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"code": "P38",
"name": "Омфалит новорожденного с небольшим кровотечением или без него",
"icd_name": "Омфалит новорожденного с небольшим кровотечением или без него",
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"lead": "Нарушение здоровья, относящееся к группе инфекционные болезни, специфичные для перинатального периода",
"description": "Омфалит – инфекция пуповинного остатка и пупочной ранки, приводящая к воспалению кожи и подкожной клетчатки, нарушению процессов эпителизации.",
"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>",
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"code": "P57",
"name": "Ядерная желтуха",
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"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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"lead": "Нарушение здоровья, относящееся к группе хромосомные аномалии, не классифицированные в других рубриках",
"description": "Синдром Эдвардса — это генетическое заболевание, характеризующееся дублированием (трисомией) 18 хромосомы и проявляющееся целым рядом характерных пороков развития у плода во время беременности, часто приводящих к смерти ребенка или его инвалидизации. \r\n\r\nСиндром Патау – хромосомное заболевание, обусловленное наличием дополнительной копии 13-ой хромосомы (трисомия по 13-ой хромосоме). \r\n \r\n\r\n ",
"etiology": "<p>Причиной синдрома Эдвардса является наличие дополнительной 18-й хромосомы (трёх вместо двух в норме для диплоидного набора) в кариотипе зиготы. </p>\r\n<p>Основой для развития синдрома Патау служит присутствие в кариотипе дополнительной копии 13-ой хромосомы. Точные причины утроения хромосом не установлены. Известно лишь, что генетический сбой может произойти во время формирования гамет или уже на этапе образования зиготы. Прослеживается связь между частотой развития патологии у плода и возрастом матери. </p>\r\n<p>Роль других факторов (инфекций, соматических заболеваний матери, вредных привычек, экологического неблагополучия и пр.) достоверно не определена. </p>",
"pathogenesis": "<p>Лишняя хромосома обычно появляется до оплодотворения. У человека нормальные половые клетки — гаметы — содержат по 23 хромосомы (гаплоидный набор) и, сливаясь, они дают кариотип зиготы — 46 хромосом. К появлению лишней хромосомы у гамет обычно приводит нерасхождение хромосом при мейотическом делении, вследствие чего в половой клетке оказывается 24 хромосомы. В случае, если такая клетка встретит при оплодотворении гамету от противоположного пола, они образуют зиготу с трисомией. </p>\r\n<p>В одном случае из десяти наблюдается мозаицизм в явлении трисомии 18: лишнюю хромосому несут не все клетки организма. Это говорит о том, что нерасхождение произошло на ранней стадии развития зародыша, а все клетки с трисомией — потомки неправильно поделившейся клетки зародыша. </p>",
"diagnostics": "<p>На первом этапе скрининга производится определение биохимических маркеров (бета-ХГЧ, РАРР-А и др.) и УЗИ-исследование, на основании которых рассчитывается риск рождения больного ребенка для данной женщины. </p>\r\n<p>Женщинам, попавшим в группы риска, предлагается проведение инвазивной пренатальной диагностики: биопсии ворсин хориона (8-12 недели), амниоцентеза (забор околоплодных вод) на 14-18 недели или кордоцентеза (взятие крови плода из пуповины) после 20-й недели беременности. В полученных образцах материала плода проводится поиск трисомии по 13-ой хромосоме методом кариотипирования с дифференциальной окраской хромосом или КФ-ПЦР. </p>\r\n<p>Если дородовая диагностика по каким-либо причинам не проводилась, хромосомная аномалия может быть заподозрена у новорожденного неонатологом на основании ярких клинических признаков и дерматографических изменений. Однако цитогенетический диагноз трисомии может быть получен только после определения хромосомного набора ребенка. </p>\r\n<p>Новорожденные с предполагаемым или установленным диагнозом нуждаются в углубленном комплексном обследовании для выявления тяжелых пороков развития (эхокардиографии, УЗИ органов брюшной полости и почек, нейросонографии, КТ головного мозга и др.). </p>",
"treatment": "<p>Лечения хромосомных заболеваний в настоящее время не существует. </p>\r\n<p>Проводятся пластическиу операции по устранению щели на небе и губе, и ликвидации лишних пальцев; осуществляются множественные хирургические вмешательства для удаления патологий внутренних органов; обеспечивается тщательный уход, полноценное питание и постоянный контроль за малышом; общеукрепляющие мероприятия для поддержания функционирования поражённых органов; ограничение ребёнка от заражения инфекционными или воспалительными заболеваниями.</p>",
"prevention": "<p>Специфической профилактики не существует. С целью своевременного выявления хромосомной патологии у плода не следует пренебрегать антенатальным скринингом, входящим в программу введения беременности.</p>",
"clinical_picture": "<h3><strong>Синдром Эдвардса </strong></h3>\r\n<p>Во время беременности наблюдается малый вес плода, многоводие, небольшая плацента и наличие одной артерии плаценты. </p>\r\n<p>Новорожденные имеют изменение формы черепа, маленькие рот и челюсть, лицевой дисфорфизм, дефекты глаз (косоглазие, опущение века, третье веко, пучеглазие) и низкие деформированные ушные раковины. Также наблюдаются количественные аномалии пальцев рук и ног, деформация стопы («стопа-качалка»). </p>\r\n<p>Из дефектов внутренних органов наиболее часто встречаются пороки сердца и сосудов, мочеполовой системы, желудочно-кишечного тракта, дыхательной системы. </p>\r\n<p>Синдром Эдвардса характеризуется умственной отсталостью и задержкой в развитии. Большая часть детей умирает в первые месяцы жизни. </p>\r\n<h3><strong>Синдром Патау</strong></h3>\r\n<p>Дети с синдромом Патау небольшого роста, с микроцефалией (маленьким черепом), имеют покатый лоб, суженные глазные щели, маленькие глаза, миеломенингоцеле (спиномозговая грыжа), помутнение роговицы, запавшая переносица и широкое основание носа, деформированные ушные раковины, расщелина верхней губы и нёба, полидактилия (увеличение количества пальцев), короткая шея, флексорное (сгибательное) положение кистей, сморщенная кожа задней поверхности шеи. </p>\r\n<p>Характерна умственная отсталость. Внутренние органы имеют дефекты: пороки сердца, сосудов, поджелудочной железы, селезенки, почек. </p>\r\n<p>Во время беременности в большинстве случаев наблюдается многоводие. </p>\r\n<p> </p>",
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