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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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