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Complications of purulent infection

Sepsis

Local purulent-inflammatory processes are capable of progressing into a generalized form, causing severe complications up to mediastinitis, meningitis, and sepsis. The progression of the infection is promoted by altered virulence of the flora and an inadequate hyperergic immune response.

Microbial associationsMost commonly, inflammation is caused by a combination of 3–4 strains of aerobic and anaerobic bacteria.
Occult bacteremiaIn septicopyemia, microorganisms can be cultured in only 1/3 to 1/4 of all blood cultures.
MortalityBefore the antibiotic era, it reached 80% in purulent phlegmon; now it has decreased to 15%.
Septic spleenIn sepsis, the spleen yields abundant pulp scrapings, and its weight can reach 1,500 grams.
4 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Odontogenic infections and their threats

Purulent-inflammatory diseases of the maxillofacial region remain a serious problem in purulent surgery. In 90–96% of cases, the infection is of odontogenic or stomatogenic origin, and only a small fraction is associated with hematogenous or lymphogenous spread.

The irrational use of antibacterial drugs has led to changes in the properties of pathogenic microflora. Today, inflammation is more commonly caused by microbial associations containing both aerobes and anaerobes. Entering into synergistic relationships, bacteria increase the severity of the disease, reduce treatment efficacy, and contribute to the chronization of the process. In unfavorable cases, formidable complications arise: mediastinitis, facial vein thrombophlebitis, meningitis, and sepsis.

Clinical and anatomical forms of sepsis

Sepsis is a systemic hyperergic reaction to infection with profound microcirculatory impairment. According to its rate of development, it can be fulminant, acute, subacute, and chronic. There are four main clinical and morphological forms:

  • Septicemia
  • Septicopyemia
  • Bacterial (septic) endocarditis (as an independent form)
  • Chronic sepsis (sepsis lenta)
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Septicemia: toxic-allergic shock

Septicemia is an acute form of sepsis without the formation of purulent metastases. Gram-negative microflora play a leading role in its pathogenesis. Patients develop severe endotoxemia and a systemic inflammatory response leading to septic shock: blood pressure drops, tissue perfusion suffers, and DIC syndrome and multiple organ failure progress. Due to vasculitis with fibrinoid necrosis, hemorrhagic syndrome is prominent.

Why doesn't pus form? The disease runs a fulminant course, and the patient often dies within 1–3 days. Metastases do not have time to form, and the body loses the ability to mount an adequate leukocytic response (incomplete phagocytosis predominates in neutrophils — endocytobiosis). For the same reason, neither splenic nor lymph node hyperplasia has time to develop.

Septicopyemia: generalization with metastases

Septicopyemia is characterized by the presence of purulent metastases and a less violent allergic reaction. It is most often caused by Gram-positive flora (staphylococci, streptococci) as well as Candida fungi. The key sign of this form is the presence of a primary purulent focus at the entry gate, accompanied by purulent lymphangitis and thrombophlebitis.

Via the bloodstream, pus spreads through the body, forming embolic abscesses:

  1. In the kidneys (embolic purulent nephritis).
  2. In the bone marrow (osteomyelitis).
  3. In the liver and lungs (suppuration of infarcts, pleural empyema).

A feature of such metastases is the prolonged absence of a protective capsule around the abscess. Heart involvement is characteristic in the form of acute septic polypous-ulcerative endocarditis with purulent deposits on the valves. In immunopoietic organs, pronounced hyperplasia is observed: a tense "septic spleen" with myeloid metaplasia is formed.

Purulent-resorptive fever vs. Sepsis

Previously, chronic purulent exhaustion was mistakenly equated with chronic sepsis. Today, purulent-resorptive fever is recognized as an independent disease. Its main difference is the secondary nature of immune suppression against the background of constant intoxication without true septic hyperergy.

Differential diagnosis is based on two principles:

  • Response to sanitation: in purulent-resorptive fever, removal of the focus rapidly improves the patient's condition; in sepsis, surgical sanitation often no longer affects the generalized course.
  • Symptom correlation: the severity of general symptoms and fever in purulent-resorptive fever strictly depend on the status of the primary focus, whereas in sepsis no such relationship exists.
How to memorize

To avoid confusing the two acute forms of sepsis, pay attention to the roots: Septicemia — emphasis on "cemia" (blood, toxins, fulminant shock, hemorrhages), no purulent metastases. Septicopyemia — emphasis on "pyemia" (pus), a primary purulent focus and purulent metastases throughout the body are invariably present.

Class and exam questions

What is cryptogenic sepsis?

This is a diagnosis established when clinicians or pathologists fail to detect the primary septic focus that served as the entry gate for the infection.

Why is endocarditis in septicopyemia distinguished from bacterial endocarditis?

Acute polypous-ulcerative endocarditis in septicopyemia is characterized by specific purulent deposits on the heart valves — a direct consequence of pus metastasis. Independent bacterial endocarditis has a different pathogenesis.

What morphological changes occur in parenchymal organs during sepsis?

Due to severe intoxication, vascular lesions, and increasing hypoxia, pronounced fatty degeneration and interstitial stromal inflammation develop in parenchymal organs. The picture of "shock lung" with coalescent hemorrhages forms in the lungs.

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What else to study on this topic

  • Mechanisms of DIC syndrome and septic shock development in septicemia
  • Pathomorphology of "shock lungs" in adult respiratory distress syndrome
  • Macro- and microscopic picture of the "septic spleen"
  • The role of anaerobic flora in aggravating odontogenic inflammatory processes
  • Sepsis lenta: pathogenesis and morphology of subacute bacterial endocarditis

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