Composition and properties of purulent exudate
Pus is a thick, creamy fluid whose color varies in various shades of bluish-green. The exudate has a specific odor.
It consists of three main groups of components:
- Liquid part: formed from blood plasma. Contains albumins, globulins, biologically active substances, and complement components.
- Solid elements: include a moderate amount of fibrin threads, microorganisms, and tissue detritus (remnants of destroyed structures in the focus of inflammation).
- Cellular composition: the absolute majority (17–29%) consists of neutrophilic leukocytes. Upon entering tissues from the blood, they live for about 8–12 hours, after which they die, turning into pus corpuscles. The cell structure is diverse and depends on the time of their entry into the focus. Macrophages, lymphocytes, and eosinophilic granulocytes are also present in the exudate.
Pus performs two crucial pathophysiological functions:
- Histolysis (tissue lysis): the exudate is extremely rich in enzymes, especially proteases. They break down dystrophically altered and dead structures, including tough elastic and collagen fibers. Therefore, purulent inflammation is always accompanied by tissue liquefaction.
- Bactericidal action: pus destroys bacteria and inhibits their growth. This occurs due to cellular factors (phagocytosis and microbial killing by polymorphonuclear leukocytes) and humoral factors (immunoglobulins, complement). Bactericidal substances are produced by living cells, released upon the decay of dead leukocytes, and supplied with plasma.
Clinical and morphological forms of suppuration
The process can be acute or chronic, affecting absolutely any tissues and organs. Four main morphological forms are distinguished:
- Abscess — a localized accumulation 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 according to the nature of tissue changes:
- Soft phlegmon: active lysis of necrotic tissues predominates in the focus.
- Hard phlegmon: characterized by the development of coagulation necrosis of the inflamed tissue. Subsequently, these dense necrotic masses are gradually rejected.
Phlegmon is dangerous due to severe complications:
- Vascular: when the process extends to arteries, thrombosis occurs, leading to necrosis of the affected tissues (a classic example is gangrenous appendicitis). Involvement of veins and lymphatic pathways causes purulent thrombophlebitis and lymphangitis.
- Contact spread: under the influence of gravity, pus flows down into lower regions along adipose layers, musculo-fascial sheaths, and neurovascular bundles. This forms accumulations of pus without a capsule — cold abscesses (or gravitational abscesses).
- Extension to adjacent organs: for example, the development of acute purulent inflammation of the mediastinal fat tissue — purulent mediastinitis.
- Hemorrhages: specific to hard phlegmon at the time of rejection of coagulated masses.
- General: severe intoxication that always accompanies a purulent process.
Phlegmon outcomes are divided into favorable (the process is walled off, the surgeon removes the pus, and the surgical wound heals with the formation of a coarse scar) and unfavorable (the infection becomes generalized, leading to the development of sepsis).
Hemorrhagic inflammation
Hemorrhagic inflammation is not a strictly independent form. It is a severe variant of serous, fibrinous, or purulent inflammation (e.g., serous-hemorrhagic).
Pathogenesis of the process lies in a sharp increase in the permeability of the microvasculature. Because of this, massive erythrocyte diapedesis occurs, and the exudate becomes saturated with blood.
Etiology is always associated with extremely pronounced bodily intoxication. Such inflammation is characteristic of severe forms of influenza and highly dangerous infections: smallpox, anthrax, plague. The addition of a hemorrhagic component always drastically worsens the course of the disease.
An interesting feature: if atmospheric oxygen gains access to the erythrocytes in the exudate, hemoglobin undergoes chemical transformations, causing the masses to turn black (this phenomenon gave rise to the historical name "black smallpox").
In the framework of differential diagnosis, it is important to remember: if, during purulent inflammation, enzymes erode the wall of a blood vessel (arrosion) 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 etiology of the causative agent.
Microscopic picture (using dysentery as an example)
As part of the study of exudative inflammation, the microscopic picture of dysentery is often considered. In this pathology, diphtheritic inflammation develops in the large intestine. On a micro-slide stained with hematoxylin and eosin, deep necrosis of the mucosal membrane and underlying submucosal layer is clearly visualized. The affected tissues undergo marked imbibition—they are densely soaked with fibrinous exudate.
Briefly: answers to topical questions
What layers form the wall of a chronic abscess?
The wall of a chronic abscess is formed by two layers.
- Inner layer — faces directly into the abscess cavity, consisting of maturing granulations, accumulations of fibrin, and tissue detritus.
- Outer layer — consists of mature connective tissue that walls off the focus of inflammation from surrounding structures.
The formation of a full-fledged two-layered capsule begins on the third day. The inner layer is also called the pyogenic membrane because it produces exudate, whereas in immunodeficiency, an imperfect capsule prone to lysis is formed.
In which natural body cavities does empyema most commonly develop?
Empyema is an accumulation of pus in natural body cavities or hollow organs. The presented materials mention the following localizations:
- Pleural cavity — a special form of exudative pleurisy with the accumulation of purulent exudate.
- Gallbladder — occurs when the cystic duct is obstructed and pus accumulates in its cavity, serving as a complication of acute cholecystitis.
What outcomes are typical for an acute abscess?
Both favorable and unfavorable variants of the termination of the inflammatory process are typical for an abscess. The following main outcomes are distinguished:
- Spontaneous drainage — release of purulent exudate onto the body surface, into closed cavities, or into hollow organs. With complete drainage, the walls collapse, and scarring occurs.
- Fistula formation — formation of a narrow channel in case of incomplete drainage and failure of the walls to collapse, leading to transition into a chronic form.
- Encapsulation — a rare phenomenon accompanied by thickening of the pus.
- Petrification — deposition of calcium salts in the lesion focus.
To easily remember the 4 main forms of purulent inflammation, use the acronym FAER: Phlegmon, Abscess, Empyema, Wound (purulent).
Class and exam questions
How does purulent inflammation fundamentally differ from other types?
The obligatory presence of histolysis—enzymatic tissue digestion by proteases, which are contained in large quantities in the purulent exudate.
What are pus corpuscles?
These are dead polymorphonuclear leukocytes (neutrophils) that migrated to the focus of inflammation and disintegrated after 8–12 hours.
How to distinguish hemorrhagic inflammation from bleeding in a purulent wound?
Hemorrhagic inflammation occurs due to erythrocyte diapedesis against the background of high capillary permeability. Bleeding in a purulent focus is a consequence of arrosion (destruction) of the vessel wall by purulent enzymes, i.e., a complication.
What else to study on this topic
- Mechanisms of phagocytosis and killing of microorganisms by polymorphonuclear leukocytes.
- Differences between diphtheritic and croupous inflammation (using dysentery as an example).
- Pathogenesis of sepsis as a systemic complication of phlegmon.
- Morphology of an abscess and the stages of its capsule formation.
- Features of the cellular composition during the transition of purulent inflammation into a chronic form.
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