SEPSIS

SEPSIS

Sepsis is general infectious disease caused by infections getting into the organism and differs from other infectious diseases.

·        Sepsis is severe disease with high lethality. The death rate in sepsis is very high. The incidence of sepsis has increased recently which is associated with the appearance of antibiotic-resistant strains of bacteria and administration of cytostatic preparations causing immune system insufficiency.

·        Epidemiological feature is polyetiology (except viruses), not infectious illness. Sepsis may be cause by different causative agents (staphylococci, streptococci, pneumococci, meningococci, blue pus bacilli, tuberculosis mycobacteria, typhoid bacilli, fungi and other agents, except for viruses).

·        Sepsis is not contagious; it cannot be reproduced experimentally.

·        Clinical features - irrespective of the character of the activator displays of illness are stereotyped, are stipulated by generalization of infection and inadequate reaction of organism on the infection.

·        The course of the disease is not cyclic, as it is observed in many infections.

·        There is no certain incubate period. The duration of the disease is different (from some days to several months and even years), that is why some forms of the disease may be defined, i.e. very acute, acute, subacute, and chronic.

·        Immunologic peculiarity of the sepsis is that immunity is not formed at this disease; inadequate reaction on the activator develops, hyperergic reaction prevails.

·        Morphological feature is the fact that the local and general changes have no specific features as it is observed in many infections.

Pathogenesis

·        Sepsis is a special form of interaction of macro- and microorganism, significance of which is equivalent.

·        Hyperergic reaction of the organism on infects and absence of immunity stimulates generalization of infection, acyclic course, prevalence of general reaction and losses of the ability to locate infection.

Morphology

1. Local changes.

·        Local changes occur by the primary focus of infection (portal of entry) or at some distance, in some cases it is absent.

·        Usually it is a focus of purulent inflammation, sometimes with no changes.

·        The infection propagates from the focus through the lymph and blood vessels.

·        Lymphangitis, lymphothrombosis and lymphadenitis, but also phlebitis and thrombophlebitis quickly develop.

·        There is purulent thrombophlebitis, progressing to thrombobacterial embolism.

2. General changes

·        General changes at sepsis have degenerative, inflammatory and hyperplastic character.

·        Degenerative changes develop in parenchymatous organs and often finish by the necrosis.

·        The inflammatory processes in parenchymatous organs and vessels occur.

·        Inflammatory changes are represented by interstitial septic nephritis, hepatitis, myocarditis, and acute polypous-ulcerative endocarditis with the tissue melting and tearing off of the valve.

·        Vasculitis, intoxication, increasing of vascular permeability, anemia stimulates the hemorrhagic syndrome.

·        Hyperplastic processes develop in blood-creating and lymphatic tissues.

·        Hyperplastic processes in sepsis are observed mainly in the hemopoietic and lymphoid tissue.

·        Bone marrow hyperplasia occurs in the flat bones. The yellow bone marrow of the tubular bones becomes red.

·        In blood leukocytosis and, sometimes, immature leukocytes are found, the so-called leukemoid reaction develops.

·        Peripheral lymphonodes are increased; spleen is acutely increased, flabby on cut and of red color. Spleen produces large scrap of pulp (“septic splenitis”).

·        Hyperplastic processes in histiocyte-macrophage system are the cause of the liver enlargement.

·        Hemolytic jaundice may result from hemolytic action of some bacterial toxins.

Classification of sepsis

A number of features are taken into account in classification.

I. According to the etiology: staphylococcal, blue pus bacillus and association of these microorganisms, meningococcal, pneumococcal, gonococcal, colibacillary, anthracic, tuberculous.

II. According to portal of entry of infectious agent (location of the septic focus).

·        Therapeutic (parainfectious).

·        Tonsilogenic sepsis.

·        Surgical.

·        Uterine.

·        Otogenic.

·        Odontogenic.

·        Umbilical.

·        Pulmonary.

·        Cryptogenous (portal of entry of infectious agent is absent).

III. According to the clinical-morphologic forms of sepsis: septicemia, septicopyemia, septic endocarditis and chronic septicemia.

Septicemia

·        It is a form of sepsis, for which toxicosis (high temperature, delirium) are characteristic, increased reactivity of organism (hyperergia), absence of purulent metastases and rapid course.

·        The etiology is frequently streptococcus.

·        Primary septic focus is frequently absent.

·        The skin and sclera are usually yellow (hemolytic jaundice).

·        Hemorrhagic syndrome is well pronounced (petechial rash, hemorrhages to the serous and mucous membranes and internal organs).

·        Hyperplasia of lymphoid and hemopoietic system is typical: the spleen is enlarged, with pulp scraping (“septic spleen”). The lymph nodes are also enlarged.

·        Proliferation of lymphoid and reticular cells as well as accumulation of mature and immature blood cells are found in the spleen and lymph nodes.

·        Increased hemopoiesis with formation of a large number of immature forms is noted in the bone marrow of the flat bones and in the diaphyses of the bones.

·        The foci of extramedullar hemopoiesis appear.

·        Interstitial inflammation develops in the parenchymal organs (heart, liver, kidneys). The stroma of the organs is edematous; infiltration by neutrophils, lymphocytes, and histiocytes is noted.

·        Septicemia is also characterized by increased vascular permeability, fibrinoid changes in the vessels, allergic vasculitis that is responsible for hemorrhagic syndrome.

Septicopyemia

·        It is the form of sepsis, main attributes of which are purulent processes in the entrance of infection and bacterial embolism with formation of abscesses in many organs and tissues.

·        In contrast to septicemia, hyperergy signs are moderate; the course of the disease is not very acute.

·        The development is assosiated with staphylococcus and blue pus bacillus.

·        At the dissection there is primary septic focus, it is usual in the entrance of infection with purulent lymphangitis and lymphadenitis.

·        The purulent thrombophlebitis in the primary septic focus is a source of thrombobacterial embolism, which causes the creation of metastatic abscesses in organs.

·        At first metastatic abscesses appear in the lungs, then in the liver, kidneys (apostematous nephritis), subcutaneous fat, bone marrow (purulent osteomyelitis), synovial membranes (purulent arthritis), the heart valves (acute septic polypous-ulcerative endocarditis).

·        Besides, purulent pleuritis and pericarditis develop in the cases of lung abscess. In liver abscess, purulent peritonitis develops. Kidney abscesses are complicated with peri- and paranephritis; skin abscess is complicated with phlegmon.

·        Hyperplastic processes in blood-creating lymphatic tissue are expressed more poorly. The lymphatic nodes are not increased.

·        Spleen is septic.

·        Interstitial inflammation in parenchymatous organs is moderate or is absent.

Septic (bacterial) endocarditis

·        It is the form of sepsis, for which septic lesion of valves of the heart is characteristic.

·        Hyperergia occurs and it can be considered to be bacterial septicemia.

·        The presence of primary septic focus on valves of the heart stimulates hyperergic damage of cardiac - vascular system.

·        The most often causative agents are staphylococcus albus, aureus, streptococcus viridian, and enterococcus.

·        In the basis of hyperergia reactions of hypersensitivity lays, stimulated by toxic immune complexes circulating in the blood, containing antigen of activator and causing to generalized vasculitis.

·        Increasing of vascular pemerability, thromboembolic syndrome, cellular reactions of stroma are marked.

Classification

According to the character of course:

·        Acute (about 2 weeks).

·        Subacute (till 3 months).

·        Chronic (months and years).

Depending on the presence of the background disease, septic endocarditis (especially subacute and acute) is divided into 2 types:

·        On unchanged valves (intact valves) -primary septic endocarditis (Chernogybov’s disease), in 20- 30 % of cases.

·        Developed on changed valves (defective) - secondary septic endocarditis in 70-80 % of cases.

Morphology

·        Polypous-ulcerative endocarditis develops on both sclerotic and intact valves.

·        Large thromboembolic polyp-shaped plaques appear on sclerotic valves.

·        The plaques are easily crumbled and are saturated with calcium, which is characteristic for the disease.

·        After removal of the plaques, ulcerative defects are seen in the sclerotic and deformed cusps of the valves.

·        Thrombotic plaques are located not only on the cusps but also on the parietal endocardium.

·        When the aortic valves are injured, the disease involves the aortic intima.

·        The spleen is enlarged due to prolonged pulp hyperplasia; there are infarcts in the organ.

·        Immune-complex diffuse glomerulonephritis develops in the kidneys. Infarctions and postinfarction scars are frequently observed.

·        Interstitial inflammatory processes, vasculitis, hemorrhages, infarctions are observed in different organs.

·        The foci of softening and hemorrhages are observed in the brain due to vascular changes (vasculitis, aneurysm) and thromboembolism.

·        The so-called peripheral signs of septic endocarditis are

a) Petechial hemorrhages in the conjunctiva near the internal angle of the lower eyelid (“Lukin-Libman spots”).

b) Nodular thickening on the palm surface of the hand (“Osler’s nodes”).

c) Thickening of the nail phalanges (“drum sticks”).

d) Necrotic foci in the subcutaneous fat.

e) Hemorrhages to the skin and subcutaneous fat (Jeinway’s spots).

f) Jaundice.

·        Thromboembolic complications are frequent, as the source of thromboembolism; thromboendocarditis is most commonly localized in the left heart.

·        Thromboembolism frequently becomes generalized and dominates in the clinical picture of the disease.

·        The embolisms give the rise to infarctions in the lungs, spleen, kidneys, retina, and skin necrosis, gangrene of the extremities, intestine, foci of softening in the brain.

·        In spite of the presence of streptococci in the thrombi, suppuration in the tissue is absent which suggests hyperergic reaction of the organism in septic endocarditis.

Chronic septicemia

·        This form of sepsis is characterised by durably availability, not healing primary septic focus.

·        These septic foci can be found in carious teeth, tonsils but more frequently they are large suppurations resulting from wounds.

·        Extensive purulent processes, causing to intoxication, progressing exhaustion (cachexia) and amyloidosis take place.

·        In organs and tissues there is atrophy, dehydration are expressed.

·        Brown atrophy is found in the liver, myocardium, and striated muscles.

·        The spleen is decreased.