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Acute Inflammation

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Original Author(s): Jess Speller
Last updated: 19th June 2021
Revisions: 8

Original Author(s): Jess Speller
Last updated: 19th June 2021
Revisions: 8

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Inflammation describes the tissue response to injury and is a series of processes initiated to limit tissue damage. Acute inflammation is an innate, immediate and stereotyped response in the short term following tissue injury.

This article discusses the potential causes and signs of acute inflammation, relevant tissue changes and immune cells involved. Finally, It will outline some clinical conditions in which this process occurs.

Causes and Features

Acute inflammation occurs in response to a variety of situations where there may be tissue damage. Common causes include infection, hypersensitivity reactions, physical or chemical agents and tissue necrosis.

Acute inflammation has five main features:

  • Rubor (redness)
  • Tumour (swelling)
  • Calor (heat)
  • Dolor (pain)
  • Loss of function

    Fig 1 – Image of a toe with acute inflammation.

Tissue Changes

Blood flow changes

In the first few seconds following injury, there is transient arteriolar vasoconstriction to control any blood loss followed by arteriolar vasodilation to enhance blood flow in nearby capillaries and tissues. This provides blood components for managing the primary injury and initiating repair. The higher blood flow causes the signs of rubor and calor.

Mast cells, basophils and platelets at the injury site release histamine. This leads to the blood vessels becoming more permeable and the formation of an exudate (protein-rich fluid) within the tissues. The circulation is also slowed which, in combination with fluid exudation, increases the concentration of red blood cells within circulation near the injury site. These two changes lead to the sign of tumour.

Exudation of fluid

Exudation of fluid occurs due to Starling’s Law. Vasodilation of arterioles leads to increased hydrostatic pressure and, as a result, higher fluid movement out of vessels.  In addition to this, increased vessel permeability allows proteins to move into the interstitium, leading to increased colloid pressure and further increasing fluid movement out of vessels.

This increase in tissue fluid also leads to increased lymphatic drainage, which can help remove damaging substances and causative microbes.

Exudation occurs as a result of several mechanisms:

  • Endothelial contraction, mediated by histamine and leukotrienes
  • Cytoskeletal reorganisation, mediated by cytokines, IL-1 and TNF-α.
  • Direct injury, from toxic burns or chemicals.
  • Leukocyte-dependent injury, due to toxic oxygen species or enzymes from leukocytes.
  • Increased transcytosis (channels across endothelial cytoplasm), mediated by VEGF.

This fluid allows plasma proteins, such as fibrin, to be delivered directly to the injury site.

Cellular Phase of Acute Inflammation

The main immune cells involved in acute inflammation are neutrophils. The stasis of circulation allows neutrophils to line up along the endothelium near the injury site, known as margination. Next, they roll along the endothelium, sticking intermittently.

Following rolling, they attach more avidly to the endothelium, known as adhesion. Finally, the neutrophils migrate through the blood vessel walls. Neutrophils can leave blood vessels through relaxation of inter-endothelial cell junctions and digestion of the vascular basement membrane.

Neutrophils move to areas of damage via chemotaxis. This is often following a concentration gradient of chemotaxins, including  C5a, LTB4 and bacterial peptides.

Neutrophils are necessary as they can phagocytose pathogens and cellular debris to remove them, facilitated by opsonins. Further detail on the process of phagocytosis can be found here.

Fig 3 – Electron micrograph showing margination of neutrophils in acute inflammation.

How does Acute Inflammation Help?

The changes that occur in acute inflammation help with controlling the infection and restoring tissues to their normal state:

  • Exudation of fluid helps deliver plasma proteins to injury sites. It, furthermore, dilutes toxins and increases lymphatic drainage.
  • Infiltration of neutrophils leads to the removal of pathogens and cellular debris.
  • Vasodilation, much like exudation, helps to increase the delivery of necessary proteins and cells and to increase tissue temperature.
  • Pain and loss of function help to enforce rest and lower the risk of further tissue damage.

Clinical Relevance

Liver Abscess

Acute inflammation can be the result of infection, as is the case in an abscess. An abscess is a painful collection of pus within the tissue that is often due to a bacterial infection. When this occurs in the liver, it results in right upper quadrant pain, hepatomegaly, fever, night sweats, nausea and vomiting, weight loss and jaundice.

Blood tests will often show a raised white cell count, abnormal liver function tests and a positive blood culture. In addition to this, the abscess can be identified using ultrasound or through a CT scan.

Treatment involves antibiotics,  along with supportive measures such as fluids, pain relief and abscess drainage. Drainage is usually guided by ultrasound or CT and can be either aspirated or drained via a catheter; depending on the abscess size. If the abscess ruptures, open surgery may be necessary.

Complications of liver abscesses include sepsis, abscess rupture, peritonitis, and secondary infection with further abscesses.

Fig 4 – CT scan showing a large liver abscess. The red arrow is pointing to the abscess.

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