Her hemoglobin continued to decrease steadily, despite administration of a peak cell injection. Partial thromboplastin time, international normalized ratio, prothrombin time, and total bilirubin levels were within normal limits during hospitalization ( Table 1).īetween the first and second day of NAC administration, the patient’s hemoglobin and hematocrit levels decreased markedly from 12.6 g/dL and 35% to 4.5 g/dL and 13%, respectively. Liver function tests showed elevated alanine aminotransferase and aspartate aminotransferase (22 and 12 times the upper limit of normal, respectively) until the second day of poisoning and a gradual decrease to normal by the seventh day. Biochemistry showed hypernatremia and increased blood urine and creatinine from the first day onward ( Table 1).Ībbreviations: INR, international normalized ratio PTT, partial thromboplastin time PT, prothrombin time ALKP, alkaline phosphatase SGOT, serum glutamic oxaloacetic transaminase SPGT, serum glutamic pyruvic transaminase. On the second day, generalized edema was observed. The patient also became oliguric, with a urine output of less than 250 mL in 24 hours. On the first day, there was a gradual increase in edema around the eyes and face. Her arterial blood gas measurements indicated metabolic acidosis and respiratory alkalosis that was resistant to treatment in the first 18 hours, but was controlled by ventilation and infusion of sodium bicarbonate. Her breath sounds were decreased on auscultation of the lungs. Respiratory tract secretions increased significantly, and the patient had dyspnea, tachypnea, and shallow breathing early on. Computed tomography of the brain showed signs of edema. She was intubated and transferred to the intensive care unit, where she died 12 days later.Īccording to the clinical evaluations, the patient’s pupils were normal, symmetric, and reactive to light until the third day, when they became mydriatic and reacted slowly to light thereafter.

However, her level of consciousness decreased to 7/15 on the Glasgow Coma Scale, her hypotension became severe, her radial pulse became unpalpable, and her respiratory rate increased to 32 per minute. After administration of NAC 100 g, the patient’s pupils were normal, symmetric, and reactive to light. Suspecting a drug allergy, the physician stopped administration of NAC, but further investigation revealed that a nurse had administered NAC 100 g (instead of 10 g) as the loading dose. The patient developed agitation, nausea, vomiting, dyspnea, tachypnea, hypotension (blood pressure 80 mmHg), drowsiness, and periorbital edema. Following administration of activated charcoal, in view of the toxic dose of acetaminophen ingested, treatment with NAC was started, with a 10 g loading dose of NAC 150 mg/kg given over 30 minutes, followed by a 9.5 g maintenance dose with 500 mL of 5% dextrose water administered over 20 hours. She had normal arterial blood gas and vital signs. Clinical symptoms, laboratory test results, are presented and discussed.įour hours after taking 50 acetaminophen 325 mg tablets, a 23-year-old alert female patient weighing 65 kg presented to the emergency ward with weakness, lethargy, nausea, and dizziness. Here we report a rare case of iatrogenic NAC overdose due to an error made during preparation of the solution. 6 – 8 Due to the complexity of preparation of NAC as well as its side effects, mistakes are possible. However, despite its efficacy in reducing mortality due to acetaminophen poisoning, intravenous NAC can cause anaphylactoid reactions. 7 – 9 NAC solution has been used for over two decades in emergency wards in Iran. 4 – 6 Their NAC regimen was 150 mg/kg body weight given over 15–30 minutes, 50 mg/kg over 4 hours, and 100 mg/kg over 16 hours, with the final dose of 100 mg/kg repeated three times until liver aminotransferase levels reverted to normal.

1 – 3 Previous studies reported that a sterile 20% solution of N-acetylcysteine (NAC) administered intravenously was effective in the treatment of acetaminophen overdose. However, acetaminophen overdose is common in patients who present to hospital emergency rooms, and in many cases causes liver and renal necrosis. Acetaminophen is a widely used analgesic and antipyretic agent.

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