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Acute inflammation is the early (almost immediate) response of a tissue to injury. It is nonspecific and may be evoked by any injury short of one that is immediately lethal. Acute inflammation may be regarded as the first line of defense against injury and is characterized by changes in the microcirculation: exudation of fluid and emigration of leukocytes from blood vessels to the area of injury. Acute inflammation is typically of short duration, occurring before the immune response becomes established, and it is aimed primarily at removing the injurious agent.

Until the late 18th century, acute inflammation was regarded as a disease. John Hunter (1728–1793, London surgeon and anatomist) was the first to realize that acute inflammation was a response to injury that was generally beneficial to the host: “But if inflammation develops, regardless of the cause, still it is an effort whose purpose is to restore the parts to their natural functions.”

Clinically, acute inflammation is characterized by 5 cardinal signs: rubor (redness), calor (increased heat), tumor (swelling), dolor (pain), and functio laesa (loss of function) (Figure 3-1). The first four were described by Celsus (ca 30 bc–38 ad); the fifth was a later addition by Virchow in the nineteenth century. Redness and heat are due to increased blood flow to the inflamed area; swelling is due to accumulation of fluid; pain is due to release of chemicals that stimulate nerve endings; and loss of function is due to a combination of factors. These signs are manifested when acute inflammation occurs on the surface of the body, but not all of them will be apparent in acute inflammation of internal organs. Pain occurs only when there are appropriate sensory nerve endings in the inflamed site—for example, acute inflammation of the lung (pneumonia) does not cause pain unless the inflammation involves the parietal pleura, where there are pain-sensitive nerve endings. The increased heat of inflamed skin is due to the entry of a large amount of blood at body core temperature into the normally cooler skin. When inflammation occurs internally—where tissue is normally at body core temperature—no increase in heat is apparent.

Figure 3–1.

Cardinal signs of acute inflammation. Note swelling and redness of the skin around an infected burn. Marked tenderness, increased local temperature, and loss of function were also present.

The morphologic and functional changes in acute inflammation were described in the late nineteenth century by Cohnheim, who demonstrated the vascular changes of injury in the vessels of a frog tongue. The two main components of the acute inflammatory response are the microcirculatory response and the cellular response.

Microcirculatory Response

Vasodilation and Stasis

The first change in the microcirculation is a transient and insignificant vasoconstriction, which is then followed by marked, active dilation of arterioles, capillaries, ...

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