Composition and Properties of Purulent Exudate
Pus is a thick, creamy fluid with shades varying from bluish-green and a specific odor.
It consists of three main groups of components:
- Fluid phase: Formed from blood plasma. Contains albumins, globulins, biologically active substances, and complement components.
- Solid elements: Include a moderate number of fibrin strands, microorganisms, and tissue detritus (remnants of destroyed structures from the inflammatory focus).
- Cellular composition: The absolute majority (17–29%) consists of neutrophilic leukocytes. Entering tissues from the blood, they live for about 8–12 hours before dying and transforming into pus corpuscles. Cell structures vary depending on the timing of their arrival at the focus. Macrophages, lymphocytes, and eosinophilic granulocytes are also present in the exudate.
Pus performs two critical pathophysiological functions:
- Histolysis (tissue lysis): The exudate is extremely rich in enzymes, especially proteases. They break down dystrophically altered and dead structures, including robust elastic and collagen fibers. Therefore, purulent inflammation is always accompanied by tissue melting.
- Bactericidal action: Pus destroys bacteria and inhibits their growth. This occurs via cellular factors (phagocytosis and microbial killing by polymorphonuclear leukocytes) and humoral factors (immunoglobulins, complement). Bactericidal substances are produced by living cells, released during the breakdown of dead leukocytes, and supplied by plasma.
Clinical and Morphological Forms of Suppuration
The process can be acute or chronic, affecting any tissues and organs. There are four main morphological forms:
- Abscess — a localized collection of pus.
- Phlegmon — a diffuse purulent inflammation.
- Empyema — an accumulation of pus in natural body cavities.
- Purulent wound (and its variant — acute ulcers).
Phlegmon: Types and Severe Complications
Phlegmon is classified by the nature of tissue changes:
- Soft phlegmon: Active lysis of necrotic tissue predominates in the focus.
- Hard phlegmon: Characterized by the development of coagulation necrosis of the inflamed tissue. Subsequently, these dense necrotic masses are gradually sloughed off.
Phlegmon is dangerous due to severe complications:
- Vascular: When the process spreads to arteries, thrombosis occurs, leading to necrosis of affected tissues (a classic example is gangrenous appendicitis). Involvement of veins and lymphatic pathways causes purulent thrombophlebitis and lymphangitis.
- Contiguous spread: Driven by gravity, pus drains into lower anatomical compartments along fat planes, muscle-tendon sheaths, and neurovascular bundles. This forms pus collections without a capsule known as sinus tracts / undermining phlegmons (or "cold abscesses").
- Spread to adjacent organs: For example, the development of acute purulent inflammation of the mediastinal adipose tissue — purulent mediastinitis.
- Hemorrhage: Specific to hard phlegmon at the time of sloughing of coagulated masses.
- Systemic: Severe intoxication that always accompanies the purulent process.
Outcomes of phlegmon are divided into favorable (the process is localized, the surgeon removes the pus, and the surgical incision heals with coarse scar formation) and unfavorable (infection generalizes, leading to sepsis).
Hemorrhagic Inflammation
Hemorrhagic inflammation is not strictly an independent form. It is an exacerbated variant of serous, fibrinous, or purulent inflammation (e.g., serous-hemorrhagic).
Pathogenesis lies in a sharp increase in the permeability of the microvasculature. This causes massive erythrocyte diapedesis, and the exudate becomes saturated with blood.
Etiology is always associated with extremely pronounced systemic intoxication. Such inflammation is characteristic of severe influenza and highly dangerous infections: smallpox, anthrax, plague. The addition of a hemorrhagic component always drastically worsens the disease course.
An interesting feature: if atmospheric oxygen gains access to the erythrocytes in the exudate, hemoglobin undergoes chemical alterations, causing the masses to turn black (this phenomenon gave rise to the historical term "black smallpox").
In differential diagnosis, it is important to remember: if enzymes erode a blood vessel wall (arrosion) during purulent inflammation and bleeding begins, this is regarded as a complication of the purulent process rather than true hemorrhagic inflammation. The outcome of the pathology depends directly on the causative pathogen.
Microscopic Appearance (Using Dysentery as an Example)
When studying exudative inflammation, the microscopic picture of dysentery is frequently examined. In this pathology, diphtheritic inflammation develops in the large intestine. On a hematoxylin and eosin-stained slide, deep necrosis of the mucosa and underlying submucosa is clearly visualized. The affected tissues undergo marked imbibition — they are densely infiltrated with fibrinous exudate.