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PH-FD22

Haemorrhagic and gangrenous inflammation

Why some inflammations fill with blood and others rot: how toxins and severe vessel injury let red cells into the exudate, and how anaerobic bacteria turn dead, poorly supplied tissue into foul, gas-filled gangrene.

By the end, you can

  • Explain how severe endothelial injury lets red cells into an exudate, and why a haemorrhagic exudate signals a dangerous process.
  • Relate examples of haemorrhagic inflammation (anthrax, plague, severe influenza, haemorrhagic fevers, pancreatitis) to their mechanisms.
  • Explain how anaerobic bacteria cause gangrenous (putrefactive) inflammation in dead or poorly supplied tissue.
  • Describe gas gangrene and necrotising fasciitis, and why they spread so fast.
  • Distinguish dry, wet and gas gangrene by their colour, smell, edge and crepitus.
  • Recognise the classic appearances, types and tests of haemorrhagic and gangrenous inflammation, and explain how debridement, amputation, antibiotics, antitoxins and hyperbaric oxygen act on them.

What it is

Haemorrhagic inflammation is inflammation whose exudate is rich in red cells, because toxins, enzymes or the infection itself have badly damaged the vessel walls; it is usually mixed with another exudate (serous, fibrinous or purulent). Gangrenous (putrefactive) inflammation is inflammation in which anaerobic, putrefying bacteria invade dead or poorly supplied tissue and decompose it, with a foul smell, gas and dark discoloration.

4 types to tell apart
Haemorrhagic inflammation
Red cells dominate the exudate: anthrax, plague, severe influenza pneumonia, viral haemorrhagic fevers, meningococcal sepsis; and without infection in acute haemorrhagic pancreatitis.
Gangrenous (putrefactive) inflammation
Anaerobes such as clostridia, Bacteroides and Fusobacterium decompose dead tissue: gangrenous appendicitis or cholecystitis, strangulated bowel, gangrene of the lung, wet gangrene of a limb, noma.
Gas gangrene and necrotising fasciitis
Rapidly spreading, toxin-driven necrosis of muscle (clostridial myonecrosis) or along the fascia (necrotising fasciitis).
Dry, wet and gas gangrene
Clinical terms for dead tissue: dry gangrene is ischaemic necrosis without infection; wet gangrene is dead tissue invaded by bacteria; gas gangrene is clostridial infection with gas in the tissue.

US spelling: haemorrhagic → hemorrhagic.

Normal function

Intact vessels and well-oxygenated tissue

Red cells stay in the blood because the endothelium, its junctions and its basement membrane form a continuous wall. Even the gaps of ordinary acute inflammation let fluid, proteins and white cells through but few red cells, and platelets and clotting seal any small breach at once.

Living tissue with a good blood supply also resists anaerobic bacteria. Oxygen keeps the oxidation–reduction (redox) potential too high for strict anaerobes to grow, and the bring white cells, antibodies and complement, while resident patrol. Dead or poorly perfused tissue loses both protections.

Point to it on the model