200. Pathological anatomy of septicemia and septicopyemia.

Septicemia is the most acute form of sepsis, which lasts 2-3 days and ends in death.

Septicemia is often associated with streptococcus. Upon autopsy of deceased patients from septicemia, the septic focus is usually absent or weakly expressed, the entrance gate of infection is not detected. The skin and sclera are often jaundiced (hemolytic jaundice), signs of hemorrhagic syndrome are clearly expressed in the form of petechial rash on the skin, hemorrhages in serous and mucous membranes, in internal organs. Moderate hyperplasia of lymphoid and hematopoietic tissues is characteristic, while the spleen is slightly enlarged, gives a small scraping of the pulp. In the spleen and lymph nodes, not only the proliferation of lymphoid and reticular cells is found, but also clusters of mature and immature forms of hematopoiesis cells. In the bone marrow of flat bones and the diaphysis of tubular bones, increased hematopoiesis is noted with the formation of young forms of hematopoiesis cells. Intrauterine inflammation develops in parenchymal organs — heart, liver, kidneys (see Fig. 24-36). The stroma of these organs is edematous and infiltrated by neutrophils, lymphocytes, and histiocytes. Septicemia is characterized by increased vascular and tissue permeability, fibrinoid changes in the walls of blood vessels, allergic vasculitis, which is largely associated with manifestations of hemorrhagic syndrome.

Septicopyemia is a form of sepsis, the leading signs of which are purulent processes at the gates of infection and bacterial embolism ("pus metastasis") with the formation of ulcers in organs and tissues. Unlike septicemia, hyperergia is moderate, and the course of the disease is relatively mild. The main role in the development of septicopyemia belongs to Staphylococcus and Pseudomonas aeruginosa. Upon autopsy of a patient who died of septicopyemia, as a rule, a septic focus is found, usually located at the gate of infection, with purulent lymphangiitis and lymphadenitis. Moreover, the lymph node is often in a state of purulent melting. In the area of the septic focus, purulent thrombophlebitis is found — a source of thrombobacterial embolism, often in the veins of a large circle of blood circulation. As a result, the first metastatic ulcers appear in the lungs. In pulmonary thrombophlebitis, ulcers appear in the organs of the large circulatory system — the liver (liver abscesses), kidneys (purulent nephritis), subcutaneous tissue, bone marrow (purulent osteomyelitis), synovial membranes (purulent arthritis), heart valves (acute septic polypous ulcerative endocarditis). Hyperplasia of lymphatic (immunocompetent) and hematopoietic tissues. The lymph nodes are moderately enlarged, but the spleen is typically septic, significantly enlarged, and myeloid metaplasia is observed in the spleen and lymph nodes. Interstitial inflammation in parenchymal organs is moderate or absent.

201. Acute infective endocarditis: pathomorphological characteristics, complications, causes of death in patients.

Acute infectious endocarditis (duration about 2 weeks).

The main changes concern the heart valves. Isolated valvular endocarditis prevails. Polypous ulcerative endocarditis occurs on sclerosed and non-sclerosed valves (Fig. 12-1). At the same time, extensive thrombotic overlays in the form of polyps usually appear on sclerosed valves, which easily crumble and are soaked with lime early, which is characteristic of this disease. After removal of these overlays, ulcerative defects are found in the sclerosed and deformed valve flaps, sometimes superficial, sometimes with a violation of the integrity of the valve, the formation of acute aneurysms of the flaps or their massive destruction. Thrombotic overlays are also located on the parietal endocardium, and when the aortic valves are affected, they spread to the intima of the aorta.

Microscopic examination reveals that the process begins with the formation of foci of valve necrosis, around which infiltration from lymphoid cells, histiocytes, and multinucleated macrophages is observed; neutrophils are absent or very few. Bacterial colonies are found among the infiltrate cells. Massive thrombotic overlays appear in the areas of necrosis, which are organized. The growing granulation tissue deforms the valves during maturation, which leads to the formation of a heart defect. If endocarditis has developed on the vicious valves, then their sclerosis increases. Hypertrophy of muscle fibers occurs in the myocardium, the severity of which in the walls of a particular cavity of the heart depends on the nature of the defect. Plasma impregnation and fibrinoid necrosis of the walls, endo- and perivasculitis are found in the myocardial vessels.

Complications: The formation of a heart defect, namely stenosis of the affected valve, however, since purulent melting is present, it is possible to detach the valve leaf, with a transition to insufficient valve function. Thromboembolism and tissue embolism are also possible, as a result of which abscesses form in other organs. Circulatory insufficiency, cardiac arrhythmias and conduction disorders.

Causes of death: heart failure, cerebral vascular thromboembolism, pulmonary vascular thromboembolism.