Disease List

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                            "name": "отравление"
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                            "name": "Отказ от пищи"
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            "etiology": "<p>У новорождённого развитие омфалита чаще всего происходит из-за попадания инфекции в незажившую пупочную рану. Это может произойти при перевязке пуповины или несоблюдении правил при обработке пупка мамой в период новорождённости. Также некоторые внешние факторы могут провоцировать возникновение омфалита у новорождённого:  </p>\r\n<ul>\r\n<li>Наличие внутриутробной инфекции в детском организме; </li>\r\n<li>Нарушение правил гигиены при уходе за заживающей пупочной раной; </li>\r\n<li>Неправильная обработка, использование запрещённых средств, купание в загрязнённой воде;  </li>\r\n<li>Применение необработанных и непродезинфицированных предметов ухода; </li>\r\n<li>Новорожденные с гипоксией и аномалиями развития, в первую очередь это аномалии самого пупка; </li>\r\n<li>Наличии пеленочного дерматита или других инфекционных заболеваний кожи у новорожденного (пиодермии, фолликулита). </li>\r\n</ul>\r\n<p>Возбудителями омфалита чаще всего оказываются стафилококки, стрептококки, примерно в 30% случаев - грамотрицательные микроорганизмы (кишечная палочка, клебсиелла и др.). </p>",
            "pathogenesis": "<p>По причинам возникновения омфалит может быть первичным (при инфицировании пупочной ранки) или вторичным (в случае присоединения инфекции на фоне имеющихся врожденных аномалий - свищей). Вторичный омфалит у ребенка развивается в более поздние сроки и протекает более длительно. </p>\r\n<p>По характеру и степени воспалительных изменений в области пупка различают катаральный или простой омфалит («мокнущий пупок»), флегмонозный и гангренозный (некротический) омфалит  </p>\r\n<p>Возбудитель (преимущественно стафилококк) проникает в ткани, прилежащие к пупку, через культю пуповины или через ранку после её отпадения. Инфекция может распространяться и фиксироваться в пупочных сосудах (чаще в артериях, реже в венах), вызывая продуктивное, гнойное или некротическое воспаление. Распространение воспаления приводит к развитию флегмоны в области пупка. При вовлечении в процесс пупочной вены возникает флебит (воспаление стенки сосуда), который может распространиться по воротной вене во внутрипечёночные её разветвления. Нередко при этом по ходу вен образуются гнойные очаги, иногда уже после заживления пупочной раны </p>",
            "diagnostics": "<p>Диагностика заболевания не представляет трудностей и основывается на характерных местных признаках заболевания (наличие отделяемого из пупочной ранки, покраснение кожи вокруг нее). </p>\r\n<p>При развитии гнойной, флегмонозной или некротической форм возможны воспалительные изменения в общем анализе крови (повышение уровня лейкоцитов и СОЭ). </p>\r\n<p>При неэффективности назначенного лечения проводится исследование – посев отделяемого из пупка с определением чувствительности микроорганизмов к антибиотикам (в зависимости от его результатов подбирается другой антибиотик). </p>\r\n<p>Дополнительные исследования проводятся при возникновении осложнений: </p>\r\n<ul>\r\n<li>УЗИ брюшной полости (при подозрении на перитонит (воспаление брюшной полости)); </li>\r\n<li>УЗИ мягких тканей (при подозрении на флегмону брюшной стенки – гнойное воспаление подкожной клетчатки). </li>\r\n</ul>",
            "treatment": "<p> Местное лечение:  </p>\r\n<ul>\r\n<li>Удаление пупочного отделяемого и обработки пупочной ранки антисептическими растворами (перекисью водорода, бриллиантовым зеленым); </li>\r\n<li>в случае гнойной формы местно назначаются антибактериальные мази, а также применяется дренирование раны (установка в рану специальной трубки для оттока гноя наружу с ее помощью); </li>\r\n<li>иссечение некротизированных тканей; </li>\r\n<li>применяется также физиолечение (УФО – ультрафиолетовое облучение, УВЧ – ультравысокочастоная терапия). </li>\r\n</ul>\r\n<p>Системное лечение: </p>\r\n<ul>\r\n<li>антибиотики широкого спектра действия с учетом чувствительности флоры; </li>\r\n<li>витаминотерапия; </li>\r\n<li>дезинтоксикационная терапия; </li>\r\n<li>средства, повышающие иммунитет. </li>\r\n</ul>",
            "prevention": "<p>Профилактика омфалита предполагает соблюдение асептики при обработке пуповины, ежедневном уходе за пупочной ранкой, соблюдение гигиены ухаживающим персоналом. Категорически недопустимо насильственно срывать корочки с пупочной ранки, закрывать ее повязкой или подгузником, заклеивать лейкопластырем, поскольку это провоцирует мокнутие и инфицирование. В случае покраснения пупочной ранки, появления отечности и отделяемого следует незамедлительно проконсультироваться у педиатра. <br class=\"SCXW172751371\" /> </p>",
            "clinical_picture": "<p>При катаральном омфалите пупочная ранка не затягивается, из нее начинает выделяться скудный секрет серозного (прозрачного), кровянистого или серозно-гнойного характера. Ранка периодически затягивается корочками, однако после их отторжения дефект не эпителизируется. Пупочное кольцо гиперемировано (красное) и отечно. При длительном мокнутии (в течение 2-х и более недель) может происходить избыточное разрастание молодой соединительной ткани (грануляций) с формированием на дне пупочной ранки грибовидного выпячивания – фунгуса пупка, который еще более затрудняет заживление. Общее состояние новорожденного (аппетит, физиологические отправления, сон, прибавка в массе) при простой форме омфалита обычно не нарушено; иногда отмечается небольшое повышение температуры. </p>\r\n<p>Флегмонозный омфалит характеризуется распространением воспаления на окружающие ткани и обычно является продолжением «мокнущего пупка». Кожа вокруг пупка гиперемирована, подкожная клетчатка отечна и возвышается над поверхностью живота. Рисунок венозной сети на передней брюшной стенке усилен, наличие красных полос свидетельствует о присоединении воспаления лимфатических сосудов. </p>\r\n<p>Кроме мокнутия пупочной ранки, отмечается пиорея – истечение гнойного отделяемого и выделение гноя при надавливании на околопу­почную область. Возможно образование на дне пупочной ямки язвочки, покрытой гнойным налетом. При флегмонозном омфалите состояние младенца ухудшается: температура тела повышается до 38°С, выражены признаки интоксикации (вялость, плохой аппетит, срыгивания, диспепсия), замедляется нарастание массы тела. У недоношенных детей локальные изменения при омфалите могут быть выражены минимально, зато на первый план обычно выходят общие проявления, молниеносно развиваются осложнения. </p>\r\n<p>Некротический омфалит встречается редко, обычно у ослабленных детей (с иммунодефицитом, гипотрофией и т.д.). При этом расплавление клетчатки распространяется в глубину. В области пупка кожа приобретает темно-багровый, синюшный оттенок. При некротическом омфалите воспаление практически всегда переходит на пупочные сосуды. В некоторых случаях могут некротизироваться все слои передней брюшной стенки с развитием контактного перитонита. Гангренозный омфалит имеет наиболее тяжелое течение: температура тела может снижаться до 36°С, ребенок истощен, заторможен, не реагирует на окружающие раздражители. </p>\r\n<p> </p>",
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            "code": "P57",
            "name": "Ядерная желтуха",
            "icd_name": "Ядерная желтуха",
            "gender": 1,
            "age_min": 0,
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            "slug": "p57_yadernaya_zheltuha",
            "lead": "Нарушение здоровья, относящееся к группе геморрагические и гематологические нарушения у плода и новорожденного",
            "description": "Ядерная желтуха – патологическое состояние, которое может возникнуть у новорожденных в результате билирубиновой интоксикации. Билирубин появляется в базальных ганглиях и ядрах ствола мозга, что приводит к нарушениям мозговых функций. ",
            "etiology": "<p>Причинами ядерной желтухи могут стать следующие факторы: </p>\r\n<ul>\r\n<li>травмы головного мозга новорожденного; </li>\r\n<li>рождение раньше срока; </li>\r\n<li>недостаток ферментов, связывающих и выводящих билирубин; </li>\r\n<li>критическое нарушение обменных процессов у новорожденного; </li>\r\n<li>подкожные кровоизлияния у младенца; </li>\r\n<li>несовместимость резус-факторов матери и ребенка; </li>\r\n<li>серьезные патологии эндокринной системы матери; </li>\r\n<li>последствия приема сильнодействующих препаратов в период беременности; </li>\r\n<li>внутриутробные заболевания инфекционного характера; </li>\r\n<li>заболевания крови (матери и ребенка). </li>\r\n</ul>",
            "pathogenesis": "<p>Заболевание развивается в связи с неспособностью организма новорожденного справиться с высокой концентрацией билирубина в крови. В норме реакции распада преобладают в первые дни жизни ребенка. Именно с этим связана физиологическая желтуха новорожденных, но в норме новорожденный справляется, и симптомы исчезают в течение нескольких дней или недель. Ядерная желтуха новорожденных характеризуется чрезмерной гипербилирубинемией, вследствие чего желчный пигмент начинает проходить через гематоэнцефалический барьер, окрашивая базальные ядра, ядра мозжечка и черепно-мозговых нервов в желтушный цвет. </p>\r\n<p>Для развития ядерной желтухи новорожденных необходимо множество условий. В частности, гематоэнцефалический барьер пропускает только свободный билирубин, то есть тот, который не связан с альбуминами и не подвергнутый конъюгации в печени. Значит, одним из факторов, способствующих развитию данного состояния, является гипопротеинемия (снижение белков-переносчиков). По этой причине симптомы чаще наблюдаются у детей с отеками, обширной кефалогематомой и т. д. Гипоксическое, инфекционное или травматическое повреждение мозга, имевшее место внутриутробно или в родах, значительно повышает проницаемость гематоэнцефалического барьера. То же касается недоношенности, когда мозговые структуры к моменту рождения остаются незрелыми. </p>\r\n<p>Гемолитическая болезнь новорожденных всегда является фактором повышенного риска ядерной желтухи новорожденных, поскольку в этом случае концентрация несвязанного билирубина быстрее всего достигает предельно допустимых значений и начинает превышать их, способствуя проникновению билирубина в вещество мозга. В таких случаях состояние развивается стремительно, часто с летальным исходом или глубокой инвалидизацией.  </p>",
            "diagnostics": "<p>Подозрение на ядерную желтуху возникает у врача еще на этапе визуального обследования новорожденного. Для подтверждения диагноза малышу назначаются лабораторные исследования и комплексное обследование внутренних систем организма. </p>\r\n<p>В некоторых случаях возникает необходимость в дополнительной консультации с профильными специалистами. </p>\r\n<p>Диагностика ядерной желтухи включает в себя следующие процедуры: </p>\r\n<ul>\r\n<li>определение уровня билирубина - при ядерной желтухе более 256 мкмоль/л у доношенных и более 171 мкмоль/л у недоношенных детей. </li>\r\n<li>пробы Кумбса - определение наличия антител к эритроцитам; </li>\r\n<li>биохимический анализ крови и мочи; </li>\r\n<li>общий анализ крови и мочи; </li>\r\n<li>УЗИ печени и селезенки; </li>\r\n<li>УЗИ головного мозга. </li>\r\n</ul>",
            "treatment": "<p>Одним из этапов лечения ядерной желтухи новорожденных является фототерапия. Доказано, что излучение видимого спектра, особенно голубого цвета, способствует переходу токсичного непрямого билирубина в его изомер, который может выводиться печенью и почками без связывания с альбуминами крови.  </p>\r\n<p>Если на фоне фототерапии уровень билирубина не снижается, показано переливание плазмы  крови. Перелитые вместе с плазмой белки способствуют связыванию избыточного билирубина с последующим выведением его из организма. </p>\r\n<p>При неэффективности перечисленных методов лечения или стремительном прогрессировании симптоматики проводится обменно-заменное переливание крови.  </p>\r\n<p>Применяются медикаменты, которые способствуют более быстрому выведению билирубина из тела младенца (препараты с желчегонным действием), энтеросорбенты. </p>\r\n<p>По показаниям проводится противосудорожная терапия.</p>",
            "prevention": "<p>Профилактика состояния возможна в первые дни жизни. Профилактическая фототерапия проводится всем новорожденным с уровнем билирубина в крови выше 200 мкмоль/л, а также всем недоношенным новорожденным, детям, перенесшим внутриутробные инфекции, гипоксию плода, родовые травмы и др.</p>",
            "clinical_picture": "<p>Гипербилирубинемия в первые дни и недели жизни заметна по желтой окраске кожных покровов и склер. В данном случае этот признак выражен в значительной степени. Кожа малыша имеет ярко-желтый оттенок уже в первый день жизни, в отличие от физиологической желтухи, которая развивается спустя 5-7 дней после рождения. Состояние чаще возникает остро в течение первой недели жизни. Выделяют две стадии: асфиксическую и спастическую. Первая стадия ядерной желтухи новорожденных характеризуется появлением приступов апноэ (ребенок не дышит) разной продолжительности. Мышечный тонус снижен, отмечаются отдельные подергивания. Ребенок вялый, плохо сосет. </p>\r\n<p>Спастическая стадия ядерной желтухи новорожденных представлена выраженным гипертонусом мышц разгибателей вплоть до опистотонуса. Голова ребенка непроизвольно резко запрокидывается назад, глаза закатываются вверх (симптом «заходящего солнца»). Дыхание нарушено, отмечаются частые приступы апноэ. Могут наблюдаться тонические судороги и пронзительный крик, связанный с напряжением мышц и отчасти с болевым синдромом, сопровождающим гипертонус. В тяжелых случаях ядерной желтухи новорожденных мышечное напряжение распространяется на конечности с их резким выпрямлением и пронацией сжатых кулачков. </p>\r\n<p>В течение нескольких недель состояние ребенка улучшается. Симптомы ослабевают, судороги и гипертонус отмечаются реже. Однако к концу первого года жизни в 80% случаев развивается мышечная ригидность, судороги вновь учащаются. Прогрессируют симптомы поражения черепно-мозговых нервов, что клинически проявляется снижением зрения и слуха. Часто развивается косоглазие и тугоухость. Массивное поражение нейронов неизбежно отражается на умственном развитии. У детей, перенесших ядерную желтуху новорожденных, впоследствии нередко диагностируется синдром дефицита внимания с гиперактивностью (СДВГ), а также умственная отсталость. </p>",
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            },
            "code": "P75*",
            "name": "Мекониевый илеус (E84.1+)",
            "icd_name": "Мекониевый илеус (E84.1+)",
            "gender": 0,
            "age_min": 0,
            "age_max": 1,
            "cause": [
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            "periodicity": 1,
            "slug": "p75*_mekonievyy_ileus_e84_1",
            "lead": "одна из клинических форм муковисцидоза, характеризующаяся непроходимостью подвздошной кишки на фоне ее обтурации уплотненными мекониальными массами",
            "description": "",
            "etiology": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Задержка отхождения мекония свыше 24 часов после рождения указывает на патологию пищеварительного тракта и представляет опасность для жизни ребёнка. Основные причины:&nbsp;</span></p>\r\n<ul>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Врождённые дефекты кишечника с нарушением проходимости &ndash; атрезия участка тонкой или толстой кишки, ануса, кольцевидная поджелудочная железа, мембрана в двенадцатиперстной кишке. Дефекты пищеварительного тракта часто возникает на фоне хромосомных аномалий и сочетается с пороками развития других органов.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Муковисцидоз &ndash; тяжёлое полиорганное заболевание с аутосомно-рецессивным типом наследования. Секрет поджелудочной железы становится вязким, уменьшается продукция ферментов, усиливается всасывание жидкости из просвета кишечника. Изменяется консистенция мекония, нарушается его отхождение.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Функциональная незрелость органов пищеварения &ndash; снижение секреции и перистальтики у недоношенных младенцев приводит к застою кала.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Синдром мекониевой пробки &ndash; скопление мекония в толстой кишке из-за нарушения моторики. Патология встречается у детей, рождённых от женщин с сахарным диабетом и гипермагниемией.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Болезнь Гиршпрунга &ndash; врождённое недоразвитие или отсутствие нервных сплетений кишечника, регулирующих моторику. В результате возникает обструкция поражённого участка. Отделы кишечника, расположенные выше, переполняются каловыми массами и расширяются.</span></li>\r\n</ul>\r\n<p>&nbsp;</p>",
            "pathogenesis": "",
            "diagnostics": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Для подтверждения диагноза и выявления причины патологии назначают следующие исследования:&nbsp;</span></p>\r\n<ul>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Обзорная рентгенограмма живота &ndash; на снимке видны раздутые кишечные петли. Наличие газа и плотного мекония даёт характерную рентгенологическую картину: симптом матового стекла и мыльного пузыря.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Ирригография &ndash; в прямую кишку с помощью клизмы вводят гастрографин (контрастное вещество) и выполняют рентгенограмму. При мекониевом илеусе толстая кишка пустая, узкая (микроколон), в дистальном отделе подвздошной кишки видны дефекты наполнения &ndash; плотные комочки мекония. С помощью исследования определяют место закупорки кишечника.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Компьютерная томография &ndash; метод диагностики причины кишечной непроходимости, проводят рентгеновское исследование с разных ракурсов, затем получают трёхмерное изображение на компьютере.&nbsp;</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">УЗИ &ndash; показывает структурные изменения органов брюшной полости, псевдокисты, кальцинаты в брюшной полости. Потовая проба &ndash; определение содержания хлоридов в секрете потовых желёз. Это основной лабораторный метод диагностики муковисцидоза. Тест проводят всем детям с мекониевой непроходимостью.</span></li>\r\n</ul>\r\n<p>&nbsp;</p>",
            "treatment": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Тактика лечения мекониального илеуса зависит от тяжести состояния ребенка, наличия или отсутствия осложнений. При неосложненном варианте заболевания проводится промывание кишечника гиперосмолярным раствором (цистографином). Высокое осмотическое давление раствора позволяет &laquo;стягивать&raquo; в просвет кишечника жидкость из окружающих тканей, тем самым разжижая густые мекониальные массы и способствуя их отхождению. Промывание осуществляется не более 2-3 раз.</span></p>\r\n<p>&nbsp;</p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">При тяжелом общем состоянии ребенка, развитии осложнений или отсутствии эффекта от промывания кишечника гипертоническим раствором выполняют хирургическое вмешательство путем срединной лапаротомии. После вскрытия брюшной полости для упрощения манипуляций уплотненным меконием в просвет подвздошной кишки шприцем вводят цистографин. Далее при помощи эластического катетера, введенного в аппендикс, осуществляют эвакуацию размягченного секрета через анальное отверстие. При неэффективности данной манипуляции показано раскрытие просвета кишки и механическое удаление мекониальных масс с последующим восстановлением целостности пищеварительного тракта. В некоторых случаях формируют проксимальную стому, выводя кишку на переднюю брюшную стенку. При необходимости проводят симптоматическое лечение.</span></p>",
            "prevention": "<p>&nbsp;</p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Специфической профилактики мекониального илеуса и муковисцидоза не разработано. Неспецифические превентивные меры включают в себя медико-генетическое консультирование семейных пар, планирование беременности, регулярное посещение женской консультации, прохождение всех необходимых исследований в период гестации, обследование больных с подозрением на муковисцидоз.</span></p>",
            "clinical_picture": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Клиническая картина мекониального илеуса развивается в первые 24-48 часов после родов. В норме у новорожденного первородные каловые массы отходят на первые, редко &ndash; на вторые сутки. При данной форме муковисцидоза отхождения кала не происходит. Примерно через 1-2 дня ухудшается общее состояние ребенка &ndash; он становится беспокойным, нарушаются сон и аппетит, возникает необоснованный плач. На 2 день (иногда &ndash; с момента рождения) появляется срыгивание, частая рвота желудочным содержимым, нередко &ndash; с примесью желчи или фекальных масс. Спустя некоторое время возникают бледность и снижение тургора кожных покровов, расширение вен передней брюшной стенки и вздутие живота. Ребенок постепенно становится апатичным и малоподвижным. Присоединяются синдромы интоксикации и дегидратации: повышение температуры тела, выраженная жажда, сухость кожи, снижение АД, повышение ЧД и ЧСС и т. д. Часто присоединяются интеркуррентные заболевания &ndash; пневмонии, бронхиты и другие.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\">&nbsp;</p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Примерно в 50% случаев мекониальный илеус является причиной атрезии, перфорации или незавершенного поворота кишечника. Это обусловлено заворотом растянутых и ослабленных петель, формированием псевдоклапана и нарушением кровоснабжения стенок пищеварительного канала. При длительной ишемии возникает инфаркт кишечника с последующим заращением просвета (атрезией) или перфорацией кишки, развитием мекониевого перитонита или псевдокисты.</span></p>\r\n<p>&nbsp;</p>",
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            "published": 1,
            "parent": null,
            "block_rubric": 173,
            "standards": []
        },
        {
            "id": 7195,
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                {
                    "id": 14360,
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