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Hydrogen sulfide poisoning treated with hyperbaric oxygen
The~ournaiofEmergencyMedune, Vol.3, pp 23-25. 1985
PrInted in theUSA ??CopyrIght 6 1985 Pergamon Press Ltd
HYDROGEN SULFIDE POISONING TREATED WITH HYPERBARIC OXYGEN Daniel D. Whitcraft III, MD, FACEP, Todd D. Bailey, George B. Hart, MD, FACS
MD,
and
Memorial MedIcal Center of Long Beach, Long Beach, Callfornla Reprint Address. Daniel D. Whitcraft, Ill, MD, Memorial Medical Center of Long Beach P.0 Box 1428, Long Beach, CA 90801-1428
Cl Abstract-Hydrogen sulfide inhalation injury can be life threatening. The toxic gas is produced, sometimes unexpectedly, from a wide variety of sources. Because its mechanism of toxicity is similar to that of cyanide, hydrogen sulfide poisoning is commonly treated with the nitrite component of the cyanide antidote kit. In this case report, hyperbaric oxygen was successfully used to treat hydrogen sulfide intoxication. Further evaluation of hyperbaric oxygen therapy as adjunctive treatment of hydrogen sulfide poisoning is recommended. 0 Keywords-hyperbaric oxygen; hydrogen sulfide; inhalation injury; syncope; methemoglobinemia
introduction Hydrogen sulfide is a malodorous gas commonly found in petroleum refining, rayon and heavy-water manufacturing, sewer gas, manure, silos, and in the fishing and tanning industry.’ Like cyanide, its toxicity is generally thought to be due to inactivation of cytochrome oxidase A3, and acute poisonings have been treated with nitrite-in-
duced methemoglobinemia. We describe the first reported use of hyperbaric oxygen for hydrogen sulfide poisoning.
Case Report A 2%year-old male collapsed after breathing fumes from a gas leak, which were later verified to be hydrogen sulfide. Four coworkers became unconscious trying to aid him. He arrived in the emergency department of Long Beach Memorial Hospital unconscious 30 minutes after the accident. Respirations were shallow but he was not cyanotic. Blood pressure was 130/90 mm Hg and pulse rate 96 beats per minute and regular. Neurologic examination demonstrated pupils to be 5 mm, round, and reactive to light, flaccidity, absent deep tendon reflexes, and normal Babinski reflexes. Gag reflex and cornea1 reflex were present. A chest radiograph demonstrated pulmonary edema. The ECG and cross table cervical spine film showed nothing abnormal. Initial arterial blood gas determination taken on 100% 0, after endotracheal intubation
~
of the most critical and challenging areas confronting the emergency department staff -is coordinated by Kenneth Kulig, MD of the Rocky Mountain Poison
=zxz==
Center.
Toxicology-one
RECEIVED: 15 August
1984; ACCEPTED: 24 December 1984 0736-467905 $3.00 + .OO 23
24
Daniel D. Whitcraft Ill, Todd D. Bailey, George B. Hart
showed a pH of 7.34; Po2, 190; O2 saturation, 99%; HCO,, 20; and Pco2, 35. A complete blood count revealed WBC, 22,800; hemoglobin, 16.3 g/dL; and hematocrit, 46.9%; PMN, 82; bands, 8; lymphocytes, 6%; and monocytes, 4%. Serum calcium was 9.4 mg/dL; Na, 138 mEq/L; K, 3.6 mEq/L; Cl, 104 mEq/L; CO,, 24 mEq/L. The serum glucose was 148 mg/dL; BUN, 11 mg/dL; creatinine, 1.1 mg/dL. The patient was given intravenously (IV) 250 mg of aminophylline over 20 minutes, 1.75 g IV push of pyridoxine (as a possible sulfide acceptor), and 300 mg of sodium nitrite. The patient opened and closed his eyes on command at one hour after exposure but did not voluntarily move his extremities. Decerebrate posturing of his right arm occurred following painful stimuli. He was taken to the baromedical unit, and placed inside a compression chamber set at 2.5 atmospheres absolute 0, (ATA) for 90 minutes. The patient began to move his extremities, and his level of consciousness dramatically improved after decompression. He was extubated after the treatment and was able to transfer himself to the stretcher and hospital bed. Three hours after leaving the emergency department he was awake, alert, and eating a soft diet. He was treated with two more go-minute periods of 2.5 ATA. The patient was discharged after 48 hours. Although he is back at work, he continues to complain of mild leg weakness and intermittent headaches. The four would-be rescuers had each been unconscious from one to three minutes, but recovered spontaneously with oxygen therapy and monitoring only. Their symptoms of headache, cough, dizziness, nausea, and eye irritation cleared after 24 hours.
Discussion Hydrogen sulfide is a colorless gas, heavier than air, and noted for an odor resembling rotten eggs. A potential victim, however, might not sense this characteristic smell be-
cause of rapid paralysis of the olfactory nerve when exposed to high concentrations of the gas. Hydrogen sulfide is liberated from decomposing protein and is a byproduct of petroleum refining, tanning, and manufacture of heavy water.’ It is found in septic tanks, sewers, and mines and has been documented to have caused severe poisoning in a community hospital where sulfuric acid (H2S04) solution was being used to clean the cast room drain trap.* At 0 to 25 ppm the odor is detectable, and exposure above 50 ppm produces symptoms that progress from irritation of the mucous membranes, headache, nausea, cough, dizziness, and dyspnea to pulmonary edema, seizures, coma, and death. Although the duration of exposure to hydrogen sulfide certainly affects outcome, the primary determinant of the severity of the poisoning is probably the intensity of the initial exposure. Sudden collapse and death occur at 500 to 1,000 ppm. The first acid dissociation constant of hydrogen sulfide is 10 to 7 mol/L, so that in body fluids dissociated and undissociated hydrogen sulfide exist in approximately equal proportions. The undissociated acid penetrates biologic membranes more rapidly than the (HS-) anion; however, it is thought that the (HS-) anion is responsible for the inhibition of the function of cytochrome oxidase.3 When the mitochondrial electron transport system is unable to function properly, cellular respiration continues anaerobically with production of organic acid by-products. Hydrogen sulfide is normally detoxified by undergoing spontaneous oxidation4 to sulfate or thiosulfate, although a reaction with endogenous disulfide bonds has been postulated. The appropriate initial treatment must include vigorous prehospital and emergency basic and advanced life support. Amy1 nitrite by inhalation followed by sodium nitrite intravenously are then employed. Nitrites induce methemoglobin, which combines with hydrogen sulfide to form sulfmethemoglobin. This is the same principle
Sulfide Poisoning Treated with HBO
25
by which cyanide is detoxified through formation of cyanomethemoglobin. Hyperbaric oxygen is the supersaturation of the tissues with oxygen given under pressure for short periods of time (90 to 120 minutes). Henry’s Law states that the degree to which a gas enters into physical solution in body fluids is directly proportional to the partial pressure of the gas to which the fluid is exposed. Hyperbaric oxygen at 3 ATA (FiO,-2,200 mm Hg) allows 6 vol % O2 to be dissolved in the plasma to meet the body’s resting requirement.5 This amount of dissolved oxygen in the blood may exert a protective effect. As hydrogen sulfide is a pulmonary irritant, the increased PO* may be beneficial treatment for the chemical pneumonitis through the fluid medium of the swollen alveolar cells, as stated in Henry’s Law.6.7 Moreover, the dissolved oxygen in the plasma supports metabolism without hemoglobin,8 and it also accelerates the reduction of methemoglobin, which results from the antidote.g
Lastly, the elimination of the hydrogen sulfide may be accelerated as it is in carbon monoxide intoxication.”
Hydrogen
Conclusion
Two recent case reports of survival after severe hydrogen sulfide poisoning2 I’noted longer periods of in-hospital convalescence than our patient experienced. We postulate that hyperbaric oxygen treatment may have diminished the number and severity of symptoms, shortened the length of convalescence, and possibly been responsible for the rapid improvement of initial symptoms. A victim of hydrogen sulfide poisoning should not be put in a hyperbaric chamber without vigorous supportive therapy being first performed. Patients with known hydrogen sulfide poisoning who continue to have significant symptomology after the initial management should be considered for treatment with hyperbaric oxygen.
REFERENCES 1. Burnet WW, King EG, Grace M, et al: Hydrogen sulfide poisoning: Reviewing five years experience. _I Can Med Assoc 1977; 117:1277-1280. 2. Peters JW: Hydrogen sulfide poisoning in a hospital setting. JAMA 1981; 246:1588-1589. 3. Smith RP, Gosselin RE: Hydrogen sulfide poisoning. J Occup Med 1979; 21:93-97. 4. Evans CL: The toxicity of hydrogen sulfide and other sulfides. Exp Physiol 1967; 52:231-248. 5. Bassett BE, Bennett PB: Introduction to the physical and physiological bases of hyperbaric therapy, in Davis JC, Hunt TK (eds): Hyperbaric Oxygen Therapy. Maryland, Undersea Medical Society, 1977, pp. 19-20. 6. Schwartz Sl, Breslau RC, Kutner F, et al: Effects of drugs and hyperbaric oxygen environment on experimental kerosene pneumonitis. Dis Chest 1965; 41:353-359.
7. Gorman JF, Glow DE, Rejent M, Stansell G, et al: Hyperbaric oxygen therapy for chemical pneumonitis: Experimental and clinical observations. Surgery 1968; 64:1027-1032. 8. Boerema I, Meijne NC, Brummelkamp WK, et al: Life without blood. J Cardiovasc Surg 1960; 1:133-146. 9. Goldstein GM, Doull J: Treatment of nitrite-induced methemoglobinemia with hyperbaric oxygen. ProcSocExpBiolMed 1971; 138:137-139. 10. Pace N, Strajman E, Walker EL: Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science 1950; 111:652-654. 11. Stine RS, Slosberg B, Beacham BE: Hydrogen sulfide intoxication: A case report and discussion of treatment. Ann Intern Med 1976; 85:756-758.
PrInted in theUSA ??CopyrIght 6 1985 Pergamon Press Ltd
HYDROGEN SULFIDE POISONING TREATED WITH HYPERBARIC OXYGEN Daniel D. Whitcraft III, MD, FACEP, Todd D. Bailey, George B. Hart, MD, FACS
MD,
and
Memorial MedIcal Center of Long Beach, Long Beach, Callfornla Reprint Address. Daniel D. Whitcraft, Ill, MD, Memorial Medical Center of Long Beach P.0 Box 1428, Long Beach, CA 90801-1428
Cl Abstract-Hydrogen sulfide inhalation injury can be life threatening. The toxic gas is produced, sometimes unexpectedly, from a wide variety of sources. Because its mechanism of toxicity is similar to that of cyanide, hydrogen sulfide poisoning is commonly treated with the nitrite component of the cyanide antidote kit. In this case report, hyperbaric oxygen was successfully used to treat hydrogen sulfide intoxication. Further evaluation of hyperbaric oxygen therapy as adjunctive treatment of hydrogen sulfide poisoning is recommended. 0 Keywords-hyperbaric oxygen; hydrogen sulfide; inhalation injury; syncope; methemoglobinemia
introduction Hydrogen sulfide is a malodorous gas commonly found in petroleum refining, rayon and heavy-water manufacturing, sewer gas, manure, silos, and in the fishing and tanning industry.’ Like cyanide, its toxicity is generally thought to be due to inactivation of cytochrome oxidase A3, and acute poisonings have been treated with nitrite-in-
duced methemoglobinemia. We describe the first reported use of hyperbaric oxygen for hydrogen sulfide poisoning.
Case Report A 2%year-old male collapsed after breathing fumes from a gas leak, which were later verified to be hydrogen sulfide. Four coworkers became unconscious trying to aid him. He arrived in the emergency department of Long Beach Memorial Hospital unconscious 30 minutes after the accident. Respirations were shallow but he was not cyanotic. Blood pressure was 130/90 mm Hg and pulse rate 96 beats per minute and regular. Neurologic examination demonstrated pupils to be 5 mm, round, and reactive to light, flaccidity, absent deep tendon reflexes, and normal Babinski reflexes. Gag reflex and cornea1 reflex were present. A chest radiograph demonstrated pulmonary edema. The ECG and cross table cervical spine film showed nothing abnormal. Initial arterial blood gas determination taken on 100% 0, after endotracheal intubation
~
of the most critical and challenging areas confronting the emergency department staff -is coordinated by Kenneth Kulig, MD of the Rocky Mountain Poison
=zxz==
Center.
Toxicology-one
RECEIVED: 15 August
1984; ACCEPTED: 24 December 1984 0736-467905 $3.00 + .OO 23
24
Daniel D. Whitcraft Ill, Todd D. Bailey, George B. Hart
showed a pH of 7.34; Po2, 190; O2 saturation, 99%; HCO,, 20; and Pco2, 35. A complete blood count revealed WBC, 22,800; hemoglobin, 16.3 g/dL; and hematocrit, 46.9%; PMN, 82; bands, 8; lymphocytes, 6%; and monocytes, 4%. Serum calcium was 9.4 mg/dL; Na, 138 mEq/L; K, 3.6 mEq/L; Cl, 104 mEq/L; CO,, 24 mEq/L. The serum glucose was 148 mg/dL; BUN, 11 mg/dL; creatinine, 1.1 mg/dL. The patient was given intravenously (IV) 250 mg of aminophylline over 20 minutes, 1.75 g IV push of pyridoxine (as a possible sulfide acceptor), and 300 mg of sodium nitrite. The patient opened and closed his eyes on command at one hour after exposure but did not voluntarily move his extremities. Decerebrate posturing of his right arm occurred following painful stimuli. He was taken to the baromedical unit, and placed inside a compression chamber set at 2.5 atmospheres absolute 0, (ATA) for 90 minutes. The patient began to move his extremities, and his level of consciousness dramatically improved after decompression. He was extubated after the treatment and was able to transfer himself to the stretcher and hospital bed. Three hours after leaving the emergency department he was awake, alert, and eating a soft diet. He was treated with two more go-minute periods of 2.5 ATA. The patient was discharged after 48 hours. Although he is back at work, he continues to complain of mild leg weakness and intermittent headaches. The four would-be rescuers had each been unconscious from one to three minutes, but recovered spontaneously with oxygen therapy and monitoring only. Their symptoms of headache, cough, dizziness, nausea, and eye irritation cleared after 24 hours.
Discussion Hydrogen sulfide is a colorless gas, heavier than air, and noted for an odor resembling rotten eggs. A potential victim, however, might not sense this characteristic smell be-
cause of rapid paralysis of the olfactory nerve when exposed to high concentrations of the gas. Hydrogen sulfide is liberated from decomposing protein and is a byproduct of petroleum refining, tanning, and manufacture of heavy water.’ It is found in septic tanks, sewers, and mines and has been documented to have caused severe poisoning in a community hospital where sulfuric acid (H2S04) solution was being used to clean the cast room drain trap.* At 0 to 25 ppm the odor is detectable, and exposure above 50 ppm produces symptoms that progress from irritation of the mucous membranes, headache, nausea, cough, dizziness, and dyspnea to pulmonary edema, seizures, coma, and death. Although the duration of exposure to hydrogen sulfide certainly affects outcome, the primary determinant of the severity of the poisoning is probably the intensity of the initial exposure. Sudden collapse and death occur at 500 to 1,000 ppm. The first acid dissociation constant of hydrogen sulfide is 10 to 7 mol/L, so that in body fluids dissociated and undissociated hydrogen sulfide exist in approximately equal proportions. The undissociated acid penetrates biologic membranes more rapidly than the (HS-) anion; however, it is thought that the (HS-) anion is responsible for the inhibition of the function of cytochrome oxidase.3 When the mitochondrial electron transport system is unable to function properly, cellular respiration continues anaerobically with production of organic acid by-products. Hydrogen sulfide is normally detoxified by undergoing spontaneous oxidation4 to sulfate or thiosulfate, although a reaction with endogenous disulfide bonds has been postulated. The appropriate initial treatment must include vigorous prehospital and emergency basic and advanced life support. Amy1 nitrite by inhalation followed by sodium nitrite intravenously are then employed. Nitrites induce methemoglobin, which combines with hydrogen sulfide to form sulfmethemoglobin. This is the same principle
Sulfide Poisoning Treated with HBO
25
by which cyanide is detoxified through formation of cyanomethemoglobin. Hyperbaric oxygen is the supersaturation of the tissues with oxygen given under pressure for short periods of time (90 to 120 minutes). Henry’s Law states that the degree to which a gas enters into physical solution in body fluids is directly proportional to the partial pressure of the gas to which the fluid is exposed. Hyperbaric oxygen at 3 ATA (FiO,-2,200 mm Hg) allows 6 vol % O2 to be dissolved in the plasma to meet the body’s resting requirement.5 This amount of dissolved oxygen in the blood may exert a protective effect. As hydrogen sulfide is a pulmonary irritant, the increased PO* may be beneficial treatment for the chemical pneumonitis through the fluid medium of the swollen alveolar cells, as stated in Henry’s Law.6.7 Moreover, the dissolved oxygen in the plasma supports metabolism without hemoglobin,8 and it also accelerates the reduction of methemoglobin, which results from the antidote.g
Lastly, the elimination of the hydrogen sulfide may be accelerated as it is in carbon monoxide intoxication.”
Hydrogen
Conclusion
Two recent case reports of survival after severe hydrogen sulfide poisoning2 I’noted longer periods of in-hospital convalescence than our patient experienced. We postulate that hyperbaric oxygen treatment may have diminished the number and severity of symptoms, shortened the length of convalescence, and possibly been responsible for the rapid improvement of initial symptoms. A victim of hydrogen sulfide poisoning should not be put in a hyperbaric chamber without vigorous supportive therapy being first performed. Patients with known hydrogen sulfide poisoning who continue to have significant symptomology after the initial management should be considered for treatment with hyperbaric oxygen.
REFERENCES 1. Burnet WW, King EG, Grace M, et al: Hydrogen sulfide poisoning: Reviewing five years experience. _I Can Med Assoc 1977; 117:1277-1280. 2. Peters JW: Hydrogen sulfide poisoning in a hospital setting. JAMA 1981; 246:1588-1589. 3. Smith RP, Gosselin RE: Hydrogen sulfide poisoning. J Occup Med 1979; 21:93-97. 4. Evans CL: The toxicity of hydrogen sulfide and other sulfides. Exp Physiol 1967; 52:231-248. 5. Bassett BE, Bennett PB: Introduction to the physical and physiological bases of hyperbaric therapy, in Davis JC, Hunt TK (eds): Hyperbaric Oxygen Therapy. Maryland, Undersea Medical Society, 1977, pp. 19-20. 6. Schwartz Sl, Breslau RC, Kutner F, et al: Effects of drugs and hyperbaric oxygen environment on experimental kerosene pneumonitis. Dis Chest 1965; 41:353-359.
7. Gorman JF, Glow DE, Rejent M, Stansell G, et al: Hyperbaric oxygen therapy for chemical pneumonitis: Experimental and clinical observations. Surgery 1968; 64:1027-1032. 8. Boerema I, Meijne NC, Brummelkamp WK, et al: Life without blood. J Cardiovasc Surg 1960; 1:133-146. 9. Goldstein GM, Doull J: Treatment of nitrite-induced methemoglobinemia with hyperbaric oxygen. ProcSocExpBiolMed 1971; 138:137-139. 10. Pace N, Strajman E, Walker EL: Acceleration of carbon monoxide elimination in man by high pressure oxygen. Science 1950; 111:652-654. 11. Stine RS, Slosberg B, Beacham BE: Hydrogen sulfide intoxication: A case report and discussion of treatment. Ann Intern Med 1976; 85:756-758.