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The article presents comparative evaluation of serum total oxidizing and total anti-oxidizing activity in reanimation patients with severe cranio-cerebral injury and ischemic and hemorrhagic strokes. Due to irregularity of experimental groups in a number of demographic and clinical indicators the new estimated indicator was proposed. The normalized coefficient of oxidation made it possible to apply comparative evaluation of expression of oxidative anti-oxidative imbalance in these groups. The characteristics are presented concerning the oxidative derangements in the studied groups during acute period of disease.

Fifty-three patients aged 17-65 years who had severe brain injury (SBI) were examined and randomized to 2 groups: 1) 16 patients without complications; 2) 37 patients developed pneumonia (35.2%), bronchitis (32.4%), meningitis (10.8%), meningitis concurrent with pneumonia (8.1%), bedsores concurrent with bronchitis (13.5%) on days 4-7. The authors studied the immune status: the subpopulation composition of lymphocytes (CD+, a marker of adult lymphocytes; CD+, a marker of T helper/inductor cells, CD8+, a marker of cytotoxic lymphocytes, CD16+, a marker of natural killer cells, CD20+, a marker of B lymphocytes) by the indirect immunofluorescence technique using monoclonal antibodies; the functional activity of lymphocytes from the expression of activation antigens, such as CD71+, CD25+, HLA-DR; serum immunoglobulins (IgG, IgA, and IgM) by the immunoturbidimetric technique using the test systems (Spinreakt, Spain). A control group included 23 apparently healthy individuals. Immunosuppression developing as significant T lymphopenia due to lower CD4+ and CD8+ lymphocytes, as well as impaired humoral immunity with inadequate IgG generation was detected in the acute phase of SBI. The indicators reflecting the development of secondary pyoseptic complications were elevated CD3+, CD4+, and CD8+ lymphocytes on day 7 and the higher lymphocytic expression of the activation antigens CD25+ and CD71+. The findings show that the diagnostic markers, such as CD3+, CD4+, CD8+, CD25+, and CD71+ lymphocytes, should be included into a comprehensive examination of patients with SBI.

External respiratory function was examined in 79 patients with spinal cord damage at the cervical and thoracic levels before and 1-3, 5-7 days after surgery. They also underwent cliniconeurological and neurophysiological studies. Two groups were identified. These included: 1) patients with spinal cord damage at the C1-5 level and 2) those with this condition at the C6-Th8 level. According to spinal cord conduction disturbance, the groups were divided into two subgroups: a and b. External respiration was investigated after removing a respirator from the patient. Prior to surgery, subgroup 1a had respiratory disorders by the mixed type; subgroups 1b, 2a, and 2b had restrictive respiratory disorders. Postoperatively, all the patients had mixed neurogenic external respiratory disorders that were more significant in subgroups 1a and 2a. In the postoperative period, respiratory disorders became worse and were of mixed nature, which was associated with deteriorated spinal cord function at surgery. Subsequently, there was their regression by day 7. Patients with significant respiratory disorders must be managed in an intensive care unit.

The authors analyze mortality rates during 338,000 anesthetic procedures. Mortality was 0.02%. Epidural, spinal, and plexus anesthesias were 15% of the total number of anesthetic procedures. In this group, mortality was twice less [0.01% (6 patients)] than that under general anesthesia. Under regional anesthesia, all deaths were associated with the induction of epidural anesthesia. A human factor is of profound importance for fatal cases under regional anesthesia. Regional anesthetic techniques are safer than general anesthetic ones.

Many authors point to the peritoneum-blood barrier damage factor in the pathogenesis of abdominal sepsis and peritonitis. The study was undertaken to define the types of blood-peritoneal barrier damage, by providing evidence for a differential approach to intensive care. For this, immunochemical permeability markers and the clinical and laboratory criteria for sepsis were studied in 106 patients. The patients with generalized peritonitis from the sepsis group showed a compensated type of barrier damage. Those with septic shock exhibited its decompensated type. The described types may serve as a criterion for the differential correction of intensive care in abdominal sepsis.

Antithrombotic mechanisms were studied in 156 patients with severe brain injury (SBI) on days 1, 3, 5, 7, and 9 after injury. It was found that the acute period of SBI was marked by a reduction in the athrombogenic potential through both the consumption of physiological anticoagulants, antiaggregants, the components of the plasmin system and the elevated levels of fibrinolytic inhibitors. The inhibitory mechanism responsible for impaired fibrinolysis predominated when infectious complications of SBI developed.

Estimates of the relative-entry coefficient, molecular profile of the cerebrospinal fluid and of the molecular blood profile based on the comparison of concentrations of proteins with different physical-and-chemical properties enable an evaluation of the function of the hematoencephalic barrier in victims with craniocerebral trauma in critical state. It was possible to state, with such approach in use, that the regulatory and protective functions of the hematoencephalic barrier were changing differently in favorable and unfavorable trauma outcomes, which must be duly considered in choosing a treatment tactics for the above category of victims.

The clinical, immunobiochemical and hemostasiological parameters of the systemic inflammatory response (SIR) were studied in 51 patients with diffusive peritonitis. The study showed that lactoferrin, plasminogen/plasmin and alpha 2-macroglobulin can be used, in a set, as informative indices of SIR. A reduced content of lactoferrin, a smaller concentration of proteases inhibitor alpha 2-macroglobulin and a higher relation between plasminogen and plasmin correlate with an unfavorable outcome of the disease beginning from the 1st postoperative day. An activity of Willebrandt's factor is a diagnostic and prognostic marker, which determines a lesion to the endothelium system.

Permeability of the blood-brain barrier was studied by comparing the molar concentrations of albumin and alpha 2-macroglobulin in the spinal fluid and blood of patients with severe brain injury. If the outcome was good, the selective permeability of the barrier was shown to be fully retained, which meant that its regulatory and protective functions remained normal. If the outcome was poor, the selective permeability changed to a greater extent and the alterations found suggested that the regulatory function of the barrier was preserved with simultaneous loss of its protective properties. More marked changes in the function of blood-brain barrier and in the protein composition of spinal fluid occurred with simultaneously elevated intracranial pressure.

Transfusion of fresh-frozen plasma with fraxiparin is the most rational basic therapy for the first and third clinical pathogenetic variants of subacute disseminated intravascular coagulation in multiple-modality treatment of severe craniocerebral injury. In the second variant of this condition, high doses of proteinase inhibitors in combination with minimum heparin doses are the most rational.

Sixty-one patients with severe craniocerebral injuries were examined on days 1-3 after the injury. Consciousness was no more than 8 points by the Glasgow Coma Scale. The patients were divided into 2 groups: 1) favorable outcomes and 2) unfavorable outcomes. Gaseous composition of arterial and venous blood was analyzed in all patients, intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were measured, artificial ventilation of the lungs (AVL) and noninvasive monitoring of cerebral oxygenation (CO) were carried out. The results indicate that continuous monitoring of CPP and CO helps control the time course of cerebral blood flow, thus promoting early detection and effective treatment of cerebral ischemia in critical patients.

In tick-borne encephalitis certain immunopathological reactions develop in the tissues of the central nervous system; alpha 2-macroglobulin may serve as the marker of the activity of these reactions. The dynamic study of liquor taken from 16 patients with the meningeal and focal forms of tick-borne encephalitis (TBE), 8 patients with severe craniocerebral traumas accompanied by meningitis and 10 patients with osteochondrosis was made. As revealed in this study, in TBE patients the level of alpha 2-macroglobulin increases 3.5-fold and remains stable during the acute period of the disease.

Investigation of pulmonary hemodynamics were carried out in 26 victims operated on for brain compression with intracranial (epi-, subdural, and intracerebral) hematomas in combination with severe contusions during different regimes of artificial ventilation of the lungs (VCV, VCV + PEEP, PCV). Intracranial pressure and cerebral perfusion pressure were evaluated. The results indicate that in patients with severe craniocerebral injury PCV decreased systolic pulmonary artery pressure, total pulmonary resistance, central venous pressure, intracranial pressure, increased cerebral perfusion pressure, and therefore the pressure cyclic mode is pathogenetically validated in this patient population.

To study blood-brain barrier permeability and proteolytic changes in in patients with severe brain injury and to evaluate their impact on its course and outcome, the concentrations of albumin, plasminogen (plasmin), alpha 2-macroglobulin, alpha 2-antiplasmin, and alpha 1-antitrypsin were examined in 58 victims by enzyme immunoassay. The control group comprised 20 patients examined for lumbar discal hernia. The studies indicate that early severe brain injury showed blood-brain barrier dysfunction whose severity can be detected by the spinal fluid levels of albumin, plasminogen, and alpha 2-macroglobulin. Proteolytic changes in spinal fluid are determined by its albumin, plasminogen (plasmin), alpha 2-macroglobulin, alpha 2-antiplasmin, and alpha 1-antitrypsin concentrations and affect the development of secondary brain lesion and they are of practical value.

Detection of clinical and pathogenetic variants of the DIC syndrome for development of its differentiated therapy in multiple-modality treatment of severe craniocerebral injury was the purpose of this study. A total of 170 patients with grave craniocerebral injury were examined. The hemostasis system was studied by the following methods: analysis of platelet hemostasis, general coagulation tests, fibrinolysis evaluation, detection of physiological anticoagulants and markers of intravascular blood coagulation and fibrinolysis. Based on the clinical (intra- and extracranial) symptoms and results of studies of the hemostasis system, 3 clinical pathogenetic variants of the DIC syndrome were distinguished, which should be borne in mine when treating patients with severe craniocerebral injury developing the DIC syndrome.

The CSF levels of albumin, alpha 2-microglobulin and IgG were studied in patients with severe brain injury. Elevated CSF levels of albumin and alpha 2-microglobulin were found in more severe patients. The level of IgG level was within the normal range. Endogenic protease-bound alpha 2-microglobulin may cause secondary cerebral tissue lesion, by closing the vicious circle.

The permeability of the blood-brain barrier for the cerebrospinal fluid marker proteins has been assessed in patients with grave craniocerebral injuries. The content of albumin and alpha 2-macroglobulin in the survivors decreased with time and by day 7 after the injury was virtually normal. In patients who died the content of these proteins was reliably increased starting from day 1. By day 7 the content of albumin in the cerebrospinal fluid approached the norm in this group, whereas the content of alpha 2-macroglobulin remained increased. The level of IgG surpassed the normal value on day 1 only in the patients who died, and later it did not differ from the norm in both groups.

The described case with a severe craniocerebral injury in a patient with hemophilia A demonstrated that the initial hypocoagulation does not preclude the development of intravascular blood coagulation. Therefore, in patients with severe brain injury, a more rapid reduction of antihemophilic globulin A is possible, in comparison with that occurring during planned surgery, and, hence, higher doses of cryoprecipitate and longer duration of its infusion are needed. Moreover, this case demonstrated that even in patients with a slight form of hemophilia A the treatment with cryoprecipitate should be continued till the levels of thrombinemia markers are reduced and the concentration of antihemophilic globulin A in the blood stabilized at a level of at least 10%; the dose of infused cryoprecipitate should be reduced gradually.

Fibrinolysis components were studied in 32 patients with slight and 38 ones with grave craniocerebral injuries on days 1, 3, 5, and 7 after the injury. No expressed disorders of blood fibrinolytic activity were revealed in patients with slight injuries. Grave craniocerebral injuries were associated with disorders of the plasmin system. Depression of the external and internal mechanisms of fibrinolysis were the most manifest starting from day 3 and caused by a number of factors characteristic of the developing disseminated intravascular blood coagulation syndrome and, possibly, by impaired regulation of the plasmin system by the central nervous system.

The hemostasis parameters are compared in 32 patients with slight (14-15 Glasgow score) and 114 with grave craniocerebral injury (3 to 7 Glasgow score) on days 1, 3, 5, and 7 after the injury. Assessment of hemostasiograms revealed a regular development of disseminated intravascular blood coagulation (DIC) in patients with grave craniocerebral injury, whereas in patients with slight injury the changes in the hemostasis system were compensatory. Early (starting from day 1) addition of anticoagulants, disaggregants, and fresh-frozen plasma to treatment protocols are advisable for patients with grave craniocerebral injuries.

The paper summaries authors' experience with lifetime and postmortem pulmonary changes in 223 victims with severe craniocerebral injury, as well as the data available in literature on this point. The investigations have shown that microcirculatory disorders make a great contribution to the development of pulmonary complications and revealed specific feature of the natural history of the shock lung in patients with severe craniocerebral injury. The paper provides strong evidence for the neurotrophic pattern of pulmonary complications and proposes a scheme of their development in this injury.

Changes of the bronchial tree revealed during sanative fiber bronchoscopy in the first 24 hours of the acute period of severe craniocerebral trauma were studied in 57 patients. Analysis of the results made it possible to identify the components of the obstructive syndrome, its dependence on the side and level of injury to the brain, to determine the terms of disappearance of the bronchial obstruction and the number of sanative endoscopies. Comparison with the results of treatment of 75 similar patients without bronchoscopy showed the role of the obstructive syndrome in the development of pneumonia in severe craniocerebral trauma.

The results of endoscopic studies of the bronchial tree have been assessed in 150 patients during the acute period of craniocerebral trauma. A correlation has been established between the side and degree of the brain stem damage and the onset of asymmetrical bronchomalacia. The development and signs of the obstructive syndrome within a 2-week post-traumatic period have been demonstrated. The incidence of destructive pneumonia has reduced four-fold. It is concluded that endoscopy of the bronchial tree is highly effective for the prevention of pneumonia in the acute period of severe craniocerebral trauma.