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Hydrogen sulphide
Poisonous substances
Hydrogen sulphide
Supplemental oxygen should then be administered to the casualty. Although 100% oxygen had no beneficial effect in one experimental study,11 in another it was of benefit.12 In the same study hyperbaric oxygen (3 ATA) alone or with co-administration of sodium nitrite reduced the mortality substantially12; hyperbaric oxygen has been used to treat patients with life-threatening symptoms.13,14 There is limited experimental evidence that pre-treatment with sodium nitrite reduces mortality in hydrogen sulphide poisoning; 11 in another study sodium nitrite was of no benefit.12 However, it has been argued that nitrite could be effective only for a few minutes after exposure.15 Clinical benefit has been claimed.16 ◆
Allister Vale
Abstract References 1 Dorman DC, Moulin FJM, McManus BE, et al. Cytochrome oxidase inhibition induced by acute hydrogen sulfide inhalation: correlation with tissue sulfide concentrations in the rat brain, liver, lung, and nasal epithelium. Toxicol Sci 2002; 65: 18–25. 2 Beauchamp Jr RO, Bus JS, Popp JA, et al. A critical review of the literature on hydrogen sulfide toxicity. Crit Rev Toxicol 1984; 13: 25–97. 3 Guidotti TL. Hydrogen sulphide. Occup Med (Oxf) 1996; 46: 367–71. 4 International Programme on Chemical Safety. In: Chou C-H SJ, ed. Concise international chemical assessment document no. 53. Hydrogen sulfide: human health aspects. Geneva: World Health Organization, 2003. 5 Tanaka S, Fujimoto S, Tamagaki Y, et al. Bronchial injury and pulmonary edema caused by hydrogen sulfide poisoning. Am J Emerg Med 1999; 17: 427–29. 6 Burnett WW, King EG, Grace M, Hall WF. Hydrogen sulfide poisoning: review of 5 years’ experience. Can Med Assoc J 1977; 117: 1277–80. 7 Gaitonde UB, Sellar RJ, O’Hare AE. Long term exposure to hydrogen sulphide producing subacute encephalopathy in a child. Br Med J 1987; 294: 614. 8 Tvedt B, Skyberg K, Aaserud O, et al. Brain damage caused by hydrogen sulfide: a follow-up study of six patients. Am J Ind Med 1991; 20: 91–101. 9 Hirsch AR. Hydrogen sulfide exposure without loss of consciousness: chronic effects in four cases. Toxicol Ind Health 2002; 18: 51–61. 10 Schneider JS, Tobe EH, Mozley Jr PD. Persistent cognitive and motor deficits following acute hydrogen sulphide poisoning. Occup Med (Oxf) 1998; 48: 255–60. 11 Smith RP, Kruszyna R, Kruszyna H. Management of acute sulfide poisoning. Effects of oxygen, thiosulfate, and nitrite. Arch Environ Health 1976; 31: 166–69. 12 Bitterman N, Talmi Y, Lerman A, et al. The effect of hyperbaric oxygen on acute experimental sulfide poisoning in the rat. Toxicol Appl Pharmacol 1986; 84: 325–28. 13 Whitcraft III DD, Bailey TD, Hart GB. Hydrogen sulfide poisoning treated with hyperbaric oxygen. J Emerg Med 1985; 3: 23–25. 14 Smilkstein MJ, Bronstein AC, Pickett HM, Rumack BH. Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. J Emerg Med 1985; 3: 27–30. 15 Beck JF, Bradbury CM, Connors AJ, Donini JC. Nitrite as antidote for acute hydrogen sulfide intoxication? Am Ind Hyg Assoc J 1981; 42: 805–9. 16 Huang C-C, Chu N-S. A case of acute hydrogen sulfide (H2S) intoxication successfully treated with nitrites. J Formos Med Assoc 1987; 86: 1018–20.
Hydrogen sulphide is a potent inhibitor of cytochrome oxidase A3 and a mucous membrane irritant at lower concentrations. Cyanosis, confusion, pulmonary oedema, coma, convulsions and respiratory arrest are common in severe poisoning and neurological and neuropsychiatric sequelae have been observed. Rescue, resuscitation if necessary, and the administration of oxygen are the mainstay of treatment.
Keywords cytochrome oxidase A3 inhibitor; neuropsychiatric sequelae; pulmonary oedema; sodium nitrite; subacute encephalopathy
Hydrogen sulphide is a colourless gas. Workers in the petrochemical and gas industries and in tanning are at particular risk of exposure. The gas is also found in mines and sewers, and is liberated from decomposing fish (a hazard in fishing boats if the hold is filled with ‘trash’ fish used for making fish meal) and liquid manure systems. Mechanisms of toxicity: hydrogen sulphide is an even more potent inhibitor of cytochrome oxidase A3 than cyanide.1 In addition, at lower concentrations, the gas is a mucous membrane irritant.2 Features: exposure to high concentrations, particularly if repeated, can cause olfactory nerve paralysis; consequently, the characteristic smell is not detected by those exposed and a lack of a history of a ‘smell of rotten eggs’ does not exclude the diagnosis. Low concentrations cause blepharospasm, pain and redness in the eyes, blurred vision and the seeing of coloured haloes around lights.3,4 Headache, nausea, dizziness, drowsiness, sore throat and cough may also occur. Cyanosis, confusion, pulmonary oedema, coma and convulsions are common with higher concentrations.2,5 Mortality was 6% in 221 cases;6 death is usually from respiratory arrest or traumatic injury. Subacute encephalopathy7 and delayed neuropsychiatric sequelae have been reported.8–10 Management: casualties should be moved into fresh air. Rescuers must wear breathing apparatus, because of the risk of sudden respiratory arrest. Since the victims of severe poisoning die from respiratory arrest, prompt establishment of a clear airway and adequate ventilation by whatever means is available is imperative.
Allister Vale MD FRCP FRCPE FRCPG FFOM FAACT FBTS is Director of the National Poisons Information Service (Birmingham Unit) and the West Midlands Poisons Unit at City Hospital, Birmingham, UK. Competing interests: none declared.
MEDICINE 35:12
623
© 2007 Published by Elsevier Ltd.
Hydrogen sulphide
Supplemental oxygen should then be administered to the casualty. Although 100% oxygen had no beneficial effect in one experimental study,11 in another it was of benefit.12 In the same study hyperbaric oxygen (3 ATA) alone or with co-administration of sodium nitrite reduced the mortality substantially12; hyperbaric oxygen has been used to treat patients with life-threatening symptoms.13,14 There is limited experimental evidence that pre-treatment with sodium nitrite reduces mortality in hydrogen sulphide poisoning; 11 in another study sodium nitrite was of no benefit.12 However, it has been argued that nitrite could be effective only for a few minutes after exposure.15 Clinical benefit has been claimed.16 ◆
Allister Vale
Abstract References 1 Dorman DC, Moulin FJM, McManus BE, et al. Cytochrome oxidase inhibition induced by acute hydrogen sulfide inhalation: correlation with tissue sulfide concentrations in the rat brain, liver, lung, and nasal epithelium. Toxicol Sci 2002; 65: 18–25. 2 Beauchamp Jr RO, Bus JS, Popp JA, et al. A critical review of the literature on hydrogen sulfide toxicity. Crit Rev Toxicol 1984; 13: 25–97. 3 Guidotti TL. Hydrogen sulphide. Occup Med (Oxf) 1996; 46: 367–71. 4 International Programme on Chemical Safety. In: Chou C-H SJ, ed. Concise international chemical assessment document no. 53. Hydrogen sulfide: human health aspects. Geneva: World Health Organization, 2003. 5 Tanaka S, Fujimoto S, Tamagaki Y, et al. Bronchial injury and pulmonary edema caused by hydrogen sulfide poisoning. Am J Emerg Med 1999; 17: 427–29. 6 Burnett WW, King EG, Grace M, Hall WF. Hydrogen sulfide poisoning: review of 5 years’ experience. Can Med Assoc J 1977; 117: 1277–80. 7 Gaitonde UB, Sellar RJ, O’Hare AE. Long term exposure to hydrogen sulphide producing subacute encephalopathy in a child. Br Med J 1987; 294: 614. 8 Tvedt B, Skyberg K, Aaserud O, et al. Brain damage caused by hydrogen sulfide: a follow-up study of six patients. Am J Ind Med 1991; 20: 91–101. 9 Hirsch AR. Hydrogen sulfide exposure without loss of consciousness: chronic effects in four cases. Toxicol Ind Health 2002; 18: 51–61. 10 Schneider JS, Tobe EH, Mozley Jr PD. Persistent cognitive and motor deficits following acute hydrogen sulphide poisoning. Occup Med (Oxf) 1998; 48: 255–60. 11 Smith RP, Kruszyna R, Kruszyna H. Management of acute sulfide poisoning. Effects of oxygen, thiosulfate, and nitrite. Arch Environ Health 1976; 31: 166–69. 12 Bitterman N, Talmi Y, Lerman A, et al. The effect of hyperbaric oxygen on acute experimental sulfide poisoning in the rat. Toxicol Appl Pharmacol 1986; 84: 325–28. 13 Whitcraft III DD, Bailey TD, Hart GB. Hydrogen sulfide poisoning treated with hyperbaric oxygen. J Emerg Med 1985; 3: 23–25. 14 Smilkstein MJ, Bronstein AC, Pickett HM, Rumack BH. Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. J Emerg Med 1985; 3: 27–30. 15 Beck JF, Bradbury CM, Connors AJ, Donini JC. Nitrite as antidote for acute hydrogen sulfide intoxication? Am Ind Hyg Assoc J 1981; 42: 805–9. 16 Huang C-C, Chu N-S. A case of acute hydrogen sulfide (H2S) intoxication successfully treated with nitrites. J Formos Med Assoc 1987; 86: 1018–20.
Hydrogen sulphide is a potent inhibitor of cytochrome oxidase A3 and a mucous membrane irritant at lower concentrations. Cyanosis, confusion, pulmonary oedema, coma, convulsions and respiratory arrest are common in severe poisoning and neurological and neuropsychiatric sequelae have been observed. Rescue, resuscitation if necessary, and the administration of oxygen are the mainstay of treatment.
Keywords cytochrome oxidase A3 inhibitor; neuropsychiatric sequelae; pulmonary oedema; sodium nitrite; subacute encephalopathy
Hydrogen sulphide is a colourless gas. Workers in the petrochemical and gas industries and in tanning are at particular risk of exposure. The gas is also found in mines and sewers, and is liberated from decomposing fish (a hazard in fishing boats if the hold is filled with ‘trash’ fish used for making fish meal) and liquid manure systems. Mechanisms of toxicity: hydrogen sulphide is an even more potent inhibitor of cytochrome oxidase A3 than cyanide.1 In addition, at lower concentrations, the gas is a mucous membrane irritant.2 Features: exposure to high concentrations, particularly if repeated, can cause olfactory nerve paralysis; consequently, the characteristic smell is not detected by those exposed and a lack of a history of a ‘smell of rotten eggs’ does not exclude the diagnosis. Low concentrations cause blepharospasm, pain and redness in the eyes, blurred vision and the seeing of coloured haloes around lights.3,4 Headache, nausea, dizziness, drowsiness, sore throat and cough may also occur. Cyanosis, confusion, pulmonary oedema, coma and convulsions are common with higher concentrations.2,5 Mortality was 6% in 221 cases;6 death is usually from respiratory arrest or traumatic injury. Subacute encephalopathy7 and delayed neuropsychiatric sequelae have been reported.8–10 Management: casualties should be moved into fresh air. Rescuers must wear breathing apparatus, because of the risk of sudden respiratory arrest. Since the victims of severe poisoning die from respiratory arrest, prompt establishment of a clear airway and adequate ventilation by whatever means is available is imperative.
Allister Vale MD FRCP FRCPE FRCPG FFOM FAACT FBTS is Director of the National Poisons Information Service (Birmingham Unit) and the West Midlands Poisons Unit at City Hospital, Birmingham, UK. Competing interests: none declared.
MEDICINE 35:12
623
© 2007 Published by Elsevier Ltd.