Septicopyemia
This is a form of sepsis in which the generalization of the process occurs through metastatic spread of pus. Pathogenetically, septicemia may only be a brief preceding stage of this condition.
The key sign of septicopyemia is the presence of a purulent septic focus at the portal of entry of the infection, which is accompanied by purulent thrombophlebitis, lymphangitis, and lymphadenitis.
Main morphological manifestations:
- Purulent metastases: embolic abscesses containing the pathogen appear in the kidneys, bone marrow, liver, and lungs. An important feature: a capsule does not form around these septic abscesses for a very long time.
- Cardiac involvement: acute septic polypous-ulcerative endocarditis develops with purulent deposits on the valves (unlike bacterial endocarditis, where there is no suppuration).
- Changes in immunogenesis organs: pronounced splenomegaly (spleen weight reaches 500–1500 g). The capsule is tense, the pulp yields abundant scrapings ("septic spleen"). Hyperplasia is observed in the lymph nodes and bone marrow.
- Parenchyma and vessels: systemic vasculitis with hemorrhagic syndrome, fatty degeneration of organs against the background of increasing hypoxia and intoxication.
Septic (bacterial) endocarditis
This is an independent form of sepsis in which the primary focus is localized on the leaflets of the heart valves. Two main forms are distinguished:
- Primary (Chernogubov's disease) — develops on intact (unchanged) valves, occurring in 25% of cases.
- Secondary — develops against the background of prior diseases, most commonly rheumatic valve involvement (about 70% of cases), as well as atherosclerosis, syphilis, or congenital malformations.
Pathogenesis and local changes The disease is based on the circulation of immune complexes (CIC) and hypersensitivity reactions. Microorganism colonies, foci of necrosis, and polypoid thrombotic deposits are visible on the valve leaflets. Macrophage infiltration forms around them, while neutrophilic leukocytes are absent. The process may be complicated by leaflet perforation, valve rupture, and thromboembolic syndrome.
Characteristic tetrad of lesions in endocarditis:
- Valvular endocarditis.
- Vasculitis (including microaneurysms in the brain, Janeway lesions on the skin, and Osler's nodes / Libman–Sacks spots on the mucosa).
- Kidney damage (immune-complex diffuse glomerulonephritis) and spleen involvement.
- Thromboembolic syndrome (infarcts without suppuration).
Purulent-resorptive fever and chronosepsis
The term "purulent-resorptive fever" was proposed by I.V. Davydovsky to describe the condition in severe injuries to large bones. Due to the continuous absorption of pus and toxins, prolonged intoxication, protein loss, and traumatic exhaustion develop. Secondary amyloidosis frequently joins.
Differences from sepsis: In purulent-resorptive fever, the main feature of sepsis — peculiar hyperergy — is absent. Furthermore, if the purulent focus is sanitized in time (e.g., by amputation), mortality drops sharply. In true sepsis, removal of the focus often does not halt the progression of the disease. In modern practice, the only form of sepsis running a chronic course is recognized to be subacute bacterial endocarditis (sepsis lenta).
Therapeutic pathomorphosis of sepsis
The widespread use of antibiotics and modern detoxification has altered the clinical and morphological picture of sepsis:
- The course of septicopyemia has become prolonged and wave-like.
- Connective tissue capsules now manage to form around abscesses.
- Alterative-exudative vasculitides have been replaced by chronic productive ones (leading to vascular sclerosis).
- In the treatment of endocarditis, combating acquired heart defects, immune-complex glomerulonephritis, and multiple organ failure comes to the forefront rather than fighting the infection itself.
Briefly: answers to topical questions
What specific renal changes develop in subacute bacterial endocarditis?
In subacute bacterial endocarditis, the following develop in the kidneys:
- Immune-complex diffuse glomerulonephritis.
- Diffuse proliferative glomerulonephritis as a manifestation of immune reactions.
- Renal infarcts associated with thromboembolic syndrome; suppuration of the infarcts does not occur within pyogenic infection thromboemboli.
- Post-infarction scars.
Also, subacute infective endocarditis can be a cause of secondary nephrotic syndrome.
What clinical and anatomical forms of sepsis are distinguished depending on the localization of the infection's portal of entry?
Depending on the localization of the primary focus and the portal of entry, the following historical forms of sepsis are distinguished:
- Therapeutic (parainfectious) — develops against the background of other diseases.
- Surgical (wound) — the portal of entry is a wound (including burn sepsis).
- Uterine (gynecological) — the source is located in the uterus or appendages.
- Umbilical — the focus is localized in the umbilical stump.
- Tonsillogenic — the source is in the tonsils or oral cavity.
- Odontogenic — associated with dental caries and its complications.
- Otogenic — occurs in purulent otitis media.
- Urogenital — the focus is in the kidneys or urinary tract.
- Cryptogenic — the source and portal of entry are unknown.
In modern clinical practice, this classification is not used.
What pathogenesis stages and morphological changes are characteristic of septic shock?
The sources do not single out separate stages of septic shock pathogenesis. The following mechanisms are described: release predominantly of endotoxins, activation of complement, coagulation, and fibrinolysis systems, and stimulation of nitric oxide and cytokine production. This leads to acute circulatory failure; in severe cases, tissue hypoperfusion and DIC syndrome are noted.
Morphological changes include:
- Microcirculatory disorders: stasis, blood sludging, vascular endothelial damage.
- Diapedetic hemorrhages and pronounced hemorrhagic syndrome.
- Small multiple foci of necrosis.
- Changes in "shock organs": in the kidneys — an ischemic cortex and hyperemic medulla; in the lungs — "shock lungs" with coalescing multiple hemorrhages.
To memorize the tetrad of lesions in bacterial endocarditis, use the acronym "EVPS": Endocarditis, Vasculitis, Renal/splenic lesions, Thromboembolic syndrome.
Class and exam questions
What is the difference between septic abscesses in septicopyemia and regular abscesses?
In septicopyemia, a connective tissue capsule does not form around embolic abscesses for a very long time, which distinguishes them from abscesses of other etiologies.
How to distinguish acute septic endocarditis in septicopyemia from bacterial septic endocarditis?
In septicopyemia, purulent deposits form on the valves. In primary bacterial endocarditis, thrombotic deposits without neutrophilic leukocytes are present in the septic focus.
What are Osler's nodes and what conditions are they characteristic of?
This is the result of microembolism of the vessels of the palmar surface of the hands with the development of inflammation and sclerosis. A characteristic sign of subacute and protracted septic endocarditis.
What else to study on this topic
- Morphological characteristics of «shock lungs» in sepsis
- Features of immune complex glomerulonephritis in septic endocarditis
- Pathogenesis of thromboembolic syndrome in bacterial endocarditis
- Causes and mechanisms of traumatic exhaustion in purulent-resorptive fever
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