Acute Inflammation

Original Author: Ollie Jones
Last Updated: November 9, 2016
Revisions: 15

Inflammation refers to the initial physiological response to tissue damage, such as that caused by mechanical, thermal, electrical, irradiation, chemical, or infection.

It can be acute (lasting for a few days) or chronic (in response to an ongoing and unresolved insult). Inflammation is associated with permanent tissue damage and fibrosis.

In this article, we shall look at the processes involved in acute inflammation.


Characteristic Features

Acute inflammation begins within seconds to minutes following injury to tissues. It is characterised by four key features (Latin terms in brackets):

  • Redness (rubor) – secondary to vasodilatation and increased blood flow.
  • Heat (calor) – localised increase in temperature, also due to increased blood flow.
  • Swelling (tumour) – results from increased vessel permeability, allowing fluid loss into the interstitial space.
  • Pain (dolor), caused by stimulation of the local nerve endings, from mechanical and chemical mediators.
Fig. 1 - Redness (rubor) and swelling (tumour) - characteristic features of acute inflammation.

Fig. 1 – Redness (rubor) and swelling (tumour) – characteristic features of acute inflammation.


Phases of Acute Inflammation

Acute inflammation can be discussed in terms of two stages; (1) the vascular phase, which is followed by; (2) the cellular phase.

Vascular Phase

In the vascular phase, small blood vessels adjacent to the injury dilate (vasodilatation) and blood flow to the area increases (rubor and calor). The endothelial cells initially swell, then contract to increase the space between them, thereby increasing the permeability of the vascular barrier. This process is regulated by chemical mediators (see appendix).

Exudation of fluid leads to a net loss of fluid from the vascular space into the interstitial space, resulting in oedema (tumour).

The formation of increased tissue fluid acts as a medium for which inflammatory proteins (such as complement and immunoglobulins) can migrate through. It may also help to remove pathogens and cell debris in the area through lymphatic drainage.

Cellular Phase

The predominant cell of acute inflammation is the neutrophil. They are attracted to the site of injury by the presence of chemotaxins – chemicals released into the blood immediately after the insult.

The migration of neutrophils occurs in four stages:

  • Margination – cells line up against the endothelium.
  • Rolling – close contact with and roll along the endothelium.
  • Adhesion – connecting to the endothelial wall.
  • Emigration – cells move through the vessel wall to the affected area.

Once in the region, neutrophils recognise the foreign body and begin phagocytosis – the process whereby the pathogen is engulfed and contained with a phagosome. The phagosome is then destroyed via oxygen-independent mechanisms (e.g. lysozymes), or oxygen-dependent mechanisms (e.g. free radical formation).

Fig 2 - The features of acute inflammation; vessel vasodilation, exudate formation and neutrophil migration.

Fig 2 – The features of acute inflammation; vessel vasodilation, exudate formation and neutrophil migration.


Outcomes

Following the process of acute inflammation, there are several possible results:

  • Complete resolution – with total repair and destruction of the insult.
  • Fibrosis and scar formation – occurs in cases of significant inflammation, and may impair the function of the tissue.
  • Chronic inflammation – from a persisting insult.
  • Formation of an abscess

Abscess Formation

An abscess is a mass of necrotic tissue, with dead and viable neutrophils suspended in a liquefied tissue necrosis. It forms when the primary insult is a pyogenic bacterium, and extensive tissue necrosis occurs.

The initial inflammatory exudate forces the tissue apart, leaving a centre of necrotic tissue with the neutrophils and pathogens. Over time, the acute inflammation will cease and the abscess will be replaced by scar tissue.

An abscess can be a source for systemic dissemination of a pathogen, with the abscess acting as a harbour for the infection. It can also cause continually rising pressures within the tissue, resulting in pain and damage to local structures.

Fig 3 - Remnant of a drained pulmonary abscess at post-mortem

Fig 3 – Remnant of a drained pulmonary abscess at post-mortem


Appendix – Chemical Mediators

Table 1 – Chemical Mediators in Acute Inflammation
Mechanism Involved Mediators
Vasodilatation Histamine, Bradykinin, Complement (C3a, C5a), Leukotrienes (LTC4, LTD4), Prostaglandins (PGI2, PGE2, PGD2, PGF2)
Mast cell degranulation Complement (C3a, C5a)
Chemotaxis Interleukins (IL-8), PAF, Complement (C5a), Histamine
Lysosomal granule release Complement (C5a), Interleukins (IL-8), PAF
Phagocytosis Complement (C3b)
Pain Prostaglandins (PGE2), Bradykinin, Histamine
Fever Interleukins (IL-1, IL-6), TNF-α, Prostaglandins (PGE2)

Further Reading

C-reactive protein (CRP) measurement in geriatric patients hospitalized for acute infection
Ticinesi A et al., European Journal of Internal Medicine

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