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Infectious Diseases · Infections of the Integumentary System and Sepsis

Classification of sepsis

Sepsis

Sepsis is an acyclic generalized infectious disease that develops upon the massive invasion of bacteria and their toxins from the primary focus into the bloodstream. The process unfolds against the background of decreased immunoreactivity of the body in the form of hyperergic systemic inflammation and leads to multiple organ dysfunction.

Diagnostic criteriaFocus of infection, signs of SIRS, and the development of organ-system dysfunction
Main pathogensOpportunistic flora, often aerobes from normal automicroflora
Key featureInability to self-cure and a progressive malignant course
Mortality rateRemains at 30–50% despite the development of therapeutic methods
5 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Clinical and morphological forms

According to the pathomorphological and clinical picture, the generalized process is traditionally divided into several main variants. The differences lie in the presence or absence of purulent metastases, as well as the nature of internal organ damage.

  • Septicemia. A form without the formation of secondary purulent metastases. Pronounced microcirculatory disorders, severe hemorrhagic syndrome (due to vasculitis and DIC syndrome), and damage to "shock organs" come to the foreground. Ischemia of the cortex is observed in the kidneys, distress syndrome with confluent hemorrhages in the lungs, and foci of necrosis and cholestasis in the liver.
  • Pyosepticemia. Characterized by the formation of purulent-inflammatory secondary (metastatic) foci in tissues. Patients exhibit abscesses of the brain, myocardium, lungs, embolic purulent nephritis, and suppurative thrombophlebitis.
  • Bacterial (septic) endocarditis. Distinguished as a separate form with predominant involvement of the valve apparatus (e.g., septic polypous-ulcerative endocarditis).
  • Chronic sepsis. A protracted variant of the infection's course.

Regardless of the form, general signs of severe intoxication include depression of hematopoiesis, dystrophy of parenchymatous organs, and fibrinoid necrosis of vessel walls.

Etiological Classification

Sepsis is a polyetiological disease without a specific pathogen. In most cases, opportunistic aerobes without strict organ specificity serve as the source.

  1. Gram-positive flora. The leading cause of the disease. Includes staphylococci, pneumococci, listeria, and $\beta$-hemolytic streptococcus. Metastatic abscesses (pyosepticemia) occur more frequently with this flora. Infectious-toxic shock develops relatively rarely, except for cases of infection with Staphylococcus aureus, which produces an aggressive enterotoxin.
  2. Gram-negative flora. This includes *Escherichia coli*, *Pseudomonas aeruginosa*, *Neisseria meningitidis*, and *Proteus*. It is characterized by an extremely severe intoxication syndrome. Shock in this type of sepsis occurs 4–5 times more frequently than in the Gram-positive variant.
  3. Nosocomial sepsis. A specific group of infections in ICU patients. The main culprits are non-fermenting Gram-negative bacteria: Pseudomonas aeruginosa, Klebsiella pneumoniae, Acinetobacter spp. Development is promoted by prolonged mechanical ventilation and the use of third-generation cephalosporins.
  4. Rare causative agents. In individuals with profound immunodeficiencies (radiation sickness, terminal stages, HIV), the disease can be caused by saprophytes (coagulase-negative staphylococci), pathogenic fungi (*Candida*, *Aspergillus*), and actinomycetes.
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Criteria for infection generalization

For a local purulent process to be classified as sepsis, the mere presence of bacteria in the blood (bacteremia) is not enough. According to modern approaches, the diagnosis is reliable in the presence of three fundamental criteria:

  • Presence of a focus. There is a primary infectious focus from which the dissemination of the pathogen and pro-inflammatory mediators occurs.
  • Systemic inflammatory response syndrome (SIRS). Indicates that toxins and inflammatory mediators have entered the systemic circulation, causing vascular dilation, fever, and changes in the blood formula.
  • Organ-system dysfunction. Serves as proof that the infectious-inflammatory process has spread far beyond the primary focus and begun to damage the body's own tissues due to tissue hypoxia and oxidative stress.

Risk factors and epidemiology

Classification of patients into risk groups also plays an important role in management tactics. The global incidence is continuously growing (from 17 to 19 million cases annually). This is associated not with an increase in microbial aggressiveness, but with a progressive decrease in population immunoreactivity.

The high-risk group includes extremely premature newborns, the elderly, patients with oncology and diabetes mellitus. A major iatrogenic factor is the expansion of the use of invasive devices: urinary and intravascular catheters, mechanical ventilation equipment, surgical prostheses, as well as the mass and sometimes indiscriminate use of antibiotics, immunosuppressants, and corticosteroids.

Briefly: answers to topical questions

What does systemic inflammatory response syndrome (SIRS) consist of?

Systemic inflammatory response syndrome (SIRS, or SIRS) occurs as a result of vascular dilation, hypotension, hypovolemia, tissue ischemia, febrile reaction, and inflammatory blood changes. It is a criterion for the penetration of inflammatory mediators into the systemic circulation. To confirm the syndrome, at least two of the four signs must be present:

  • Disorder of thermoregulation — fever above 38 °C (or 38.5 °C in children) or hypothermia below 36 °C.
  • Heart rate alteration — resting tachycardia > 90 beats per minute (bradycardia is possible in infants under one year old).
  • Respiratory rate alteration — resting tachypnea > 20 breaths per minute.
  • Shifts in the leukocyte formula — leukocytosis > 12 × 10⁹/L, leukopenia, or a qualitative left shift of the formula (immature forms exceed 10%).

Which scales are used to assess multiple organ failure in sepsis?

To assess multiple organ/organ-system dysfunction in sepsis, the SOFA scale (Sequential Organ Failure Assessment) is used; it is employed to determine the severity of organ-system disorders and for dynamic assessment of organ dysfunction in ICU sepsis patients.

To assess the overall severity of the patient's condition, sources also indicate APACHE II (Acute Physiology And Chronic Health Evaluation) and the SAPS system.

Class and exam questions

What is the main difference between septicemia and pyosepticemia?

In septicemia, there are no secondary purulent metastases; microcirculatory disorders, damage to "shock organs," and hemorrhagic syndrome predominate. In pyosepticemia, bacteria form secondary abscesses in various tissues (e.g., brain or lung abscesses).

Which flora more frequently leads to infectious-toxic shock?

Gram-negative flora (*Escherichia coli*, *Neisseria meningitidis*, etc.) causes the development of shock 4–5 times more frequently due to potent intoxication. Among Gram-positive bacteria, a high risk of shock is primarily associated with *Staphylococcus aureus* (Staphylococcus aureus).

Can sepsis be cured without medical intervention?

No, the disease is characterized by the inability to self-cure. Due to the failure of natural resistance systems, the body is unable to localize the infection, which leads to a progressive malignant course.

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What else to study on this topic

  • Pathogenesis of systemic inflammatory response syndrome (SIRS)
  • Mechanisms of development of multiple organ dysfunction syndrome (MODS)
  • Differential diagnosis with malaria, leptospirosis, and typhoid-paratyphoid infections
  • Principles of selecting empirical antibiotic therapy
  • Surgical tactics for the elimination of the primary septic focus

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