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18
II. ДИАГНОСТИКА
UDC 616.12-007.2-089.28/.29
MORPHOLOGICAL ASSESSMENT OF AN ACUTE HEART FAILURE IN STRUCTURE OF THE GENERAL POSTOPERATIVE COMPLICATIONS AT PATIENTS WITH RHEUMATIC HEART
DISEASES
About the authors:
Evgeny A. Enin - head of the anatomico-pathological laboratory of the NSCS n/a Syzganov, a high level certificate physician. Anastasiya V. Pismareva -pathologist,
Key words:
heart failure, traumatic failure of valves, local adaptic reaction, mitral restenosis.
Авторлар туралы:
Енин Евгений Альбертович - А.Н. Сызганов атын. YfXO-нын патологанатомиялык зертханасыньщ Meœrepyrnici, жогарш санатты дэргер;
Письмарева Анастасия Владимировна - дэрГер-патологанатом.
Тушн сездер:
журек жeтicпeyшiлiгi, какпащалардыц травматикалык жeтicпeyшiлiп, жepплiктi беШмделу эсер '1, митральды рестеноз.
Enin E., Pismareva A.
National Scientific Center of Surgery named after A.N. Syzganov, Almaty, Kazakhstan naTOfloroaHaTOMMMbiK, fladopaTopwHCbi
Abstract
The results of researches showing a share and nature of morphological changes in heart at an acute heart failure in structure of the general postoperative complications at patients with rheumatic heart diseases are reflected in this publication. Research is conducted by studying of complications at 89 patients with rheumatic heart diseases who transferred various operative measures with a lethal outcome in the postoperative period.
Ревматикалыщ журек акауы бар наукастардыщ отадан кешп аскынуларына жалпы курылымдык жедел журек желспеушшпне морфологиялыщ бага
Енин Е., Писмарева А.
А.Н. Cbi3f3H0B атындаш Улттык, шлыми хирургиялык, орталык,, Алматы, К,азак,стан Pathologicoanatomic laboratory
Ацдатпа
Б±л макалада ревматикалык, журек акауы бар наукастардын отадан кешп аскынуларына жалпы курылымдык, жедел журек жeтicпeyшiлiгiнiц морфологиялык езгерютер сипаттамасы жэне керсетюш белю зерттеу нэтижeлepi ±сынылады.
Зерттеу ревматикалык журек акаулары бар эр турл'1 оталадан сон елмге ушыраган 89 наукастардын эр турл'1 аскынуларын уйрену аркылы жузешге асырылды.
Морфологическая оценка острой сердечной недостаточности в структуре общих послеоперационных осложнений у больных ревматическими пороками сердца
Об авторах:
Енин Евгений Альбертович - заведующий патологоанато-мической лабораторией, ННЦХ им. Сызганова врач высшей категории, e-mail:enin66@ mail.ru Письмарева Анастасия Владимировна - врач-патологоанатом, e-mal: anastasiyapismareva@mail.ru
Ключевые слова:
сердечная недостаточность, травматическая недостаточность клапанов, местная адаптационная реакция, митральный рестеноз.
Енин Е., Писмарева А.
Национальный научный центр хирургии им. А.Н. Сызганова, Алматы, Казахстан Патологоанатомическая лаборатория
Аннотация
В данной публикации отражены результаты исследований, демонстрирующие долю и характер морфологических изменений в сердце при острой сердечной недостаточности в структуре общих послеоперационных осложнений у больных ревматическими пороками сердца. Исследование проведено путем изучения осложнений у 89 пациентов ревматическими пороками сердца, перенесших различные оперативные вмешательства с летальным исходом в послеоперационном периоде.
ВЕСТНИК ХИРУРГИИ КАЗАХСТАНА № 2(43)*2015
There are frequent complication of cardiac operations, especially in the conditions of an artificial circulation, the acute heart failure [1,2,4,6,12,20].
The task of our researches is to study a share and nature of morphological changes in heart at an acute heart failure in structure of the general postoperative complications at patients with rheumatic heart diseases.
We studied complications of 89 patients with rheumatic heart diseases who transferred various operative measures and the death in the postoperative period. Among the dead there were 48 men and 41 women. On age the dead were distributed as follows: till 19 years there were 6 people, 20-29 years - 20, 30-39 years - 39, 40-49 years - 20, over 50 years - 4.
We have met the various types of defects: mitral stenosis (MS), including restenosis in 31 cases, MS in combination with aortic stenosis (AS) - 15, MS + TC (tricuspid stenosis) - 5 MS + AC + TS - at 9 patients, mitral insufficiency - in 19 cases, other types of multi-valve defects - at 10 cases. Thus, multivalve defects in our material occupied a large share.
Among the observed fatal complications often was heart failure, it had been met in 39 patients (43.8%). There were distinguished four forms of heart failure: 1) unrestored adequate cardiac function after a phase of intracardiac surgery, 2) lightning flowing heart failure (the first hours after surgery), 3) acute progressive heart failure (the first hours after the operation), 4), subacute and chronic heart failure, myocardial (six or more days) [3,5,10,15,17]. Acute heart failure, or first three forms, according to the above classification, were met in 29 cases, 10 deaths were caused by flowing subacute and chronic heart failure.
More than half (n=15), congestive heart failure was caused by the weight of the original state of the myocardium in patients with mitral stenosis IV stage by N.N. Bakulev, rheumatic heart disease, pregnancy-related, post-infarction aneurysm of the left atrium. The group attributed the outcome when mitral commissurotomy was performed on intensive care indications while severe pulmonary edema. Another large group of reasons that led to the development of congestive heart failure, was of various defects surgery: heart septum perforation, incorrect valve prostheses implanted with a deviation of the axis of the direction of blood flow, creating paravalvular atrioventricular fistula, not eliminated the faults of others valves, traumatic failure valves, coronary embolism.
Traumatic heart valve failure led to the death of 15 patients. The most common traumatic mitral regurgitation was observed. Postcomissural failure leads to a new kind of heart disease. Detrinated left ventricle in a very short time put in conditions requiring increased hemodynamic load performance. Will it be reconstructed or breakdown occurs adaptation mechanism largely depends on the type of set up of traumatic failure of the valve? Our investigations have shown equally often ruptures the body front and back cuspis of the mitral valve, once observed fracture annulus and perforation of the posterior leaflet. In most cases (n=10) was a rupture of fibrosis wings, and only in 5 cases - calcified. Time of death in patients with postcomissural mitral valve insufficiency was directly dependent on the type of mechanical valve rupture. If the defect was created in the middle of the body folds, or there was a break of the fibrous ring, the acute left ventricular failure developed on the operating table, and death occurred either immediately or in the next 2-3 hours after surgery, with symptoms of pulmonary edema. In the case where the break took place near the commissure, therapeutic interventions were able to transfer acute heart failure in a subacute or chronic form. In these cases, gradually, along with left ventricular, was right ventricular failure. The death of such patients often occurs from joined pneumonia, with the constant chronic congestion in the pulmonary circulation. The highest survival time of patients with traumatic mitral insufficiency was 6 years. Anatomical explanation more benign course of the second type of traumatic failure is the fact that a torn cuspis of the unit approached the chord [7,9,11,16].
At histological examination of left ventricular wall of the patients who died from acute heart failure due to rupture of the cuspis of the mitral valve, in cases of instantaneous death, was a rapid swelling of the myocardial stroma. Capillaries, veins, arterioles were paretically expanded strictly congested. Glycogen is determined only in a surface lying myocardial fibers in the form of randomly arranged small granules. Succinate dehydrogenase and cytochrome detected in the form of strips and grains that make up the long chains. There was a discrepancy between the muscle cells in the intercalated disks, which were in the form of double lanes separated by short intervals.
Within 2-3 hours after creating postcomissural valve insufficiency stromal edema persisted, dilation of blood vessels was less pronounced. Celebrating small-caliber arterial spasm. When
stained sections of iron haematoxylin by Heidenhain was seen a large number of outbreaks contracture degeneration in the form of coarse disintegration of protoplasm and reduce the abundance of bands. Observe longitudinal contraction of myofibrils with the disappearance of cross-striations. Glycogen in myocardial syncytium is usually not determined. But there is a large number of muscle segments with PAS-positive cytoplasm. The bright pink color of their remains after processing sections amylase. These areas contain increased amounts of total protein, SH-groups, increased eosinophilic, painted by Selye in orange and brick red. The same colors were painted by Selye foci of contracture dystrophy. A number of muscle fibers had basophilic protoplasm. Succinate dehydrogenase and cytochrome identified as lying randomly formazan grains lose their correct orientation in the form of bands and chains. Myoglobin in the slides was determined as polymorphic granules observed tendency to aggregation of granules. Some muscle cells myoglobin was not determined. The frozen sections stained with Sudan black visible infiltration of myocardium by fat. Reduced number of fine granules of ascorbic acid in the muscle fibers, and coarse grains is almost completely absent.
After 1-2 days there was visible polymorphic picture. Begins again detected in the myocardium of single grains of glycogen granules formazan respiratory enzyme sites formed a chain and the right band to appear larger granules of ascorbic acid. These morphological features suggest starting to adapt to the altered hemodynamics. But sometimes it develops coagulation necrosis in foci of contracture dystrophy. Around the dead muscle fibers in the stroma of the myocardium multiply mononuclear cells, fibroblasts and leukocytes. Infiltration is replaced by a more widespread small-and large-drop adipose degeneration. It continues to identify a large number of eosinophil and basophil sharply muscle fibers.
The appearance of basophilic muscle fibers to be associated with the development of local adaptive response, shortness of adaptability to the newly created vicious circulation. The same we explain the sharp decrease and then the disappearance of glycogen in the muscle fibers. Reducing the content of ascorbic acid is associated with a decrease in cell respiration, when stimulation of oxidative processes going on vigorous use of vitamin C. As an adaptive mechanism there should be considered the appearance of muscle fibers in the early stages of the changed flow of fatty infiltration. Lipids are beginning to be used as an
energy material. Further accumulation of lipids in the muscle cell in the form of small and large granules shows marked degenerative processes. This accumulation eventually causes toxic effects causing cardiac arrhythmia. Showed increased eosinophilic segments are a manifestation of the general failure of adaptive response [7,8,13,14,19].
Congestive heart failure was the cause of death of nine patients. We must say that this kind of heart failure occurs predominantly on the right ventricular type. Morphologically it appeared cavitary edema, phenomena of venous stasis of internal organs, which is transmitted and lymphatic channels. The microvasculature of the lymphatic system is dilated lymphatic capillaries, the formation of the network of lymph capillaries are not inherent in the normal "lakes", "lacunes." In lymphatic vessels wall thickening occurred due to the development of collagen fibers, was observed varicose vascular changes at near-by the valve apparatus when developed bizarre growths.
Chronic heart failure occurred in one patient after double mitral commissurotomy and subsequent development of calcification of the valve and at two patients with traumatic mitral regurgitation. Two patients with heart failure were caused by the development of the aneurysm of the left ventricle in place of the surgical wound at applying dilator. An aneurysm is diagnosed at 7 and 8 years after surgical manipulations. In 4 cases this kind of heart failure occurred after restenosis of the left atrioventricular valve.
Mitral restenosis was diagnosed in 13 cases. Calcification of the valve occurred in 6 cases, and almost constantly observed return warty valvulitis. Isolated mitral restenosis developed only in 3 patients, in 10 cases there was the rheumatic process two (8 patients) and three (two patients) valves. The most common (6 cases) mitral restenosis combined with aortic stenosis [18,19,20]. The data are likely to show that in cases of rheumatic process activation after surgery on his heart, he takes a more aggressive, with more pronounced morphological picture. To eliminate these defects, therefore, more appropriate to the "open heart."
The lung, pulmonary heart disease caused the death of 14 patients (15.6%). To the development of respiratory failure in one case resulted in a bilateral obstructive atelectasis of lower lobes of the lungs, in 2 cases - pulmonary infarction and 10 - pneumonia. Typically, pneumonia layered on existing heart failure. We observed focal bronchopneumonia, abscessed, and only in one case - rheumatic pneumonia.
Suppurative complications caused the death of 4 patients. The most severe complication was purulent sepsis. Taking into account the work of previous years, we studied pathological anatomy pseudomonas sepsis. A thorough epidemiological analysis rejects the development of self-infection and indicates the development of nosocomial infections - the question is now moving surgeons around the world. In all cases Pseudomonas aeruginosa contained in the structure of blue-yellow pigment. There have been cases of Pseudomonas sepsis and other pigments, but they proceeded smoothly. Biochemically this culture is inactive: glucose, sucrose, mannitol, lactose do not decompose. Isolates strains do not give plasmocoagulase and do not form pyocyanin. They agglutinated by rabbit's serum immunized with our strains which isolated from the blood of patients. At postmortem study it was noted that half of the patients had yellow skin and visible mucous membranes. The edges and bottom of wounds in these cases were swollen, dry, covered with a touch of dirty green. In 2 patients (from 14) there was revealed a purulent mediastinitis. Pericardial cavity was filled with blue-green pus. The amount of pus was small, and it is in the form of honeycomb, separated by thin layers. Histological examination showed that the pericardial cavity grows granulation tissue, and that the part of the epicardium grows thin connective tissue fibrils. Granulation tissue richly infiltrated by grained leukocytes. At coloring of Gram-Weigert it can be seen a large number of Gram-negative rods a very small amount of them is subject for phagocytosis. Among the granulation tissue of its large field of fibrin.
Around the ligatures that were sutured wounds of the heart, it was revealed small pustules on the type microabscesses. Wound healing is slower than usual. Wound channel filled with granulation tissue with little of its organization. There was revealed a small amount of fine connective tissue fibers only occasionally emerging in bunches. In the granulation tissue it has seen a large number of granular white blood cells and Gram-negative rods. In sepsis in the wound more pronounced necrotic component. The preparations showed large pockets of myocardial necrosis. Slow healing process to a certain extent due to the presence in the wound walls trombovasculitis, necrosis of the walls of small arteries, indicating the hyperergic nature reaction.
In the region separated into operation valve commissure were polypous lush growths of gray dull. Histological examination revealed that the
endocardium wounded in these areas and ulcer surface covered with large clots of fibrin. The bottom of the ulcers presented loose connective tissue infiltrated with round cells and a small number of granular white blood cells. In the connective tissue revealed gram-negative bacilli, but the masses of fibrin were absent. Myocardial stroma was diffusely infiltrated with sero-purulent exudate. In the surface layers of the heart muscle is often detected thrombus located in the lumens of the arteries and veins.
In 6 cases there was revealed focal pneumonia. Exudate in the alveoli was serous or serous-hemorrhagic nature and exudate contained sticks of blue-green pus. In a few fields of necrosis was observed interalveolar septs. In the vessels lumen were infected blood clots. This fact is evidence in favor of the fact that the pneumonia was metastatic by character.
The liver was flabby, nutmeg species. Microscopic examination revealed pronounced parenchymal degeneration, down to small foci of central necrosis. In the stroma there was serous exudate.
Severe morphological changes observed in the kidney. On the surface of the organ there was plenty of small pustules. Microscopically slides characterized by the presence of purulent interstitial nephritis, glomerulonephritis. Characteristically was revealing in slides in a number of different sections of the largest abscesses and infarctions. There was parenchymal degeneration of the epithelium of the convoluted tubules, was dead at 3 necrotizing nephrosis.
The brain is constantly detected subarachnoid hemorrhage. Microscopic examination of the intraorgan vessels defined infected blood clots, and in 4 cases found small abscesses in the white brain matter, containing sticks of blue-green pus. Pia mater was edematous it contained large cell round with a mixture of leukocyte infiltration.
The spleen was dramatically increased in size gave abundant scraping. Microscopy showed hyperplasia of reticular cells and plasm cells, a large amount of granular contents of leukocytes and destructed erythrocytes. There was identified different focuses of infarctions.
Adrenal insufficiency was the cause of death in 3 patients (3.3%). It should be noted that its development in the postoperative period in patients with rheumatic heart disease there is a "favorable" background. Also it is due to the phenomena of chronic stagnation in the systemic circulation and on the other - the phenomena of disorganization
of connective tissue and its subsequent scarring. Morphologically, these processes are expressed in the reduction of the number of parenchymal elements of the adrenal cortex and increased development of the stroma. The impetus for the development of adrenal insufficiency in 2 patients were bleeding into the adrenal glands (1 patient operation took place under conditions of artificial blood circulation), and 1 - stress reaction took place against the background discreetly flowing adrenal insufficiency. Clinically, in all cases severe hypotension and heart rhythm disorder were observed. Thus, from three clinical forms adrenal insufficiency: gastrointestinal, brain, cardiovascular, we met only last form - cardiovascular. Histological manifestations were delipoidisation of cortical cells, necrobiosis of parenchymal cells of the adrenal cortex.
Thromboembolic complications occurred in 11 cases. 3 persons have occurred embolism branches of the superior mesenteric artery, leading to gangrene of the intestine and the development of peritonitis. The source of emboli in all cases was warty overlay on the mitral valve. One patient died on 5th days after electroimpuls therapy, the other -on 4th day after closed mitral commissurotomy, at the third patient complication came a year after the elimination of mitral stenosis. Eight patients died from embolism of cerebral vessels. It was found that in 4 cases a source of embolism was warty endocarditis of the mitral valve and calcification of the mitral valve, thrombosis of the left atrial auricle and left atrial thrombi. In 2 cases there was an air embolism of cerebral vessels in the manufacture of surgical interventions on the "open-heart" with cardiopulmonary bypass. Thrombotic emboli in all cases fall in arteries supplying the left hemisphere of the brain, while the air - in both cases were in the vessels supplying the right brain. Emboli cannot always be found in the lumen of the vessel. In such cases indirectly say about this complication detected foci of softening of the white matter of the brain. Air emboli at autopsy we found in both cases, both at macro and microscopic studies. At suspection on an air embolism in the first place been opened cranial cavity and carefully remove the dura mater. The air was detected in the arch and in the vascular plexus. Histologically it drew attention to the presence of the vessel lumen air bubbles surrounded by a zone of increased coagulation of blood plasma.
One patient died from a massive subdural hemorrhage in the brain on the fifth day after the surgery mitral valve replacement.
Bleeding and acute hemorrhagic anemia
caused the death in 12 cases. Bleeding occurred in 6 cases after surgical interventions carried out against the background of artificial haemophilia and in 6 cases after closed instrumental comissurotomy. The causes of bleeding in 9 cases had defects of surgical benefits associated with inadequate hemostasis and large vessels damage. In 2 cases there was served as the source of the bleeding wound of an intercostal artery during their intensive care in the postoperative period. Finally, in one case it was set intrapleural bleeding from crossed adhesions.
Acute liver failure was fatal complication at 4 patients. In all cases, it was combined with renal insufficiency. In 3 patients this type of complications developed after surgery performed with cardiopulmonary bypass, at 1 - after closed mitral commissurotomy. In 2 cases renal and hepatic failure occurred after massive blood transfusion: 2350ml and 3500ml. In 2 patients complications due to inadequate perfusion were developed.
Thus on the basis of the above revealed that the most frequent among the postoperative complications are cardiac insufficiency, about 43.8% due to traumatic injury valves. Acute heart failure is about 32.5%.
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