Subcutaneous Fat Necrosis of the Newborn

Clinical Features. Subcutaneous fat necrosis of the newborn usually occurs in premature or full-term infants, often after a complicated delivery by forceps or by cesarean section . Indurated, erythematous to violaceous nodules and plaques appear in the subcutis a few days to a week after birth. Rarely, in cases with numerous nodules, the lesions may discharge a caseous material . The patient's health generally is good, and the nodules resolve spontaneously after a few weeks or months. Rarely, some infants are severely ill and die . In 16 reported cases, the subcutaneous fat necrosis was associated with hypercalcemia, and 3 patients died . Thrombocytopenia, hypertriglyceridemia, and hypoglycemia have also been reported . The development of extensive fat necrosis has been reported in infants following induced hypothermia used in cardiac surgery (145) or after surface hypothermic treatment of birth asphyxia, producing hypercalcemia 7 weeks later. An underlying defect in composition and metabolism of fat has been assumed to exist in such cases. The cases need to be followed for the development of hypercalcemia, which may occur in approximately one third of cases . Subcutaneous fat necrosis has been reported also in a number of rare associations (3), including with maternal cocaine use and intrapartum administration of calcium channel blockers.

Histopathology.

 Focal areas of fat necrosis are present in the fat lobules and are infiltrated by macrophages and foreign body-type giant cells (Fig. 20-28). Fat deposits in the macrophages and giant cells contain crystalline fat, which after lipid extraction appears as needle-shaped clefts in a radial arrangement . In frozen sections, the radial clefts contain doubly refractile crystals. Calcium deposits usually are small and scattered in the necrotic fat. If the necrosis is

extensive, calcium deposits may be large and require several years to be reabsorbed.

Pathogenesis. Electron microscopic examination shows that the phagocytosis of fat crystals starts with the invasion of fat cells by cytoplasmic projections of macrophages. Subsequently, fat crystals are seen within the cytoplasm of macrophages and of foreign body-type giant cells, which result from fusion of the macrophages .

The cause of subcutaneous fat necrosis of the newbom is not known. There is debate about the role of trauma, as many of the patients have been premature infants who were born by forceps delivery or who otherwise endured a difficult delivery. However, lesions have been reported in children delivered by cesarean section .

differential Diagnosis

. Both subcutaneous fat necrosis of the newborn and sclerema neonatorum have crystalline arrays of needle-like clefts in the fat. Sclerema is a catastrophic diffuse illness that gives little time for extensive inflammation; thus, in sclerema, there is an absence of focal areas of fat necrosis with macrophages and giant cells. In sclerema, there is also an absence of calcifications and the presence of wide bands of fibrous tissue in the subcutis . Treatment of children with high doses of steroids-for example, as was done for rheumatic fever-can produce poststeroid panniculitis with subcutaneous lesions very similar histologically to those of subcutaneous fat necrosis of the newborn . The deep nodules usually occur within 1 to 30 days after the cessation of high-dose steroid treatment. Traumatic fat necrosis has focal areas of necrosis and inflammation but lacks the crystals in the fat. Localized infection can be difficult to exclude clinically, but the infants with subcutaneous fat necrosis are generally rather healthy and are not septic.