Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer !

Lesion

Acute inflammation looks different depending on what leaks out: clear fluid, fibrin, pus or a gap in the surface. The pattern points to the cause.

Updated 2026-11-01

What it is

The pattern of acute inflammation depends on how severe the injury is, where it happens and what causes it. Mild leakage gives serous fluid; larger leaks let fibrinogen out to form fibrin; pyogenic bacteria produce pus and abscesses; and loss of a surface lining leaves an ulcer. Pathologists read these patterns under the microscope, and clinicians see them as effusions, blisters, friction rubs and wounds.

Key facts

Fibrin removed by fibrinolysis allows resolution; fibrin that persists is invaded by fibroblasts and vessels (organisation) and becomes scar.
Pyogenic (pus-forming) bacteria include staphylococci, streptococci, pneumococci, gram-negative rods and anaerobes.

Structure

Serous: thin, protein-poor fluid in a body cavity or under the epidermis (blister); few cells.
Fibrinous: pink meshwork of fibrin on serosal surfaces; grossly a shaggy, ‘bread-and-butter’ look on the pericardium.
Purulent (suppurative): pus made of neutrophils, liquefied necrotic cells and oedema fluid; creamy yellow exudate.
Abscess: localised pus in a cavity; necrotic centre, rim of preserved neutrophils, then vessels and fibroblasts that wall it off.
Ulcer: local defect of an epithelial surface; an acute ulcer base has neutrophils and fibrin, a chronic one adds granulation tissue and scar.
Pseudomembranous: fibrin, neutrophils and necrotic epithelium forming an adherent membrane.

Patterns, what leaks out and classic examples

Pattern	What leaks out or is lost	Classic examples
Serous	Thin fluid from plasma or mesothelial cells	Burn or friction blister, viral blister, early pleural or pericardial effusion
Fibrinous	Fibrinogen, which polymerises into fibrin	Fibrinous pericarditis (after infarction, uraemia), lobar pneumonia, meningitis
Purulent	Neutrophils, liquefied tissue and fluid	Acute appendicitis, bacterial pneumonia, bacterial meningitis
Abscess	Walled-off pus, often Staphylococcus aureus or mixed anaerobes	Furuncle, lung abscess after aspiration, liver abscess
Ulcer	Surface epithelium	Peptic ulcer, aphthous ulcer, venous and pressure ulcers
Pseudomembranous	Fibrin and necrotic epithelium forming a membrane	Clostridioides difficile colitis, diphtheria

Clinical notes

A pericardial friction rub is the sound of fibrinous pericarditis; if the fibrin organises it leaves adhesions and can lead to constrictive pericarditis.
Antibiotics penetrate the walled-off cavity of an abscess poorly, so drainage is the mainstay of treatment.
Pus inside a pre-existing body cavity is called empyema (pleura, gallbladder).

Test yourself

Think of the answer, then tap the question to see it.

What causes the ‘bread-and-butter’ look of the pericardium after a myocardial infarction?

Fibrinous pericarditis: fibrin strands laid down on both pericardial layers that are pulled apart.

What is pus made of?

Neutrophils (many of them dead), liquefied necrotic tissue, oedema fluid and often the causative bacteria.

Why is drainage the key treatment for an abscess?

The fibrous wall and necrotic centre limit blood supply and antibiotic penetration, so the pus must be evacuated.

Add to my cards (3)

Elsewhere in DurgiPedia

Microorganisms

← All of general pathology

Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: Abscess: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Appendicitis (StatPearls (NCBI Bookshelf), 2024); Peptic Ulcer Disease (StatPearls (NCBI Bookshelf), 2024).

Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake

Representative model, for educational purposes only.