Смешанные метаболические энцефалопатии

Клинические признаки и симптомы достаточно часто позволя­ют сделать обоснованное предположение, что у больного в состо­янии ступора или комы имеет место диффузное метаболическое поражение головного мозга. Однако при лабораторном исследова­нии либо обнаруживается целый ряд изменений, ни одно из кото­рых, по-видимому, не является достаточно тяжелым, чтобы вызвать расстройство сознания, либо метаболические или токси­ческие нарушения не определяются совсем. В первом случае к тяжелой метаболической энцефалопатии, вероятно, приводит со­вокупное действие ряда легких метаболических нарушений, и течение такой энцефалопатии может иногда смягчиться с помо­щью коррекции лишь какого-либо одного из компонентов пато­генного комплекса.

Наблюдение 4—21. Больной 74 пет с диссеминированной карцино­мой предстательной железы поступил в госпиталь в состоянии спутанности сознания и дезориентации. При общем обследовании установлены нор­мальные показатели жизненных функций, кахексия и увеличение размеров печени. Больной находился в состоянии ступора, но под действием силь­ных раздражителей пробуждался. Приходя в сознание, он оставался спу­танным и дезориентированным. Дыхание 16 в 1 мин, диаметр зрачков 2 мм, реакции сохранены, движения глазных яблок при выполнении пробы «го­ловы куклы» в полном объеме. При болевых раздражениях больной адек­ватно отдергивал все конечности. Отмечались повышение глубоких сухо­жильных рефлексов и сгибательные подошвенные рефлексы. Если больной пробуждался настолько, что мог вытянуть руки, то отмечался двусторонний астериксис. Других признаков ссгментарного поражения нервной системы не было. При лабораторном исследовании выявлены следующие патологи­ческие изменения: гемоглобин 8 г/100 мл, кальций 11,5 мг/100 мл, уровень Щелочной фосфатазы в целом повышен, слегка увеличены значения фер­ментов печени. В газовом составе крови — напряжение кислорода 55 мм рт. ст., рН 7,49, напряжение углекислого газа 30 мм рт. ст. На рентгенограм­ме грудной клетки обнаружен небольшой инфильтрат в средней доле пра­вого легкого. Был поставлен диагноз смешанной метаболической энцефало­патии, причиной которой была совокупность анемии, гипоксии, метастазов в печень и гиперкальциемии.

Введение кислорода через носовые проходы повысило напряжение кис­лорода артериальной крови, к изменению клинической картины не приве­ло. В результате переливания крови в двойной дозе уровень гемоглобина

повысился до 10 г/100 мл; когда переливание объединили с введением кислорода, больной проснулся и, хотя был дезориентирован во времени, со­хранял живую реакцию на окружающее, и поведение его было адекватным. К моменту восстановления состояния бодрствования изменения уровня кальция в плазме крови и нарушения функции печени, по данным лабора­торных проб, не наблюдалось.

Более трудная ситуация возникает в случаях, когда ни мета­болические, ни токсические нарушения не определяются. В этих условиях первым шагом в диагностике должно быть прекраще­ние приема всех лекарств, получаемых больным в последние 48ч. Отменив седативные или наркотические препараты, необходимо проверить количество тромбоцитов и коагулограмму. У некоторых из этих больных впоследствии обнаруживался синдром диссеми-нированного внутрисосудистого свертывания с неврологической симптоматикой, появляющейся до возникновения признаков на­рушения свертывающей системы крови. У других больных суще­ствовавший до обследования биохимический дефект может оста­вить резидуальное поражение головного мозга даже в том случае, если лежавшие в его основе биохимические нарушения подверг­лись коррекции. Это происходит, например, при отравлении окисью углерода или при гипогликемии. У некоторых больных причиной нарушений может быть поступление в организм лекарств, химические свойства которых не определяются обыч­ными лабораторными методами. Иногда поставить диагноз не удается вообще и следует предполагать, что у больных в таких случаях имеются неопределяемые токсины или непонятные нару­шения метаболизма. Столкнувшись с такой трудностью, врач должен применить поддерживающую терапию, описанную в об­щих чертах в главе 8, и пока заболевание развивается, продол­жать кропотливый поиск причин метаболических нарушений.

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