Causes and mechanism of development
The pathogenesis is based on the absorption (resorption) of toxic products of purulent-putrefactive tissue breakdown. The primary purulent focus always plays the triggering role. The process becomes generalized when the volume of accumulated pus is too large and the protective granulation barrier fails to contain the infection in time. Further spread occurs via hematogenous or lymphogenous routes.
Development of severe toxicosis is promoted by non-absorbable substrates in the wound:
- Necrotic tissues and bone sequestra.
- Crushed fascia and tendons.
- Foreign bodies (bullets, shrapnel, clothing fragments).
The presence of such objects without adequate drainage of purulent pockets and tracking constantly maintains the systemic reaction.
Clinical Forms
Depending on the clinical course and the presence of metastases, several variants are distinguished:
- Acute sepsis (septicemia). Characterized by a sharp onset in the presence of a primary abscess. It is accompanied by drenching sweats, chills, and high fever. Patients often develop yellowish discoloration (icterus) of the sclera and skin, and an enlarged liver and spleen (hepatosplenomegaly).
- Septicopyemia. The main diagnostic criterion is the appearance of secondary (metastatic) purulent foci in the subcutaneous tissue, skin, or lungs against the background of acute septicemia.
- Fulminant form. Symptoms progress catastrophically fast. Furuncles or carbuncles of the face often act as the primary source. Pronounced facial edema occurs (the eye on the affected side may close completely), the pulse accelerates to 120–140 bpm, and the temperature reaches 40 °C. Central nervous system disorders are characteristic: initial agitation is replaced by apathy, and loss of consciousness is possible by days 2–3.
Diagnostic features
The nature of the fever and laboratory parameters play a crucial role in making the diagnosis.
Temperature curve:
- In septicemia, the difference between morning and evening temperature is minimal (0.5–1 °C).
- In septicopyemia, the fever is undulating: opening a metastasis leads to a drop to subfebrile levels, while the formation of a new focus causes a spike to 39–40 °C.
- Chronic course produces an irregular curve without regular patterns.
Complete blood count: Blood changes are persistent and progressive. Anemia develops very rapidly (hemoglobin drops below 70–80 g/L, erythrocytes decrease to $3.0 \times 10^{12}$/L, anisocytosis and poikilocytosis appear). Against the background of neutrophilic leukocytosis ($8.0–15.0 \times 10^9$/L), lymphocytes and eosinophils drop sharply, down to anoxemia/aneosinophilia. ESR rises to 60–80 mm/h. Unfavorable signs: shift to the left (appearance of myelocytes and band/young forms) and toxic granulation of neutrophils.
Bacteriological culture: Blood testing is of high value, but a negative result does not refute the diagnosis. Blood sampling is performed strictly before starting antibiotic therapy (or 12 hours after drug administration), optimally at the peak of chills.
Complications and treatment
Prolonged systemic inflammatory response syndrome (SIRS) leads to multiple organ dysfunction. Interstitial nephritis, hepatitis, ulcerative-necrotic colitis, and splenomegaly develop. Abscesses, infarctions, or pneumonia may occur in the lungs.
Specific complications drastically worsen the prognosis:
- Bacterial-toxic (septic) shock. Acute circulatory failure due to the massive impact of toxins on cellular metabolism.
- Septic endocarditis. Primarily affects the bicuspid (mitral) valve. Detached thrombi can cause organ infarctions or limb gangrene.
- Septic hemorrhages. Can be diapedetic (due to increased vessel wall permeability) or arrosive (destruction of the vessel by pus).
Principles of treatment: The basis of therapy is timely surgical intervention. It is necessary to perform a complete debridement of the primary and secondary foci: excise non-viable tissues, open tracking, and ensure adequate drainage. Detoxification and antibacterial conservative therapy are applied only in conjunction with surgical treatment.
You can memorize the stages of the process's development by the acronym: Focus $\rightarrow$ SIRS $\rightarrow$ MODS $\rightarrow$ Metastases. First, a primary abscess appears, then a systemic inflammatory response, which progresses to multiple organ dysfunction syndrome and ends with the seeding of purulent metastases.
Class and exam questions
What is the difference between septicemia and septicopyemia?
Septicemia is characterized by acute toxicosis without the formation of secondary foci. In septicopyemia, against the background of acute infection, new purulent metastases form in various organs (skin, lungs), resulting in a characteristic undulating fever.
Does a sterile blood culture rule out the diagnosis of sepsis?
No. Bacteriological examination is very informative, but the absence of microbial growth in the test tube (especially if the patient has already started taking antibiotics) does not rule out the clinical diagnosis of generalized infection.
What belongs to unfavorable changes in blood tests?
A poor prognostic sign is the appearance of toxic granulation of neutrophils, the complete disappearance of eosinophils (aneosinophilia), and a severe left shift in the leukocyte formula with the appearance of myelocytes and young forms.
What else to study on this topic
- Pathogenesis and stages of bacterial-toxic shock
- Features of the development of septic endocarditis
- Mechanisms of diapedetic and arrosive hemorrhages
- Multiple organ dysfunction syndrome (MODS) in surgery
- Rules for primary surgical debridement of purulent wounds
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Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"
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