Search PubMed⌕ Search

Biomedical subjects

I E Galankina

Publications and source records attributed to I E Galankina.

At least 19 recordsLinked to original sources
PubMed2006

[Structure of hospital lethality in polytrauma and ways to reduce it].

Case histories of 276 patients and autopsy protocols for patients who had died of polytrauma in 2002-2003 were analyzed. It was found that hospital polytrauma lethality is characterized by two peaks: within the first 24 hours after trauma (34.3% of the victims) and on day 4 and later after polytrauma (53.2%). Acute blood loss and shock are the cause of early lethality. In the period from 1 to 3 days after trauma the main causes of death are edema and dislocation of the brain in patients with dominating craniocerebral injury. Late mortality (on day 4 and later) is associated with infectious complications. The overall lethality after polytrauma decreased from 26-30% to 18.5-18.9% for the recent 10 years due to shortening of presurgical period, "cell-saver" use, improvement of anesthetic and intensive care management, mini-invasive osteosynthesis, timely prevention and treatment of brain edema, preventive use of last generation antibiotics and immune correction.

Aged↗
PubMed2004

[The endoscopic and morphological diagnostics of gastroesophageal reflux].

The experiences with endoscopic examinations of 140 patients with gastroesophageal reflux followed by the development of reflux-esophagitis (RE) of different degree are presented. The authors describe the complicated and uncomplicated forms of RE. The uncomplicated forms include RE with unimpaired integrity of the epithelium, erosive RE, erosive-ulcerous RE. The complicated forms include peptic ulcer of the esophagus, peptic stricture and Barrett esophagus. The degree of RE was found to depend on the character and degree of impairment of the obturating function of the cardia. The morphological examination of the esophagus mucosa was performed in 35 patients. Morphological heterogeneity of the so called "catarrhal RE" was shown that makes the expedience of using this term in clinical practice doubtful. Exact endoscopic and morphological criteria of the differential diagnostics of erosive and erosive-ulcerous RE, erosive-ulcerous RE and peptic ulcer of the esophagus are described.

Acute Disease↗
PubMed2003

[Instrumental diagnosis of reflux esophagitis].

One hundred and forty patients with clinical symptoms of gastroesophageal reflux disease were examined. Instrumental examination included esophagogastroduodenoscopy (140 patients) with target biopsy (44 patients), x-ray study of the esophagus and stomach (95), intragastric pH-metry (74), esophagomanometry (67). It is demonstrated that all the patients with clinical picture of gastroesophageal reflux disease suffer from reflux-esophagitis (RE) of various severity. Definite morphological equivalents correspond to each of endoscopic forms of RE. Complex instrumental diagnosis of RE must include intragastric pH-metry and esophagomanometry in line with esophagogastroduodenoscopy and morphological study. It is necessary to perform x-ray study in peptic strictures of the esophagus and in combination of RE with large axial hiatal hernias. Cardial or cardial-fundal hiatal hernia, increase of intragastric pressure and hyperacidity promote development of the most severe (destructive) forms of RE.

Adult↗
PubMed1996

[Healing of extensive acute gastric ulcer after chemical burn by Helium-Neon laser (endoscopic and morphologic investigation)].

The paper provides the results of endoscopic and morphologic follow-up of healing of extensive corrosive gastric ulcer in He-Ne laser therapy of 34 patients (512 gastric biopsies). Laser radiation of ulcer reduces frequency of stenosis in healing outcome as well as treatment duration, creates conditions for healing without leukocytic fusion of necrotic tissues. Effectivity of laser therapy is determined by the time of its start and regularity.

Acute Disease↗
PubMed1991

[Coronary thrombosis, mechanisms of thrombolysis and the tactics in radiographically guided endovascular treatment of patients with acute myocardial infarction].

The radio-angiographic features of coronary blood flow were studied in 119 patients in the first 24 hours of a macrofocal myocardial infarction. In 100 (84%) patients with recognized occlusion of the coronary artery responsible for the infarction the semeiotics of the occluding coronary thrombosis is described, and the characteristics of the residual stenoses after intracoronary thrombolysis were studied. In more than 60% of cases the radiographic features of these stenoses were found to be similar to those of primarily revealed stenoses responsible for infarction of the coronary arteries in degree, form, and the presence of mural thrombus. The mechanism of the formation of these stenoses was of a common character--lysis of the occluding thrombus, which was medicinal in the first case and spontaneous in the second. Medicinal thrombolysis is an analogue of the natural physiological mechanism--spontaneous coronary thrombolysis. It was established that the process of medicinal lysis of the coronary thrombus, a mural thrombus among others, is fully completed by the end of the second day of myocardial infarction. The obtained information makes it possible to formulate some principles of radiologically-guided intravascular treatment of patients with myocardial infarction.

Adult↗
PubMed1990

[Mechanisms of the development of hemorrhagic myocardial infarction and the criteria of angiographic diagnosis].

Unlike ischemic myocardial infarction, hemorrhagic myocardial infarction develops with active involvement of vessels of microcirculation and veins which are implicated in the process concurrently with great coronary artery occlusion or immediately after blood flow normalization. Morphological changes found in the vessels of microcirculation and veins suggest that the majority of them have advanced spasm. This leads to abnormal blood outflow from the hemorrhagic myocardial infarction zone, which is followed by extensive blood interstitial saturation with continuous blood inflow (ante- and retrogradely). Angiography reveals hypervascularization in the area of evolving infarction (a late arterial period), intensive contrast (a parenchymatous period), contrast agent extravasation and its prolonged elimination from the distal channel (a venous period).

Angiography↗
PubMed1988

[Complications of x-ray endovascular recanalization and their role in thanatogenesis].

In line with clinical benefits observed in the diagnosis and treatment of arteriopathies, invasive methods currently introduced in a wide practice entail some negative sequelae presenting with specific complications with occasional lethal outcomes. Because the complications are so closely related to pathogenesis and outcomes of the disease, they should be thoroughly analyzed in view of their role and place in the conceptions of thanatogenesis and pathological diagnosis in which they can be introduced as the main, concurrent or competitive disease, registered as complications depending on the role in the thanatogenesis and initial status of the patient assessed both by the clinician and the pathologist before the invasive procedure.

Angioplasty, Balloon↗
PubMed1988

[Morphologic manifestations of the medicinal lysis of a coronary artery thrombus].

Morphologic studies of coronary arterial thrombi have shown immature fibrin fibres to prevail in those, with fibrin degradation products always present. This fact suggests that fibrinolytic components of hemostasis, limiting the rates of fibrin polymerization and maturation, may participate in thrombogenesis. At the same time, macrophages that phagocytose fibrin and blood cells (platelets and erythrocytes) become activated since the early hours of the thrombus' existence. Selective administration of fibrinolytic activators destroys the fibrin network of the thrombus, blood cells are washed away by the blood flow and the thrombus diminishes in volume. At the same time, its macrophagal response is activated, and fibrin and fibrin degradation products are eliminated from the vascular lumen.

Animals↗
PubMed1988

[Morphologic characteristics of the evolution of myocardial infarct after effective thrombolytic therapy].

Stroma and vessels which remain in the zone of myocardial infarction (MI) after thrombolytic therapy has restored impaired circulation during early hours of MI onset may produce foci of necrosis responsible for accelerated MI formation both in the periphery and centre of the foci. Hemorrhagic MI development can be related to microvascular and intramural vein spasms at early stages of the blood supply recovery. Fibrinoid necrosis of the wall and thrombosis of the lumen were observed in relevant vessels later on. These were associated with disturbed blood outflow from the infarction zone and hemorrhagic saturation of the interstice and cardiomyocytes.

Aged↗
PubMed1988

[Pathomorphologic changes in the arterial wall following x-ray endovascular dilatation in chronic ischemia of the lower extremities].

Intravital and postmortem (7 and 14 cases, respectively) x-ray endovascular dilatation of the limb arteries studied morphologically is shown to induce traumatic lesion of the vascular wall presenting with plaque cracking and detachment, disintegration of the cover, necrosis of smooth muscle cells. A clear-cut change of the plaque size was not recorded. Vascular dilatation at the site of stenosis treated by the balloon may be caused mainly by the plaque cracks and detachment from the vessel wall entailing partial recovery of its elasticity. Mechanical aftereffects of the balloon introduction noted morphologically involve also smoothing of convolution of the internal elastic membrane and the absence of the typical vascular superficial microrelief.

Arteriosclerosis↗
PubMed1988

[Characteristics of cardiac insufficiency in myocardial infarction in the pre-rupture period].

Of 61 patients with myocardial infarction (MI), complicated by cardiorrhexis (CR), 72% had heart failure (HF) in the prerupture period. A small MI zone (35.8 +/- 2.6% of the left ventricular area) was marked in 29 cases of instantaneous CR. Coronary arteries (CA) outside the necrotic zone were slightly necrosed (up to 50%). These factors as well as the hyperdynamic syndrome in 75% of the patients with instantaneous CR on the 1st day and a high frequency of left ventricular aneurysms made it possible to associate HF development with myocardial dyskinesia. In prolonged MI there were several HF causes: a large MI zone (47.9 +/- 3.1%), noticeable CA stenosis outside the MI zone. However, early CR development (on the 4th day) and a high frequency of aneurysms (62%) could be indicative of a considerable contribution of dyskinesia to HF development. A variant of prolonged CR combined with dysfunction of the papillary muscles was attended by HF development in 100% of cases in an intermediate value of a MI zone and the CA state. However, dysfunction of the papillary muscles was one of the variants of myocardial dyskinesia. A conclusion was made of an important role played in HF genesis by myocardial dyskinesia binding HF and CR by the single mechanism.

Aged↗
PubMed1985

[Morphological characteristics of hemorrhagic myocardial infarction].

The main features of hemorrhagic myocardial infarction (HMI) are presented basing on the light and electron microscopic study of 32 cases. HMI is distinguished macroscopically from the ischemic infarction by its dark-red colour due to a diffuse hemorrhagic imbibition and by the clear borders already seen within, the first hours of the disease. Histologically HMI is distinct due to the fibrinoid necrosis of the walls of small arteries, capillaries and, first of all, veins with their thrombosis. This results in the increasing vessel permeability, large hemorrhages into the interstitium with the fibrin deposits and the penetration of erythrocytes and fibrin into cardiomyocytes. Pathogenetic peculiarity of HMI is the blockade of the microcirculatory and venous bed in the background of normal coronary circulation. These events develop probably primarily in natural course of HMI and secondarily when fibrinolytic therapy is used. The thrombi of big arteries found in 9 out of 32 cases seem to arise secondarily in the background of the altered venous circulation. Possible causes of the microcirculatory-venous blockade in HMI may be persistent angiospasm, alteration of the blood coagulation, complications of the fibrinolytic therapy as well as toxicoallergic reactions and microembolism.

Aged↗
PubMed1985

[Pulmonary artery aneurysm with rupture].

Literature on the rare complication--lung artery rupture--is presented. One authors' observation is described: rupture of the lung artery aneurysm in a patient with rheumatic vitium cordis. It the authors' opinion, rupture of the lung artery results from the combination of several factors: hypertension in the lung artery system, structural alterations of the artery wall with the decrease of its solidity.

Aneurysm↗
PubMed1984

[Macrofocal metabolic myocardial damage].

Eighteen observations of large-focal damage of the myocardium are analysed which macroscopically simulated myocardial infarction. Histologically the foci were represented by confluent areas of fatty and albuminous degeneration alternating with necrosis of individual cardiomyocytes. This condition is a complication of diseases having signs of intoxication, anemia, disorders of lipid metabolism and water-electrolyte balance combined with ischemic heart disease. The degree of heart function disturbance correlated with both the severity of concurrent diseases and the depth and size of cardiomyocyte damage.

Adult↗