Indurated, Purplish Plaque on a Newborn FREE

A female neonate carried to term and born weighing 2.87 kg was delivered spontaneously to a 29-year-old woman with no medical illness. The infant had meconium aspiration at delivery and required mechanical ventilation for 2 days. Her hospital stay was complicated by the development of pneumothorax and recurrent hypoglycemia. On day 4 she developed thrombocytopenia and 3 days later was noted to have an erythematous patch on her back that was diagnosed as cellulitis and treated with intravenous antibiotics. However, the lesion persisted and dermatologic review on day 9 of her life revealed an indurated, well-defined purplish plaque measuring 10.5 × 8 cm over her back (Figure 1) that was tender and warm but nonpulsatile. The remaining findings of her physical examination were normal. She had been extubated successfully with no persistent respiratory symptoms, and there was no hepatosplenomegaly or lymphadenopathy.

A . Aspirate the lesion and send for culture and cytology
B . Begin intravenous hydration and furosemide
C . Do nothing; the lesion will resolve over time
D. Obtain a biopsy of the lesion

Subcutaneous fat necrosis

D. Obtain a biopsy of the lesion

The key clinical feature in this case is recognizing that this patient could have subcutaneous fat necrosis of the newborn, which may occur during the first few days to weeks of life.² Differential diagnosis includes sclerema neonatorum, cellulitis, histiocytosis, and sarcoma. Distinguishing among these conditions would require performing a skin biopsy, which is the preferred course of action in this case.

Subcutaneous fat necrosis of the newborn is a rare disorder that usually affects full-term neonates.³ It is a form of panniculitis and consists of either single or multiple well-circumscribed, erythematous, indurated, nodular areas of fat necrosis.³ It is occasionally tender to palpation. The common sites of occurrence include the cheeks, back, buttocks, arms, and thighs. Predisposing factors include maternal gestational diabetes mellitus, preeclampsia, or cocaine or calcium blocker use; delivery complications including hypothermia, hypoxemia, infections, or trauma; and newborn anemia or thrombocytosis.² Birth asphyxia and meconium aspiration were the most frequently recognized etiologic associations in a series of 11 patients.⁴

Differential diagnosis includes sclerema neonatorum, cellulitis, histiocytosis, benign tumors (hemangiomas and infantile myofibromatosis), and malignant tumors (sarcoma, neuroblastoma, leukemia).³ There have also been reports of newly recognized subcutaneous fat necrosis in the setting of hypothermia in the neonatal intensive care unit.³ Definitive diagnosis is made by skin biopsy, which shows needle-shaped clefts within fat cells and foamy histiocytes, fat necrosis and granulomatous infiltrate of lymphocytes, and histiocytes and multinucleated giant cells.⁵

The pathogenesis of this condition is unknown. One possible mechanism is crystallization of neonatal fat during cold stress, with consequent adipocyte necrosis. Other proposed mechanisms include immaturity of the enzymatic systems involved in fatty acid metabolism and hypoxic injury to subcutaneous fat owing to local trauma during delivery.⁶

Subcutaneous fat necrosis of the newborn is usually self-limited. Rare life-threatening complications include hypercalcemia. The mean time from the development of lesions to the diagnosis of hypercalcemia is 24 days. Hypercalcemia is mostly moderate and without clinical symptoms. However, kidney calcium deposits occur. Elevated serum calcium levels can be detected up to 3 months after diagnosis. Other complications include dyslipidemia, thrombocytopenia, hypoglycemia, and rarely, progression to subcutaneous atrophy.

Treatment is aimed at prevention and management of the complications. Analgesia is given if the lesion is painful. If the fat liquefies, aspiration of fluctuant material may be necessary for decompression, but this is seldom required.⁷ Patients should be monitored for hypercalcemia; treatment includes intravenous hydration and furosemide. Corticosteroids, calcitonin, and bisphosphonate may be needed.^7- 8

In this patient, histologic examination of the skin biopsy revealed septal and lobular inflammatory infiltrate of lymphocytes, plasma cells, histiocytes, and a few eosinophils wedged in between the subcutaneous fat cells. The fat cells contained fine eosinophilic cytoplasmic strands forming clefts (Figure 2). These findings were diagnostic of subcutaneous fat necrosis of the newborn. She was treated conservatively and monitored for complications of the condition. She was discharged well on day 14 of life. Her hypoglycemia and thrombocytopenia resolved before discharge. Her serum calcium level remained within the reference range on follow-up.