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},
"code": "T58",
"name": "Токсическое действие окиси углерода",
"icd_name": "Токсическое действие окиси углерода",
"gender": 0,
"age_min": 0,
"age_max": 100,
"cause": [
3,
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],
"periodicity": 1,
"slug": "t58_toksicheskoe_deystvie_okisi_ugleroda",
"lead": "Нарушение здоровья, относящееся к группе токсическое действие веществ, преимущественно немедицинского назначения",
"description": "Отравление в результате токсического действия окиси углерода (СО) является одной из наиболее распространенных и тяжелых форм химической патологии. Отравление СО обуславливает серьезные поражения систем и органов человека. Отравление сопровождается непосредственными и отсроченными осложнениями, значительно утяжеляющими течение заболевания. Последствия перенесенного отравления часто приводят к потере трудоспособности и инвалидизации пострадавших. ",
"etiology": "<p>Опасность отравлений оксидом углерода обусловлена тем, что токсикант не определяется органолептически, в связи с чем контакт с этим веществом остается до определенного времени незаметным для пострадавшего. </p>\r\n<p>Отравления окисью углерода могут быть следствием несчастных случаев в быту, на производстве. Наиболее частым бытовыми ситуациями являются «угорание» в помещениях с неисправными отопительными приборами, при использовании угольных брикетов в примитивных печах для обогрева альпинистских палаток, хижин, жаровен с тлеющими углями, самоваров, при длительном горении керосиновых ламп, мазутных или керосиновых отопительных и нагревательных приборов в невентилируемых помещениях, при утечке бытового газа пропана, в котельных бытовых и производственных зданий и т.д., в банях «по-черному». </p>\r\n<p>Одной из современных причин отравления, как в быту, так и на производстве, служит вдыхание выхлопных газов автомобилей и другого автотранспорта, электрогенераторов в плохо вентилируемых помещениях, в том числе в подвалах гаражей и даже в салонах автомобилей с работающим двигателем, находящихся на открытом воздухе. </p>\r\n<p>Эксплуатация двигателей внутреннего сгорания в условиях высокогорья значительно увеличивает риск отравления. Отравления угарным газом более часто возникают в помещениях с недостаточным движением воздуха (капонирах, тоннелях и др.). Источником оксида углерода могут быть возгорания на энергетических станциях, в том числе работающих с использованием атомной энергии, у космонавтов при авариях на космических станциях (возгорание, разгерметизация). Известны случаи острых отравлений окисью углерода у подводников при попадании выхлопных газов в отсеки подводных лодок. </p>\r\n<p>Отравление окисью углерода возможно у лиц, имеющих профессиональный контакт с продуктами горения (спасатели, пожарные, утилизаторы мусора, повара, строительные рабочие и др.), а также у регулировщиков уличного движения и у сотрудников автостоянок при определенных климатических условиях, способствующих концентрации окиси углерода в нижних слоях атмосферы. </p>\r\n<p>Возможны групповые и массовые отравления окисью углерода. Случаи групповых отравлений нередки в больших закрытых помещениях, ресторанах, ночных клубах, крытых катках, церквях, жертвами отравления становятся многие десятки людей всех возрастов. </p>\r\n<p>Монооксид углерода - один из главных поражающих факторов во время стихийных бедствий, таких как крупные лесные пожары, извержения вулкана и т.п. При горении напалмовых зажигательных смесей образуются высокие концентрации окиси углерода и углекислого газа. </p>",
"pathogenesis": "<p>Окись углерода (СО) обладает большим сродством к гемоглобину, чем кислород, в 250-300 раз. Она вступает с кислородом в конкурентные отношения, вытесняя его из оксигемоглобина, образуя более стойкое соединение - карбоксигемоглобин (СО Нb). </p>\r\n<p>Образующийся карбоксигемоглобин приводит к понижению кислородной емкости крови и развитию гипоксии (снижению содержания кислорода в организме). Развившаяся кровяная гипоксия ведет к одышке. </p>\r\n<p>Повышенная вентиляция в легких приводит к избыточному удалению из организма углекислоты. Это в свою очередь приводит к гипокапнии (снижению СО2 в организме), что еще в большей степени ухудшает распад оксигемоглобина и отдачу кислорода тканями. </p>\r\n<p>Особенно чувствительным к гипоксии является дыхательный центр. Сначала наблюдается его возбуждение, перевозбуждение, затем угнетение и паралич. Поэтому неслучайно при отравлении СО смерть чаще всего наступает при картине остановки дыхания. </p>",
"diagnostics": "<p>Анамнез, в том числе профессиональный, свидетельствующий о пребывании пострадавшего в условиях возможного образования окиси углерода. </p>\r\n<p>Для первоначальной оценки глубины расстройств сознания целесообразно использовать оценочную шкалу ком Глазго. Помимо этого, целесообразно проводить нейропсихологическое тестирование и нейровизуализацию, которым придается важное значение для оценки действия СО на центральную нервную систему. </p>\r\n<p>Химико-токсикологическая диагностика. </p>\r\n<p>Основой диагностики отравлений монооксидом углерода является измерение уровня HbCO крови, обозначаемого в процентах к общему гемоглобину. Этот тест рассматриваются как наиболее точный индикатор повышенной нагрузки на организм окиси углерода. </p>\r\n<p>Диагностическую ценность может составить определение содержания СО в воздухе помещения, однако, в большинстве случаев это бесполезно после прекращения образования газа и проветривания помещения. </p>\r\n<p>Целесообразно проведение тропонинового теста для подтверждения гипоксического повреждения миокарда и оценки риска сердечной смерти вследствие отравления угарным газом. С этой же целью необходимо исследовать кровь и мочу на миоглобин, в особенности, в случае отравления, сопровождавшегося потерей сознания и наличии внешних признаков позиционной травмы. </p>\r\n<p>Методы инструментальной диагностики направлены на оценку тяжести поражения органов и систем и выявления осложнений: </p>\r\n<ul>\r\n<li>ЭКГ - необходимо выполнять всем с целью выявления поражения сердца, обусловленного оксидом углерода; </li>\r\n<li>метод электроэнцефалографии (ЭЭГ) - используется для диагностики нарушений функциональной активности мозга, а также с целью дифференциальной диагностики комы используют; </li>\r\n<li>рентгенография органов грудной клетки позволяет подтвердить наличие острого токсического отека легких; </li>\r\n<li>при наличии позиционной травмы целесообразно УЗИ почек. </li>\r\n<li> </li>\r\n</ul>",
"treatment": "<p>Основное назначение специфической терапии отравления - создание условий для максимально быстрого удаления СО из организма и восстановления нормального функционирования гемоглобина. </p>\r\n<p>Общепринятым антидотным средством является кислород, влияющий на патогенез отравления и способствующий обратному распаду HbCO (карбоксигемоглобина) и образованию HbO2 (оксигемоглобина). Наиболее эффективной является гипербарическая оксигенация (ГБО), которая позволяет значительно ускорить (в 10–15 раз) распад HbCO и увеличить количество кислорода, свободно растворенного в плазме. </p>\r\n<p>В качестве специфического средства, предназначенного для лечения острого отравления CO, в последние годы применяется Ацизол. Этот препарат способствует более эффективной диссоциации оксигемоглобина, повышает сродство гемоглобина к кислороду и одновременно уменьшает относительное сродство гемоглобина к оксиду углерода; повышает устойчивость клеток к гипоксии. Помимо лечебного ацизол может использоваться как профилактическое средство сотрудниками МЧС, пожарными в случае работы в очаге пожара. </p>\r\n<p>В дальнейшем проводят мероприятия по профилактике и лечению отека мозга, коррекции КОС, профилактике пневмоний, возмещению энергетических потребностей организма, профилактике и лечению поражения почек. </p>",
"prevention": "<p>Профилактика сводится главным образом к усовершенствованию вентиляционных установок, герметизации производственных процессов, соблюдению правил личной гигиены, организация газоспасательной службы, систематические анализы воздуха на угарный газ в производственных помещениях. </p>",
"clinical_picture": "<p>Клинические проявления интоксикации зависят от дозы (концентрации газа во вдыхаемом воздухе) и продолжительности воздействия СО. Имеет значение и скорость нарастания концентрации CO во вдыхаемом воздухе (градиент концентрации). </p>\r\n<p>В первые минуты, реже часы отравления кожные покровы и видимые слизистые бывают алыми, позднее становятся бледными и синюшными. </p>\r\n<p>Психосенсорные расстройства: головная боль в височной и лобной областях, часто опоясывающая (симптом «обруча»), головокружение, тошнота, рвота, шум в ушах, мерцание в глазах, может появиться чувство слабости и страха, жажда. </p>\r\n<p>Психические расстройства: состояние, сходное с опьянением, резкое возбуждение или оглушенность, потеря рассудка, оценки ситуации, маниакальное беспокойство, делириозное расстройство сознания, зрительно-слуховые галлюцинации, агрессивные эмоции, неадекватная обнаженность влечений. </p>\r\n<full></full>\r\n<p>Неврологические расстройства: шаткость походки, нарушение координации движений. Снижается ощущение боли. В дальнейшем, при сохранении сознания, оцепенелость, слабость и безучастность (или даже ощущение приятной истомы). Затем нарастают сонливость и оцепенение или же спутанность сознания. В типичных случаях пострадавший теряет сознание. В зависимости от скорости нарастания концентрации окиси углерода во вдыхаемом воздухе возможно быстрое (апоплектическое) или постепенное развитие комы. Коматозное состояние протекает с повышением мышечного тонуса. Возможно появление преходящей очаговой неврологической симптоматики. Зрачки суживаются или расширяются, может быть преходящая анизокория (разный диаметр зрачков). Иногда наблюдаются тонические судороги. Гипергидроз (повышенная потливость). Выявляются отек зрительного нерва и кровоизлияния в сетчатку глаза. </p>\r\n<p>Расстройство функции дыхания выражается обычно в увеличении числа дыханий, одышке, сменяющейся в дальнейшем редким дыханием, что обусловлено развивающейся гипокапнией. </p>\r\n<p>Может повышаться температура тела до 38-40°C; тенденция к тахикардии и артериальной гипертензии, покраснение и жжение кожи лица, дрожь. </p>\r\n<p>Выход из коматозного состояния происходит, как правило, в течение нескольких часов, реже более суток. На выходе возможны проявления острого интоксикационного психоза. Обнаруживаются признаки астеновегетативного синдрома, корсаковского амнестического синдрома (расстройство ориентировки в окружении, во времени, месте). Выявляются стойкие поражения периферических нервов по типу моно-/ полинейропатии и полирадикулоневрита. </p>\r\n<p> </p>",
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