Sepsis

For medical students2 min readUpdated 2026-10-10

Sepsis is a severe generalized infection developing against the background of altered immune reactivity. In pathology, several distinct forms of the disease are distinguished, among which septicopyemia and septic (bacterial) endocarditis are of primary importance.

PathogensMost commonly staphylococci and streptococci, less frequently Gram-negative flora and fungi

Blood culturesYield positive results in only one-third of cases in septicopyemia

Cardiac involvementIn endocarditis, the mitral (40%) and aortic (30%) valves are most commonly affected

Difference from feverPurulent-resorptive fever is treated by source debridement; sepsis is not always resolved this way

Septicopyemia

This is a form of sepsis in which the generalization of the process occurs via metastatic spread of pus. Pathogenetically, septicemia may serve only as a short preceding stage of this condition.

A key feature of septicopyemia is the presence of a purulent septic focus at the portal of entry of the infection, 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. Important feature: a connective tissue capsule fails to form around these septic abscesses for a very long time.
Cardiac involvement: acute septic polypous-ulcerative endocarditis develops with purulent deposits on the valves (in contrast to bacterial endocarditis, where suppuration is absent).
Changes in immunogenesis organs: marked splenomegaly (spleen weight reaches 500–1,500 g). The capsule is tense, and the pulp yields abundant scraping ("septic spleen"). Hyperplasia is observed in the lymph nodes and bone marrow.
Parenchyma and vessels: systemic vasculitis with hemorrhagic syndrome, fatty change (steatosis) of organs against the background of progressive hypoxia and intoxication.

Septic (Bacterial) Endocarditis

This is an independent form of sepsis in which the primary focus is localized on the heart valve cusps. Two main forms are distinguished:

Primary (Chernogubov's disease) — develops on intact (unaltered) valves, occurring in 25% of cases.
Secondary — arises against the background of prior diseases, most commonly rheumatic valve disease (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 (ICs) and hypersensitivity reactions. Microorganism colonies, foci of necrosis, and polypoid thrombotic deposits are visible on the valve cusps. Macrophage infiltration forms around them, while neutrophilic leukocytes are absent. The process may be complicated by cusp perforation, valve avulsion, and thromboembolic syndrome.

Characteristic tetrad of lesions in endocarditis:

Valvular endocarditis.
Vasculitis (including cerebral microaneurysms, Janeway lesions on the skin, and Osler's nodes / Roth spots / Lukin-Libman spots on the mucosa).
Renal involvement (immune complex diffuse glomerulonephritis) and splenic 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 seen in severe injuries to large bones. Due to the constant absorption of pus and toxins, prolonged intoxication, protein loss, and traumatic exhaustion develop. Secondary amyloidosis frequently supervenes.

Differences from Sepsis: Purulent-resorptive fever lacks the defining feature of sepsis — distinctive hyperergy. Furthermore, if the purulent focus is surgically debrided in a timely manner (e.g., via amputation), mortality drops sharply. In true sepsis, removing the focus often fails to halt disease progression. In modern practice, the only form of sepsis that runs a protracted chronic course is recognized as 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 protracted and wave-like.
A connective tissue capsule now successfully forms around abscesses.
Alterative-exudative vasculitides have been replaced by chronic productive vasculitides (leading to vascular sclerosis).
In the treatment of endocarditis, management shifts focus from combating the infection itself to treating acquired heart defects, immune complex glomerulonephritis, and multiple organ dysfunction syndrome (MODS).

Mnemonic

To memorize the tetrad of lesions in bacterial endocarditis, use the acronym "EVPT": Endocarditis, Vasculitis, Renal/splenic involvement, Thromboembolic syndrome.

Frequently asked questions

What specific renal changes develop in protracted bacterial endocarditis?

In protracted bacterial endocarditis, the following changes develop in the kidneys:

Immune complex diffuse glomerulonephritis.
Diffuse proliferative glomerulonephritis as a manifestation of immune reactions.
Renal infarcts associated with thromboembolism; suppuration of infarcts does not occur despite the pyogenic nature of the emboli.
Post-infarction scars.

Additionally, subacute infective endocarditis can cause secondary nephrotic syndrome.

What clinical and anatomical forms of sepsis are distinguished based on the localization of the portal of entry?

Depending on the localization of the primary focus and portal of entry, historical forms of sepsis include:

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 adnexa.
Umbilical — the focus is localized in the umbilical stump.
Tonsillogenic — the source is in the tonsils or oral cavity.
Odontogenic — associated with caries and its complications.
Otogenic — arises from 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 largely replaced by etiology-based approaches.

What pathogenetic stages and morphological changes are characteristic of septic shock?

Pathogenetic mechanisms include the release of predominantly endotoxins, activation of the complement, coagulation, and fibrinolysis systems, and stimulation of nitric oxide and cytokine production. This leads to acute circulatory failure; severe cases show tissue hypoperfution and DIC syndrome.

Morphological changes include:

Microcirculatory disturbances: stasis, blood sludging, vascular endothelial damage.
Diapedetic hemorrhages and pronounced hemorrhagic syndrome.
Multiple small foci of necrosis.
Changes in "shock organs": in the kidneys — ischemic cortex and hyperemic medulla; in the lungs — "shock lung" with coalescing multiple hemorrhages.

How do septic abscesses in septicopyemia differ from regular abscesses?

In septicopyemia, a connective tissue capsule fails to form around embolic abscesses for a very long time, distinguishing them from abscesses of other etiologies.

How do you distinguish acute septic endocarditis in septicopyemia from bacterial septic endocarditis?

In septicopyemia, purulent deposits form on the valves. In primary bacterial endocarditis, the septic focus exhibits thrombotic deposits without neutrophilic leukocytes.

What are Osler's nodes and what are they characteristic of?

They are the result of microembolism of vessels in the palmar surface of the hands, accompanied by inflammation and sclerosis. They are a characteristic sign of subacute and protracted septic endocarditis.

Go deeper

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