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N-Acetylcysteine in the Treatment of Human Arsenic Poisoning

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N-Acetylcysteine in the Treatment of Human Arsenic Poisoning J Am Board Fam Pract: first published as 10.3122/jabfm.3.4.293 on 1 October 1990. Downloaded from N-Acetylcysteine In The Treatment Of Human Arsenic Poisoning Debra S. Martin, M.D., Stephen E. Willis, M.D., and David M. Cline, M.D. Abstract: A 32-year-old man was brought to the emergency department 5 1/2 hours after ingesting a potentiaIly lethal dose (900 mg) of sodium arsenate ant poison in a suicide attempt. The patient deteriorated progressively for 27 hours. After intramuscular dimercaprol and supportive measures failed to improve his condition, he was given N-acetylcysteine intravenously. The patient showed remarkable clinical improvement during the following 24 hours and was discharged from the hospital several days later. (J Am Board Fam Pract 1990; 3:293-6.) Arsenic has been used since medieval times, known use of intravenous NAC in a patient with both as medicine and poison. Although its me­ arsenic poisoning. dicinal use has declined, arsenic can still be found as an ingredient in certain homeopathic Case Report formulas, I which are available in some health A 32-year-old man was brought to the emer­ food stores. Arsenic also is present in high con­ gency department by ambulance 5 hours after centrations in many easily obtainable ant kill­ he ingested approximately 900 mg of sodium ers, and this source is responsible for most toxic arsenate - five times the lethal doseJ,6 - in a human ingestions. 2 Other sources include in­ suicide attempt. He was lethargic but arousable secticides, herbicides, and rodenticides. Com­ by voice and answered questions appropriately. mon symptoms of arsenic poisoning are metal­ He stated that he vomited 1 hour after the in­ lic taste, nausea, vomiting, abdominal pain, and gestion and developed diarrhea 3 hours later. diarrhea. Depending on severity, patients may His pulse rate was 145/min, respirations were experience vasodilation, circulatory collapse, 24/min, blood pressure was 74/50 mmHg, and seizures, and acute tubular necrosis. 3 In 1988 an electrocardiographic monitor showed sinus there were 527 reported arsenic exposures in tachycardia. In addition to lethargy and hypo­ http://www.jabfm.org/ the United States, of which 280 required treat­ tension, his skin was cool but not cyanotic, and ment. Forty-three patients required hospitali­ no blood was present in the mouth or nares. His zation, and there were no reported deaths from neck was supple without jugular venous disten­ arsenIc. exposure. 4 tion. Cardiopulmonary examination was nota­ Intramuscular dimercaprol (BAL) followed by ble only for tachycardia, and deep palpation oral D-penicillamine is the currently recom­ showed mild epigastric tenderness. The genita­ on 29 September 2021 by guest. Protected copyright. mended treatment for acute arsenic ingestionS; lia were unremarkable, and the rectal examina­ however, both drugs have important adverse ef­ tion was hemoccult negative. Pulses were equal fects, and neither may be effective in severe poi­ in all extremities. There were no focal neuro­ sonings. Animal studies have shown N-acetyl­ logic deficits. cysteine (NAC) to be effective in treating arsenic A toxicology screen and random urine and se­ ingestion. A MEDLINE literature search cover­ rum arsenic levels were requested, and a 24-hour ing the past 15 years did not show any reported urine arsenic collection was started. Initial labo­ cases of NAC therapy in the treatment of human ratory studies showed: sodium, 142 mEq/L (142 arsenic poisoning. We are reporting the first mmol/L); potassium, 2.7 mEq/L (2.7 mmol/L); chloride, 106 mEq/L (106 mmol/L); CO2, 25 mEq/L (25 mmol/L); creatinine, 2.1 mg/dL From the Department of Family Medicine and the Depart­ (185.64 J.1mol/L); glucose, 163 mg/dL (9.05 ment of Emergency Medicine, East Carolina University, School mmol/L); prothrombin time, 13.2 seconds; partial of Medicine, Greenville, NC. Address reprint requests to Ste­ phen E. Willis, M.D., East Carolina University, Brody Building thromboplastin time, 44 seconds. Blood chemis­ 4N7H, Greenville, NC 27H5H-4354. try panel, urinalysis, and complete blood count N-Acetylcysteine in Arsenic Poisoning 293 J Am Board Fam Pract: first published as 10.3122/jabfm.3.4.293 on 1 October 1990. Downloaded from were normal except for phosphorus, which was for conjunctivitis, rhinorrhea, and a sterile ab­ 2.5 mg/dL (0.81 mmol/L). scess at the BAL injection site. Repeated serum Tn the emergency department, the patient re­ glutamic-oxaloacetic transaminase (SGOT) and ceived a bolus of 250 mL normal saline, saline coagulation studies were begun 24 hours after gastric lavage (2 liters), 50 g of activated charcoal, ingesting the poison (Figure 1). The maximum and 5 mg/kg of intramuscular BAL. He vomited elevation of the SGOT was 125 U/L at approxi­ the activated charcoal shortly after transfer to the mately 84 hours after ingestion. intensive care unit, and attempts at placement of Consultation with the National Capitol Poison a nasogastric tube were unsuccessful because of Center, Washington, D.C., was obtained because persistent vomiting. A dopamine intravenous the patient's condition remained critical despite drip was started after numerous normal saline aggressive therapy and BAL chelation every 4 boluses failed to bring the systolic blood pressure hours. A physician at the poison center recom­ to 90 mmHg. The patient had a net positive fluid mended using intravenous NAC. The first dose input of 8 liters within the first 24 hours and was a small test dose, without any adverse efFects developed a right pleural effusion, ascites, and approximately 27 hours after ingestion. The dos­ mild anasarca. age ofNAC (4 grams every 4 hours) was based on Urine alkalinization was initiated to prevent 70 mg/kg/dose. The oral form of NAC was mixed hemolysis; however, this was discontinued 14 in 250 mL of normal saline and then millipore hours after ingestion when the urine output de­ filtered. Based on instructions from the physician creased to less than 30 mLlhr. The patient had at the poison center, we administered a total of hemodialysis because of decreased urine output 18 doses of NAC by continuous intravenous and elevated serum creatinine. After dialysis, he infusion. continued to be hypotensive, requiring dopamine Within 24 hours after the IV NAC was started, for 36 hours - up to 9.3 j.1g/kg/min. During the the prothrombin and partial thromboplastin first 24 hours, the patient complained of persist­ times returned to normal. The relations between / ent nausea and vomiting, penile burning, and in­ prothrombin time, partial thromboplastin time, termittent paresthesias of the distal extremities. and treatment with NAC are shown in Figure 1. His physical examination was unchanged except The patient's clinical status also improved; dopa­ mine was discontinued, and his blood pressure and urine output remained stable. On day 4, the http://www.jabfm.org/ 15.0 100.0 patient was tolerating a clear liquid diet, and BAL - Protlme was discontinued. Oral D-penicillamine therapy ........ Control Pro time 14.5 --- PTT 89.4 (500 mg every 6 hours) was started. IV NAC was _. - Control PTT discontinued, and we ordered oral NAC 4 grams 14.0 every 4 hours. This treatment was discontinued 78.9 :S UJ after 2 doses, because he refused to ingest oral 13.5 10 0. NAC. The remainder of his hospital course was on 29 September 2021 by guest. Protected copyright. Q) 68.3 0 D . ~ unremarkable. After spending 2 days in the psy­ 13.0 E 0... ...0 chiatric unit, the patient was discharged, com­ Q. ~ 57.7 ~ plaining only of a mild headache. 12.5 ~... 10 After discharge from the hospital, the patient 47.1 Q. 12.0 was seen in follow-up at the Eastern Carolina Family Practice Center. He remained on oral D­ 11 .5 36.6 penicillamine therapy, and serial 24-hour urine ------ collections were continued. Urinary arsenic lev­ 11.0 ........-l..---L_..I.---I._.l.--l..---L_..I.---I.---I 26.0 els for the first 11 days of treatment are shown in 012 3 .. 5 6 7 8 Figure 2 . HAC• HAC• Started Stopped One month after ingestion of sodium arsenate, TIME (days) the patient continued to complain of a mild, persist­ Figure 1. PT and PTI by number of days. (Note initiation and ent headache in the occipital region and intermit­ completion of NAC therapy.) tent paresthesias of his hands, feet, and arms. He 294 JABFP October-December 1990 Vol. 3 No.4 J Am Board Fam Pract: first published as 10.3122/jabfm.3.4.293 on 1 October 1990. Downloaded from tient experienced several toxic sid' eflccls of both u 7500 '2 Ql the BLand I)-penicillamine. III .( The ideal antidote for a toxic ing 'stion would 5000 :.>- efficiently eliminate the agent, pr'vent further .5 toxicity, have minimal adverse ctrects, and b :s 2500 easy to administer. For arseni . toxicity, a sour e of su lfll ydryl groups could ctrectively prevent its °1....-----.i..---'-----1.--...1..------l.--daYs 2.0 4.0 8.0 8.0 10.0 inactivation of enzymes by dehydrogenation D8Ys (oxidation). Arsenic dehydrogenates sulfhydryl groups of many vital enzymes, resulting in cell Figure 2. Urinary arsenic levels by number of days. I 6 death. • Glutathione protects systems from oxi­ dation by providing sulfllydryl groups. In aceta­ minophen overdoses, toxicity is believed to occur was referred to a neurologist because the symp­ when glutathione fails to provide enough sulfhy­ toms suggested polyneuropathy. Electradiagnos­ dryl groups. NA prevents acetaminophen toxic­ tic studies were normal, and the neurologist ity by providing a sourcc of cysteine for glutathi­ thought that the patient may have been experi­ one synthesis.9 encing an acute myasthenic reaction to D-peni­ Recent studies of laboratory mice have shown ci llamine.
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