Acute Inflammation - Introduction

Introduction

• Acute inflammation is characterised sudden onset and may last for a few hours to a few days.
• Vascular, humoral and cellular alterations cause the 5 cardinal signs as a result of exposure of tissues to various causes.
• Acute inflammation can:
  1. Be fatal
  2. Resolve by regeneration in association with the host defence mechanisms.
     • May be assisted by therapeutic measures.
  3. Undergo repair by fibrosis.
  4. Become chronic.
     • First goes through a subacute phase.
     • Is dependent upon the persistence of the agent and the amount of damage caused.

Sequence of Events

• The following sequence of events is provoked by the presence of the irritant.

1. Momentary vasoconstriction
   • Following contact with the irritant, there is momentary vasoconstriction of the blood vessels in the affected area.
   • This is reversed within minutes.
2. Dilation of the blood vessels
   • Initially, dilation of the capillaries is caused by the release of chemical mediators.
   • Arterioles then dilate under the influence of a local axon reflex.
   • This gives rise to an initial acceleration of the blood flow to the area.
     • This later gives way to a slowing of blood flow, caused by alterations in vascular endothelial permeability and the filling of previously closed capillaries.
3. Exudation of fluid
   • Follwing the slowing of blood flow and altered capillary permeability, a protein-rich fluid is exudated.
4. Margination of leukocytes
   • Circulating white blood cells are attracted to the altered endothelial surfaces.
5. Emigration of leukocytes
   • Leukocytes migrate through the altered endothelium to reach the injured area.
   • This is an active process - chemotaxis.
     • The cells are attracted to the endothelium by release of proteins, and further into the tissues by factors released from cells in the damaged area.
     • The emigrated leukocytes and components of the fluid exudate are also chemotactic.
     • More cells and fluid are attracted to the area.
6. Emigration of red blood cells
   • Erythrocytes migrate through the gaps in the altered endothelium to the damaged tissue.
7. Induction of an increase in temperature
   • This may occur either locally or systemically.
   • A systemic rise in temperature is known as pyrexia.
     • Occurs in generalise acute inflammation.
     • Pyrogens act on the temperature control centres in the hypothalamus, and are released from:
       • Neutrophils, eosinophils and macrophages
         • Particulary neutrophils when they begin to phagocytose.
       • The cellular coat of gram-negative organisms.
       • Necrosis of damaged tissue cells.
       • Antigen-antibody complexes.
       • Tumours.
         • Particularly those which have metastasised
         • It may be difficult to separate this from the pyrexia caused by the central necrosis in such tumours.

Cells

Graph illustrating the cellular response to inflammation

• The classical cells of acute inflammation are neutrophils, eosinophils, macrophages, mast cells and basophils.
  • Macrophages are a common feature of acute and chronic inflammation.