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      Pharmacological treatment of inhalation injury after nuclear or radiological incidents: The Chinese and German approach

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          Abstract

          Inhalation injury is often associated with burns and significantly increases morbidity and mortality. The main toxic components of fire smoke are carbon monoxide, hydrogen cyanide, and irritants. In the case of an incident at a nuclear power plant or recycling facility associated with fire, smoke may also contain radioactive material. Medical treatments may vary in different countries, and in this paper, we discuss the similarities and differences in the treatments between China and Germany. Carbon monoxide poisoning is treated by 100% oxygen administration and, if available, hyperbaric oxygenation in China as well as in Germany. In addition, antidotes binding the cyanide ions and relieving the respiratory chain are important. Methemoglobin-forming agents (e.g., nitrites, dimethylaminophenol) or hydroxocobalamin (Vitamin B12) are options. The metabolic elimination of cyanide may be enhanced by sodium thiosulfate. In China, sodium nitrite with sodium thiosulfate is the most common combination. The use of dimethylaminophenol instead of sodium nitrite is typical for Germany, and hydroxocobalamin is considered the antidote of choice if available in cases of cyanide intoxications by fire smoke inhalation as it does not further reduce oxygen transport capacity. Systematic prophylactic use of corticosteroids to prevent toxic pulmonary edema is not recommended in China or Germany. Stable iodine is indicated in the case of radioiodine exposure and must be administered within several hours to be effective. The decorporation of metal radionuclides is possible with Ca (DTPA) or Prussian blue that should be given as soon as possible. These medications are used in both countries, but it seems that Ca (DTPA) is administered at lower dosages in China. Although the details of the treatment of inhalation injury and radionuclide(s) decorporation may vary, the general therapeutic strategy is very similar in China and Germany.

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          Hyperbaric oxygen for acute carbon monoxide poisoning.

          Patients with acute carbon monoxide poisoning commonly have cognitive sequelae. We conducted a double-blind, randomized trial to evaluate the effect of hyperbaric-oxygen treatment on such cognitive sequelae. We randomly assigned patients with symptomatic acute carbon monoxide poisoning in equal proportions to three chamber sessions within a 24-hour period, consisting of either three hyperbaric-oxygen treatments or one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air. Oxygen treatments were administered from a high-flow reservoir through a face mask that prevented rebreathing or by endotracheal tube. Neuropsychological tests were administered immediately after chamber sessions 1 and 3, and 2 weeks, 6 weeks, 6 months, and 12 months after enrollment. The primary outcome was cognitive sequelae six weeks after carbon monoxide poisoning. The trial was stopped after the third of four scheduled interim analyses, at which point there were 76 patients in each group. Cognitive sequelae at six weeks were less frequent in the hyperbaric-oxygen group (19 of 76 [25.0 percent]) than in the normobaric-oxygen group (35 of 76 [46.1 percent], P=0.007), even after adjustment for cerebellar dysfunction and for stratification variables (adjusted odds ratio, 0.45 [95 percent confidence interval, 0.22 to 0.92]; P=0.03). The presence of cerebellar dysfunction before treatment was associated with the occurrence of cognitive sequelae (odds ratio, 5.71 [95 percent confidence interval, 1.69 to 19.31]; P=0.005) and was more frequent in the normobaric-oxygen group (15 percent vs. 4 percent, P=0.03). Cognitive sequelae were less frequent in the hyperbaric-oxygen group at 12 months, according to the intention-to-treat analysis (P=0.04). Three hyperbaric-oxygen treatments within a 24-hour period appeared to reduce the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning. Copyright 2002 Massachusetts Medical Society
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            Cardiovascular manifestations of moderate to severe carbon monoxide poisoning.

            We describe the cardiovascular manifestations of carbon monoxide (CO) poisoning. Carbon monoxide poisoning is a common cause of toxicologic morbidity and mortality. Although the neurologic sequelae of CO poisoning have been well described, the cardiovascular consequences are limited to isolated case reports. We reviewed the cardiovascular manifestations of 230 consecutive patients treated for moderate to severe CO poisoning in the hyperbaric oxygen chamber at Hennepin County Medical Center (HCMC), a regional center for treatment of CO poisoning. The mean age was 47.2 years with 72% men. Ischemic electrocardiogram (ECG) changes were present in 30% of patients, whereas only 16% had a normal ECG. Cardiac biomarkers (creatine kinase-MB fraction or troponin I) were elevated in 35% of patients. In-hospital mortality was 5%. Cardiovascular sequelae of CO poisoning are frequent, with myocardial injury assessed by biomarkers or ECG in 37% of patients. Patients admitted to the hospital with CO poisoning should have a baseline ECG and serial cardiac biomarkers.
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              Elevated blood cyanide concentrations in victims of smoke inhalation.

              The nature of the toxic gases that cause death from smoke inhalation is not known. In addition to carbon monoxide, hydrogen cyanide may be responsible, but its role is uncertain, because blood cyanide concentrations are often measured only long after exposure. We measured cyanide concentrations in blood samples obtained at the scene of residential fires from 109 fire victims before they received any treatment. We compared the results with those in 114 persons with drug intoxication (40 subjects), carbon monoxide intoxication (29 subjects), or trauma (45 subjects). The metabolic effect of smoke inhalation was assessed by measuring plasma lactate at the time of admission to the hospital in 39 patients who did not have severe burns. The mean (+/-SD) blood cyanide concentrations in the 66 surviving fire victims (21.6 +/- 36.4 mumol per liter, P less than 0.001) and the 43 victims who died (116.4 +/- 89.6 mumol per liter, P less than 0.001) were significantly higher than those in the 114 control subjects (5.0 +/- 5.5 mumol per liter). Among the 43 victims who died, the blood cyanide concentrations were above 40 mumol per liter in 32 (74 percent), and above 100 mumol per liter in 20 of these (46 percent). There was a significant correlation between blood cyanide and carbon monoxide concentrations in the fire victims (P less than 0.001). Plasma lactate concentrations at the time of hospital admission correlated more closely with blood cyanide concentrations than with blood carbon monoxide concentrations. Plasma lactate concentrations above 10 mmol per liter were a sensitive indicator of cyanide intoxication, as defined by the presence of a blood cyanide concentration above 40 mumol per liter. Residential fires may cause cyanide poisoning. At the time of a patient's hospital admission, an elevated plasma lactate concentration is a useful indicator of cyanide toxicity in fire victims who do not have severe burns.
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                Author and article information

                Contributors
                tiantianyan27031@163.com
                guoanlin169@163.com
                1597163656@qq.com
                andreas.Lamkowski@med.uni-muenchen.de
                MatthiasPort@bundeswehr.org
                AlexisRump@bundeswehr.org
                Journal
                Mil Med Res
                Mil Med Res
                Military Medical Research
                BioMed Central (London )
                2095-7467
                2054-9369
                31 March 2019
                31 March 2019
                2019
                : 6
                : 10
                Affiliations
                [1 ]Military Burn Center, the 990th Hospital of the Joint Logistics Support Forces of Chinese PLA (the 159th Hospital of Chinese PLA), Zhumadian, 463000 Henan China
                [2 ]ISNI 0000 0004 1936 9748, GRID grid.6582.9, Bundeswehr Institute of Radiobiology, ; Munich, Germany
                Article
                200
                10.1186/s40779-019-0200-2
                6454727
                30961671
                3d8962ae-1c32-4420-bf80-5aebd81f7bfa
                © The Author(s). 2019

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 11 November 2018
                : 25 March 2019
                Categories
                Review
                Custom metadata
                © The Author(s) 2019

                fire smoke,inhalation injury,carbon monoxide,cyanide,radionuclide incorporation,decorporation

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