You are in: eMedicine Specialties > Dermatology > DISEASES OF THE SUBCUTANEOUS TISSUE Subcutaneous Fat Necrosis of the NewbornArticle Last Updated: Mar 23, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Howard Pride, MD, Associate Professor, Departments of Pediatrics and Dermatology, Geisinger Medical Center Howard Pride is a member of the following medical societies: American Academy of Dermatology and Society for Pediatric Dermatology Editors: Daniel Mark Siegel, MD, MS, Director, Procedural Dermatology Fellowship Program, Clinical Professor of Dermatology, Department of Dermatology, State University of New York Downstate; David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic; Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University; William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System Author and Editor Disclosure Synonyms and related keywords: obstetric trauma, obstetrical trauma, meconium aspiration, neonatal asphyxia, neonatal hypothermia, neonatal peripheral hypoxemia, SCFN INTRODUCTIONSection 2 of 11
  BackgroundSubcutaneous fat necrosis of the newborn (SCFN) is an uncommon disorder characterized by firm, erythematous nodules and plaques over the trunk, arms, buttocks, thighs, and cheeks of full-term newborns. The nodules and plaques appear in the first several weeks of life. SCFN usually runs a self-limited course, but it may be complicated by hypercalcemia and other metabolic abnormalities. PathophysiologyThe exact pathogenesis of SCFN in not known. It is postulated that cold or stress-induced injury to immature fat results in the development of solidification and necrosis. A granulomatous infiltrate forms subsequently and nonrenal absorption of calcium increases. No other organ systems are involved, unless hypercalcemia intervenes. FrequencyUnited StatesFrequency is unknown; SCFN is rare. InternationalFrequency is unknown; SCFN is rare. Mortality/MorbidityThis is a harmless, self-limited condition. Significant morbidity (seizures, blindness, failure to thrive) and even mortality (from infection and cardiac arrest) can result from the associated hypercalcemia. RaceRace does not play a role in this condition. SexSex does not play a role in this condition. AgeSCFN occurs in the first several weeks of life. Hypercalcemia, if it occurs, begins in children aged 1-2 months. CLINICALSection 3 of 11
HistoryNewborns who develop SCFN usually are healthy and full-term at delivery but have had some antecedent obstetric trauma, meconium aspiration, asphyxia, hypothermia, or peripheral hypoxemia. Within the first several weeks of life, hard, indurated nodules and plaques with ill-defined overlying erythema develop on the trunk, arms, buttocks, thighs, or cheeks. The lesions are not warm or painful. Congenital ulceration has been reported. PhysicalThe infants usually appear well and are afebrile. The condition begins as an area of edema and progresses to variably circumscribed nodules and plaques that have a deep, indurated feel, implying a panniculitis. The overlying skin may be red, purple, or flesh-colored and may look taut and shiny. Lesions may become fluctuant and spontaneously drain necrotic fat. If mild hypercalcemia is present, findings might be absent, or the child may display weight loss, irritability, apathy, or hypotonia. Examination may reveal growth and mental retardation, hypertension, seizure activity, and tissue calcification with more severe hypercalcemia. CausesThe cause of SCFN is unknown. Neonatal stress and hypothermia from various sources, such as Rh factor incompatibility, meconium aspiration, placenta previa, umbilical cord prolapse, anoxia, seizures, preeclampsia, maternal cocaine abuse, and hypothermic cardiac surgery, play some role in instigating the process. One infant developed SCFN after icebag placement for treatment of supraventricular tachycardia. Three possible mechanisms for the development of the necrosis have been proposed.
DIFFERENTIALSSection 4 of 11
Cellulitis Erysipelas Sclerema Neonatorum
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| Drug Name | Furosemide (Lasix) |
|---|---|
| Description | Increases excretion of water by interfering with chloride-binding co-transport system, which in turn inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Causes increased excretion of water, sodium, chloride, magnesium, and calcium. |
| Pediatric Dose | 1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; not to administer >q6h |
| Contraindications | Documented hypersensitivity; hepatic coma, anuria, and state of severe electrolyte depletion |
| Interactions | Metformin decreases furosemide concentrations; furosemide interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter |
Prednisone may be used if other measures fail. Interferes with metabolism of vitamin D to active form, 1,25-dihydroxyvitamin D, and also may inhibit production of metabolite by macrophages involved in granulomatous inflammatory process.
| Drug Name | Prednisone (Deltasone) |
|---|---|
| Description | May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. |
| Pediatric Dose | 4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid-qid; taper over 2 wk as symptoms resolve |
| Contraindications | Documented hypersensitivity; viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, and fungal or tubercular skin infections; GI disease |
| Interactions | Coadministration with estrogens may decrease prednisone clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
| Pregnancy | B - Usually safe but benefits must outweigh the risks. |
| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use |
| Media file 1: Ill-defined erythema overlying an indurated plaque of a newborn. | |
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| Media file 2: Bruiselike indurated plaque of subcutaneous fat necrosis of the newborn on the lower back of a newborn. | |
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| Media file 3: Ill-defined erythema and induration of subcutaneous fat necrosis of the newborn on the posterior calf of a newborn. | |
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Subcutaneous Fat Necrosis of the Newborn excerpt
Article Last Updated: Mar 23, 2007
