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. Catarrhal inflammation. A surface inflammation associated with greatly increased secretion of clear mucus. Later, polymorphs appear (common cold and some forms of colitis).
2. Hemorrhagic inflammation. Where the damage is severe, actual rupture of all blood vessels occurs, with hemorrhage the most striking feature (acute hemorrhagic pneumonia occasionally occurring in fatal cases of influenza).
3. Suppuration. There are several types of suppuration: an abscess, phlegmon, furuncle, carbuncle, cellulitis, bacterial infections of the blood.
When acute bacterial infection is accompanied by intense neutrophilic infiltrate in the inflammed tissue, it results in tissue necrosis. A cavity is formed which is called an abscess and contains purulent exudate 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. The wall of abscess is called pyogenic membrane. 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.
Phlegmon is unbounded purulent inflammation in which pus spreads diffusely between different components of tissue owing to fusion and tissue lysis. Phlegmon frequently occurs along the muscular bands, tendons, fascias, vascular-nerves bands and in subcutaneous fat. Two types of phlegmon have been described: soft and dense.
If purulent exudate appears in the human cavities it is called empyema.
Furuncle is an acute inflammation via hair follicles in the dermal tissues.
Carbuncle is seen in untreated diabetics and occurs as a located abscess in the dermis and soft tissues of the neck.
Cellulitis. It is a diffuse inflammation of soft tissues resulting from spreading effects of substances like hyaluronidase released by some bacteria.
Bacterial infections of the blood. This includes the following 3 conditions: bacteremia, septicemia, pyemia.
Bacteremia is defined as presence of small number of bacteria in the blood which don't 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.
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 toxemia, multiple small hemorrhage, neutrophilic leucocytosis and disseminated intravascular coagulation (DIC).
Pyemia 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 pyemic abscesses or septic infarcts. Pyemic 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 pyemic abscess shows a central zone of necrosis containing numerous bacteria, surrounded by a zone of suppuration and an outer zone of acute inflammatory cells. Septic infarcts result from lodgment 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.
4. Serous inflammation. Serous inflammation is marked by the outpouring of a thin fluid that, depending
on the size of injury, is derived from either the blood serum or the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities. The skin blister resulting from a burn or viral infections represents a large accumulation of serous fluid, either within or immediately beneath the epidermis of the skin.
5. Fibrinous inflammation. With more severe injuries and the resulting greater vascular permeability, larger molecules such as fibrin pass the vascular barrier. A fibrinous exudate develops when the vascular leaks are large enough or there is a pro-coagulant stimulus in the interstitium (e.g., cancer cells). A fibrinous exudate is characteristic of inflammation in body cavities, such as the pericardium and pleura. Microscopically, fibrin appears as an eosinophilic meshwork of threads, or sometimes as an amorphous coagulum. Fibrinous exudates may be removed by fibrinolysis, and other debris by macrophages. This process, called resolution, may restore normal tissue structure, but when the fibrin is not removed it may stimulate the ingrowth of fibroblasts and blood vessels and thus lead to scarring. Conversion of the fibrinous exudate to scar tissue (organization) within the pericardial sac will lead either to opaque fibrous thickening of the pericardium and epicardium in the area of exudation or, more often, to the development of fibrous strands that bridge the pericardial space.
According to the type of epithelium on which inflammatory process develops and depth of necrosis there are two types of fibrinous inflammation croupous and diphtheroid fibrinous inflammation. Usually croupous inflammation develops on the columnar epithelium. In this case the fibrinous membranes unfix easily, without any effort. Diphtheroid fibrinous inflammation develops on the squamous or intermediate epithelium, when the fibrinous membranes unfix with difficulties.
6. 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.
7. Ulcer. Ulcer is a local defect on the surface of an organ produced by inflammation. 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.
The acute inflammatory process can culminate in one of the following 4 outcomes: resolution, healing by scarring, progression to suppuration, progression to chronic inflammation.
Outcome. This means complete return to normal tissue following acute inflammation. It occurs when
tissue changes are slight and the cellular changes are reversible, e.g. resolution in lobar pneumonia.
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.
Progression to 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.
Progression to chronic inflammation. Acute inflammation may progress to chronic one in which the processes of inflammation and healing proceed side by side.
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