5. Necrosis

The extent and type of necrosis in inflammation is variable.

1. In gas gangrene, there is extensive necrosis with discolored and foul smelling tissues.

2. In acute appendicitis, there is necrosis as a result of vascular obstruction.

3. In chronic inflammation such as tuberculosis, there is characteristic caseous necrosis.

MORPHOLOGY OF ACUTE INFLAMMATION

Inflammation of an organ is usually named by adding the suffix- 'itis' to its Latin name e.g. ap­pendicitis, hepatitis, cholecystitis, meningitis etc. A few morphologic varieties of acute inflamma­tion are described below:

1. PSEUDOMEMBRANOUS INFLAMMA­TION. It is inflammatory response of mucous surface (oral, respiratory, bowel) to toxins of diph­theria or irritant gases. As a result of denudation of epithelium, plasma exudes on the surface where it coagulates, and together with necrosed epithe­lium, forms false membrane that gives this type of inflammation its name.

2. ULCER. Ulcers are local defects on the sur­face of an organ produced by inflammation. Com­mon sites for ulcerations are the stomach, duode­num, intestinal ulcers in typhoid fever, intestinal tuberculosis, bacillary and amoebic dysentery, ulcers of legs due to varicose veins etc. In the acute stage, there is infiltration by polymorphs with vasodilatation while long-standing ulcers develop infiltration by lymphocytes, plasma cells and macrophages with associated fibroblastic prolif­eration and scarring.

3. Suppuration (abscess formation).

When acute bacterial infection is accompanied by intense neutrophilic infiltrate in the inflamed tissue, it results in tissue necrosis. A cavity is formed which is called an abscess and contains purulent exudates or pus and the process of abscess formation is known as suppuration. The bacteria which cause suppuration are called pyogenic.

Pus is creamy or opaque in appearance and is composed of numerous dead as well as living neutrophils, some red cells, fragments of tissue debris and fibrin. In old pus, macrophages and cholesterol crystals are also present.

An abscess may be discharged to the surface due to increased pressure inside or may require drainage by the surgeon. Due to tissue destruc­tion, resolution does not occur but instead heal­ing by fibrous scarring takes place.

Some of the common examples of abscess formation are as under:

(i) Boil or furuncle which is an acute inflamma­tion via hair follicles in the dermal tissues.

(ii) Carbuncle is seen in untreated diabetics and occurs as a loculated abscess in the dermis and soft tissues of the neck.

4. CELLULITIS. It is a diffuse inflammation of soft tissues resulting from spreading effects of substances like hyaluronidase released by some bacteria.

5. BACTERIAL INFECTION OF THE BLOOD. This includes the following 3 conditions:

(i) Bacteremia is defined as presence of small number of bacteria in the blood which do not mul­tiply significantly. They are commonly not de­tected by direct microscopy. Blood culture is done for their detection e.g. infection with Salmonella typhi, Escherichia coli, Streptococcus viridans,

(ii) Septicemia means presence of rapidly mul­tiplying, highly pathogenic bacteria in the blood e.g. pyogenic cocci, bacilli of plague etc. Septicemia is generally accompanied by systemic effects like toxaemia, multiple small hemorrhages, neutrophilic leucocytosis and disseminated intravascular coagulation (DIC).

(iii) Pyaemia is the dissemination of small septic thrombi in the blood which cause their effects at the site where they are lodged. This can result in pyaemic abscesses or septic infarcts.

(a) Pyaemic abscesses are multiple small abscesses in various organs such as in cerebral cortex, myocardium, lungs and renal cortex, resulting from very small emboli fragmented from septic thrombus. Microscopy of pyaemic abscess shows a central zone of necrosis containing numerous bacteria, surrounded by a zone of suppuration and an outer zone of acute inflammatory cells.

(b) Septic infarcts result from lodgement of larger fragments of septic thrombi in the arteries with relatively larger foci of necrosis, suppuration and acute inflammation e.g. septic infarcts of the lungs, liver, brain, and kidneys from septic thrombi of leg veins or from acute bacterial endocarditis.

SYSTEMIC EFFECTS OF ACUTE INFLAMMATION

The account of acute inflammation given up to now above is based on local tissue responses. However, acute inflammation is associated with systemic effects as well. These include fever, leucocytosis and lymphangitis-lymphadenitis.

1. Fever occurs due to bacteremia. It is thought to be mediated through release of factors like prostaglandins, interleukin-1 and tumor necrosis factor in response to infection.

2. Leucocytosis commonly accompanies the acute inflammatory reactions, usually of the range of 15,000-20,000/l. When the counts are higher than this with 'shift to left' of myeloid cells, the blood picture is described as leukemoid reac­tion. Usually, in bacterial infections there is neutrophilia; in viral infections lymphocytosis; and in parasitic infestations, eosinophilia. Typhoid fe­ver, an example of acute inflammation, however, induces leucopenia with relative lymphocytosis.

3. Lymphangitis-lymphadenitis is one of the im­portant manifestations of localized inflammatory injury. The lymphatics and lymph nodes that drain the inflammed tissue show reactive inflammatory changes in the form of lymphangitis and lymphadenitis. This response represents either a nonspecific reaction to mediators released from inflammed tissue or is an immunologic response to a foreign antigen. The affected lymphnodes may show hyperplasia of lymphoid follicles (follicular hyperplasia) and proliferation of mononuclear phagocytic cells in the sinuses of lymphnode (sinus histiocytosis).

FATE OF ACUTE INFLAMMATION

The acute inflammatory process can culminate in one of the following 4 outcomes:

1. Resolution

2. Healing by scarring

3. Progression to suppuration

4. Progression to chronic inflammation.

1. RESOLUTION. It means complete return to normal tissue following acute inflammation. This occurs when tissue changes are slight and the cellu­lar changes are reversible e.g. resolution in lobar pneumonia.

2. HEALING BY SCARRING. This takes place when the tissue destruction in acute inflammation is extensive so that there is no tissue regeneration but actually there is healing by fibrosis.

3. SUPPURATION. When the pyogenic bacte­ria causing acute inflammation result in severe tis­sue necrosis, the process progresses to suppuration. Initially, there is intense neutrophilic infiltration. Subsequently, mixture of neutrophils, bacteria, frag­ments of necrotic tissue, cell debris and fibrin com­prise pus which is contained in a cavity to form an abscess. The abscess, if not drained, may get organized by dense fibrous tissue, and in time, get calcified.

4. CHRONIC INFLAMMATION. The acute inflammation may progress to chronic inflamma­tion in which the processes of inflammation and healing proceed side by side.

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