Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes.In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.It is usually associated with trauma of the pancreas or acute pancreatitis. It can also occur in the breast, the salivary glands and neonates after a traumatic delivery. Signs and symptoms
Signs and symptoms of fat necrosis are presented below:

masses that seem to be irregular beneath the skin, by touch these should feel smooth and rounded. tenderness in areas with masses
skin tethering
dimpling
nipple retraction

Causes
Fat necrosis occurs primarily in the breast and pancreas. Breast lesions are mostly caused by adipose tissue trauma or post-surgical complications (e.g. hypoxia). Pancreatic lesions arise as a result of the pathological release of pancreatic enzymes which digest surrounding adipose tissue. Fat necrosis is also a feature of some diseases that cause inflammation of subcutaneous fat (panniculitis). Examples of causes include but are not limited to:

Breast trauma (e.g. seat belt injury from a car accident)
Breast surgery
Fine needle aspiration biopsy and cytology (FNAB, FNAC)
Radiotherapy
Lumpectomy
Reduction mammoplasty
Breast reconstruction
Pancreatic disease
Acute pancreatitis
Pancreatic cancer
Pancreatic injury
Some forms of panniculitis
Subcutaneous fat necrosis of the newborn
Weber–Christian disease
Polyarteritis nodosa

Pathophysiology
Fat necrosis is the pattern of damage associated with the destruction of adipose tissue by trauma, hypoxia, or lipase digestion (e.g. pancreatitis). In the classic case of fat necrosis in severe acute pancreatitis, the necrosis arises because adipocytes in the peritoneum are broken and digested by inappropriately activated pancreatic enzymes.
With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations. It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration. Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.In nephrotic syndrome, SBP can frequently affect children but only very rarely can it affect adults. Diagnosis
Infection of the peritoneum causes an inflammatory reaction with a subsequent increase in the number of neutrophils in the fluid. Diagnosis is made by paracentesis (needle aspiration of the ascitic fluid); SBP is diagnosed if the fluid contains neutrophils at greater than 250 cells per mm3 (equals a cell count of 250 x106/L) fluid in the absence of another reason for this (such as inflammation of one of the internal organs or a perforation).The fluid is also cultured to identify bacteria. If the sample is sent in a plain sterile container, 40% of samples will identify an organism, while if the sample is sent in a bottle with culture medium, the sensitivity increases to 72–90%. Prevention
All people with cirrhosis might benefit from antibiotics (oral fluoroquinolone norfloxacin) if:

Ascitic fluid protein <1.0 g/dL.