![]() ![]() An electrocardiogram (ECG) of the patient showed normal sinus rhythm and tachycardia.Īn intravenous line was obtained and hydration coupled with other supportive measures was started. The patient reported tobacco use but no history of alcohol abuse or addiction to illicit drugs.Īfter admission to the emergency department, primary blood work revealed leukocytosis and metabolic acidosis (laboratory data are summarized in Table 1). Physical examination other than an evident tachycardia was otherwise normal. Peripheral perfusion was assessed using capillary refill time and was normal. ![]() Pulse oximetry showed 97% oxygen saturation with a regular pulse. Upon arrival, the patient had an oral temperature of 37.2☌, pulse rate of 110 beats per minute, respiratory rate of 18 breaths per minute, blood pressure recording of 110/70, and a Glasgow Coma Scale (GCS) score of 15/15. ![]() Immediately after the ingestion of the powder, gastric irrigation and activated charcoal administration were undertaken in a primary health care facility, and the patient was then referred to our center due to the development of refractory nausea and severe vomiting. The patient was admitted to our center approximately 7 h after ingestion of the substance. In this report, we aim to discuss plasmapheresis as an acceptable alternative measure in patients with cyanide poisoning, and in centers where cyanide antidote kits are not available.Ī 39‐year‐old male patient was brought to the emergency department with severe nausea and vomiting after intentional ingestion of two spoonsful of cyanide salt which had been obtained from a friend in the jewelry industry. Other measures such as hemodialysis and plasmapheresis may be used on a case by case basis to eliminate toxic substances from the circulation. Antidote kits are used in emergency settings and have proven efficacy in improving survival however, these kits may not be available at all centers. 4 Management of cyanide poisoning mainly consists of supportive measures in order to preserve organ perfusion and maintain proper homeostasis. Several studies have pointed to lactate levels as a sensitive marker in cyanide poisoning. 4 Cellular hypoxia leads to anaerobic cellular metabolism, accumulation of lactic acid, and eventually, lactic acidosis. Rapid development of hypotension, shock, bradycardia, and ultimately death may ensue. Patients with acute cyanide poisoning can present with headache, confusion, vertigo, palpitations, respiratory distress, and hyperventilation. 4 Rapid diagnosis of cyanide poisoning may not be possible due to its nonspecific presentations, limited availability of blood cyanide level kits, and their time‐consuming nature. Cyanide‐induced hypoxia eventually leads to neurologic and cardiovascular compromise. 2, 3 By disrupting the enzymatic pathways involved in cellular respiration, cyanide hinders the utilization of oxygen by cells, leading to adenosine triphosphate (ATP) depletion, and ultimately, cellular dysfunction. Thus, it is a common cause of intoxication among workers in the jewelry industry. 1 Cyanide salts are widely used in the jewelry industry and are not readily available to the public. Cyanide is a well‐known cause of intoxication and a historically recognized substance for suicide.
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