Classification and General Features
The type of exudative inflammation is determined by the composition of the exudate. There are four main types:
- Serous.
- Fibrinous.
- Purulent.
- Putrid (gangrenous).
There are also variants that are not classified as independent types because they represent admixtures to the primary exudate. These include hemorrhagic inflammation (admixture of erythrocytes), catarrhal (admixture of mucus), and mixed (combination of different exudates).
The course of the process is most often acute; chronic forms are less common. In most cases, inflammation ends in restitutio ad integrum — complete restoration of the damaged tissue. Less commonly, scar tissue forms at the site of the lesion.
Serous Inflammation
This form produces a turbid fluid containing a moderate number of cells (lymphocytes, leukocytes, desquamated epithelium). Biochemically, the exudate is characterized by a protein content of up to 2.5% (albumin-to-globulin ratio from 0.55:1 to 2.7:1).
Causes:
- Viral infections (influenza, herpes, viral hepatitis, chickenpox) — the most common cause.
- Bacteria and allergens.
- Burns (thermal, chemical, radiation).
- Action of endo- and exotoxins causing plasmorrhagia.
Localization and Manifestations: The process affects mucous, serous, and synovial membranes, the skin (blister formation), renal glomeruli capsules, liver perisinusoidal spaces, and the stroma of parenchymatous organs. The main function of this exudate is to flush toxins and microorganisms from surfaces.
Clinically, the process is accompanied by fever, moderate leukocytosis, and an elevated ESR. The danger of serous inflammation lies in fluid accumulation: in the meninges, it leads to brain compression; in the pleural cavity, to lung collapse (atelectasis); and infiltration of the interalveolar septa causes acute respiratory distress syndrome. The outcome is usually favorable, but transition to diffuse sclerosis is possible in parenchymatous organs.
Fibrinous Inflammation
Characterized by the formation of a dense exudate with a high fibrin content. The mechanism is associated with tissue necrosis and platelet aggregation: under the action of tissue thromboplastin, fibrin precipitates, impregnating dead tissues and forming a light-gray membrane. Microorganisms actively multiply beneath this membrane, releasing toxins.
Etiology includes exposure to viruses, allergens, toxins, and bacteria (e.g., Corynebacterium diphtheriae, Shigella, Mycobacterium tuberculosis, coccal flora).
Depending on the depth of necrosis and the type of epithelium, two forms are distinguished:
- Croupous inflammation (from Scot. croup — film). Develops on mucous or serous membranes covered by a single-layer epithelium with a thin connective tissue base (trachea, bronchi, peritoneum, pleura). Necrosis is superficial, the membrane is thin and easily separated without forming ulcers. Example: lobar pneumonia.
- Diphtheritic inflammation (from Greek diphthera — leather/membrane). Occurs on stratified squamous non-keratinizing or transitional epithelium, as well as on single-layer epithelium with a loose, wide lamina propria (pharynx, esophagus, uterus, urinary bladder). Necrosis is deep, and the thick membrane is firmly fused to the tissues. Its detachment leaves deep ulcers.
Outcomes: Clearing of the focus occurs via autolysis — hydrolases of polymorphonuclear leukocytes (neutrophils) dissolve the fibrin. The croupous form usually ends in complete restitution. Diphtheritic inflammation heals via substitution (imperfect regeneration) with scar formation. If fibrin is not resorbed, it activates fibroblasts, leading to organization of the exudate — replacement by connective tissue. On serous membranes, this leads to adhesions, fibrous bands (shwarts), and cavity obliteration.
Catarrhal Inflammation (Catarrh)
A specific variant that develops exclusively on mucous membranes. Its main feature is an admixture of mucus to any other type of exudate (serous, purulent, hemorrhagic).
Causes of catarrh include infections, allergic reactions (e.g., serous catarrh in allergic rhinitis), as well as chemical and thermal irritants. Example: purulent catarrh of the tracheal and bronchial mucosa.
Acute catarrh lasts 2–3 weeks and usually resolves without consequences. In chronic courses, irreversible changes develop in the mucous membrane: it may thin (atrophy) or, conversely, thicken (hypertrophy).