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        Traumatic Fat Necrosis:

              

(Diagram: Traumatic fat necrosis in the breast. Necrotic area is surrounded by lipid filled macrophages and foreign-body giant cells).

 Visit: Necrosis  

Traumatic fat necrosis is usually seen in the female breast especially, if  the breast is heavy and pendulous. 

Subcutaneous fat necrosis may follow trauma, particularly to the shins.

Essentially it results from the rupture of adipocytes with release of their contents.

This is sometimes discharged through a surface wound.

The released fat undergoes lipolysis and is converted to fatty acids and glycerol.

Clinically the lesion appears as a hard lump in the breast, which may give the impression that a malignant neoplasm is present.

On slicing the excised specimen one may see a small central cystic area in which some oily droplets are present. At the periphery the adipose tissue is much firmer and also more opaque than usual.

Histological examination of conventionally prepared material shows the presence of numerous granular macrophages which contain phagocytosed lipid.

Fatty acid crystals are also often present and these excite a foreign body giant cell reaction (multinucleate cells formed as a result of the fusion of macrophages).

In subcutaneous lesions cases coming to biopsy often show fat cysts of varying size with surrounding fibrosis.

The microcysts sometimes show lipomembranous (membranocystic) change.

There are often small collections of foam cells, a mild patchy lymphocytic infiltrate and some hemosiderin.

 In earlier lesions there is fat necrosis with cystic spaces and numerous neutrophils in the adjacent fat.

A similar appearance follows surgical disruption of the subcutis.

Sometimes collections of fat cells, often necrotic, can be seen within the dermis, apparently in the process of being eliminated through a break in the dermis.

Normal subcutaneous fat, necrosis of adipocytes and classification of the panniculitides.Semin Cutan Med Surg. 2007 Jun;26(2):66-70.

The panniculitides represent a group of heterogeneous inflammatory diseases that involve the subcutaneous fat. The specific diagnosis of these diseases requires histopathologic study because different panniculitides usually show the same clinical appearance, which consists of erythematous nodules on the lower extremities. However, the histopathologic study of panniculitis is difficult because of an inadequate clinicopathologic correlation and the changing evolutive nature of the lesions. In addition, large scalpel incisional biopsies are required. From histopathologic point of view, all panniculitides are somewhat mixed because the inflammatory infiltrate involves both the septa and lobules. However, nearly always the differential diagnosis between a mostly septal and a mostly lobular panniculitis is straightforward at scanning magnification on the basis of the structures more intensely involved by the inflammatory infiltrate. Mostly septal panniculitides with vasculitis are actually more vasculitis than panniculitis and include superficial thrombophlebitis and cutaneous polyarteritis nodosa. Mostly septal panniculitides with no vasculitis include erythema nodosum, necrobiosis lipoidica, deep morphea, subcutaneous granuloma annulare, rheumatoid nodule, and necrobiotic xanthogranuloma. Mostly lobular panniculitis with vasculitis is only represented by erythema induratum of Bazin. In contrast, mostly lobular panniculitides without vasculitis comprise a large series of disparate disorders, including sclerosing panniculitis, calciphylaxis, sclerema neonatorum, subcutaneous fat necrosis of the newborn, poststeroid panniculitis, lupus erythematosus profundus, pancreatic panniculitis, alpha(1)-antitrypsin deficiency panniculitis, subcutaneous Sweet syndrome, infective panniculitis, factitial panniculitis, lipodystrophy, traumatic panniculitis, subcutaneous sarcoidosis, and sclerosing postirradiation panniculitis. Finally, some cutaneous lymphomas may simulate panniculitis, both from clinical and histopathologic points of view and, for that reason, they will be included in this review, although they are not inflammatory processes, but authentic lymphocytic neoplasms involving subcutaneous tissue.

           

               Pancreatic Fat Necrosis:

               

(Diagram: Fat necrosis in acute pancreatitis. The release and activation of lipolytic pancreatic enzymes results in the necrosis  of surrounding adipose tissue. The hydrolysis of the triglycerides releases free fatty acids, which precipitate as calcium soaps in  the necrotic debris).

Another type of fat necrosis is seen in the peritoneal cavity as a consequence of acute hemorrhagic pancreatitis.

In pancreatitis the enzymes secreted by the exocrine pancreas are released from the acini and ducts and thus reach the interstitial tissues.

The proteolytic and lipolytic enzymes damage the cell membranes and convert the intracellular triglyceride into  glycerol and fatty acids.

These latter combine with calcium in the interstitial fluid to form soaps which appear as small, intensely white and opaque patches on the adipose tissue of the pancreas, omentum and other areas of the peritoneum.

                  

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