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      S2k guideline diagnosis and treatment of carbon monoxide poisoning Translated title: S2k-Leitlinie Diagnostik und Therapie der Kohlenmonoxidvergiftung

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          Abstract

          Carbon monoxide (CO) can occur in numerous situations and ambient conditions, such as fire smoke, indoor fireplaces, silos containing large quantities of wood pellets, engine exhaust fumes, and when using hookahs.

          Symptoms of CO poisoning are nonspecific and can range from dizziness, headache, and angina pectoris to unconsciousness and death.

          This guideline presents the current state of knowledge and national recommendations on the diagnosis and treatment of patients with CO poisoning.

          The diagnosis of CO poisoning is based on clinical symptoms and proven or probable exposure to CO. Negative carboxyhemoglobin (COHb) levels should not rule out CO poisoning if the history and symptoms are consistent with this phenomenon. Reduced oxygen-carrying capacity, impairment of the cellular respiratory chain, and immunomodulatory processes may result in myocardial and central nervous tissue damage even after a reduction in COHb.

          If CO poisoning is suspected, 100% oxygen breathing should be immediately initiated in the prehospital setting.

          Clinical symptoms do not correlate with COHb elimination from the blood; therefore, COHb monitoring alone is unsuitable for treatment management. Especially in the absence of improvement despite treatment, a reevaluation for other possible differential diagnoses ought to be performed.

          Evidence regarding the benefit of hyperbaric oxygen therapy (HBOT) is scant and the subject of controversy due to the heterogeneity of studies.

          If required, HBOT should be initiated within 6 h.

          All patients with CO poisoning should be informed about the risk of delayed neurological sequelae (DNS).

          Zusammenfassung

          Kohlenmonoxid (CO) kann in zahlreichen Situationen und Umgebungen auftreten, beispielsweise Brandrauch, Feuerstellen in geschlossenen Räumen, Silos mit großen Mengen an Holzpellets; Motoren-Abgase und der Gebrauch von Wasserpfeifen.

          Die Symptome einer Kohlenmonoxidvergiftung sind unspezifisch und können Schwindel, Kopfschmerz, Angina pectoris bis zu Bewusstlosigkeit und Tod umfassen.

          Diese Leitlinie legt den aktuellen Stand der Erkenntnisse und der nationalen Empfehlungen in der Diagnostik und Behandlung von Patienten mit Kohlenmonoxidvergiftungen dar.

          Die Diagnose einer Kohlenmonoxidvergiftung erfordert klinische Symptome und eine nachgewiesene oder wahrscheinliche Exposition mit Kohlenmonoxid. Ein negativer CO-Hämoglobin (Hb)-Nachweis soll nicht zum Ausschluss einer Kohlenmonoxidvergiftung führen, wenn Anamnese und Symptome übereinstimmend sind. Durch eine reduzierte Sauerstofftransportkapazität, die Beeinträchtigung der zellulären Atmungskette und immunmodulatorische Prozesse kann es auch nach Reduktion des CO-Hb zu myokardialen und zentralnervösen Gewebeschäden kommen.

          Bei Verdacht auf eine Kohlenmonoxidvergiftung soll präklinisch sofort mit einer 100% Sauerstoffatmung begonnen werden.

          Die klinische Symptomatik der Patienten korreliert nicht mit der CO-Hb Clearance aus dem Blut. CO-Hb-Kontrollen allein sind für eine Therapiesteuerung ungeeignet. Insbesondere bei fehlender Besserung unter Therapie sollte eine Reevaluation für andere möglicherweise vorliegende Differentialdiagnosen erfolgen.

          Die Evidenz zum Nutzen der hyperbaren Sauerstofftherapie (HBOT) ist aufgrund der heterogenen Studienlage niedrig und wird kontrovers diskutiert.

          Der Beginn einer HBOT soll gegebenenfalls innerhalb von 6 Stunden erfolgen.

          Jeder Patient mit Kohlenmonoxidvergiftung soll über das Risiko eines verzögert einsetzenden neurologischen Defizites (delayed neurological sequelae, DNS), aufgeklärt werden.

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          Most cited references102

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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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            Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy

            Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15–40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.
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              Clinical practice. Carbon monoxide poisoning.

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                Author and article information

                Journal
                Ger Med Sci
                Ger Med Sci
                GMS Ger Med Sci
                GMS German Medical Science
                German Medical Science GMS Publishing House
                1612-3174
                04 November 2021
                2021
                : 19
                : Doc13
                Affiliations
                [1 ]German Interdisciplinary Association of Critical Care and Emergency Medicine (DIVI)
                [2 ]German Society of Medical Intensive Care and Emergency Medicine (DGIIN)
                [3 ]Bundesvereinigung der Arbeitsgemeinschaften der Notärzte Deutschlands (BAND)
                [4 ]German Association for Emergency Medicine (DGINA)
                [5 ]German Society of Anaesthesiology and Intensive Care Medicine (DGAI)
                [6 ]GIZ-Nord Poisons Center, University Medical Center Göttingen (GIZ-Nord)
                [7 ]Bundesverband der Ärztlichen Leiter Rettungsdienst Deutschland (ÄLRD)
                [8 ]The German Society of Anaesthesiology and Intensive Care Medicine (DGAI)
                [9 ]German Respiratory Society (DGP)
                [10 ]German Society for Diving and Hyperbaric Medicine (GTÜM)
                [11 ]AMEOS Klinikum Bernburg, Germany
                [12 ]Society for Neonatology and Pediatric Intensive Care Medicine (GNPI)
                [13 ]German Society of NeuroIntensive Care and Emergency Medicine (DGNI)
                [14 ]Bundeswehrkrankenhaus Ulm, Germany
                [15 ]The Association of the Scientific Medical Societies in Germany (AWMF)
                Author notes
                *To whom correspondence should be addressed: Björn Jüttner, Department of Anaesthesiology and Intensive Care Medicine, Hannover Medical School, Carl-Neuberg-Str. 1, 30625 Hannover, Germany, E-mail: juettner.bjoern@ 123456mh-hannover.de
                Article
                000300 Doc13 urn:nbn:de:0183-0003009
                10.3205/000300
                8607608
                34867135
                c1467856-17e5-4000-96ee-eb69e35aa15f
                Copyright © 2021 Jüttner et al.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

                History
                : 15 July 2021
                Categories
                Article

                Medicine
                carbon monoxide poisoning,etiology,prevention,prehospital management,oxygen breathing,initial in-hospital care,hyperbaric oxygen therapy,hbot,co hemoglobin,delayed neurological sequelae (dns),rehabilitation

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