particularly with smaller doses, stimulates central nervous system driven hyperventilation, leading to respiratory alkalosis (supported by blood gas data from the second case—not shown). In a pure respiratory alkalosis, we would have expected our patient’s blood pCO2 to be less than 10 mm Hg, given that pH was 7·846. It is possible that HCO3 formation in the stomach could have contributed to our patient’s initially raised blood pCO2. In the stomach, HCl is depleted in gastric secretions because it reacts with KCN. Each mmol of H secreted will generate 1 mmol of HCO3, leading to a transient increase in plasma HCO3. In KCN ingestion, there is no stimulus for HCO3 secretion in the duodenum because of gastric acid depletion and quick absorption of HCN. The net result is an increase in plasma HCO3 concentration. Severe metabolic acidosis, with raised lactate, occurred quickly, because KCN inhibits the electron transport chain and anaerobic respiration. Hydroxocobalamine 5–10 g is the recommended treatment. We gave our patient an initial dose of 2·5 g hydroxocobalamine because of the potential for mass casualties and low stores of antidote. Only prompt diagnosis and antidote can resolve severe CN poisoning.