However, therapeutic strategies are still debated. Many antidotes are available and efficient. A plasma lactate concentration > or = 10 mmol/L in fire victims without severe burns and > or = 8 mmol/L in pure cyanide poisoned patients is a sensitive and specific indicator of cyanide intoxication. The biological hallmark is lactic acidosis. Clinical features include coma, respiratory arrest and cardiovascular collapse. Understanding both available antidotes and their respective benefits, contraindications is highly essential for intensivists.Cyanide poisoning may result from different exposures: residential fires, industrial accidents, drug and plant intoxication. Out of two antidotes, hydroxocobalamin is claimed to have fewer adverse events than the cyanide antidote kit 6. Cyanide poisoningis treatable when quickly recognized and treated with antidote. Unfortunately, there is no test for rapid confirmation of cyanide toxicity, so treatment must be based on a presumptive diagnosis 3. Clinical presentation of acute cyanide exposure varies depending on amount starting from dizziness to loss of consciousness, cardiac and respiratory failure, hypoxic brain injury, and dose-dependent death within minutes to hours 5. Inhibition of oxygen utilization causes sudden surge of anerobic metabolism 4. Once in the bloodstream, cyanide rapidly reacts with ferric ions of cytochrome oxidase a, a mitochondrial enzyme responsible for oxidative phosphorylation in the final pathway of cellular respiration. It's molecular structure consists of a cyano group (a carbon triple-bonded to nitrogen) C≡N in combination with potassium or hydrogen 3. She improved gradually over night and was extubated the next day.Ĭyanide is a deadly poison, utilized in some pharmaceutical and chemical industries, and is rarely available for public access 1, 2. Over next few hours patient started improving in terms of blood pressure, ABG and sensorium with continuation of other conservative treatments. Antidote for cyanide was administered with sequential injection of 3% sodium nitrite 600 mg IV over 3 minutes, followed by 25% sodium thiosulfate 25 g IV over 30 minutes at 2:40 pm. Family was counseled regarding the most probable diagnosis as cyanide poisoning, urgency of situation, time and unavailability for confirmatory tests and the antidotes available. Upon questioning she confirmed nonverbally, an intentional consumption of substance, and that to be cyanide through. Around this time the patient started regaining consciousness partially, despite continued severe metabolic acidosis. A strong suspicion of cyanide poisoning was made but could not be confirmed because of unavailability of rapid laboratory testing. Simultaneous venous blood gas analysis from the central vein and arterial blood gas testing revealed similar and high values of SCvO 2 and SPaO 2 (92% and 97% respectively). The family had no knowledge regarding access to substances that can cause cyanide poisoning. Carbon monoxide poisoning was ruled out with the sudden onset. We suspected a carbon monoxide poisoning or cyanide poisoning. ![]() We got bright red blood, which was mimicking an arterial sample, but venous placement of cannula was reconfirmed with a USG and free flow of fluid method and subsequently with blood gas analysis. Central venous cannulation with ultrasound guidance was tried via left internal jugular vein in view of ongoing resuscitation and use of vasopressors. ![]() Urine toxicology, electrolyte, renal and liver function markers and urgent CT brain was ordered. Investigations to evaluate sudden onset unconsciousness and shock were initiated with a differential diagnosis including anaphylactic shock, vasovagal episode, massive stroke or substance abuse. Arterial blood gas reports at 1:50 pm revealed a severe acidosis of combined respiratory and metabolic origin with lactate 15 mmol/l and bicarbonate 6 mmol/l. She was intubated, connected to the ventilator and resuscitated with crystalloids and noradrenalin through a wide bore peripheral cannula. On arrival at the emergency room, she had a barely palpable pulse and unrecordable blood pressure. She was found unresponsive around 1:15 pm after having gone to the restroom at 1:10 pm and had been conscious and alert prior to this episode. A 36 year female without comorbidities was brought to the emergency room unconscious and in respiratory distress at 1:40 pm.
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