PEDIATRICS Vol. 113 No. 4 April 2004, pp. 927-929
Severe Hydrogen Sulfide Exposure in a Working Adolescent
Heikki E. Nikkanen, MD*,
and
Michele M. Burns, MD*
* Division of Emergency Medicine-Medical Toxicology, Department of Medicine, Children’s Hospital, Boston, Massachusetts
Department of Emergency Medicine, Brigham and Women’s Hospital, Boston, Massachusetts
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ABSTRACT
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We describe an occupational exposure to hydrogen sulfide gas in a 16-year-old boy. While cleaning the reoxygenation tank of a fish hatchery, he and an adult supervisor lost consciousness. The adult died, and the adolescent regained consciousness briefly when emergency medical services personnel administered oxygen. At a local emergency department, he was intubated for respiratory distress. He was transferred to a tertiary care facility for additional management and, over the next 2 weeks, had a recovery to normal function.
Hydrogen sulfide is a colorless, malodorous gas that results from the decay of organic material. It is a byproduct of industry and agriculture. The mechanism of its toxicity is related primarily to inhibition of oxidative phosphorylation, which causes a decrease in available cellular energy. Although there is some anecdotal evidence to suggest that the early use of hyperbaric oxygen is beneficial, supportive care remains the mainstay of therapy. This report highlights the sources of exposure, management, and need for more stringent application of safety regulations in industries in which adolescents are employed.
Key Words: adolescent • occupational • hydrogen sulfide • inhalation exposure • toxicity • poisoning
Abbreviations: H2S, hydrogen sulfide
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CASE REPORT
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A 16-year-old boy was employed at a university aquaculture research facility for the summer. Half the halibut in the salt-water hatchery died. The water in the hatchery was tested and found to have a hydrogen sulfide (H2S) level of 4 mg/L, which is considered toxic to fish. There was a noticeable odor of H2S in the air. The system was drained, and the odors dissipated. The boy descended to the bottom of a 16-foot-deep tank to clean out some sludge. Soon after beginning work, he collapsed. His adult supervisor climbed down to rescue him, but rapidly lost consciousness and did not recover. The adolescent regained consciousness after high-flow oxygen was administered by emergency medical services, and he climbed out of the tank with assistance.
On arrival to a local emergency department, he was noted to have labored breathing and a persistent cough. His oxygen saturation was 88% on nonrebreather mask. His mental status was depressed, and he exhibited jerking movements of his arms and legs. He was intubated for respiratory distress. Results of arterial blood gas analysis after intubation were pH of 7.16, PO2 of 80 mm Hg, PCO2 of 43 mm Hg, and HCO3 of 28 mEq/L. His serum chemistries were significant for a glucose level of 185 mg/dL, potassium of 5.3 mEq/L, and bicarbonate of 18 mEq/L. Complete blood count showed a white blood cell count of 2900 cells per microliter, hematocrit of 50.8%, and platelet count of 221 000 cells per µL.
He was transferred to a tertiary care facility because of concerns about his respiratory status. His temperature was 36.9°C, his heart rate was 118 beats per minute, and his blood pressure was 104/62 mm Hg. Mechanical ventilator settings were placed at pressure support of 26 mm Hg, positive end expiratory pressure of 14 mm Hg, and a rate of 26 breaths per minute. An electrocardiogram showed 2 mm ST segment depression in leads II, III, and aVF, suggestive of inferior myocardial ischemia.
His treating physicians were concerned that he might need high-frequency oscillatory ventilation and possibly extracorporeal membrane oxygenation, which the facility could not provide. For this reason, he was transferred to a pediatric intensive care unit with this capability. There, he received high-frequency oscillatory ventilation therapy for <1 day, with no need for extracorporeal membrane oxygenation. On hospital day 4, the peak inspiratory pressures required for adequate oxygenation remained 
30 mm Hg. Portable chest radiographs revealed bilateral hilar infiltrates. Creatine kinase MB isoenzyme fraction reached a maximum of 3.1%, and troponin I reached a maximum of 2.39 ng/mL on hospital day 1. The urine thiosulfate level was 0.7 µmol/mg Cr (reference range: <0.4 µmol/mg Cr) on hospital day 1.
On hospital day 10, corticosteroid therapy was started for the treatment of noncardiogenic pulmonary edema. By hospital day 13, his blood gas on 55% fraction of inspired oxygen had improved to pH 7.44, PCO2 to 47.3 mm Hg, PO2 to 98.9 mm Hg, and HCO3 to 31 mEq/L. He was extubated shortly thereafter.
Over the following week, his oxygen requirement decreased to room air. He had only partial recall of the details of the exposure. He was discharged on hospital day 22 to a rehabilitation facility. At the time of this writing, he has returned to school and has regained normal function.
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DISCUSSION
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H2S is a colorless, heavier-than-air gas, with a characteristic odor of rotten eggs. It is a byproduct of the decay of organic material and, as such, is present in many industrial processes such as extraction of natural gas, paper manufacturing, leather processing, and storage of animal or vegetable matter. It is also present in sewers in a high concentration.
H2S exposures occur almost exclusively by the inhalational route. Once absorbed, the compound is distributed in the blood and taken up preferentially by the brain, liver, kidneys, pancreas, and small intestine.1 Metabolism occurs along 3 pathways: oxidation to sulfate, methylation, and reaction with metalloproteins. It is this last process that is responsible for the most serious toxic effects. Metabolites are subsequently excreted renally.
After contact with mucous membranes, H2S reacts with water to generate sodium sulfate, which is an irritant.2 Within the lungs, in addition to its irritant effects, H2S impairs the function of alveolar macrophages and cilia. Avid binding to mitochondrial cytochrome c oxidase slows oxidative phosphorylation, producing cellular hypoxia. However, unlike cyanide and other cellular asphyxiants, H2S rapidly dissociates from the mitochondria.
Clinical effects of H2S depend on the concentration and duration of exposure. Interestingly, a phenomenon known as "olfactory extinction" exists, which describes the loss of perception of the odor as the level increases. This is thought to be caused by paralysis of the olfactory nerve (Table 1). Blurry vision and halos around light sources (known as "gas eye"), as well as keratoconjunctivitis, are common ocular findings. Respiratory sequelae range from sore throat and cough to hemoptysis and pulmonary edema. Central nervous system effects include headache, agitation, convulsions, loss of consciousness, and respiratory center paralysis.1
Laboratory studies are generally not of help in making the rapid diagnosis of H2S poisoning. Urine thiosulfate and serum sulfmethemoglobin levels can be determined, but the results are generally not rapidly available. There is no clear correlation between these levels and severity of illness. As with any poison that interrupts cellular respiration, decreased oxygen utilization will result in a decrease in the PO2 gradient between arterial and venous blood. However, this is neither sensitive nor specific for H2S. Chest radiography may show pulmonary edema; computed tomography of the brain may show lesions in the basal ganglia. Interestingly, copper or silver metal, such as coins or jewelry, exposed to a high concentration of H2S often turn a black color, providing a clue to the nature of the injury.3 At autopsy, the brain may have a striking, black discoloration.
Foremost in the treatment of victims of H2S exposure is removal from the environment. However, the rapidity with which this toxin acts dictates that would-be rescuers wear proper protective gear to avoid being affected. A number of case reports describe scenarios in which significant numbers of would-be rescuers become victims themselves.4,5 Supportive measures including airway protection and administration of oxygen are the mainstay of hospital treatment. There is anecdotal evidence that hyperbaric oxygen may be helpful, especially if instituted early.6–10 A number of antidotes have been studied in animals, including nitrites and thiosulfates; however, they are of unclear benefit, and no human studies have been done to show clinical applicability.5,11
This case report highlights the ubiquity of H2S in industry as well as its rapid and lethal effects. It is difficult to detect, and removal from the environment and protection of rescuers are of paramount importance. Workers in industries in which H2S exists should be taught about the nature of the hazard. They should be trained frequently in the use of detection equipment, protective gear, and safety procedures. After an exposure, care is largely supportive.
In addition, this article emphasizes the importance of implementing occupational health regulations in the nascent aquaculture industry and especially where adolescents are concerned. In 2000, between 6 and 7 million children and adolescents were employed in the United States. An analysis of occupational toxic exposure data over the years 1993–1997 showed 8779 reported incidents involving adolescents <18 years old. Of them, 14.2% were rated as severe injury and 0.3% as life threatening, and there were 2 deaths. The true number of incidents has been estimated at 3 to 5 times this number.12 It was not illegal for the adolescent described in this article to be employed in the capacity that he was. Federal and state child labor laws should be reviewed to determine whether children are being appropriately barred from performing certain hazardous duties. Pediatricians have a duty to their patients to take an occupational history and to educate the family about potential workplace hazards.
The university to which the hatchery belongs has a protocol and program concerning work in confined spaces that could be hazardous to staff or students. However, this tank was never identified as a space that someone might enter. As a result, no signs were posted, and the protocol was not used in this situation. The state’s Department of Labor inspected the site shortly after the incident and found 12 violations of occupational safety and health rules, including the failure to evaluate the workplace to determine whether any confined spaces existed or to post any signs in such spaces. The area in which the incident occurred would have been qualified as a "permit-required" confined space, mandating that the employer evaluate it for potential hazards; develop protocols for entry into the space; provide equipment for monitoring, ventilation, communication, personal protection, and means of egress; identify employees to perform specific roles during the operation in the confined space; and develop a procedure for summoning emergency services. These actions had not been taken before the incident. The failure to protect the adolescent and adult worker seems to be due to failure to comply with existing occupational safety and health rules. Inspection of facilities and enforcement of compliance with regulations already on the books may be necessary to prevent additional incidents.
Follow-up by telephone 3 months after the incident confirmed that the patient had returned to normal functioning. Because of geographical distance and lack of baseline testing, however, no neurobehavioral testing has been planned.
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FOOTNOTES
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Received for publication Mar 13, 2003; Accepted Dec 11, 2003.
Address correspondence to Heikki E. Nikkanen, MD, 24 Grovenor Rd, #1, Jamaica Plain, MA 02130. E-mail: hnikkanen{at}partners.org
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PEDIATRICS (ISSN 1098-4275). ©2004 by the American Academy of Pediatrics
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