Case Report

Acute hydrogen sulfide toxicity due to sewer gas exposure

Abstract

Hydrogen sulfide toxicity is a known risk for individuals working in the petroleum, sewer, maritime, and mining industries. Concern regarding exposure has led to the development of safety precautions and treatment guidelines. The US government imposes Safety measures including self- contained breathing masks and exposure time limits to hydrogen sulfide gas. Current treatment methods, however, are not strongly supported by research. acute exposure to hydrogen sulfide gas still poses a significant life threat. In this report, we discuss a case of a sewer worker exposed to deadly concentrations of hydrogen sulfide. Safety precau- tions and treatment options available to those exposed to high doses of hydrogen sulfide gas are explored.

Anoxic brain injury, pulmonary edema, and death are significant outcomes from exposure to high levels of hydrogen sulfide gas. Current safety precautions and preventive measures are the best safeguards against hydro- gen sulfide poisoning. There is little evidence-based medicine, nevertheless, to guide the treatment of those exposed to hydrogen sulfide gas. Empirically grounded guidelines regarding treatment of acute poisoning is needed. Continued evaluation of case reports of those exposed to high doses of hydrogen sulfide provides important clinical scenarios for further evaluation of current treatment methods. A 34-year-old male sewer worker was found unresponsive approximately 20 ft below street level in a sewer line. There was some concern that he was not wearing the issued proper safety equipment. Coworkers found him to be unconscious, and emergency medical services (EMS) was called approxi- mately 5 to 7 minutes after last known communication. The EMS arrived on the scene within minutes and reported that a very powerful sewer gas odor was present at street level. The local fire Hazmat confirmed with EMS that the patient was exposed to hydrogen sulfide gas. Further complicating medical care, dangerous conditions made the extrication time somewhere between 45 and 50 minutes before EMS could assess the patient. EMS found the patient unresponsive with sonorous respirations, ashen gray, wet from sewer water, and emitting a strong odor of sewer gas. Oxygen was

administered via a self-contained breathing apparatus (SCUBA) mask while still below street level. Vital signs were obtained once the patient was elevated to street level, which revealed a systolic blood pressure of 170 by palpation, Pulse oximetery with nonrebreather mask at 15 L of oxygen per minute at 82%, respiratory rate of 30, and a pulse at a regular rate of 80. Bag mask valve ventilation (BMV) was initiated, and Skin color returned to normal; however, SPO2 remained in the 80% range. Intubation was attempted by EMS but was unsuccessful secondary to the patient’s clenched teeth (rapid sequence intubation [RSI] drugs are not available to local EMS). The EMS subsequently placed a nasal airway and continued BMV. Suctioning yielded pink frothy sputum. He remained in this condition and was transported to the emergency department (ED).

Upon arrival to the ED, repeat vital signs included blood pressure of 171/85, pulse rate of 86, respiratory rate of 32, pulse oximetery of 86% with continued BMV, and temperature of 36.0?C. The patient was unresponsive with sonorous respirations. Physical examination was remarkable for production of pink frothy sputum from the mouth, and breath sounds revealed diffuse rales bilaterally. He was not moving any extremities. In addition, the patient, had a clenched jaw. Pupils were equal, round, and reactive to light bilaterally without evidence of chemosis or injection. There was no obvious trauma externally.

The patient was intubated immediately using etomidate and succinycholine. He was placed on mechanical ventila- tion with the following settings: assist control, respiratory rate of 14, fraction of inspired oxygen (FIO2) of 100%, and positive end expiratory pressure of 12 cm H₂O. Pulse oximetery readings improved to 90% initially; however, it declined to 84%-86% shortly thereafter. He was given intravenous fluids. Sedation was maintained with versed and vecuronium while he was in the ED. Poisondex was reviewed, and the Poison Control Center was consulted for treatment of hydrogen sulfide toxicity. Both confirmed the use of sodium nitrite to induce methemoglobinemia. The patient was given 300 mg (0.33 mL/kg of 3% solution) of sodium nitrite by slow Intravenous push.

The chest radiograph showed the endotracheal tube present a few centimeters above the carina. An oral-gastric tube extended distally to the diaphragm, but the tip could not be visualized. Bilateral patchy mid and upper lung infiltrates,

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predominantly perihilar and greater on the left consistent with pulmonary edema, were present. Head computed tomography was negative for any acute traumatic injury or significant findings. An arterial blood gas was obtained before the administration of sodium nitrite and also while the patient was on mechanical ventilation. With assisted ventilation, the patient maintained a respiratory rate of 34 and temperature of 36.0?C, and FIO2 of 100% revealed a marked respiratory acidosis and mild metabolic acidosis. pH was 7.215; PaCO2, 49.0 mm Hg; PaO2, 58.8 mm Hg; bicarbonate, 19.4 mmol/L; HbO2 saturation 85%; carbox- yhemoglobin, 0.5%; and methemoglobin, 0.4%. Complete blood count was remarkable for leukocytosis. The basic metabolic panel was remarkable for hyperglycemia only. Urine screen was unremarkable other than being positive for benzodiazepines (the patient was given versed). Salicylate and acetaminophen levels were negative. Liver function tests were significant for elevated ALT and AST at 56 and 83 IU/ L, respectively. Lactate was elevated at 5.2 mmol/L. Repeat ABG was sent postadministration of sodium nitrite and continued to show a significant respiratory acidosis and mild metabolic acidosis (pH 7.133, PaCO2 65.0 mm Hg, PaO2

49.4 mm Hg, bicarbonate 21.2 mmol/L, HbO2 saturation 71.2%, carboxyhemoglobin 0.9%, and methemoglobin level 7.0%). The elevation in metHemoglobin levels was to be expected after the treatment with sodium nitrite.

After the patient was transferred to the medical intensive care unit (MICU), his course worsened. He remained unresponsive in the MICU supported by mechanical ventilation. When sedation was weaned, the Neurological examination was significant for intact pupillary light response, negative corneal reflex, positive dolls’ eyes, and no response to painful stimulation (including nail bed pressure), with no response to plantar stroke. Albuterol and Atrovent nebulizer treatments were administered. In addi- tion, bicarbonate was given to correct his acidosis, which continued to worsen.

Serial ABG results revealed continued respiratory acidosis with elevated PaCO2 and low PaO2. Basic metabolic panel was significant for hypocarbia at 19 mmol/L. Repeat cardiac enzymes were positive with an initial troponin of

1.35 ng/mL and declining to 0.93 ng/mL. lactic acid levels remained elevated, reaching a level of 6.7 mmol/L after initially improving to 2.6 mmol/L. The next morning, after MICU admission, the patients’ blood pressure and oxygen saturation rapidly declined, and he was found to be in ventricular fibrillation. Advanced cardiac life support protocol was initiated. The patient’s rhythm varied from ventricular fibrillation to asystole intermittently. He showed no response to the multiple doses of epinephrine and atropine that were given. He died after 30 minutes of resuscitation.

Initial reports indicate that thiosulfate blood levels were

3.5 ug/mL from the blood sample obtained before the patient was pronounced dead. It is important to note that the Upper limit of normal for thiosulfate blood levels is 2.0ug/mL.

Postmortem femoral blood levels, however, were negative for thiosulfate. Postmortem heart blood sampling was unable to be preformed. Cyanide blood levels were negative as well. The Cleveland Hazmat team reported that hydrogen sulfide gases were present in high quantities on scene- verbal reports estimated a level greater than 1000 parts per million (ppm) at the bottom of the sewer. There was a strong odor at street level, and the patient emitted a foul odor as well. This patient’s injuries are suggestive of significant exposure, with Respiratory insufficiency and pulmonary edema consistent with acute respiratory syndrome. Neuro- logical compromise is consistent with prolonged Brain hypoxia, which was aggravated by the time to patient extraction. Elevation in cardiac enzymes may have been secondary to overall metabolic acidosis. Given the clinical scenario, the most likely cause of death of this patient was indeed neurological damage secondary to acute respiratory

distress and hypoxia due to hydrogen sulfide toxicity.

Hydrogen Sulfide (H2S) is a colorless, flammable, rapidly inhaled toxic gas that is known for its characteristic smell of rotten eggs. It is found as a byproduct in several industrial settings including petroleum refineries, oil and natural gas refineries, mines, and dye-making plants. Hydrogen sulfide gas is often found in deposits of crude oil and natural gas, thereby contributing to its occurrence in the refinery process. Furthermore, hydrogen sulfide gas is a byproduct of the breakdown of organic sulfide compounds and can also be found at hazardous levels in sewers, barns, commercial fishing holds, sulfur hot springs, ships holds, and liquid manure areas [1].

Hydrogen sulfide inhibits the cytochrome oxidase system, thereby arresting aerobic cellular respiration. Cellular asphyxia ensues, and the promotion of anaerobic metabolism occurs with resultant accumulation of lactic acid leading to metabolic acidosis [2].

The characteristic rotten egg odor is detectable at levels as low as 0.025 ppm. At levels between 100 and 150 ppm, the olfactory nerve becomes paralyzed, and the characteristic scent is no longer recognized, which allows for Toxic exposures to occur. The Federal OSHA permissible exposure limit for general industry is 20 ppm during the 8-hour work shift [3]. If no other exposures occur during an 8-hour work shift, however, the permissible exposure limit can be up to 50 ppm for a single period up to 10 minutes [4]. Levels of 100 ppm pose an immediate health and life hazard, pulmonary edema may occur at levels of 300 to 500 ppm, with death occurring at levels greater than 600 to 800 ppm [3].

side effects occur from both low-level and high-level exposures of hydrogen sulfide gas. Chronic low level exposures result from hydrogen sulfide’s irritant effects and include upper airway irritation, conjunctivitis, wheezing, and green-gray lines. High-level exposures can result in cough, dyspnea, confusion, coma, seizures, loss of con- sciousness, and hemotypisis. Massive inhalation exposure may result in myocardial infarction, cardiopulmonary arrest, and death. Long-term outcome for those who survive

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massive inhalation can range from Complete recovery to severe neurological impairment [3,5]. There also have been case reports of late sequelae of interstitial fibrosis after hydrogen sulfide poisoning [6].

The “knockdown” effect describes the phenomenon of sudden loss of consciousness at high levels of hydrogen sulfide gas exposure-usually in the range of 750 to 1000 ppm. Hydrogen sulfide directly affects the brainstem through the inhibition of the cytochrome oxidase pathway and results in apnea. If the victim is immediately removed from the setting, there is potential for complete recovery. However, extended exposure to the gas results in prolonged apnea, which will lead to anoxic brain injury and also allows time for the occurrence of the severe systemic effects of pulmonary edema, coma, seizures, and myocar- dial infarction [7].

Diagnosis of hydrogen sulfide based on laboratory parameters is difficult. A complete clinical history is extremely important in aiding final assessment of hydrogen sulfide toxicity. Although not a sensitive sign, silver coins on the victim classically blacken because of the conversion of silver to silver sulfide [3]. Hydrogen sulfide is labile in vitro, and therefore, specific levels are not helpful in diagnosis. Kage et al [8] has proposed that urinary thiosulfate levels are appropriate to aid in the diagnosis of hydrogen sulfide poisoning in nonfatal cases and that blood thiosulfate levels should be used to aid in the diagnose of hydrogen sulfide poisoning in lethal cases. Neither thiosulfate levels, however, are timely in critical situations.

Treatment of massive inhalation of hydrogen sulfide toxicity is largely supportive. The initial goal of treatment should be attention to the airway, breathing, and circulation. Management of respiration includes oxygen, positive pressure ventilation, and positive end expiratory pressure if necessary. Specific treatments for hydrogen sulfide toxicity include administration of amyl nitrite, sodium nitrite, and albuterol or atrovent nebulizer treatments. Hydrogen sulfide has a greater affinity for methemoglobin than cellular cytochrome oxidases. Nitrite administration results in the formation of methemoglobin and thereby helps to reduce the metabolic toxicity of hydrogen sulfide by allowing for the conversion of hydrogen sulfide to the less toxic sulfmethemoglobin. Nitrites, nonetheless, can also result in hypotension, and methemoglobinemia will further decrease oxygen saturation. Furthermore, there is limited evidence supporting the usefulness of nitrite therapy in hydrogen sulfide poisoning. It should be used with caution. Amyl nitrite ampules may be inhaled by patients [9-11]. Sodium nitrite is administered 0.33 mL/kg of 3% solution slow intravenous push to a maximum of 10 mL. It is important to note that thiosulfate should not be used in the treatment of hydrogen sulfide poisoning. Bronchodilators like albuterol may be given to reduce the bronchospasm associated with the irritant effects of hydrogen sulfide gas. Hyperbaric oxygen therapy has been documented as a therapeutic option

in case reports; however, this mode of treatment is largely anecdotal and lacks strong supportive evidence [5,3].

preventive measures are extremely important in pre- venting lethal exposure to hydrogen sulfide toxicity. Measures include following federal guidelines on limiting exposure at the work place, including wearing protective respiratory equipment and being aware of the potential for exposure based on the environmental setting. As men- tioned previously, proper use of protective equipment may have prevented this tragic death. General medical care guidelines, however, are not grounded in research with human subjects. Hydrogen sulfide toxicity is an important area of research and discussion because it effects many industrial workers and residents living near areas of hydrogen sulfide gas emission.

Acknowledgment

The authors thank Dawn A. Smith for proofreading this manuscript.

Chaethana Yalamanchili MD Michael D. Smith MD

Department of Emergency Medicine MetroHealth Medical Center Cleveland, OH 44109, USA

E-mail address: [email protected] doi:10.1016/j.ajem.2007.08.025

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