Studying an opportunity to optimize the treatment of the patients with severe traumatic brain injuries is a topical issue in modern neurosurgery. Traumatic tension pneumocephalus is one of life-threatening conditions which accompanies severe TBI and is often complicated with posttraumatic liquorrhea and mass effect. Materials and methods. We carried out systematic search in Russian and foreign medical databases (Medline, Russian Science Citation Index, EMedicine, UMKB) concerning our theme. We included the following words in our search request: tension pneumocephalus, mass effect, valve mechanism, treatment. The result of conducted review of literature was writing the clinic lecture, studying current status of the problem of etiopathogenesis, diagnostics and surveillance of the patients with tension pneumocephalus. The article presenas clinical case of successful surgical treatment of a patient with traumatic tension pneumocephalus. Conclusion. There are no uniform standards of urveillance of the patients with tension pneumocephalus. Based on our own experience, we determined that minimally invasive surgery is a method of choice among reconstructive craniofa-cial surgeries in the treatment of patients with traumatic tension pneumocephalus. It decreases the risks of intra- and postoperative complication. Compliance, using external ventricular drainage and repeated lumbar punctures with prevention of inflammatory complications helped stopping nasal liquorrhea and eliminating mass effect which caused absolute regression of neurological signs
В работе излагаются результаты многолетних экспериментальных исследований системной и региональной гемодина мики, выполненных на разных животных (собаки, кошки, крысы) с использованием различных моделей умирания. Установлено, что восстановление кровообращения у животных, перенесших 5 минутную клиническую смерть, имеет стадийный характер с первоначальной кратковременной гиперперфузией, сменяющейся гипоперфузией и последую щей постепенной нормализацией кровотока. Показано, что в период начальной перфузии происходит перераспреде ление потоков крови, в результате которого кровообращение централизуется. Установлено, что избыточная гиперпер фузия мозга сопровождается резкой активацией свободнорадикальных процессов, ухудшением неврологического восстановления и выживаемости животных. Ограничение избыточной гиперперфузии мозга путем временного исклю чения части объема циркулирующей крови, а также фармакологическая коррекция реперфузионной активации липо пероксидации (фридокс, эмоксипин) существенно улучшают процессы неврологического восстановления и уменьша ют постреанимационную летальность. Ключевые слова: перераспределение потоков, реперфузионная активация липопероксидации, неврологическое восстановление, выживаемость животных.The paper describes the results of long term experimental studies of systemic and regional hemodynamics in different animals (dogs, cats, rats), by using various models of dying. Recovery of circulation in the animals that had experi enced 5 minute clinical death has been ascertained to be phasic with primary short term hyperperfusion changing into hypoperfusion, followed by a gradual blood flow normalization. In early perfusion, the flows of blood are shown to be redistributed, causing circulation to be centralized. Excess cerebral hyperperfusion is accompanied by a drastic acti vation of free radical processes, deteriorated neurological recovery, and decreased survival. Restriction of excess cere bral hyperperfusion via temporary exclusion of a portion of the circulating blood volume, as well as correction of reper fusion activation of lipid peroxidation with drugs (fridox, emoxipin) substantially improve the processes of neurological recovery and lowers postresuscitative mortality. Key words: flow redistribution, reperfusion activation of lipid peroxidation, neurological recovery, animal survival.В работе обобщены результаты многолетних эксперимен тальных исследований сотрудников Кемеровской медицин ской академии и Филиала НИИ Общей реаниматологии, вы полненных с использованием различных моделей клинической смерти (острая одномоментная и пролонгиро ванная кровопотеря, электротравма, сдавление грудной клет ки, отравление угарным газом) на разных животных (собаки, кошки, крысы). Установлены общие закономерности восста новления системной гемодинамики и мозгового кровообраще ния оживляемого организма, механизмы развития и патогене тическая значимость ранней постреанимационной гипер и гипоперфузии.Системная гемодинамика. Первоначально развивающая ся при возобновлении сердечной деятельности кратковр...
The article presents a literature review on the VATS treatment of spontaneous pneumothorax as a complication of bullous lung emphysema. The review considers questions of etiology, diagnostics and therapeutic tactics in VATS treat-ment of spontaneous pneumothorax with bullous emphysema. The main target of surgeons is not only elimination of spontaneous pneumothorax, but quick exposure of lung parenchyma pathology in order to predict possible reoccurrence of spontaneous pneumothorax. Video-assisted thoracoscopy in this case is a mini-invasive, less traumatic and highly efficient method of treatment of spontaneous pneumothorax. Anti-relapsing surgical interventions with pleurodesis are unanimously considered to be necessary. An integrated and differentiated approach to the treatment of spontane-ous pneumothorax as a result of bullous emphysema helps to determine diagnostic and therapeutic tactics of VATS treatment and choice of pleurodesis induction leading to improved treatment outcomes in this category of patients.
Н а р у ш е н и я г е м о д и н а м и к и. Г и п о к с и я
Aim. To assess myocardial contractile function in dogs after clinical death following acute myocardial infarction and to determine its role in the development of hemodynamic derangements after cardiopulmonary resuscitation. Methods. 180 dogs included in the experiment received pentobarbital anesthesia to assess contractile function and systemic hemodynamics after a 5-min clinical death caused by myocardial infarction. Results Dogs had phase changes in the myocardial contractile function with its initial increase, subsequent depression and normalization in the early postresuscitation period after myocardial infarction. Depressed cardiac contractile function was accompanied by a decrease in the myocardial functional reserve. A similar tendency was found in the restoration of systemic hemocirculation. Conclusion. Similar phase alterations in the myocardial contractile function and systemic hemodynamics developed in the postresuscitation period of acute myocardial infarction. Immediately after recovery, the parameters of systemic hemoperfusion increased due to the activation of the cardiac contractile function. The subsequent initial (3 – 60 min) decrease in the volumetric perfusion parameters was mainly caused by the depressed cardiac contractile function. Rhythm disturbances affected on-going circulatory insufficiency 4 - 5 hours after the recovery. The subsequent progressive decrease in the volumetric perfusion was caused by the extracardiac factors.
Aim. To determine the role of volume imbalance and alterations in the rheological properties of blood in the pathogenesis of postresuscitation hemocirculatory disorders in dogs after clinical death due to acute myocardial infarction.Methods. Changes in systemic hemodynamics, volume and dynamic viscosity of circulating blood within a 5-minute period after clinical death due to myocardial infarction were evaluated in a dog model. 152 dogs received pentobarbital anesthesia.Results. In the early postresuscitation period after myocardial infarction dogs developed phase changes in systemic hemodynamics, volume and dynamic viscosity of circulating blood with an increase in the target indicators, followed by their decrease and final normalization as compared to the baseline. The development of postresuscitation systemic hyperperperfusion (1–3 min) was associated with significantly increased blood volume and its components. The subsequently decreased perfusion volume (5–30 min) was caused by depressed contractile function of the heart. The further progression (1–9 hours) of the hypoperfusion syndrome was mainly attributed to hypovolemia, increased dynamic viscosity of the blood and the viscoelastic properties of the red blood cells. The contribution of heart rhythm disturbances (polytopic ventricular extrasystoles) to the development of circulatory failure 4–5 hours after the successful resuscitation was determined. The subsequent hemodynamic improvements were associated with the normalization of the circulating plasma volume and hemorheological properties of the blood.Conclusion. Staged disorders of the systemic circulation formed in the recovery period after clinical death following acute myocardial infarction. They were accompanied by the alterations in the volume and dynamic viscosity of the circulating blood. Immediately after the revival, elevated values of the hemodynamic parameters were attributed to the increased blood flow as well as to the increased in plasma and globular components. The initial (5–30 min) decrease in the cardiac output was caused by impaired myocardial contractility. After a recovery period of 1–9 hours, a progressive decrease in the perfusion volume demonstrated a direct linear relationship with a deficit of blood flow and its plasma component. Heart rhythm disturbances contributed to the development of insufficient blood circulation in the 4–5-hour recovery period. Thus, hypovolemia and the hyperviscous syndrome associated with it significantly contributed to the development of insufficient systemic circulation within the 1–9-hour recovery period after clinical death provoked by myocardial infarction.
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