Subcutaneous Fat Necrosis of the Newborn

Updated: May 15, 2018
  • Author: Sungat K Grewal; Chief Editor: William D James, MD  more...
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Subcutaneous fat necrosis of the newborn (SFNN) is an uncommon disorder characterized by firm, mobile, erythematous nodules and plaques over the trunk, arms, buttocks, thighs, and cheeks of full-term newborns. [1, 2] The nodules and plaques appear in the first several weeks of life. Subcutaneous fat necrosis of the newborn usually runs a self-limited course, but it may be complicated by hypercalcemia and other metabolic abnormalities. [1, 2]



The exact pathogenesis of subcutaneous fat necrosis of the newborn (SFNN) is not known. It is postulated that cold or stress-induced injury to immature fat cells results in the development of solidification and necrosis. A granulomatous infiltrate forms, which, through various pathways, may lead to life-threatening hypercalcemia. Staining of biopsy specimens demonstrates increased levels of 1alpha-hydroxylase within the granulomatous infiltrate, as is seen in other granulomatous conditions such as sarcoidosis. [3] Alpha-hydroxylase promotes the conversion of 25 OH D3 to its active form 1,25 OH 2D3; the latter increases intestinal absorption of calcium and calcium mobilization from bones, potentially leading to hypercalcemia. [1, 4, 5] Elevated levels of prostaglandin (PG) E2 have been reported in subcutaneous fat necrosis of the newborn. [6] and may contribute to hypercalcemia through a different pathway.

Alternative explanations for hypercalcemia include the release of calcium from necrotic fat cells or elevated parathyroid hormone (PTH) levels that indirectly increase serum calcium by promoting osteoclast activity. [7] A child with cyanotic heart disease treated with prostaglandins (intravenous PGE1) to maintain patent ductus arteriosus developed subcutaneous fat necrosis of the newborn; when the PGE1 was discontinued, the subcutaneous fat necrosis of the newborn resolved. [6] Elevated prostaglandins contribute to the inflammatory cascade that follows, marked by thrombocytopenia, high acute-phase reactants such as C-reactive protein, and fever. [8, 9] The latter has been attributed to increased levels of PGE2 and granuloma production of interleukin 1.



The cause of subcutaneous fat necrosis of the newborn (SFNN) is not known. Hypothermia is a common antecedent. The brown fat of neonates has a greater ratio of saturated palmitic acid to unsaturated oleic acid. Palmitic acid has a higher melting point than oleic acid, making it more susceptible to solidification and crystallization in response to lowered temperature. Many cases of subcutaneous fat necrosis of the newborn have been reported in newborns who sustained perinatal hypoxic-ischemic injury and were treated by hypothermia to prevent encephalopathy and serious brain injury. [10, 11, 12, 13] Cases of subcutaneous fat necrosis of the newborn have been reported after both whole-body cooling [14, 15, 16]  and selective head-cooling. [17] One infant developed subcutaneous fat necrosis of the newborn after ice-bag placement for the treatment of supraventricular tachycardia [18] and  another after hypothermic cardiac surgery. [1, 19]

Other neonatal stresses that have been associated with subcutaneous fat necrosis of the newborn include cesarean delivery, [1, 4, 20, 21] Rh factor incompatibility, meconium aspiration, [21] placenta previa, umbilical cord prolapse, anoxia, seizures, [21] preeclampsia, maternal cocaine abuse, [22] gestational diabetes, [23] maternal use of calcium antagonists during pregnancy, [24] familial dyslipidemia, and a family history of thrombophilia. [23] Some evidence implicates a maternal hypercoagulable state such as protein C deficiency and antiphospholipid syndrome. [23] Local pressure trauma during delivery from forceps, from prolonged labor, and from being large for gestational age (macrosomia) may play a role. [20, 21]




Frequency is unknown; subcutaneous fat necrosis of the newborn (SFNN) is rare.


Race does not play a role.


Sex does not play a role.


Subcutaneous fat necrosis of the newborn (SFNN) occurs in the first several weeks of life. [1, 2, 4] Hypercalcemia, if it occurs, begins in children aged 1-2 months.



Overall, the prognosis for subcutaneous fat necrosis of the newborn (SFNN) is excellent. Self-resolution without sequelae is the norm. It is a harmless, self-limited condition. As the lesions regress, hypertriglyceridemia may result from the mobilization of fatty acids from the affected adipose tissue. There may be atrophic scars.

The areas of fat necrosis may rarely progress to scarring or ulceration. Some degree of subcutaneous atrophy is common. [23] Soft tissue calcification may last for years. Nephrocalcinosis without evidence of adverse renal outcomes has been reported to persist up to 4 years after follow-up. [25]  Rarely, significant morbidity (seizures, blindness, failure to thrive) and even mortality (from infection and cardiac arrest) can result from the associated hypercalcemia. [1, 26]


Patient Education

Parents should be informed of the early signs of hypercalcemia so they can seek prompt medical attention.