Novel treatment of dihydrogen sulfide inhalation using hyperbaric oxygen during mass casualty.

Hydrogen sulfide (H2S) is a toxic gas produced via breakdown of organic matter. Hydrogen sulfide exposure can cause symptoms ranging in severity from mild effects (dizziness, headache, nausea) to severe lactic acidosis, respiratory failure, pulmonary edema, cardiac arrhythmias and death. Treatment modalities include oral countermeasures and 100% FiO2 with supportive therapy. However, case studies utilizing hyperbaric oxygen (HBO2) therapy have been reported with general benefit seen in severe cases of toxicity. In this report, cases of mild to moderate H2S toxicity occurred aboard a U.S. Navy ship, resulting in a mass casualty incident of more than 30 patients. Patient symptoms included dizziness, headaches, nausea, vomiting, and one patient with altered mental status. Most patients' symptoms resolved after several hours of supportive therapy, but six patients had symptoms refractory to 100% FiO2 at 1 atm. These six patients received HBO2 therapy with a USN Treatment Table 9 after consultation with the local emergency room and hyperbaric assets. Four separate chambers were utilized, including two chambers onboard USN ships and the local explosive ordnance disposal (EOD) chamber. Complete resolution of symptoms in all six patients was achieved within the first breathing period. Patients were monitored after treatment aboard the USN ship medical department. No patients required emergency department care. These cases demonstrate an expanded use of HBO2 to include moderate cases of H2S toxicity refractory to first-line therapy.

Outbreak of Mysterious Illness Among Hospital Staff: Poisoning or Iatrogenic Reinforced Mass Psychogenic Illness?

BACKGROUND: Hospitals are rarely reported as settings for mass psychogenic illness (MPI). The present report scrutinizes an outbreak of probable MPI among hospital staff, with medical intervention reinforcing the course of the illness. CASE REPORT: Four of seven staff members in an emergency department became acutely ill with nonspecific symptoms. After uneventful observation they were discharged, but symptoms worsened at reassembly for debriefing. Poisoning with hydrogen sulfide was suspected, and the victims were transferred by helicopter for hyperbaric oxygen (HBO) treatment. During the following 9 days, 14 possible poisoning victims were identified, 6 of whom were transferred for HBO. After hospital stays with repeated HBO treatment and examinations without identification of significant physical disease, the majority of the 10 HBO-treated victims remained symptomatic, some on prolonged sick leave. The ward was closed for several weeks during comprehensive but negative investigations for toxic chemicals. Clinical data and lack of indication of chemical exposure, together with an attack pattern with only some individuals becoming ill in a shared environment, suggest MPI. Iatrogenic influence from dramatic intervention was probably a strong driving force in the outbreak. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Awareness of MPI may prevent unnecessary and potentially harmful treatment as well as improve health care resilience, particularly with respect to preparedness. Outbreaks of illness in a group of symptomatic victims without indication of significant physical disease should be managed by observation and limited intervention.

High-dose hydroxocobalamin administered after H2S exposure counteracts sulfide-poisoning-induced cardiac depression in sheep.

CONTEXT: Severe H2S poisoning leads to death by rapid respiratory and cardiac arrest, the latter can occur within seconds or minutes in severe forms of intoxication. OBJECTIVES: To determine the time course and the nature of H2S-induced cardiac arrest and the effects of high-dose hydroxocobalamin administered after the end of sulfide exposure. MATERIALS AND METHODS: NaHS was infused in 16 sedated mechanically ventilated sheep to reach concentrations of H2S in the blood, which was previously found to lead to cardiac arrest within minutes following the cessation of H2S exposure. High-dose hydroxocobalamin (5 g) or saline solution was administered intravenously, 1 min after the cessation of NaHS infusion. RESULTS: All animals were still alive at the cessation of H2S exposure. Three animals (18%) presented a cardiac arrest within 90 s and were unable to receive any antidote or vehicle. In the animals that survived long enough to receive either hydroxocobalamin or saline, 71% (5/7) died in the control group by cardiac arrest within 10 min. In all instances, cardiac arrest was the result of a pulseless electrical activity (PEA). In the group that received the antidote, intravenous injection of 5 g of hydroxocobalamin provoked an abrupt increase in blood pressure and blood flow; PEA was prevented in all instances. However, we could not find any evidence for a recovery in oxidative metabolism in the group receiving hydroxocobalamin, as blood lactate remained elevated and even continued to rise after 1 h, despite restored hemodynamics. This, along with an unaltered recovery of H2S kinetics, suggests that hydroxocobalamin did not act through a mechanism of H2S trapping. CONCLUSION: In this sheep model, there was a high risk for cardiac arrest, by PEA, persisting up to 10 min after H2S exposure. Very high dose of hydroxocobalamin (5 g), injected very early after the cessation of H2S exposure, improved cardiac contractility and prevented PEA.

[Study on the standard of health protection zone for petroleum processing industry].

OBJECTIVE: To establish health protection zone standards for petroleum processing industry. METHODS: The intensity of characteristic pollutants from fugitive emission were estimated by the inverse method of ground concentration through field survey and monitoring for representative petroleum processing industry, which was calculated health protection zone by using the model of atmospheric diffusion. RESULTS: Characteristic pollutant of fugitive emission source from petroleum processing industry was confirmed as hydrogen sulfide. When local average wind speed in the past five years was less than 2, 2-4 m/s and more than 4 m/s respectively and meanwhile the scale of petroleum processing industry was less than 8 million tons, the recommended value of health protection zone were 900, 800, 700 m respectively. Besides, when the scale of petroleum processing industry was more than 8 million tons and in the same wind speed level, the recommended value of health protection zone were 1200, 1000, 900 m respectively. CONCLUSIONS: Recommended value of health protection zone for petroleum processing industry was reasonable and feasible through revising and improving of the version of 1987's standard.

[Effect of oxygen therapy on the morphology of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication].

OBJECTIVE: To evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication. METHODS: One hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3), the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope. RESULTS: The results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E. CONCLUSION: Hydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria, alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.

Low-level hydrogen sulfide and central nervous system dysfunction.

Forty-nine adults living in Lovington, Tatum, and Artesia, the sour gas/oil sector of Southeastern New Mexico, were tested for neurobehavioral impairment. Contributing hydrogen sulfide were (1) an anaerobic sewage plant; (2) two oil refineries; (3) natural gas/oil wells and (4) a cheese-manufacturing plant and its waste lagoons. Comparisons were to unexposed Wickenburg, Arizona, adults. Neurobehavioral functions were measured in 26 Lovington adults including 23 people from Tatum and Artesia, New Mexico, and 42 unexposed Arizona people. Participants completed questionnaires including chemical exposures, symptom frequencies and the Profile of Mood States. Measurements included balance, reaction time, color discrimination, blink reflex, visual fields, grip strength, hearing, vibration, problem solving, verbal recall, long-term memory, peg placement, trail making and fingertip number writing errors (FTNWE). Average numbers of abnormalities and test scores were adjusted for age, gender, educational level, height and weight, expressed as percent predicted (% pred) and compared by analysis of variance (ANOVA). Ages and educational attainment of the three groups were not statistically significantly different (ssd). Mean values of Lovington residents were ssd from the unexposed Arizona people for simple and choice reaction times, balance with eyes open and closed, visual field score, hearing and grip strength. Culture Fair, digit symbol substitution, vocabulary, verbal recall, peg placement, trail making A and B, FTNWE, information, picture completion and similarities were also ssd. The Lovington adults who averaged 11.8 abnormalities were ssd from, Tatum-Artesia adults who had 3.6 and from unexposed subjects with 2.0. Multiple source community hydrogen sulfide exposures impaired neurobehavioral functions.

Neurologic sequela of hydrogen sulfide poisoning.

A 25-year-old man, a field operator in a petroleum refinery was found unconscious. He was exposed to hydrogen sulfide and presented with Glasgow Coma Score of 5, severe hypoxemia on arterial blood gas analysis, normal chest radiography, and normal blood pressure. On hospital day 7, his mental state became clear, and neurologic examination showed quadriparesis, profound spasticity, increased tendon reflexes, abnormal Babinski response, and bradykinesia. He was also found to have decreased memory, attention deficits and blunted affect, which suggested general cognitive dysfunction, but which improved soon. MRI scan showed abnormal signals in both basal ganglia and motor cortex, compatible with clinical findings of motor dysfunction.

Hyper rigs.

What's red and white and huge all over? Monster ambulances built by Braun Northwest of Chehalis, Wash., for a Russian mining company.

[Hyperbaric oxygen for hydrogen sulfide poisoning].

Hydrogen sulfide (H2S) is a toxic gas produced in decaying substances containing organic sulfur. Exposure to the gas causes severe disturbances in the central nervous and respiratory systems. The mechanism of toxicity is disruption of the electron transport chain in mitochondria, resulting in intracellular hypoxia. Treatment of H2S poisoning includes mechanical ventilation with 100% oxygen and immediate administration of sodium nitrate. Treatment with hyperbaric oxygen (HBO) has been studied in animal models, and has also been used in a number of patients. However, the clinical effectiveness of this mode of therapy has not been clearly proven. Having recently treated a case of H2S poisoning, we suggest HBO to reduce mortality.

Use of hyperbaric oxygen in toxicology.

HBO has become recognized as a potential treatment for a variety of toxins. HBO is helpful because it provides an excess of dissolved oxygen, which not only can sustain life in the absence of hemoglobin, but in some cases can actually increase the clearance of toxins. In addition, it is now apparent that HBO serves more complex roles in toxicological injuries, such as modifying PMN-endothelial interactions and preventing oxidative tissue injury. The major drawback of HBO therapy is the lack of controlled clinical trials, partly due to the rarity of most of the toxins discussed. In fact, the field of hyperbaric medicine has come under increasing criticism for this failure. There is a physiologic basis for use of HBO in the toxins discussed. Unfortunately, only for CO is patient volume adequate for studies to document efficacy. Regarding the other toxins mentioned, the use of HBO should be reserved for carefully selected cases in which patients have failed routine care or are at risk for delayed effects.

Hydrogen sulfide poisoning treated with hyperbaric oxygen.

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.

Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning.

The optimum therapy for hydrogen sulfide poisoning is unclear. Adjuncts used in the treatment of cyanide poisoning have been advocated because of the shared mechanism of toxicity between hydrogen sulfide and cyanide. Following success in cyanide poisoning, hyperbaric oxygen therapy (HBO) has been suggested for use in treating hydrogen sulfide poisoning. A case of severe hydrogen sulfide poisoning was successfully treated with HBO after standard therapy was apparently ineffective. HBO as a therapeutic adjunct in hydrogen sulfide poisoning and the rationale for its use are discussed.