Basin-scale reconstruction of euxinia and Late Devonian mass extinctions.

The Devonian-Carboniferous transition marks a fundamental shift in the surface environment primarily related to changes in ocean-atmosphere oxidation states1,2, resulting from the continued proliferation of vascular land plants that stimulated the hydrological cycle and continental weathering3,4, glacioeustasy5,6, eutrophication and anoxic expansion in epicontinental seas3,4, and mass extinction events2,7,8. Here we present a comprehensive spatial and temporal compilation of geochemical data from 90 cores across the entire Bakken Shale (Williston Basin, North America). Our dataset allows for the detailed documentation of stepwise transgressions of toxic euxinic waters into the shallow oceans that drove a series of Late Devonian extinction events. Other Phanerozoic extinctions have also been related to the expansion of shallow-water euxinia, indicating that hydrogen sulfide toxicity was a key driver of Phanerozoic biodiversity.

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.

Acute myocardial injury following hydrogen sulfide poisoning.

BACKGROUND: Hydrogen sulfide poisoning can cause severe myocardial injury, but the damage is subtle and can be easily misdiagnosed. This report presents the dynamic observation of myocardial injury associated with hydrogen sulfide poisoning. CASE REPORT: Two young men presented with symptoms of "lightning-like" death immediately after entering a tank. They were found and rescued in 20 min at a time when they were already in a coma. Case 1 had no spontaneous breathing and pulse, while case 2 had spontaneous breathing and a pulse. Upon transfer to a local hospital, case 1 received continuous cardiopulmonary resuscitation which led to the recovery of his heart rate 3 min after arriving at the hospital. However, the patient remained in a Glasgow coma scale of 3. He was transferred to our hospital where he, unfortunately, died on the seventh day due to multiple organ failure. Case 2 was also transferred to the intensive care unit in our hospital and on the fourth day of hospitalization, the patient presented ST-segment elevation and dynamic changes in markers of myocardial injury. Changes in electrocardiogram and markers of myocardial injury were monitored and examination improved through conventional echocardiography, coronary artery CT, radionuclide myocardial perfusion imaging, and two-dimensional speckle tracking imaging strain. The treatment gradually improved the patient's myocardial injury and was discharged from the hospital. CONCLUSION: Hydrogen sulfide poisoning can cause damage to myocardial function and the damage can be more insidious in nature and with a delayed onset. Recovery from myocardial damage can be very slow.

[Characteristics analysis and control countermeasures of acute hydrogen sulfide poisoning in fishing boats in a city from 2009 to 2018].

Objective: To conduct a characteristic analysis of the case of acute hydrogen sulfide poisoning in fishing boats for nearly ten years in a city, and to research on prevention and control measures, so as to provide scientific basis for formulating prevention strategies. Methods: In July 2018, collecting the data of acute hydrogen sulfide poisoning in fishing boats recorded by the Oceanic and Fishery Department & Health Sector from January 1, 2009 to June 30, 2018, the accident characteristics of acute hydrogen sulfide poisoning in fishing boats was analyzed, and compared the differences of hydrogen sulfide poisoning under different classification statistics. Results: In the past ten years, there were 14 acute poisonings in the city, 34 people were poisoned and 12 deaths (the case fatality rate was 35.3%) . According to the types of fishing vessels, the majority number of acute hydrogen sulfide poisoning incidents, poisoned persons and deaths occurred on fishing boats, accounted for 71.4% (10/14) , 76.5% (26/34) and 75.0% (9/12) respectively. From the location of the accident, 85.7% (12/14) of the acute hydrogen sulfide poisoning incidents occurred outside the fishing port. Fisher's exact test showed that the case fatality rate in within the fishing port was higher than that outside the fishing port (P=0.008) . From the cause of direct poisoning, the first three reasons were enter the fish room to rescue, enter the fish room to move fresh catch, to clean the fish room. The poisoning showed seasonal changes, Fisher's exact test showed that the fatality rate in summer was significantly higher than that in spring (P=0.044) , but there was no statistical significance in other seasons (P>0.05) . Conclusion: The acute hydrogen sulfide poisoning of fishing boats in this city has a high case fatality rate, frequent collective poisoning, and showed seasonal changes. Blind rescue, incomplete facilities, and inadequate system are important factors leading to poisoning, so daily measures and rescue measures should be strengthened to reduce the occurrence of poisoning and casualties.

Hydrogen sulfide gas poisoning in fish garbage room: A report of a fisherman.

We report the case of a fisherman who was exposed to high concentrations of hydrogen sulfide (H2S) gas from the fish garbage room. The patient survived and was discharged with full recovery from the hospital. H2S is a colourless, foul smelling and highly toxic gas next to carbon monoxide, which causes inhalation death. It is a by-product of various industrial processes particularly involves exposure from agriculture, petrochemical industry and organic matter decomposition from sewage processing. It is a by-product of H2S has been referred as the "knock down gas" because inhalation of high concentrations can cause immediate loss of consciousness and death. Although early use of amyl nitrate and hyperbaric oxygen shows some benefit in literature, supportive care remains the mainstay of treatment. Emergency physicians and pre-hospital care personnel are not very familiar with such exposure due to its rarity. This becomes more relevant in the developing world settings where there are rising concerns about the unsafe exposure to hazardous chemicals and its impact on human health. Emergency physicians working in Pakistan should be aware of this entity especially in regard to fishermen presenting to the Emergency Department with such a clinical presentation and its toxic manifestations. This incident also illustrates the need of enforcement of health and safety regulations in the fishing industry.

[The correlation between CT score of lung injury and oxygenation index in patients with acute hydrogen sulphide poisoning].

Objective: To explore correlation between chest CT score and oxygenation index in patients with acute hydrogen sulphide poisoning, whether CT score can be applied to assess acute lung injury after acute hydrogen sulfide poisoning and provide basis and reference. Methods: The clinic and a series of CT datas of 32 acute hydrogen sulphide poisoning cases were retrospectively analysed and compared, According to GBZ31-2002 (the diagnostic standard of occupational H(2)S acute poisoning) , these patients were divided into 2 grouds including moderate groud and severe groud; The CT score were improved, referenceing the scoring criteria of the chest X-ray; The difference of the CT score and the oxygenation index were analyzed between moderate and severe group in the acute phase and the disperse phase; The correlation between CT score and oxygenation index were analyzed. Results: The CT score in moderate poisoning group were lower than severe group (2.26±1.37 vs 10.44±2.55, 1.34±0.65 vs 4.55±2.45, all P<0.05) in the acute phase and the dissipation phase.The oxygen index of the 19 cases in the acute phase were 307.55±28.29, and the oxygen index of the 8 cases in the dissipation phase was 435.75±37.00; The oxygen index of the 9 cases in the acute phase and the dissipation phase were respectively 193.17±36.41, 347.67±44.49. The oxygen partial pressure and oxygenation index in severe group were significantly lower than those in moderate group (all P<0.01) in the acute phase and the dissipation phase. Pearman correlation analysis showed that the CT score were negatively correlated to the oxygen index in the acute phase and the dissipation phase, respectively (r=-0.97、-0.75, all P<0.01) . Conclusions: The CT score of lung injury and oxygenation index is negatively correlated. The CT score can be used to evaluate the degree of lung injury, and can be used in the evaluation of acute lung injury after acute hydrogen sulfide poisoning.

[An investigation of an accident of occupational acute hydrogen sulfide poisoning].

Objective: To investigate an accident of occupational acute hydrogen sulfide poisoning, and to analyze related clinical data. Methods: An investigation was performed for an accident of occupational acute hydrogen sulfide poisoning in a place in Shandong, China, in July 2016, and related clinical data were summarized. Results: This was a typical accident of occupational acute hydrogen sulfide poisoning, and a lack of occupational protection and illegal operation were the major causes of this accident. Of all five patients, four experienced coma, toxic encephalopathy, and respiratory failure and were cured at last, and one had cortical syndrome after long-term treatment and died of pulmonary infection seven months later. Conclusions: In case of occupational acute hydrogen sulfide poisoning, rescuers should help the persons who are poisoned reasonably and meanwhile ensure their own safety.

Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity.

We have previously reported that methylene blue (MB) can counteract hydrogen sulfide (H2S) intoxication-induced circulatory failure. Because of the multifarious effects of high concentrations of H2S on cardiac function, as well as the numerous properties of MB, the nature of this interaction, if any, remains uncertain. The aim of this study was to clarify 1) the effects of MB on H2S-induced cardiac toxicity and 2) whether L-type Ca(2+) channels, one of the targets of H2S, could transduce some of the counteracting effects of MB. In sedated rats, H2S infused at a rate that would be lethal within 5 min (24 µM·kg(-1)·min(-1)), produced a rapid fall in left ventricle ejection fraction, determined by echocardiography, leading to a pulseless electrical activity. Blood concentrations of gaseous H2S reached 7.09 ± 3.53 µM when cardiac contractility started to decrease. Two to three injections of MB (4 mg/kg) transiently restored cardiac contractility, blood pressure, and V̇o2, allowing the animals to stay alive until the end of H2S infusion. MB also delayed PEA by several minutes following H2S-induced coma and shock in unsedated rats. Applying a solution containing lethal levels of H2S (100 µM) on isolated mouse cardiomyocytes significantly reduced cell contractility, intracellular calcium concentration ([Ca(2+)]i) transient amplitudes, and L-type Ca(2+) currents (ICa) within 3 min of exposure. MB (20 mg/l) restored the cardiomyocyte function, ([Ca(2+)]i) transient, and ICa The present results offer a new approach for counteracting H2S toxicity and potentially other conditions associated with acute inhibition of L-type Ca(2+) channels.

A Case of Survival: Myocardial Infarction and Ventricular Arrhythmia Induced by Severe Hydrogen Sulfide Poisoning.

Most cases of acute hydrogen sulfide (H2S) poisoning in China are caused by sewage processing. With the rapid development of urbanization in China, H2S poisoning is showing an increasing trend. Here, we report a case of survival from severe H2S poisoning. A 40-year-old worker was found in the underground sewer lines. He was unresponsive with bilaterally dilated pupils and had poor oxygen saturation. After intubation, he was transferred to the intensive care unit. He developed respiratory failure, acute myocardial infarction, ventricular arrhythmia and left ventricular function impairment, requiring artificial ventilation with highly concentrated oxygen, hyperbaric oxygen treatment and drug therapy. Consequently, he completely recovered from the respiratory and cardiac failure. Cases of survival after severe H2S intoxication have been rarely reported. Such exposures may bring about severe myocardial impairment, which is most likely to benefit from angiotensin-converting enzyme inhibition and ß-blocker.

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.

The impact of newspaper reporting of hydrogen sulfide suicide on imitative suicide attempts in Japan.

PURPOSE: An analysis model based on monthly or fortnight data is inadequate to precisely evaluate the impact of media reporting of suicide on suicide rates as well as the time lag from exposure to the report of a suicide. Thus, we used daily time-series data and examined the association between newspaper articles on suicide and suicide attempts in Japan. METHODS: The Box-Jenkins transfer function model was applied to daily time-series data for the period March 27-May 21, 2008. RESULTS: Newspaper articles on suicide using hydrogen sulfide at (t - 1) were related to suicide attempts at (t) (ps < 0.001 and 0.05). Newspaper articles on suicides using hydrogen sulfide on the front page at (t - 1) were related to suicide attempts at (t) (p < 0.00). The magnitude of the impact of newspaper articles about suicide at (t - 1) or (t - 3) on "copy-cat" suicide attempts became greater as the number of news articles violating the media suicide recommendations increased. CONCLUSIONS: The time lag between exposure to newspaper reports of suicide and attempts was 1 or 3 days, and the magnitude of the impact of front page articles was about four times as great as that of suicide articles in general.

[Sewer gas induced myocardial toxicity].

We report the case of a 19 year-old worker who collapsed after acute exposure to sewer gas. He rapidly developed cardiorespiratory failure with electrocardiographic, echocardiographic and laboratory findings of myocardial involvement. The mainstay of the therapy was mainly supportive treatment with a successful outcome.

[Sargassum seaweed assaults the French West Indies]. / Algues sargasses à l'assaut des Antilles.

SARGASSUM SEAWEED AS SAULTS THE FRENCH WEST INDIES. Since 2011, Martinique and the islands of Guadeloupe have been affected by repeated groundings, culminating in an exceptional wave in 2018. While the sargassum ( Sargassum natans and S. fluitans ) involved in these phenomena are neither toxic nor urticating, indirect toxicity linked to the presence of microorganisms and heavy metals (arsenic, mercury, etc.) in sargassum clusters has been described. Similarly, after a 24 to 48 hours stay on the shore, sargassum algae enter a putrefaction cycle responsible to produce hydrogen sulfide (H2S) and ammonia (NH3). The acute toxicity of these gases is well known. However, very few data are available on the clinical effects of prolonged exposure to low doses of H2S and NH3. Our team has recently described the syndromic features of chronic exposure, supposing for deleterious effects on the cardiovascular, respiratory and neurological systems.

ALGUES SARGASSES À L'ASSAUT DES ANTILLES. Depuis 2011, la Martinique et les îles de la Guadeloupe sont touchées par des échouements à répétition d'algues sargasses qui ont culminé avec une vague exceptionnelle en 2018. Si les sargasses (Sargassum natans et S. fluitans) impliquées dans ces phénomènes ne sont ni toxiques ni urticantes, une toxicité indirecte liée à la présence de micro-organismes et de métaux lourds (arsenic, mercure…) dans les amas de sargasses est décrite. De même, après un séjour de vingt-quatre à quarante-huit heures sur le littoral, les algues sargasses entrent dans un cycle de putréfaction responsable de la production d'hydrogène sulfuré (H2S) et d'ammoniac (NH3). La toxicité aiguë de ces gaz est bien connue. Il existe en revanche très peu de données disponibles sur les effets cliniques d'une exposition prolongée à de faibles doses d'H2S ou NH3. Notre équipe a récemment décrit le tableau syndromique de l'exposition chronique et suppose des effets délétères sur le système cardiovasculaire, respiratoire et neurologique.

Suicide with hydrogen sulfide.

This presentation will address the recent rise of suicide deaths resulting from the asphyxiation by hydrogen sulfide (H2S) gas.Hydrogen sulfide poisoning has been an infrequently encountered cause of death in medical examiner practice. Most H2S deaths that have been reported occurred in association with industrial exposure.More recently, H2S has been seen in the commission of suicide, particularly in Japan. Scattered reports of this phenomenon have also appeared in the United States.We have recently observed 2 intentional asphyxial deaths in association with H2S. In both cases, the decedents committed suicide in their automobiles. They generated H2S by combining a sulfide-containing tree spray with toilet bowl cleaner (with an active ingredient of hydrogen chloride acid). Both death scenes prompted hazardous materials team responses because of notes attached to the victims' car windows indicating the presence of toxic gas. Autopsy findings included discoloration of lividity and an accentuation of the gray matter of the brain. Toxicology testing confirmed H2S exposure with the demonstration of high levels of thiosulfate in blood.In summary, suicide with H2S appears to be increasing in the United States.

Suicide by hydrogen sulfide inhalation.

The authors report a case of suicide by hydrogen sulfide in Australia. A young woman was located in a car wearing protective eyewear. A tub of foamy yellow substance and a quantity of hydrochloric acid and lime sulfur were also located in the rear of the vehicle. Morphological findings at autopsy were nonspecific. Toxicologic analysis of a specimen of leg blood detected elevated levels of methemoglobin. If Australia follows a similar trend to Japan and the United States, it is possible that incidences of such cases will rise, probably because of Internet dissemination. From a public health perspective, emergency service providers and forensic case workers should be aware of the potential hazards to themselves and others when dealing with such cases.

A fatal work-related poisoning by hydrogen sulfide: report on a case.

Hydrogen sulfide (H2S) is a colorless and potentially deadly gas that may cause rapid loss of consciousness and respiratory depression without warning. Although occupational exposure to H2S and the medical management of H2S-associated toxicity are widely established, it remains a problem in the sour gas industry and in other industrial settings, predominantly in new workers. In this article, the authors report a fatal case of a factory worker who died after breathing in H2S while undertaking a task that he was not trained to perform. Toxicological assessment supported by autopsy findings and circumstantial data was essential to clarify the cause of death, determined as H2S poisoning. This case emphasizes the need to develop work safety initiatives, improve on-the-job training, and introduce more consciousness to put on protective equipment for workers; indeed, correct training and education for workers regarding safety in the workplace may help to reduce worker fatalities.

Delayed myocardial injury following acute hydrogen sulfide intoxication.

INTRODUCTION: Hydrogen sulfide is a toxic, colorless gas produced by decaying organic matter. Its toxic effects are due to blocking of cellular respiratory enzymes, leading to anoxia. CASE PRESENTATION: We report a 28-year-old man who attempted suicide using hydrogen sulfide gas. When the emergency service arrived, his friend was dead and the patient was unconscious. He received supportive treatment and survived. In this patient both skeletal muscle and myocardial injury was observed after hydrogen sulfide intoxication. Skeletal muscle damage occurred first, because enzymes peak consisted of creatine phosphokinase, aspartate aminotransferase, and myoglobin was observed on hospital day 4. Myocardial injury was apparent on hospital day 15, because the subsequent enzymes peak was comprised of cardiac enzymes and associated electrocardiographic abnormalities. On hospital day 3, myocardial injury was detected and it evolved over the next 3 weeks to recover completely. CONCLUSION: The mechanisms of rhabdomyolysis and myocardial injury resulting from hydrogen sulfide poisoning are not known, but may be related to cellular anoxia or a direct toxic effect. This case highlights not only the risk of delayed cardiac damage, but also rhabdomyolysis, and emphasizes that careful monitoring of cardiac function and of the levels of skeletal muscle-related enzymes is essential for victims of hydrogen sulfide poisoning.