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"code": "T79.4",
"name": "Травматический шок",
"icd_name": "Травматический шок",
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"slug": "t79.4_travmaticheskiy_shok",
"lead": "патологическое состояние, которое возникает вследствие кровопотери и болевого синдрома при травме",
"description": "<p> </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;\">Травматический шок — тяжёлое, угрожающее жизни больного, патологическое состояние, возникающее при тяжёлых травмах, таких как переломы костей таза, тяжёлые огнестрельные ранения, черепно-мозговая травма, травма живота с повреждением внутренних органов, операциях, большой потере крови.</span></p>",
"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;\">Травматический шок развивается при всех видах тяжелых травм, вне зависимости от их причины, локализации и механизма повреждения. Его причиной могут стать ножевые и огнестрельные ранения, падения с высоты, автомобильные аварии, техногенные и природные катастрофы, несчастные случаи на производстве и т. д. Кроме обширных ран с повреждением мягких тканей и кровеносных сосудов, а также открытых и закрытых переломов крупных костей (особенно множественных и сопровождающихся повреждением артерий) травматический шок могут вызывать обширные ожоги и отморожения, которые сопровождаются значительной потерей плазмы.</span></p>\r\n<p> </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;\">В основе развития травматического шока лежит массивная кровопотеря, выраженный болевой синдром, нарушение функции жизненно важных органов и психический стресс, обусловленный острой травмой. При этом потеря крови играет ведущую роль, а влияние остальных факторов может существенно различаться. Так, при повреждении чувствительных зон (промежности и шеи) возрастает влияние болевого фактора, а при травме грудной клетки состояние больного усугубляется нарушением функции дыхания и обеспечения организма кислородом.</span></p>",
"pathogenesis": "<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;\">Пусковой механизм травматического шока в значительной степени связан с централизацией кровообращения – состоянием, когда организм направляет кровь к жизненно важным органам (легким, сердцу, печени, мозгу и т.д.), отводя ее от менее важных органов и тканей (мышц, кожи, жировой клетчатки). Мозг получает сигналы о нехватке крови и реагирует на них, стимулируя надпочечники выбрасывать адреналин и норадреналин. Эти гормоны действуют на периферические сосуды, заставляя их сужаться. В результате кровь оттекает от конечностей и ее становится достаточно для работы жизненно важных органов.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </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;\">Спустя некоторое время механизм начинает давать сбои. Из-за отсутствия кислорода периферические сосуды расширяются, поэтому кровь оттекает от жизненно важных органов. При этом из-за нарушений тканевого обмена стенки периферических сосудов перестают реагировать на сигналы нервной системы и действие гормонов, поэтому повторного сужения сосудов не происходит, и «периферия» превращается в депо крови. Из-за недостаточного объема крови нарушается работа сердца, что еще больше усугубляет нарушения кровообращения. Падает артериальное давление. При значительном снижении АД нарушается нормальная работа почек, а чуть позже – печени и кишечной стенки. Из стенки кишок в кровь выбрасываются токсины. Ситуация усугубляется из-за возникновения многочисленных очагов омертвевших без кислорода тканей и грубого нарушения обмена веществ.</span></p>\r\n<p> </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;\">Из-за спазма и повышения свертываемости крови часть мелких сосудов закупоривается тромбами. Это становится причиной развития ДВС-синдрома (синдрома диссеминированного внутрисосудистого свертывания), при котором свертывание крови сначала замедляется, а затем практически исчезает. При ДВС-синдроме может возобновиться кровотечение в месте травмы, возникает патологическая кровоточивость, появляются множественные мелкие кровоизлияния в кожу и внутренние органы. Все перечисленное приводит к прогрессирующему ухудшению состояния больного и становится причиной летального исхода.</span></p>",
"diagnostics": "<p> </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;\">Травматический шок диагностируют при выявлении соответствующей симптоматики, наличии свежей травмы или другой возможной причины возникновения данной патологии. Для оценки состояния пострадавшего производят периодические измерения пульса и артериального давления, назначают лабораторные исследования. Перечень диагностических процедур определяется патологическим состоянием, вызвавшим развитие травматического шока.</span></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;\">На этапе первой помощи необходимо провести временную остановку кровотечения (жгут, тугая повязка), восстановить проходимость дыхательных путей, выполнить обезболивание и иммобилизацию, а также предупредить переохлаждение. Перемещать больного следует очень осторожно, чтобы не допустить повторной травматизации.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </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;\">В стационаре на начальном этапе реаниматологи-анестезиологи осуществляют переливание солевых (лактасол, раствор Рингера) и коллоидных (реополиглюкин, полиглюкин, желатиноль и т. д.) растворов. После определения резуса и группы крови продолжают переливание указанных растворов в сочетании с кровью и плазмой. Обеспечивают адекватное дыхание, используя воздуховоды, оксигенотерапию, интубацию трахеи или ИВЛ. Продолжают обезболивание. Выполняют катетеризацию мочевого пузыря для точного определения количества мочи.</span></p>\r\n<p> </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;\">Оперативные вмешательства проводят по жизненным показаниям в объеме, необходимом для сохранения жизнедеятельности и предотвращения дальнейшего усугубления шока. Осуществляют остановку кровотечения и обработку ран, блокаду и иммобилизацию переломов, устранение пневмоторакса и т. д. Назначают гормонотерапию, и дегидратацию, применяют препараты для борьбы с гипоксией головного мозга, корректируют обменные нарушения.</span></p>",
"prevention": "<p><span id=\"docs-internal-guid-a21c2c70-7fff-984b-8c63-0474020fdeaf\"><span style=\"font-size: 7pt; font-family: Verdana; background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; vertical-align: baseline; white-space: pre-wrap;\">Своевременное выявление признаков травматического шока и вовремя принятые профилактические меры позволяют предотвратить его переход в более тяжелую стадию еще на доврачебном периоде оказания помощи пострадавшему. </span></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;\">В эректильной фазе пациент возбужден, жалуется на боль, может кричать или стонать. Он тревожен и испуган. Нередко наблюдается агрессия, сопротивление обследованию и лечению. Кожа бледная, артериальное давление немного повышено. Отмечается тахикардия, тахипноэ (учащение дыхания), дрожание конечностей или мелкие подергивания отдельных мышц. Глаза блестят, зрачки расширены, взгляд беспокойный. Кожа покрыта холодным липким потом. Пульс ритмичный, температура тела нормальная или немного повышенная. На этой стадии организм еще компенсирует возникшие нарушения. </span></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;\">Грубые нарушения деятельности внутренних органов отсутствуют, ДВС-синдрома нет.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </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;\">С наступлением торпидной фазы травматического шока пациент становится апатичным, вялым, сонливым и депрессивным. Несмотря на то, что боль в этот период не уменьшается, больной перестает или почти перестает о ней сигнализировать. Он больше не кричит и не жалуется, может лежать безмолвно, тихо постанывая, или вовсе потерять сознание. Реакция отсутствует даже при манипуляциях в области повреждения. Артериальное давление постепенно снижается, а частота сердечных сокращений увеличивается. Пульс на периферических артериях ослабевает, становится нитевидным, а затем перестает определяться.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </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;\">Глаза больного тусклые, запавшие, зрачки расширенные, взгляд неподвижный, под глазами тени. Отмечается выраженная бледность кожных покровов, цианотичность слизистых, губ, носа и кончиков пальцев. Кожа сухая и холодная, упругость тканей снижена. Черты лица заострены, носогубные складки сглажены. Температура тела нормальная или пониженная (возможно также повышение температуры из-за раневой инфекции). Пациента бьет озноб даже в теплом помещении. Нередко наблюдаются судороги, непроизвольное выделение кала и мочи.</span></p>\r\n<p> </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;\">Выявляются симптомы интоксикации. Больной мучается от жажды, язык обложен, губы запекшиеся, сухие. Может наблюдаться тошнота, а в тяжелых случаях даже рвота. Из-за прогрессирующего нарушения работы почек количество мочи уменьшается даже при обильном питье. Моча темная, концентрированная, при тяжелом шоке возможна анурия (полное отсутствие мочи).</span></p>",
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"lead": "Роговичный (корнеальный) рефлекс — это реакция, в ходе которой смыкается глазная щель. Если он ослаблен или отсутствует, это может говорить об органических поражениях лицевого или тройничного нерва, стволовой части головного мозга, а также может указывать на наличие заболеваний роговицыСлабая или нулевая реакция роговицы на внешнее воздействие может быть обусловлена множеством заболеваний и аномальных состояний организма. Невозможно поставить диагноз только по результату одного этого теста, но он является важной основой для дополнительного неврологического обследования. Как правило, после исследования, в зависимости от результатов, можно предполагать следующие патологии:\r\n\r\nПри отсутствии реакции специалист может поставить предварительный диагноз – деформация варолиевого моста. Варолиев мост – это один из отделов головного мозга, который относится (вместе с мозжечком) к заднему мозгу. Его функция состоит в том, чтобы передавать информацию из спинного мозга в головной. Он управляет лицевым и тройничным нервами.\r\nПри снижении рефлекса в сторону органов слуха можно предполагать наличие невриномы слухового нерва. Это доброкачественная опухоль, которая проявляется снижением слуха в одной из половин лица, болезненными ощущениями и нарушением функции глотания. Опухоль удаляют хирургически или при помощи радиотерапии. Иногда невринома требует лишь наблюдения.\r\nНеобязательно нарушение реакции роговицы на прикосновение является результатом внутренних патологий. Корнеальный рефлекс может быть снижен или вовсе пропасть и в том случае, если пациент в больших количествах принимает лекарства, которые обладают очень мощным седативным свойствам. К таким средствам относятся бензодиазепины, барбитураты, некоторые нейролептики и антидепрессанты, а также алкоголь. Также на рефлекс могут влиять противорвотные средств и анальгетики.\r\nПри черепно-мозговой травме врач может выявить как оживление, так и угнетение реакции. В первом случае наблюдаются улучшения и возможен скорый выход из комы, второй случай более тяжёлым: обыкновенно угнетение наблюдается при переломе височной кости.",
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"lead": "Диплопия (нем. Diplopie, англ. Diplopia), широко известная также как двойное зрение (нем. Doppelbilder, англ. double vision), — одновременное представление двух изображений одного объекта, которые могут быть смещены по горизонтали, вертикали, диагонали (то есть по вертикали и горизонтали одновременно) или повёрнуты относительно друг друга[1]. Это, как правило, результат нарушения функции глазодвигательных мышц (нем. Augenmuskeln, англ. extraocular muscles, EOM), когда оба глаза по-прежнему функционируют, но они не могут сходиться к нужному целевому объекту[1]. Проблемы с EOM могут быть из-за механических проблем, нарушений нервно-мышечного соединения, нарушений в черепных нервах (III, IV, и VI), которые стимулируют мышцы, а иногда и нарушения, вовлекающие супрануклеарные глазодвигательные пути или заглатывание токсинов[2].\r\n\r\nДиплопия может быть одним из первых признаков системного заболевания[en], в частности мышечного или неврологического процесса[3], и это может нарушить баланс движения и/или способность чтения у человека[1][4].",
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"lead": "Диссоциированная потеря чувствительности - это модель неврологического повреждения, вызванного поражением единственного в спинной мозг , который включает сохранение тонкого прикосновения и проприоцепции с избирательной потерей боли и температуры\r\n\r\nПонимание механизмов, лежащих в основе этих избирательных поражений, требует краткое обсуждение задействованной анатомии .\r\n\r\nСнижение боли и температуры связано с повреждением латеральных спиноталамических трактов , которые пересекают центральную часть спинного мозга близко к уровню, на котором они входят в него, и перемещаются вверх по позвоночному столбу. сторона, противоположная той, которую они иннервируют (т. е. поднимаются контралатерально). Обратите внимание, что поражение латерального спиноталамического тракта на определенном уровне не приведет к потере чувствительности дерматома того же уровня; это связано с волокнами тракта Лиссауэра , которые передают нейрон на один или два уровня выше пораженного сегмента (таким образом, минуя сегментарное поражение на противоположной стороне).\r\n\r\nПотеря тонкого прикосновения и проприоцепции происходит из-за повреждения спинных столбцов , которые не пересекают пуповину до ствола мозга , и поэтому перемещаются вверх по столбцу на с той же стороны, что и иннервируемая (т. е. восходят ипсилатерально).\r\n\r\nЭто означает, что поражение спинных столбов вызовет потерю осязания и проприоцепции ниже поражения и с той же стороны, что и поражение, в то время как поражение спиноталамических трактов вызовет потерю боли и температуры ниже поражения. и на противоположной стороне.\r\n\r\nДиссоциированная потеря чувствительности всегда предполагает очаговое поражение в спинном мозге или стволе мозга.\r\n\r\nРасположение поражений спинного мозга влияет на внешний вид - например, центральное поражение ( например, при сирингомиелии ) будет нокаутировать нейроны второго порядка спиноталамического тракта, когда они пересекают центр спинного мозга, и вызовет потерю боли и температуры без потери тонкого прикосновения или проприоцепции.\r\nВикипедия site:wikichi.ru",
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"lead": "Дизартрия (из др.-греч. δυσ- — приставка, означающая затруднённость, расстройство + ἀρθρόω — «сочленяю, соединяю») — нарушение произносительной стороны речи, обусловленное недостаточностью иннервации речевого аппарата. При дизартрии, в отличие от афазии, ограничена подвижность органов речи (мягкого нёба, языка, губ), из-за чего затруднена артикуляция. У взрослых дизартрия не сопровождается распадом речевой системы: нарушением восприятия речи на слух, чтения, письма. В детском же возрасте дизартрия нередко приводит к нарушению произнесения слов и, как следствие, к нарушению чтения и письма, а иногда к общему недоразвитию речи. Выявление дизартрии требует неврологического обследования, по результатам которого назначаются лечение и логопедическая коррекция.Дизартрия не является самостоятельным заболеванием, хотя у некоторых больных может быть наиболее заметным проявлением поражения нервной системы. Наблюдается при травмах и опухолях нервной системы, нарушениях мозгового кровообращения, нейроинфекциях, демиелинизирующих заболеваниях и др. У детей дизартрия часто сочетается с другими проявлениями дизонтогенеза, вызванного действием пре- и перинатальных факторов, входит в структуру нарушений при детских церебральных параличах.Значительное нарушение звукопроизношения легко распознаётся, поскольку речь смазанная, глухая, часто с носовым оттенком («Говорит, как с кашей во рту»). Лёгкие нарушения артикуляции выявляются при специальном логопедическом обследовании.Форма дизартрии зависит от места поражения нервной системы. Предложены разные классификации дизартрий, однако основной и наиболее распространённой в мире является клинико-неврологическая классификация, предполагающая выделение 6 форм (и одной смешанной):\r\n\r\nвялая — обусловлена периферическим парезом или параличом мышц, принимающих участие в артикуляции, вследствие поражения языкоглоточного, блуждающего и подъязычного нервов и/или их ядер, а также нарушения нервно-мышечной передачи. Часто сочетается с расстройствами глотания. Является одной из составляющих бульбарного синдрома;\r\nспастическая — обусловлена двусторонним центральным парезом или параличом мышц, иннервируемых языкоглоточным, блуждающим и подъязычным нервами, вследствие двустороннего поражения передних центральных извилин и/или корково-ядерных путей. Является одной из составляющих псевдобульбарного синдрома;\r\nодносторонняя верхнемотонейронная — обусловлена преимущественно односторонним центральным парезом или параличом мышц, иннервируемых языкоглоточным, блуждающим и подъязычным нервами, вследствие одностороннего поражения передних центральных извилин и/или корково-ядерных путей;\r\nатактическая — обусловлена поражением мозжечка или его проводящих путей; характеризуется растянутой, скандированной речью с нарушением модуляции и меняющейся громкостью;\r\nгиперкинетическая — вид экстрапирамидной дизартрии, возникающий при поражении подкорковых узлов и их нервных связей. Является одним из вариантов гиперкинезов, часто сочетается с гиперкинезами другой локализации. Речь смазанная, невнятная с носовым оттенком, резко нарушена просодика, интонационно-мелодическая структура речи, её темп;\r\nгипокинетическая — вид экстрапирамидной дизартрии, возникающий при поражении подкорковых узлов и их нервных связей. Чаще всего наблюдается при паркинсонизме, характеризуется замедленной невыразительной речью, нарушениями модуляции голоса;\r\nсмешанная — часто наблюдается при травмах нервной системы, диффузном и многоочаговом её поражении, когда имеет место сочетание разных механизмов дизартрии.Диагноз дизартрии (МКБ-10: R47.1) устанавливается врачом (как правило, невропатологом). При этом учитывается заключение логопеда. Логопед, в свою очередь, исследует не только особенности и характеристики нарушения звукопроизношения, но и все другие стороны речи.Поскольку дизартрия не является самостоятельным заболеванием и может наблюдаться при многих расстройствах нервной системы, содержание и очерёдность лечебных мероприятий определяются врачом после установления клинического диагноза, с учётом возраста и состояния больного. Во многих случаях требуется комплексное (лечебное и логопедическое) воздействие.\r\n\r\nВ детской логопедической практике важная роль отводится общему развитию всех сторон речи: словаря, грамматического строя, фонематического слуха, поскольку дети, страдающие дизартрией, испытывают в школьные годы трудности в усвоении письменной речи. В некоторых случаях целесообразно обучение таких детей в дошкольном периоде в логопедических группах детского сада.",
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"lead": "Конфабуля́ции (лат. confābulārī — болтать, рассказывать) — ложные воспоминания, в которых факты, бывшие в действительности либо видоизменённые, переносятся в иное (часто в ближайшее) время и могут сочетаться с абсолютно вымышленными событиями[1].\r\n\r\nВ классическом понимании, введённом в психиатрию в 1866 году К. Л. Кальбаумом, конфабуляции являются видом парамнезий, заключающихся в том, что больной сообщает о вымышленных событиях, никогда не имевших места в его жизни[2][3]. Этим конфабуляции отличаются от псевдореминисценций — другого вида парамнезий, при которых происходит смещение в памяти событий, действительно происходивших, но в другое время[4][5]. Конфабуляции иногда образно называют «галлюцинациями воспоминания» (в отличие от псевдореминисценций — «иллюзий воспоминания»). Однако в современной психиатрии существует тенденция объединять конфабуляции и псевдореминисценции под общим термином «конфабуляции»[6].\r\n\r\nТаким образом, под конфабуляциями принято понимать расстройства памяти, нередко сопровождающие прогрессирующую амнезию: события, действительно имевшие место, амнезируются («забываются»), а возникающие пробелы в памяти восполняются вымыслами[1]. Конфабуляции могут заполнять пробелы памяти больного, тем не менее наличие пробелов памяти для формирования конфабуляций совсем не обязательно: они могут формироваться при отсутствии амнезии и гипомнезии. Содержание конфабуляций часто фантастическое, но это не всегда обязательно. Кроме того, возможен и наплыв конфабуляций, сопровождающийся дезориентировкой (конфабуляционная спутанность)[1].",
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