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Казахстанский мед портал информационных систем » Статьи » ДИАГНОСТИКА И ТЕРАПИЯ ПЛАЦЕНТАРНОЙ НЕДОСТАТОЧНОСТИ

ДИАГНОСТИКА И ТЕРАПИЯ ПЛАЦЕНТАРНОЙ НЕДОСТАТОЧНОСТИ

ДИАГНОСТИКА И ТЕРАПИЯ ПЛАЦЕНТАРНОЙ НЕДОСТАТОЧНОСТИ

Профессор В.Н. Серов
Научный центр акушерства, гинекологии и перинатологии РАМН, Москва Плацентарная недостаточность (ПН) определяется как причина задержки развития плода, внутриутробной гипотрофии и гипоксии и в конечном итоге - возможности внутриутробной гибели плода. При патологическом течении беременности - гестозе, внутриутробной инфекции, экстрагенитальных заболеваниях, всегда в той или иной степени отмечается ПН. Однако компенсаторные изменения в плаценте чаще всего сдерживают развивающуюся патологию. При тяжелой патологии происходит задержка развития плода, его гибель на различных сроках беременности или рождение плода с гипотрофией и гипоксией.
Принципиально важным вопросом является отношение к ПН, как к самостоятельному клиническому синдрому или симптомокомплексу, сопровождающему основное патологическое состояние. Анализ литературы показывает, что чаще всего ПН рассматривается отдельно от той причины, которой она обусловлена. Констатируется нарушение кровообращения в сосудах фетоплацентарного комплекса вследствие гиповолемии, тромбоза и повышения резистентности сосудов и делается вывод о недостаточном снабжении плода кислородом, наличии трофической недостаточности. После чего следуют рекомендации по улучшению микроциркуляции и доставке кислорода. Однако в тени остаются причины, вызвавшие ПН, и лечение основного заболевания не всегда связывают с профилактикой и лечением ПН.

Предполагается, что ПН является универсальной при различных заболеваниях гестозе, инфекции, аутоиммунной патологии. Работы последних лет по инфекции, антифосфолипидному синдрому, привычному невынашиванию беременности свидетельствуют о различных компенсаторных возможностях при ПН, свойственных различным патологическим состояниям. Известно, что у женщин даже с тяжелыми пороками сердца рождаются маловесные, но вполне жизнеспособные дети, в то время как при тяжелом гестозе внутриутробная гибель плода и синдром задержки развития плода (СЗРП) характеризуют тяжесть самого гестоза. Особенно быстро СЗРП, его внутриутробная гибель, интранатальная и постнатальная смерть наступают при антифосфолипидном синдроме, для которого характерны не только гемодинамические, но и внутрисосудистые нарушения с генерализованными тромбозами в фетоплацентарном комплексе. Если сосудистая недостаточность компенсируется новообразованием ворсин плаценты, увеличивая площадь газообмена, то распространенный тромбоз препятствует компенсаторным реакциям в плаценте.

Пока идет накопление данных об особенностях ПН, но уже сейчас можно говорить, что многое зависит от основного заболевания, лечение которого существенно влияет на развитие ПН. Следовательно, отдельно рассматривать лечение фетоплацентарной недостаточности можно лишь в ограниченном объеме, так как лечение основного заболевания существенно влияет на ПН.

Диагностика ПН основана на выявлении признаков синдрома задержки развития плода или хронической и острой гипоксии плода. Ведущими признаками ПН являются ультразвуковые критерии биометрии плода, существенное значение имеет определение хорионического гонадотропина и плацентарного гонадотропина. Наиболее ранние проявления ПН (еще до заметной задержки развития плода) нарушения кровообращения в фетоплацентарном комплексе (в сосудах плаценты и плода).

В клинической практике наиболее часто выделяют первичную и вторичную ПН. При первичной ПН структурные изменения обнаруживаются в строении, расположении и прикреплении плаценты и созревании ворсин хориона. Вторичная ПН развивается во IIIII триместрах беременности на фоне сформировавшейся плаценты и осложненного течения беременности и характеризуется инволлюционнодистрофическими и воспалительными ее изменениями.

Как первичная, так и вторичная ПН могут иметь острое и хроническое течение. В развитии острой ПН важную роль играют нарушения маточноплацентарного кровообращения. Острая ПН чаще развивается на фоне обширных инфарктов и преждевременной отслойки нормально расположенной плаценты, вследствие чего наступает гибель плода и прерывание беременности. Хроническая ПН возникает в результате нарушения компенсаторноприспособительных механизмов в сочетании с циркуляторными расстройствами и инволюционнодистрофическими процессами [1, 2].

В клинической практике важно различать относительную и абсолютную ПН. Срыв одного из звеньев физиологической адаптации материнского организма к беременности приводит к ォдезадаптационной болезниサ, которая может проявляться гипертензивными нарушениями, острой (отслойка плаценты) или хронической ПН, внутриутробной задержкой роста плода (ВЗРП). При сохраненных компенсаторных реакциях в плаценте ее недостаточность не нуждается в лечении, а беременность в этих случаях может закончиться своевременными родами жизнеспособным и здоровым ребенком. Однако возможна и внутриутробная задержка развития плода. При неблагоприятной акушерской ситуации такая форма ПН способствует развитию гипоксии плода.

Наиболее тяжелой формой является абсолютная недостаточность плаценты, свидетельствующая об истощении компенсаторных механизмов плаценты. Эта форма патологии сопровождается ВЗРП и гипоксией плода, вплоть до его внутриутробной гибели. Беременность у таких женщин протекает на фоне угрожающего аборта или преждевременных родов. В клинической практике нередко наблюдаются переходные виды ПН.

Выделяют две основные формы хронической недостаточности плаценты:

1) нарушение питательной функции (трофическая недостаточность), при которой нарушается всасывание и усвоение питательных продуктов, а также синтез собственных продуктов обмена веществ плода;

2) дыхательная недостаточность, заключающаяся в нарушении транспорта кислорода и углекислоты.

Две формы нарушения функции плаценты могут существовать самостоятельно или сочетаться друг с другом. Они могут лежать в основе патогенеза как первичной, так и вторичной ПН.

Основные звенья патогенеза ПН

К основным звеньям патогенеза ПН относятся нарушения маточноплацентарного и плодовоплацентарного кровообращения, метаболизма, синтетической функции и состояния клеточных мембран плаценты.

Патология маточноплацентарного кровообращения характеризуется тремя важнейшими моментами: нарушением притока крови в межворсинчатое пространство, затруднением оттока крови из него и изменениями реологических и коагуляционных свойств крови матки.

Результаты изучения системных изменений при хронической ПН указывают на то, что к числу наиболее важных патофизиологических изменений в организме беременной относится гиповолемия и снижение перфузии органов. При этом возрастает чувствительность сосудистых элементов к циркулирующим прессорным агентам и происходит активация коагуляционного каскада, что ведет к одновременному снижению перфузии межворсинчатого пространства [1, 2, 3, 5].

Большая роль в нарушении гемодинамики плаценты принадлежит реокоагуляционным расстройствам. Известно, что изменения гемостаза, в частности гиперкоагуляция, занимают особое место в патогенезе ПН. Исходная физиологическая гиперкоагуляция крови, достигающая максимального развития к концу III триместра, обеспечивает локальный гемостаз в матке после родов. При беременности в организме развивается гиперволемия и снижается периферическое сосудистое сопротивление. Эти механизмы носят адаптационнозащитный характер у здоровых беременных. В случае же патологии, приводящей к активации системы гемостаза, они теряют свою защитную функцию и способствуют усугублению ПН [3, 5]. При беременности, осложненной задержкой внутриутробного развития плода, уменьшается количество проникающих в миометрий трофобластических элементов. Неполная инвазия трофобласта в спинальные артерии матери становится причиной недостаточной его перфузии и изменений секреции гуморальных факторов.

Профилактика и лечение ПН

Основными направлениями профилактики и лечения ПН и ЗВРП являются воздействия, направленные на улучшение маточноплацентарного кровообращения и микроциркуляции, нормализацию газообмена в системе матьплод, улучшение метаболической функции плаценты, восстановление нарушенной функции клеточных мембран.

В последние годы значительно расширился арсенал лекарственных средств, назначаемых для предупреждения нарушений внутриутробного роста при ПН, сопровождающейся дефицитом кислородного снабжения плода. Эффект применяемых лекарственных средств реализуется в основном на уровне микроциркуляторного русла плаценты. При этом условно выделяют средства, действующие на сосудистый компонент кровотока и на реологические свойства и антикоагулянтный потенциал крови

К числу лекарственных средств, оказывающих воздействие на сосудистый компонент маточноплацентарного сосудистого бассейна, относятся bадреномиметики. Их клинический эффект обусловлен снижением тонуса и амплитуды сокращений матки, общего периферического сосудистого сопротивления, диастолического артериального давления, учащением частоты сердечных сокращений без существенного снижения артериального давления (АД). Под их воздействием значительно возрастает пульсовое АД и минутный объем сердца, увеличивается гемоперфузия матки и фетоплацентарного бассейна. К данной группе относятся партусистен, бриканил, гинипрал. При чрезмерной активности мускулатуры матки и острой гипоксии плода внутривенное введение bадреномиметиков матери способствует улучшению маточноплацентарного кровотока. Однако при гипоксии, развившейся на фоне ПН, сопровождающейся глубокими морфологическими изменениями в плаценте, эффект от применения препаратов данной группы не достигается. Фармакологический токолиз может оказывать благоприятное влияние на маточноплацентарное кровообращение лишь при ПН функционального характера. Кроме того, применение данных препаратов при гиповолемии ограничено, поскольку сосудорасширяющий эффект при низком систолическом АД может способствовать снижению маточноплацентарного кровотока.

Улучшение транспорта кислорода к плоду может быть достигнуто использованием сосудорасширяющих средств и препаратов, нормализующих процессы микроциркуляции в плаценте и матке (например, эуфиллин, компламин).

В последние годы широкое применение в лечении плацентарной недостаточности нашли такие препараты, как актовегин, инстенон, троксевазин. По данным ряда авторов, эти препараты действуют на патогенетические звенья развития плацентарной недостаточности, включаясь в процессы метаболизма, участвуют в регуляции энергообеспечения, корригируя нарушенные компенсаторные возможности организмов матери и плода.

Для улучшения маточноплацентарного кровообращения используют внутривенные инфузии реополиглюкина, декстранов. В связи с тем, что в развитии хронической ПН существенное место занимают морфофункциональные изменения в плаценте в виде микротромбозов, гематом и инфарктов, мероприятия, направленные на улучшение реологических свойств крови, могут способствовать нормализации периферического кровотока, в том числе в бассейне маточноплацентарного круга кровообращения. К ним относится применение гепарина, а в последнее время низкомолекулярных фракций гепарина фраксипарина и др., которые могут использоваться и в амбулаторных условиях.

В последние годы для лечения ПН стали применяться эфферентные методы лечения (плазмаферез). Рекомендуют использовать ультрафиолетовое облучение крови, медицинский озон, лазерную терапию.

Как же разобраться в многочисленных рекомендациях? Следует вернуться к тому, что уже была сказано ранее. Нужно иметь в виду, что ПН возникает при различных заболеваниях, характеризуется несколькими вариантами течения и может быть выявлена на различных стадиях развития.

Недаром еще несколько лет назад считали, что ПН крайне трудно поддается лечению, и лучшим выходом из создавшегося положения считали прекращение беременности с последующим выхаживанием недоношенного ребенка. Но когда появились методы ранней диагностики ПН по состоянию кровообращения в фетоплацентарном комплексе, положение изменилось. Многие методы, улучшающие кровообращение и доставку кислорода плоду, оказались в центре внимания и стали применяться в амбулаторной практике с хорошим эффектом.

Эфферентные методы, антикоагулянты, фотомодификация крови, оксиэтилированный крахмал и ряд других терапевтических технологий рассчитаны на лечение гестоза, экстрагенитальных заболеваний, внутриутробной инфекции в условиях стационара.

Наиболее перспективны профилактика и лечение при ранних проявлениях ПН. Оправдано лечение беременных с высоким риском ПН. В первую очередь это беременные с внутриутробной инфекцией, гестозом, аутоиммунной патологией. Согласно нашим данным и сведениям литературы [4], наиболее эффективный метод лечения начальных проявлений ПН применение активатора клеточного метаболизма актовегина в сочетании с bмиметиками.

Актовегин усиливает метаболизм в клетке путем увеличения транспорта и накопления глюкозы и кислорода, стимулирует энергетические процессы, улучшает кровообращение. Фармакологические эффекты актовегина можно сформулировать в следующих положениях. Актовегин активирует процессы аэробного окисления, повышает утилизацию кислорода тканями, активизирует ферменты системы антиоксидантной защиты и повышает толерантность тканей к гипоксии.

Адреномиметики с избирательным влиянием на b2адренорецепторы, в частности, миометрия, оказывают выраженное токолитическое действие, способствующее улучшению кровообращения в плодовоплацентарном комплексе.

Под нашим наблюдением находились 66 беременных с ПН, из них с задержкой развития плода 12 степени 37 пациенток. Подавляющая часть беременных (46) страдали гестозом, у остальных регистрировалась хроническая инфекция пиелонефрит, вирусоносительство и инфекции, передающиеся половым путем. Больные получали гипотензивную и инфузионную терапию, поливитамины, беременные с влагалищной инфекцией антибиотики и антисептики местно. Большая часть больных с гестозом лечились в стационаре, лечение ПН проводилось в течение 3 недель в амбулаторных условиях. Контрольная группа состояла из 18 беременных с легким гестозом, в т.ч. в сочетании с инфекциями, передающимися половым путем (8 из 18) и с пиелонефритом (5 из 18).

Беременные основной группы получали актовегин по 2 драже (400 мг) в сутки и гинипрал по 0,5 таблетки (250 мг) 4 раза в сутки в течение 3 недель. Беременные контрольной группы получали поливитамины.

Проводилось ультразвуковое обследование, допплерометрия, определение массы плода. В основной группе отмечено улучшение плодовоплацентарного кровообращения, снижение общего периферического сопротивления. У беременных, получаших актовегин и гинипрал, масса тела новорожденных колебалась от 3200 до 3600 г, в контрольной группе 23003200 г. Гипоксия отмечалась у 5 новорожденных контрольной группы.

Таким образом, ПН развивается при осложненной беременности, особенно часто при гестозе, внутриутробной инфекции, аутоиммунной патологии. Существовавшее ранее мнение о недостаточной эффективности ПН могло объясняться поздней диагностикой. С появлением возможности для определения маточноплацентарного и плодовоплацентарного кровотока ПН стала выявляться значительно раньше, накопились данные по динамике изменений в процессе лечения.

Наряду с лечением основного заболевания появились возможности для воздействия непосредственно на ПН. Инфузионная терапия гидрооксиэтилированным крахмалом, плазмаферез, озонотерапия, низкомолекулярные гепарины, bмиметики, актовегин это неполный перечень тех средств и методов, которые используются при ПН. Однако проблема лечения ПН остается не до конца решенной, особенно в отношении направленного лечения той патологии, которая стала причиной ПН.

Литература:

1. Радзинский В.Е., Ордиянц И.М. Плацентарная недостаточность при гестозе. // Акуш. и гинек. ,1999; 1: 116.

2. Сидельникова В.М. Актуальные проблемы невынашивания беременности. М.,1999, 138 с.

3. Федорова М.В. Плацентарная недостаточноть. // Акуш. и гинек., 1997; 6: 403.

4. Шаповаленко С.А. Комплексная диагностика и лечение плацентарной недостаточности у беременных на разных стадиях гестации. // Вестник Росс. ассоциации акушеровгинекологов, 2001; 2: 437.

5. Salafia C.M. Placental pathology of fetal growth restriction. // Clin.Obstet. Gynecol, 1997; 40: 7409.

Опубликовано с разрешения администрации Русского Медицинского Журнала.

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