An unusual cause of severe lactic acidosis: cyanide poisoning after bitter almond ingestion

Dear Editor, Although cyanide exists in various alimentary sources like manioc, corn, bitter almonds, peach or apricot kernels, food-related cyanide intoxications are rare [1]. A 58-year-old healthy woman was admitted for sudden headaches, dizziness, vomiting, and generalized seizures. Prehospital medical services found her comatose (Glasgow Coma Score: 5) with bradycardia (30/min) and nonmeasurable blood pressure. She was promptly intubated and received fluids. A brain CT scan was normal. On intensive care unit (ICU) admission, her blood pressure was 80/40 mmHg, heart rate 62/min, SpO2 100% (FiO2: 100%), and temperature 37.0 C. Physical examination, electrocardiogram, and echocardiography were unremarkable. Severe lactic acidosis (arterial pH: 6.59, base deficit: 36.0 mmol/l, anion gap: 33.0 mmol/l, and plasma lactate concentration: 26.0 mmol/l) was assessed without ketosis, osmolar gap, liver or renal dysfunction. Fluids (2,000 ml), norepinephrine (0.5 mg/h), insulin, and sodium bicarbonate were infused. Routine toxicological screening was negative. Blood cyanide concentration was 2.77 mg/l (spectrophotometric method; N \0.2 mg/l; limit of detection: 0.06 mg/l) 6 h after coma onset. Hydroxocobalamin (10 g, 140 mg/kg) was immediately infused, resulting in complete recovery: lactate normalization (within 12 h, Table 1), norepinephrine weaning (20 h), acid/base balance correction (36 h), extubation (day 2), and ICU discharge (day 3). Her husband finally remembered that she had ingested a large quantity of bitter almonds (around 50) from the garden, 2 h before symptom onset. Accidental food-related cyanide poisonings are unusual [1]. Signs are delayed after ingestion, in relation to enzymatic processes producing cyanide in the gut from the ingested cyanogenic glucosides. Cyanide poisoning is rapidly fatal if not promptly treated. Clinical features are not specific, misleading the diagnosis. However, when suspicion is based on compatible circumstances, plasma lactate concentrations C8 mmol/l are an excellent predictor of blood cyanide concentrations C1 mg/l [2]. In our case, despite no relevant anamnesis, cyanide poisoning was suspected because of severe lactic acidosis with coma, hypotension, and bradycardia in the absence of sepsis. Reported symptoms of cyanide poisoning following almond/seed ingestion included headaches, dizziness, sweating, pink cyanosis, coma, seizures, hyperthermia, hypotension, polypnea, bradypnea, hypoglycemia, and lactic acidosis [3, 4]. To our knowledge, hyperlactatemia (pH 7.17, lactate: 14.3 mmol/l) was reported in only one case after ingestion of bitter almonds with laetrile tablets (containing amygdaline) given for alternative cancer treatment [3]. The present case is unique for two reasons: the severity of almondinduced lactic acidosis and its dramatic improvement after hydroxocobalamin infusion. Management of cyanide poisoning is based on advanced life support and antidotes. Despite cyanide-induced deficient cell oxygen utilization, increased oxygen delivery (FiO2: 100%) is useful to reactivate mitochondrial enzymes and other oxidative systems. Hydroxocobalamin is an effective and safe antidote binding cyanide on an equimolar ratio to form stable cyanocobalamin, which is excreted in urine [5]. Although we should