Лечение аневризм сосудов головного мозга в острой стадии субарахноидального кровоизлияния (САК), особенно на фоне церебрального вазоспазма, продолжает оставаться сложной задачей. Цель исследования-оценка динамики результатов хирургического лечения больных с аневризмами сосудов головного мозга в остром периоде САК. Материал и методы. Проведен сравнительный анализ результатов лечения пациентов, оперированных в НМИЦ нейрохирургии им. акад. Н.Н. Бурденко по поводу аневризмы на 1-21-е сутки после кровоизлияния. Для анализа выделены следующие периоды: 2006-2014 гг. (343 пациента) и 2015-2018 гг. (356 пациентов). Большинству пациентов в обоих периодах выполнены микрохирургические операции. Основным отличием между периодами являлась тактика выбора времени операции: в частности в 2015-2018 гг. операцию не откладывали у пациентов с выраженным вазоспазмом. Результаты. При анализе послеоперационной летальности установлено, что, начиная с 2006 г., имеется устойчивая тенденция к уменьшению числа больных, умерших после операции. При подсчете усредненной послеоперационной летальности за исследуемые периоды эта тенденция подтверждается-количество летальных исходов в 2015-2018 гг. статистически значимо уменьшилось по сравнению с 2006-2014 гг.-с 6,8 до 3,2%; p=0,03. В то же время возросло количество пациентов с исходом в вегетативный статус (с 0,3 до 5%). Выводы. Тактика хирургического лечения пациентов с аневризмами сосудов головного мозга в остром периоде субарахноидального кровоизлияния вне зависимости от тяжести состояния и сроков кровоизлияния не привела к ухудшению результатов лечения. Напротив, показатели послеоперационной летальности демонстрируют ее устойчивое снижение. Мы связываем этот факт с рядом изменений, произошедших в ведении и лечении больных. В частности, мы возлагаем большие надежды на разрабатываемые новые подходы к лечению вазоспазма, который остается ведущей причиной неблагоприятных исходов. Более определенные выводы будут сделаны по окончании анализа лечения соответствующих групп больных. Ключевые слова: аневризмы сосудов головного мозга, острый период субарахноидального кровоизлияния, церебральный вазоспазм, летальность при субарахноидальном кровоизлиянии.
Treatment of children in the acute stage of hemorrhage from cerebral aneurysms is based on clinical cases reported in the literature and descriptions of small series of observations. There are no studies that enable the development of evidence-based approaches to intensive care in treatment of children with aSAH. We present a clinical case with a favorable outcome of complex treatment in a child admitted to the Burdenko Neurosurgical Institute at an extremely severe condition. The efficacy of treatment was based on a timely urgent neurosurgical intervention and adequate intensive therapy in the form of extended neuromonitoring with continuous measurement of intracranial pressure, which enabled using the whole complex of measures for timely management of intracranial hypertension. A favorable outcome (a GOS score IV) after this severe aneurysmal SAH indicates that there are no absolute contraindications for neurosurgical treatment of children with cerebral aneurysms.
Acute isolated traumatic brain injury (TBI) is frequently associated with occurrence of hemostasis disorders, which may be accompanied with hemorrhagic and ischemic events in the brain matter, hence, normal functioning of the blood coagulation system is critical. Understanding of the pathophysiological mechanisms of this phenomenon might help adequate prophylaxis of secondary brain damage. Earlier, development of disseminated intravascular coagulation syndrome (DIC) has been generally considered as a mechanism of coagulation disorders during TBI. However, over the recent decades, new data emerged concerning the key role of tissue factor, systemic inflammation response, thrombocytopathy, protein C effect in the occurrence of this coagulopathy. This overview of literature is aimed at providing the new data on specific pathophysiological mechanisms underlying coagulopathy following TBI.
Acute traumatic brain injury (TBI) can be accompanied by coagulopathy. In TBI, when an increased risk of hemorrhagic lesions in the brain tissue exists, keeping the normal hemostasis is crucial.The aim: to determine the incidence of coagulopathy in the acute phase of isolated TBI and identify the correlation between the types of hemostasis disorders and the severity of TBI.Materials and methods. We analyzed 323 case records of patients with TBI hospitalized to the Neurosurgery Center ICU from 2008 to 2016, 118 of them were included in the study. Criteria for inclusion were acute isolated TBI, hospitalization in the first 72 hours after injury, young and middle-aged patients. On admission to the hospital, all patients were assessed according to the Glasgow Coma Scale (GCS) and divided into two groups: group I with severe TBI, group 2 with mild and moderate TBI. All patients underwent blood coagulation testing (APTT, PTI, fibrinogen concentration, platelet count).Results. In 63.6% of patients with acute TBI coagulopathy were found, most of them (55.1%) had hypocoagulability state and were observed in the group of severe PMT (62.5%). The most frequent signs of coagulopathy were reduced PTI of less than 70% and thrombocytopenia of less than 150×109/l. A weak correlation (R=0.276; P=0.002) was found between the development of thrombocytopenia and adverse outcomes (1–3 points according to GOS).Conclusion. on hospital admission coagulopathy was diagnosed in 63,6% of patients in the acute phase of TBI, hypocoagulability state prevailed. Coagulopathy was significantly more common in patients in the acute phase of severe TBI (GCS8 points).The mechanisms of TBI-associated coagulopathy have not yet been fully clarified. Further studies of the role of platelet, plasma and fibrinolytic components in the development of coagulopathy are warranted, which require more comprehensive methods of hemostasis investigation.
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