Hydrogen Sulfide Intoxication A Case Report and Discussion of Treatment ROBERT J. STINE, M.D.; BERNARD SLOSBERG, M.D.; and BRUCE E. BEACHAM, M.D.; Baltimore, Maryland
The toxicity of hydrogen sulfide is thought to be due primarily to reversible inactivation of the respiratory enzyme, cytochrome oxidase, with resultant inhibition of aerobic metabolism. A patient with severe hydrogen sulfide poisoning and consequent profound metabolic acidosis was treated successfully with nitrites and oxygen. The nitrite-induced methemoglobin, by competitively binding the toxic hydrosulfide anion until detoxified, presumably reactivated and protected cytochrome oxidase and thereby aided the patient's recovery by enhancing aerobic metabolism. His rapid recovery adds clinical support to the efficacy of nitrite therapy in sulfide poisoning. Therefore, we recommend that severe cases of sulfide poisoning be treated with nitrite-induced methemoglobinemia in addition to vigorous supportive care.
HYDROGEN SULFIDE is a colorless, heavier-than-air, poi-
sonous gas with a toxicity comparable to that of cyanide (1-7). It has an offensive odor at low concentrations; odor, however, is unreliable as a warning signal because at concentrations of approximately 0.015% (150 ppm) or greater, paralysis of the olfactory nerve rapidly occurs (2-7). Hydrogen sulfide is encountered in various industries, natural deposits, and sewers and septic tanks (2-4, 7). Poisoning is invariably the result of accidental exposure. We describe what is, to our knowledge, the first reported use of nitrite-induced methemoglobinemia in the management of a severe case of hydrogen sulfide poisoning and review the toxicologic mechanisms and therapy of sulfide poisoning. Case Report
A 47-year-old man was dumping a truck load of chemical waste known to be sodium sulfide, when he was overcome by acrid fumes with resultant loss of consciousness and subsequent seizurelike activity. Upon arrival in the emergency department of Baltimore City Hospital approximately 30 min after the accident, the patient was conscious but agitated, disoriented, and intensely cyanotic. He had a respiratory rate of 36/min, pulse of 160/min, and blood pressure of 150/90 mm He. An • From the Divisions of Emergency Medicine, The Baltimore City Hospitals and The Johns Hopkins University School of Medicine; Baltimore, Maryland.
756
Downloaded from https://annals.org by Tulane University user on 12/16/2018
electrocardiogram showed a supraventricular tachycardia with a rate of 160/min and left bundle branch block. A chest X ray was normal. The patient was immediately placed on 40% oxygen via face mask, and subsequent arterial blood gases showed a pH of 6.97, Po2 of 151 mm Hg, and Pco2 of 33 mm Hg. An anion gap of 41.2 meq/litre was noted. The patient was treated for hydrogen sulfide poisoning with amyl nitrite inhalations for 30 sec out of each minute for 5 min and then with 300 mg of sodium nitrite intravenously during 3 min. In addition, he received 12.5 g of sodium thiosulfate intravenously. Sodium bicarbonate was not administered. The patient was hospitalized, and a repeat ECG showed a sinus tachycardia with a rate of 110/min and resolution of the left bundle branch block. During the next few hours the patient's mental status improved, and his dyspnea and cyanosis resolved. Five hours after the accident the patient was completely oriented and lucid, and repeat arterial blood gases on 40% oxygen showed a pH of 7.41, Po,> of 205 mm Hg, and Pcoj of 29 mm Hg. The positive physical findings at that time included: an injected pharynx, bilateral subconjunctival hemorrhages, vertical and horizontal nystagmus, and motor weakness. The patient had an uncomplicated course and was discharged from the hospital 5 days after admission. One month after the accident the patient was noted to be doing well except for the following problems: intermittent frontal headaches, irritability and lack of patience, poor concentrating ability and attention span, and poor short-term memory. Cortical function tests at that time showed deficits in verbal abstraction, attention, and short-term retention. Two months after the accident the patient was still experiencing occasional headaches, but the neurologic examination was normal. Extensive investigation, including assays and chemical analyses by state officials, confirmed that the basic sodium sulfide waste solution was dumped on previously deposited acid waste material with resultant evolution of hydrogen sulfide as the offending noxious gas. Discussion
Hydrogen sulfide and soluble salts of sulfides are potent poisions. As in cyanide poisoning (8, 9 ) , the toxicity in sulfide poisoning is thought to be due primarily to reversible inhibition of the respiratory enzyme, cytochrome oxidase (6, 10-12). The mechanism is believed to be that of complex formation between the toxic hydrosulfide (HS-) anion (13) and the ferric iron of cytochrome oxidase (6, 11). As a result of inactivation of cytochrome oxidase, the respiratory electron transport chain is interrupted with resultant inhibition of aerobic metabolism (9,12). As in cyanide poisoning, the systemic manifestations Annals of Internal Medicine 85:756-758, 1976
of hydrogen sulfide intoxication result from inhibition of aerobic cellular respiration and consequently stem predominately from involvement of the organs most sensitive to oxygen deprivation, the nervous system and heart. In low concentrations of approximately 0.02% (200 p p m ) , hydrogen sulfide depresses the central nervous system; in moderate concentrations it stimulates the nervous system and respiration; and in high concentrations of 0 . 1 % (1000 ppm) or greater, it directly paralyzes the central nervous system including the respiratory center (1-5, 7 ) . Death secondary to respiratory arrest may ensue. The direct toxic action of sulfide on the heart has been associated with various arrhythmias, disorders of conduction, and disorders of ventricular repolarization (5, 7, 14). The local toxic manifestations of hydrogen sulfide result from the direct irritant effects of the gas on the membranes of the eye and respiratory tract and include respectively keratoconjunctivitis and rhinitis, pharyngitis, bronchitis, pneumonia and pulmonary edema (1-3). Sequelae, usually of a neurologic nature, have been reported (2, 3, 5 ) . Sulfide is detoxified via various oxidative mechanisms (1, 4, 6, 11, 15) with formation of nontoxic products, primarily thiosulfate and sulfate, which are excreted by the kidneys (2, 14). Other modes of elimination of sulfide of unknown significance include urinary excretion of unoxidized sulfide and pulmonary excretion of the gas (2, 6, 14). It has been shown that methemoglobin, known to bind cyanide (8, 10, 12, 13), also inactivates sulfide (10-13, 16), presumably by formation of the dissociable complex sulfmethemoglobin (10, 12, 13). One can presume that nitrite-induced methemoglobin, by competitively binding the hydrosulfide anion and then reversibly releasing the toxic anion for metabolic detoxication, should both reactivate and protect cytochrome oxidase with return of its mediated aerobic metabolism. Because the hydrosulfide and cyanide anions exert their toxic effects by the same mechanism, because each anion is inactivated by methemoglobin, and because cyanide poisoning is treated successfully with induced methemoglobinemia (8, 10, 12); it follows that induction of methemoglobinemia with nitrites should be an effective therapeutic measure in sulfide poisoning. Indeed, investigators have shown that pretreatment of animals with sodium nitrite and other agents to induce methemoglobinemia provides protection against lethal doses of sodium or hydrogen sulfide (10-13, 16). In addition, nitrite has been shown to exert a significant antidotal effect against acute sodium or hydrogen sulfide poisoning in rodents (12). The role of oxygen in the treatment of hydrogen sulfide poisoning is controversial. One can speculate that oxygen promotes oxidative detoxication of sulfide and is able to maintain life via augmentation of noncytochrome oxidasemediated, aerobic cellular respiration until the toxic hydrosulfide anion is detoxified (9, 17). Recent research, however, in contrast to previous experiments showing the efficacy of oxygen therapy in cyanide poisoning (9, 17, 18), has shown that oxygen does not protect mice against death from acute sulfide poisoning and furthermore does
not potentiate the protective effect of nitrite against sulfide poisoning (12). A review of the English literature from 1960 to present revealed only 14 case reports (2-5, 7, 19-21) of severe, life-threatening hydrogen sulfide posioning characterized by loss of consciousness and associated respiratory, or circulatory insufficiency, or both. Of these, six ( 4 3 % ) (3, 4, 7, 20) died despite vigorous resuscitative measures. Of the eight ( 5 7 % ) (2, 3, 5, 19, 21) who survived the initial resuscitation and who subsequently were hospitalized, all survived with vigorous supportive therapy (including oxygen). Recovery of normal vital signs and mental status, however, was slow (7 to 48 h) in at least six ( 7 5 % ) (2, 3, 5, 19, 21) of the patients hospitalized. As described in this paper, the efficacy of nitrites in the treatment of sulfide intoxication has a strong theoretical basis and has been shown in animal studies. Our patient had characteristic manifestations of life-threatening hydrogen sulfide poisoning, including a severe metabolic acidosis, most likely as a result of anaerobic metabolism due to inhibition of cytochrome oxidase. He recovered with treatment consisting of nitrites and general supportive care. Our case lends clinical support that nitrites can reduce recovery time, in that our patient's recovery time (5 h) was less than that of 7 5 % of reported survivors of comparable posioning treated with supportive care alone. Presumably nitrites may also reduce morbidity and sequelae, because logically a shorter recovery time should correlate with lower morbidity and less sequelae. Because our patient reached the hospital alive, he had a good chance of surviving with vigorous supportive therapy alone; but in view of presently understood mechanisms, it seems likely that nitrite therapy aided his recovery by enhancing aerobic metabolism. Likewise, one can presume that nitrites may also reduce the significant mortality associated with severe sulfide poisoning, if administered in the prehospital phase of care, such as at an industrial site. We conclude that nitrite therapy is appropriate for severe hydrogen sulfide poisoning and stress the importance of expedient administration. Therefore, we recommend that high-risk industries and areas maintain a supply of nitrites. The well-accepted dosage regimen for nitrite therapy of cyanide poisoning is likely applicable to sulfide poisoning. Thus, treatment of sulfide poisoning should be initiated with inhalations of amyl nitrite for 15 to 30 sec of each minute until 10 ml of a 3 % soultion of sodium nitrite can be injected intravenously at a rate of 2.5 to 5 ml per min (8, 13). Such dosages are considered safe ( 8 ) . Sodium nitrite injections may be repeated if necessary ( 8 ) . Additional treatment should include: closed cardiac massage as needed to maintain circulation; artificial respiration and assisted mechanical ventilation as needed to support respiration and possibly promote pulmonary excretion of the gas; administration of 100% oxygen, although its effectiveness is uncertain; and appropriate treatment of pulmonary edema, pulmonary infection, keratoconjunctivitis, and sequelae as necessary. ACKNOWLEDGMENTS: The authors thank Dr. Roger P. Smith, Stineetal.
Downloaded from https://annals.org by Tulane University user on 12/16/2018
• Hydrogen Sulfide Intoxication
757
Professor of Toxicology, Dartmouth Medical School, for his assistance and expert advice and Ms. Patricia Scardina for technical assistance. Received 23 August 1976; revision accepted 15 September 1976. • Requests for reprints should be addressed to Robert J. Stine, M.D.; Baltimore City Hospitals; 4940 Eastern Avenue; Baltimore, MD 21224.
Pharmacol Exp Ther 189:235-243, 1974 10. SMITH RP, GOSSELIN RE: The influence of methemoglobinemia
on the lethality of some toxic anions. II. Sulfide. Toxicol Appl Pharmacol 6:584-592, 1964 11. SMITH RP, ABBANAT RA: Protective effect of oxidized glutathione in acute sulfide poisoning. Toxicol Appl Pharmacol 9:209-217,1966 12. SMITH RP, KRUSZYNA R, KRUSZYNA H: Management of acute
sulfide poisoning. Effects of oxygen, thiosulfate, and nitrite. Arch Environ Health 31:166-169, 1976
References 1. HAGGARD HW: The toxicology of hydrogen sulfide. / Ind Hyg 7:113-121, 1925 2. MILBY TH: Hydrogen sulfide intoxication. Review of the literature and report of unusual accident resulting in two cases of nonfatal poisoning. J Occup Med 4:431-437, 1962
13. SMITH RP, GOSSELIN RE: On the mechanism of sulfide in-
activation by methemoglobin. Toxicol Appl Pharmacol 8:159172, 1966 14. KOSMIDER S, ROGALA E, PACHOKEK A: Electrocardiographic and
3. KLEINFELD M, GIEL C, ROSSO A: Acute hydrogen sulfide in-
4. 5. 6. 7. 8. 9.
toxication; an unusual source of exposure, lnd Med Surg 33: 656-660, 1964 ADELSON L, SUNSHINE I: Fatal hydrogen sulfide intoxication. Report of three cases occurring in a sewer. Arch Pathol 81: 375-380, 1966 KEMPER FD: A near-fatal case of hydrogen sulfide poisoning. Can Med Assoc J 94:1130-1131, 1966 EVANS CL: The toxicity of hydrogen sulphide and other sulphides. Q J Exp Physiol 52:231-248, 1967 SIMSON RE, SIMPSON GR: Fatal hydrogen sulfide poisoning associated with industrial waste exposure. Med J Aust 1:331334, 1971 CHEN KK, ROSE CL: Nitrite and thiosulfate therapy in cyanide poisoning. JAMA 149:113-119, 1952 ISOM GE, WAY JL: Effect of oxygen on cyanide intoxication. VI. Reactivation of cyanide-inhibited glucose metabolism. /
758
15. 16. 17. 18. 19.
histochemical studies of the heart muscle in acute experimental hydrogen sulfide poisoning. Arch Immunol Ther Exp (Warsz) 15:731-740, 1967 BAXTER CF, VAN REEN R: Some aspects of sulfide oxidation by rat-liver preparations. Biochim Biophys Acta 28:567-573, 1958 SMITH RP: The oxygen and sulfide binding characteristics of hemoglobins generated from methemoglobin by two erythrocytic systems. Mol Pharmacol 3:378-385, 1967 LEVINE S: Oxygen in the therapy of cyanide poisoning. JAMA 170:1585,1959 SHEEHY M, WAY JL: Effect of oxygen on cyanide intoxication. III. Mithridate. / Pharmacol Exp Ther 161:163-168, 1968 PODA GA: Hydrogen sulfide can be handled safely. Arch Environ Health 12:795-800, 1966
20. WINEK CL, COLLOM WD, WECHT CH: Death from hydrogen-
sulfide fumes (letter). Lancet 1:1096, 1968 21. THOMAN M: Sewer gas: hydrogen sulfide intoxication. Clin Toxicol 2:383-386, 1969
December 1976 • Annals of Internal Medicine • Volume 85 • Number 6
Downloaded from https://annals.org by Tulane University user on 12/16/2018
The toxicity of hydrogen sulfide is thought to be due primarily to reversible inactivation of the respiratory enzyme, cytochrome oxidase, with resultant inhibition of aerobic metabolism. A patient with severe hydrogen sulfide poisoning and consequent profound metabolic acidosis was treated successfully with nitrites and oxygen. The nitrite-induced methemoglobin, by competitively binding the toxic hydrosulfide anion until detoxified, presumably reactivated and protected cytochrome oxidase and thereby aided the patient's recovery by enhancing aerobic metabolism. His rapid recovery adds clinical support to the efficacy of nitrite therapy in sulfide poisoning. Therefore, we recommend that severe cases of sulfide poisoning be treated with nitrite-induced methemoglobinemia in addition to vigorous supportive care.
HYDROGEN SULFIDE is a colorless, heavier-than-air, poi-
sonous gas with a toxicity comparable to that of cyanide (1-7). It has an offensive odor at low concentrations; odor, however, is unreliable as a warning signal because at concentrations of approximately 0.015% (150 ppm) or greater, paralysis of the olfactory nerve rapidly occurs (2-7). Hydrogen sulfide is encountered in various industries, natural deposits, and sewers and septic tanks (2-4, 7). Poisoning is invariably the result of accidental exposure. We describe what is, to our knowledge, the first reported use of nitrite-induced methemoglobinemia in the management of a severe case of hydrogen sulfide poisoning and review the toxicologic mechanisms and therapy of sulfide poisoning. Case Report
A 47-year-old man was dumping a truck load of chemical waste known to be sodium sulfide, when he was overcome by acrid fumes with resultant loss of consciousness and subsequent seizurelike activity. Upon arrival in the emergency department of Baltimore City Hospital approximately 30 min after the accident, the patient was conscious but agitated, disoriented, and intensely cyanotic. He had a respiratory rate of 36/min, pulse of 160/min, and blood pressure of 150/90 mm He. An • From the Divisions of Emergency Medicine, The Baltimore City Hospitals and The Johns Hopkins University School of Medicine; Baltimore, Maryland.
756
Downloaded from https://annals.org by Tulane University user on 12/16/2018
electrocardiogram showed a supraventricular tachycardia with a rate of 160/min and left bundle branch block. A chest X ray was normal. The patient was immediately placed on 40% oxygen via face mask, and subsequent arterial blood gases showed a pH of 6.97, Po2 of 151 mm Hg, and Pco2 of 33 mm Hg. An anion gap of 41.2 meq/litre was noted. The patient was treated for hydrogen sulfide poisoning with amyl nitrite inhalations for 30 sec out of each minute for 5 min and then with 300 mg of sodium nitrite intravenously during 3 min. In addition, he received 12.5 g of sodium thiosulfate intravenously. Sodium bicarbonate was not administered. The patient was hospitalized, and a repeat ECG showed a sinus tachycardia with a rate of 110/min and resolution of the left bundle branch block. During the next few hours the patient's mental status improved, and his dyspnea and cyanosis resolved. Five hours after the accident the patient was completely oriented and lucid, and repeat arterial blood gases on 40% oxygen showed a pH of 7.41, Po,> of 205 mm Hg, and Pcoj of 29 mm Hg. The positive physical findings at that time included: an injected pharynx, bilateral subconjunctival hemorrhages, vertical and horizontal nystagmus, and motor weakness. The patient had an uncomplicated course and was discharged from the hospital 5 days after admission. One month after the accident the patient was noted to be doing well except for the following problems: intermittent frontal headaches, irritability and lack of patience, poor concentrating ability and attention span, and poor short-term memory. Cortical function tests at that time showed deficits in verbal abstraction, attention, and short-term retention. Two months after the accident the patient was still experiencing occasional headaches, but the neurologic examination was normal. Extensive investigation, including assays and chemical analyses by state officials, confirmed that the basic sodium sulfide waste solution was dumped on previously deposited acid waste material with resultant evolution of hydrogen sulfide as the offending noxious gas. Discussion
Hydrogen sulfide and soluble salts of sulfides are potent poisions. As in cyanide poisoning (8, 9 ) , the toxicity in sulfide poisoning is thought to be due primarily to reversible inhibition of the respiratory enzyme, cytochrome oxidase (6, 10-12). The mechanism is believed to be that of complex formation between the toxic hydrosulfide (HS-) anion (13) and the ferric iron of cytochrome oxidase (6, 11). As a result of inactivation of cytochrome oxidase, the respiratory electron transport chain is interrupted with resultant inhibition of aerobic metabolism (9,12). As in cyanide poisoning, the systemic manifestations Annals of Internal Medicine 85:756-758, 1976
of hydrogen sulfide intoxication result from inhibition of aerobic cellular respiration and consequently stem predominately from involvement of the organs most sensitive to oxygen deprivation, the nervous system and heart. In low concentrations of approximately 0.02% (200 p p m ) , hydrogen sulfide depresses the central nervous system; in moderate concentrations it stimulates the nervous system and respiration; and in high concentrations of 0 . 1 % (1000 ppm) or greater, it directly paralyzes the central nervous system including the respiratory center (1-5, 7 ) . Death secondary to respiratory arrest may ensue. The direct toxic action of sulfide on the heart has been associated with various arrhythmias, disorders of conduction, and disorders of ventricular repolarization (5, 7, 14). The local toxic manifestations of hydrogen sulfide result from the direct irritant effects of the gas on the membranes of the eye and respiratory tract and include respectively keratoconjunctivitis and rhinitis, pharyngitis, bronchitis, pneumonia and pulmonary edema (1-3). Sequelae, usually of a neurologic nature, have been reported (2, 3, 5 ) . Sulfide is detoxified via various oxidative mechanisms (1, 4, 6, 11, 15) with formation of nontoxic products, primarily thiosulfate and sulfate, which are excreted by the kidneys (2, 14). Other modes of elimination of sulfide of unknown significance include urinary excretion of unoxidized sulfide and pulmonary excretion of the gas (2, 6, 14). It has been shown that methemoglobin, known to bind cyanide (8, 10, 12, 13), also inactivates sulfide (10-13, 16), presumably by formation of the dissociable complex sulfmethemoglobin (10, 12, 13). One can presume that nitrite-induced methemoglobin, by competitively binding the hydrosulfide anion and then reversibly releasing the toxic anion for metabolic detoxication, should both reactivate and protect cytochrome oxidase with return of its mediated aerobic metabolism. Because the hydrosulfide and cyanide anions exert their toxic effects by the same mechanism, because each anion is inactivated by methemoglobin, and because cyanide poisoning is treated successfully with induced methemoglobinemia (8, 10, 12); it follows that induction of methemoglobinemia with nitrites should be an effective therapeutic measure in sulfide poisoning. Indeed, investigators have shown that pretreatment of animals with sodium nitrite and other agents to induce methemoglobinemia provides protection against lethal doses of sodium or hydrogen sulfide (10-13, 16). In addition, nitrite has been shown to exert a significant antidotal effect against acute sodium or hydrogen sulfide poisoning in rodents (12). The role of oxygen in the treatment of hydrogen sulfide poisoning is controversial. One can speculate that oxygen promotes oxidative detoxication of sulfide and is able to maintain life via augmentation of noncytochrome oxidasemediated, aerobic cellular respiration until the toxic hydrosulfide anion is detoxified (9, 17). Recent research, however, in contrast to previous experiments showing the efficacy of oxygen therapy in cyanide poisoning (9, 17, 18), has shown that oxygen does not protect mice against death from acute sulfide poisoning and furthermore does
not potentiate the protective effect of nitrite against sulfide poisoning (12). A review of the English literature from 1960 to present revealed only 14 case reports (2-5, 7, 19-21) of severe, life-threatening hydrogen sulfide posioning characterized by loss of consciousness and associated respiratory, or circulatory insufficiency, or both. Of these, six ( 4 3 % ) (3, 4, 7, 20) died despite vigorous resuscitative measures. Of the eight ( 5 7 % ) (2, 3, 5, 19, 21) who survived the initial resuscitation and who subsequently were hospitalized, all survived with vigorous supportive therapy (including oxygen). Recovery of normal vital signs and mental status, however, was slow (7 to 48 h) in at least six ( 7 5 % ) (2, 3, 5, 19, 21) of the patients hospitalized. As described in this paper, the efficacy of nitrites in the treatment of sulfide intoxication has a strong theoretical basis and has been shown in animal studies. Our patient had characteristic manifestations of life-threatening hydrogen sulfide poisoning, including a severe metabolic acidosis, most likely as a result of anaerobic metabolism due to inhibition of cytochrome oxidase. He recovered with treatment consisting of nitrites and general supportive care. Our case lends clinical support that nitrites can reduce recovery time, in that our patient's recovery time (5 h) was less than that of 7 5 % of reported survivors of comparable posioning treated with supportive care alone. Presumably nitrites may also reduce morbidity and sequelae, because logically a shorter recovery time should correlate with lower morbidity and less sequelae. Because our patient reached the hospital alive, he had a good chance of surviving with vigorous supportive therapy alone; but in view of presently understood mechanisms, it seems likely that nitrite therapy aided his recovery by enhancing aerobic metabolism. Likewise, one can presume that nitrites may also reduce the significant mortality associated with severe sulfide poisoning, if administered in the prehospital phase of care, such as at an industrial site. We conclude that nitrite therapy is appropriate for severe hydrogen sulfide poisoning and stress the importance of expedient administration. Therefore, we recommend that high-risk industries and areas maintain a supply of nitrites. The well-accepted dosage regimen for nitrite therapy of cyanide poisoning is likely applicable to sulfide poisoning. Thus, treatment of sulfide poisoning should be initiated with inhalations of amyl nitrite for 15 to 30 sec of each minute until 10 ml of a 3 % soultion of sodium nitrite can be injected intravenously at a rate of 2.5 to 5 ml per min (8, 13). Such dosages are considered safe ( 8 ) . Sodium nitrite injections may be repeated if necessary ( 8 ) . Additional treatment should include: closed cardiac massage as needed to maintain circulation; artificial respiration and assisted mechanical ventilation as needed to support respiration and possibly promote pulmonary excretion of the gas; administration of 100% oxygen, although its effectiveness is uncertain; and appropriate treatment of pulmonary edema, pulmonary infection, keratoconjunctivitis, and sequelae as necessary. ACKNOWLEDGMENTS: The authors thank Dr. Roger P. Smith, Stineetal.
Downloaded from https://annals.org by Tulane University user on 12/16/2018
• Hydrogen Sulfide Intoxication
757
Professor of Toxicology, Dartmouth Medical School, for his assistance and expert advice and Ms. Patricia Scardina for technical assistance. Received 23 August 1976; revision accepted 15 September 1976. • Requests for reprints should be addressed to Robert J. Stine, M.D.; Baltimore City Hospitals; 4940 Eastern Avenue; Baltimore, MD 21224.
Pharmacol Exp Ther 189:235-243, 1974 10. SMITH RP, GOSSELIN RE: The influence of methemoglobinemia
on the lethality of some toxic anions. II. Sulfide. Toxicol Appl Pharmacol 6:584-592, 1964 11. SMITH RP, ABBANAT RA: Protective effect of oxidized glutathione in acute sulfide poisoning. Toxicol Appl Pharmacol 9:209-217,1966 12. SMITH RP, KRUSZYNA R, KRUSZYNA H: Management of acute
sulfide poisoning. Effects of oxygen, thiosulfate, and nitrite. Arch Environ Health 31:166-169, 1976
References 1. HAGGARD HW: The toxicology of hydrogen sulfide. / Ind Hyg 7:113-121, 1925 2. MILBY TH: Hydrogen sulfide intoxication. Review of the literature and report of unusual accident resulting in two cases of nonfatal poisoning. J Occup Med 4:431-437, 1962
13. SMITH RP, GOSSELIN RE: On the mechanism of sulfide in-
activation by methemoglobin. Toxicol Appl Pharmacol 8:159172, 1966 14. KOSMIDER S, ROGALA E, PACHOKEK A: Electrocardiographic and
3. KLEINFELD M, GIEL C, ROSSO A: Acute hydrogen sulfide in-
4. 5. 6. 7. 8. 9.
toxication; an unusual source of exposure, lnd Med Surg 33: 656-660, 1964 ADELSON L, SUNSHINE I: Fatal hydrogen sulfide intoxication. Report of three cases occurring in a sewer. Arch Pathol 81: 375-380, 1966 KEMPER FD: A near-fatal case of hydrogen sulfide poisoning. Can Med Assoc J 94:1130-1131, 1966 EVANS CL: The toxicity of hydrogen sulphide and other sulphides. Q J Exp Physiol 52:231-248, 1967 SIMSON RE, SIMPSON GR: Fatal hydrogen sulfide poisoning associated with industrial waste exposure. Med J Aust 1:331334, 1971 CHEN KK, ROSE CL: Nitrite and thiosulfate therapy in cyanide poisoning. JAMA 149:113-119, 1952 ISOM GE, WAY JL: Effect of oxygen on cyanide intoxication. VI. Reactivation of cyanide-inhibited glucose metabolism. /
758
15. 16. 17. 18. 19.
histochemical studies of the heart muscle in acute experimental hydrogen sulfide poisoning. Arch Immunol Ther Exp (Warsz) 15:731-740, 1967 BAXTER CF, VAN REEN R: Some aspects of sulfide oxidation by rat-liver preparations. Biochim Biophys Acta 28:567-573, 1958 SMITH RP: The oxygen and sulfide binding characteristics of hemoglobins generated from methemoglobin by two erythrocytic systems. Mol Pharmacol 3:378-385, 1967 LEVINE S: Oxygen in the therapy of cyanide poisoning. JAMA 170:1585,1959 SHEEHY M, WAY JL: Effect of oxygen on cyanide intoxication. III. Mithridate. / Pharmacol Exp Ther 161:163-168, 1968 PODA GA: Hydrogen sulfide can be handled safely. Arch Environ Health 12:795-800, 1966
20. WINEK CL, COLLOM WD, WECHT CH: Death from hydrogen-
sulfide fumes (letter). Lancet 1:1096, 1968 21. THOMAN M: Sewer gas: hydrogen sulfide intoxication. Clin Toxicol 2:383-386, 1969
December 1976 • Annals of Internal Medicine • Volume 85 • Number 6
Downloaded from https://annals.org by Tulane University user on 12/16/2018
