The purpose of the study is a comprehensive assessment of morphological changes in the placenta and lungs to detect early signs of congenital pneumonia in extremely premature infants.

Materials and methods. Protocols of post-mortem examinations of 23 preterm newborns died from severe respiratory failure were analyzed. The average gestational age of the newborns was 26.4±2.7 weeks and the body weight at birth was 972.4±355.8 grams. In the sample, 78.3% of infants had an extremely low birth weight (ELBW). At birth, all newborns presented severe asphyxia. Newborn underwent several types of respiratory therapy since birth: Mechanical ventilation was performed in 65.2% of newborns since their birth, non-invasive ventilation was performed in 26.1% of cases, and 8.7% of patients underwent oxygenotherapy through a facial mask. In all cases, there was an unfavorable course of the neonatal period, a progressive deterioration of newborns' condition, and a lethal outcome. A comprehensive histological examination of the placenta and the lungs of deceased premature newborn infants was performed.

Results. Congenital infections of different localizations remain the leading cause of death.Congenital pneumonia and generalized infections are clinically manifested at birth by severe perinatal hypoxia and respiratory failure. In the case of congenital pneumonia, the morphological patterns are polymorphic and characterize the severity of lung damage. For some newborns, these patterns include accumulation of exudates and fibrin, segmented leukocytes, fragments of basophilic coccal microflora, and a large number of colony forming bacilli, and desquamated alveolocytes with a deformed nucleus are visualized in the deformed lumen of the alveoli and bronchi. Diffuse lymphoid-leukocyte infiltration in the septa and respiratory parts of the lungs are typical for other infants. Histological examination find lumpy or lamellar eosinophilic hyaline membranes in alveoli in specimens from these newborns. Diffuse, focal or confluent segmentonuclear infiltration in various lung structures is commonly combined with hyaline membranes of various localizations and sizes. Hyaline membranes were detected in 93.5% of cases.

Conclusion. Very early preterm delivery is associated with intrauterine pneumonia and systemic infection in extremely premature infants. Early clinical and laboratory signs of intrauterine infectious lung include severe perinatal hypoxia, very low Apgar score and laboratory test findings (hypoxaemia and decompensated metabolic lactate acidosis) that are resistant to standard resuscitation measures. Hypoxemia and decompensated metabolic acidosis persisting during the first hours of postnatal life indicate the severity of intrauterine lung damage and require a rapid change of treatment aimed at normalization of lung function, prevention of complications in the respiratory system, hemostasis and central nervous system. Clinicians should be better informed about the features of early postnatal adaptation of extremely premature infants with congenital pneumonia to provide appropriate treatment.

The purpose of the study. To describe a clinical case of sepsis in a child due to accidental ingestion of magnetic objects.

Materials and methods. Medical records of a 3-year-old patient were analyzed. Clinical presentation of diffuse purulent peritonitis was found at admission. Sepsis was diagnosed according to age-specific criteria, laboratory test findings, evidence of infection and organ dysfunction.

Results. During the surgery, diffuse fecal peritonitis was found, which had been caused by 9 unidentified magnetic foreign objects found in the intestinal lumen. The postoperative period had a severe course accompanied by developing cardiovascular, respiratory, and intestinal multiple organ failure..

Conclusion. In young children, foreign magnetic bodies can damage the gastrointestinal tract.

The purpose of the study: to assess the morphological changes in the lungs depending on the content of clozapine and its metabolites in the lungs and serum.

Materials and methods. The experiments were performed on male outbred rats weighing 290-350 g at the age of 20 weeks (n=15). The animals were divided into 3 groups: Group 1 — reference group (intact rats) (n=5); Group 2 -poisoning with clozapine (n=5); Group 3 — poisoning with a combination of clozapine with ethanol (n=5). Clozapine was administered orally at a dose of 150 mg per kg of animal's body weight under general anesthesia; alcohol was administered together with clozapine orally at a dose of 5 ml per kg of animal's body weight. Further study was carried out 24 hours after administration of drugs to animals of the 2nd and 3rd groups. After euthanasia of the animals by decapitation, tissue samples of lungs were embedded in paraffin according to the standard technique. Then 5-μm thick histological sections were made and examined using light microscopy with the aid of a Nikon Eclipse E400 microscope equipped with a video system based on the Watec 221S camera (Japan) at magnification of X200 and X400. The following pathological patterns were assessed: disorder of blood circulation (hyperemia, hemorrhage, and sludge), the presence of atelectasis and dystelectasis, the presence of emphysema, the cellular response (an increase in the white blood cell count), and desquamation of epithelium into the lumen of the bronchi. A chemical and toxicological study was performed on a high-performance liquid chromatograph with mass detector Agilent Technologies 430 Triple Quad LC/MS (Germany). To obtain chromatograms, the following software was used: Agilent Mass Hunter Workstation for series tripple Quadrapole vers. B06.00 build 6.0.6.25.4sp4.

The following software was used for processing chromatograms: Agilent Mass Hunter Quantitive Analysis vers. B 07.00 build 7.0.457.0. Serum and lung homogenate levels of clozapine, norclozapine, and clozapine-N — oxide were evaluated.

Results. In 24 hours, animals in the 2nd group exhibited atelectasis and dystelectasis in the lung tissue, and leukocyte infiltration; in the 3rd group, arterial hyperemia, cellular response (an increase in the white blood cell count), atelectasis and dystelectasis, and thickening of interalveolar septa were revealed. In 24 hours, in the lungs of animals of the 3rd group, the concentration of clozapine increased by 22.2-fold, norclozapine by 6.6-fold, and clozapine-Noxide by 6.2-fold as compared to the 2nd group; in serum it increased by 5.7-, 2.0and 4.6-fold, respectively.

Conclusion. In the case of poisoning with clozapine in combination with ethanol, a complex of pathological changes in the lungs develops, which is more severe than the isolated effect of clozapine administered as a single drug. The concentration of clozapine and its metabolites in the lung tissue and blood serum is higher when it enters the body in combination with ethanol.

Material and methods. The studies were performed on 75 white mature rats (females) weighing 180—220g. Partial hepatectomy was performed by resection of a part of the left lobe of the liver (15—20% of the organ weight). Hyperbaric oxygenation (HBO) was performed three times (3 ata, 50 min). The first, second and third sessions were performed 4—8 hours, 24 hours and 48 hours after the surgery, respectively. The urea level was determined in the tissues of visceral organs, as well as in arterial blood (aorta), portal blood, blood from renal and hepatic veins, bile from common bile duct, and in urine on the 1st, 4th and 11th days of posthyperoxic period (days 3, 7 and 14 post-surgery).

Results. Activation of the urea incretion from the operated liver to the bloodstream under hyperoxic conditions was accompanied by increased urea concentration in the arterial blood and excretion from the body with urine that was facilitated by the elimination of a stimulating effect of PHE on the reabsorption of urea in the kidneys by the HBO procedure. At the same time, the production of urea in the renal tissue was activated and further released to the circulation through the renal vein. Stimulation of the liver and intestinal urea circulation by HBO was accompanied by the preservation of the stimulating effect of PHE on its accumulation in duodenum and colon tissues. In the thyroid gland, spleen, heart, and lungs of operated rats, HBO activated the transition of the «arterial» urea from the free form to the bound one. Termination of HBO normalized the urea concentration in the arterial blood by the 11th day of the posthyperoxic period whereas urea continued to be accumulated the heart, spleen, lungs, and intestine. A preserved increased release of urea from the operated liver into the bloodstream after HBO was accompanied by partial retention in the hepatocytes of urea delivered via bloodstreem through the portal vein. On the 11th day after HBO, the repeated hyperoxic activation of the liver and intestinal urea circulation occured, as well as HBO-restored stimulation of its production in the kidneys resulted in urea release into the renal vein and excretion with urea.

Conclusion. HBO provides a correcting effect on alteration of circulating urea caused by PHE.

Purpose: evaluation of the clinical significance of parametric monitoring of the effectiveness of intensive care and rehabilitation based on the analysis of the functional state of the autonomous nervous system in patients with brain damage of different genesis.

Materials and methods. The study included 66 patients on day 20—50 after the traumatic brain injury; anoxic damage; and stroke consequences. The isolation of clinical groups and subsequent analysis of clinical status is based on the analysis of the functional state of the autonomic nervous system based on the dynamics of the heart rate variability (HRV) parameters. Findings obtained in studies of 500 patients in the postoperative period with a 5-minute HRV were tested as normal and abnormal ANS parameters [1]. Parasympathetic hyperactivity was measured within the limits for SDNN (standard deviation of all normal-to-normal R-R intervals) > 41.5 ms; for rMSSD (root-meansquare of the successive normal sinus R-R interval difference) > 42.4 ms; for pNN50% (the percentage of interval differences in successive NN intervals greater than 50 ms (NN50) / total number of NN intervals) > 8.1%; for SI (Baevsky stress index, in normalized units) < 80 n. u.; for TP (total power of variance of all NN intervals) > 2000 ms2. Sympathetic hyperactivity was determined within the limits for following parameters: SDNN, < 4.54 ms; rMSSD, < 2.25 ms; pNN50%, < 0.109%; SI, > 900 n. u.; TP < 200 ms2. Normal HRV parameters were selected within the limits of the values for: SDNN [13.31-41.4ms]; rMSSD [5.78—42.3 ms]; pNN50% [0.110—8.1%]; SI [80—900 nu]; for TP [200—2000 ms2]. To verify the parasympathetic or sympathetic hyperactivity within these limits, 3 of 5 parameters were chosen [1].

Results. Based on the dynamics of the HRV parameters before the intensive care and on days 30—60 of the intensive therapy and rehabilitation of patients with traumatic and non-traumatic brain injuries, 5 main clinical groups of patients were identified. Group 1 (n=27) consisted of patients with normal parameters of the ANS functional activity (both at the time of admission to the hospital and on the 30—60th day of the intensive therapy and rehabilitation). Group 2 (n=9) included patients with the baseline sympathetic hyperactivity of the ANS at admission to the intensive care unit and normal functional activity of the ANS on the 30—60th day of the intensive care and rehabilitation. Group 3 (n=8) included patients with baseline normal functional state of the ANS and the signs of sympathetic hyperactivity of the ANS on the 30—60th day of the intensive care and rehabilitation. Group 4 (n=15) consisted of patients with signs of sympathetic hyperactivity of the ANS both initially and on the 30—60th day of the intensive care and rehabilitation. Group 5 (n=7) included patients with signs of parasympathetic hyperactivity of the ANS (according to the parameters of HRV) both at baseline, at admission to the intensive care unit, and on the 30—60th day of the intensive care and rehabilitation.

Conclusion: The normalization of HRV parameters is accompanied by patients’ recovery from the vegetative state and coma to minimal consciousness or normal consciousness; the index of disability rate decreases, the social reintegration grows, according to the DRS scale (M. Rappaport, 1982); dependence on mechanical ventilation reduces, and the muscle tone normalizes.

The purpose of the study: scientific evidence and development of accessible morphological criteria that allow to determine the duration of dying and the rate of dying.

Materials and methods. The material of the main study included 206 identified deaths of persons with different pre-known processes of dying, which served as criterion for selection from1500 deaths (n=206, 14%). Of these, 110 cases were observed by the forensic medical expertize, 79 cases were revealed by the forensic medical examination of the dead body and 17 cases were included after the postmortem autopsy. The sample included from 30 to 57 cases subdivided in 5 groups. 53 cases were selected for the first time interval, 30 observations for the second one, 32 observations for the third one, 34 observations for the fourth one and 57 observations for the fifth time interval. The following methods were used to study the material: analysis of information about the circumstances of death (based on the records), retrospective clinical and anatomical analysis, the main (classical) method of autopsy of human corpses in sectional studies and histological examination. In addition, an immunohistochemical test, as well as morphometric, macroscopic and photographic methods were used. For the accuracy and reliability of the findings, morphological and statistical analysis was used, which included both statistical analysis of morphological characteristics and tanatogenetic analysis of the cases of the sampled material.

Study results. We developed and scientifically proved a methodology for determining 5 rates of dying according to the morphological characteristics systematized in morphological complexes: fulminant rate ≤15-30 min; fast rate >30 min — ≤2 h; moderate rate >2 — ≤6 h; slow rate >6 — ≤12 h; lingering rate >12 h. Approbation of the proposed method on the gross experimental material allowed to set the diagnostic limit of the total significance for each morphological complex, and thereby, to improve the methodology of establishing the rate of dying in accordance to the morphological characteristics for the use in forensic practice.

Conclusion. The morphological complexes of the rate of dying established in this work would serve as a base for further development of not only forensic thanatology, but also for the aim of improving the medical and preventive care.