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Infectious Diseases · Infections of the Integumentary System and Sepsis

Diagnosis of sepsis

Sepsis

Diagnosis of sepsis is based on a triad: identifying the infection source, the presence of systemic inflammatory response syndrome (SIRS), and clinical and laboratory signs of internal organ dysfunction. Identifying the causative agent in blood or other biosubstrates prior to initiating antibiotic therapy is of critical importance.

Main ruleBiomaterial for culture must be collected strictly before prescribing etiotropic antibiotic therapy.
MarkersProcalcitonin (≥10 ng/L), presepsin (P-SEP), and neutrophil CD64.
TacticsWhen sepsis is suspected, overdiagnosis is preferable to underestimating the severity of the condition.
VerificationIf opportunistic flora is isolated, the culture must be re-plated to rule out error.
4 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 criteria and septic syndrome

The diagnosis is considered confirmed if the patient simultaneously presents with three main criteria. First, the primary infection source, which determines the nature of the process. Second, systemic inflammatory response syndrome (SIRS), an indicator of inflammatory mediators entering the systemic circulation. Third, signs of organ and system dysfunction, confirming the spread of pathology beyond the portal of entry.

Typical septic syndrome manifests as acute hectic fever with wide daily fluctuations. During the temperature rise, the patient experiences severe chills, and during its drop, intense heat and profuse sweating. Intoxication progresses. Organ dysfunction manifests as hepatosplenomegaly, the development of multisegmental pneumonia, infective endocarditis, arthritis, or osteomyelitis. Hemorrhagic or pustular rashes frequently appear on the skin and mucous membranes. An unwritten rule applies in clinical practice: in the presence of an obvious purulent focus (e.g., phlegmon) and the sudden onset of septic syndrome, overdiagnosis is preferred to avoid losing time before shock develops.

Laboratory diagnostics

Tests help assess the scale of systemic inflammation and the degree of target organ damage.

  • Complete blood count (CBC): The classic picture in acute sepsis (septicopyemia) includes marked neutrophilic leukocytosis with a left shift and a significant increase in ESR. However, in fulminant forms, especially those caused by Gram-negative flora, leukopenia and neutropenia may be observed. Anemia and thrombocytopenia (down to 5–25 thousand/µL) are frequently detected, indicating the threat of DIC syndrome.
  • Biochemical analysis: A drop in albumin levels (up to the development of edema-ascites syndrome) and immunoglobulins is characteristic. Liver and kidney damage is reflected by a moderate increase in transaminases (AST, ALT), GGT, LDH, CK, alkaline phosphatase, as well as high levels of creatinine and urea. Bilirubin rises moderately: the direct fraction in cholestasis, and the indirect fraction in hemolysis.
  • Specific markers: The main indicator is a positive procalcitonin test (values of 10 ng/L and above). New markers have high diagnostic value: presepsin (P-SEP) and neutrophil CD64. They are often used dynamically to monitor treatment efficacy.
  • Urinalysis (UA): Massive proteinuria, the appearance of casts, erythrocytes, and leukocytes are noted, and isolated bacteriuria is possible even without overt signs of nephritis.
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Bacteriological method

This is the primary reliable tool for confirming the diagnosis. The method consists of isolating a pure culture of the pathogen from blood, urine, cerebrospinal fluid, or pustular skin lesions.

A critically important nuance: biosubstrates are collected strictly prior to prescribing etiotropic antibacterial therapy. If the laboratory cultures opportunistic microflora, the procedure must be repeated. Only the repeated isolation of the same microorganism eliminates the risk of accidental sample contamination. In practice, specialists consult the current International Guidelines for Management of Severe Sepsis and Septic Shock.

Differential diagnosis

The difficulty in recognizing sepsis is due to the non-specificity of SIRS and the acyclic nature of the clinical course. Symptoms can mimic many pathologies accompanied by high fever, intoxication, and rashes.

  • Infectious diseases: Malaria (strict periodicity of febrile paroxysms, connection with endemic regions), leptospirosis (intense calf muscle pain, conjunctivitis), typhus (pronounced neurological symptoms, Rosenbergs-Chiari-Avtsyn enanthema), meningococcemia (rapidly progressing purpuric rash with necrosis), brucellosis, typhoid-paratyphoid diseases, and Q fever are ruled out.
  • Non-infectious processes: Septic-like syndrome accompanies severe pancreatitis, extensive burns, polytrauma, myocardial infarction, pulmonary embolism, occult bleeding, and adrenal insufficiency. The presence of these severe conditions significantly complicates the timely diagnosis of sepsis and the development of septic shock.

Briefly: answers to topical questions

What modern scales are used to assess the degree of organ dysfunction in sepsis?

To assess the degree of organ dysfunction in sepsis, the SOFA scale (Sequential Organ Failure Assessment) is used—a score for sepsis-related organ failure designed for the dynamic assessment of organ dysfunction in patients with sepsis in the ICU.

How to memorize

Diagnostic triad: FOCUS (source) + SIRS (systemic inflammatory response) + DYSFUNCTION (organ damage distant from the focus).

Class and exam questions

What specific blood markers are used to confirm sepsis?

The procalcitonin test is most commonly used (a result of 10 ng/L or higher is considered positive). New markers—presepsin (P-SEP) and neutrophil CD64—also show high informativeness.

How does the leukocyte formula change in severe sepsis?

In a classic acute course, neutrophilic hyperleukocytosis with a left shift is observed. However, in fulminant sepsis (especially Gram-negative), the picture may paradoxically change to leukopenia and pronounced neutropenia.

Why is a repeat bacteriological examination necessary when flora is cultured?

If opportunistic flora is isolated, a repeat culture is critically important to confirm the true role of the pathogen in the development of sepsis and to rule out accidental sample contamination in the laboratory.

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What else to study on this topic

  • Clinical forms of sepsis: acute infective endocarditis, fulminant sepsis, and acute sepsis.
  • Features of the localization and development of metastatic foci in septicopyemia.
  • Pathogenesis and early signs of infectious-toxic shock (ITS).
  • Specifics of the clinical course of sepsis against the background of immunodeficiency ("pauci-symptomatic" forms).
  • Principles of choosing empiric antibacterial therapy depending on the localization of the primary focus.

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