a case report on subcutaneous fat necrosis in newborn.

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A CASE REPORT ON SUBCUTANEOUS FAT
NECROSIS IN NEWBORN.
Dr. Sindhura Kasturi, Dr. Lalat Barun Patra, Dr. Rajesh Kumar
Sethi, Dr. Debi Prasad Patra
ABSTRACT: Subcutaneous 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. Subcutaneous fat
necrosis of the newborn usually runs a self-limited course, but it may be
complicated by hypercalcemia and other metabolic abnormalities. [1]
Key words: Subcutaneous fat necrosis of the newborn (SCFN)
INTRODUCTION: Newborns who develop subcutaneous fat necrosis of the
newborn 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 days to 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. Pain may
occur, with a frequency as high as 25% in one series[2] Three possible
mechanisms for the development of the necrosis have been proposed.
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

An underlying defect in fat composition or metabolism may be present,
whereby inadequately developed enzyme systems involved in fatty acid
desaturation result in increased saturated fatty acids within the
subcutaneous tissue. Neonatal stress may exacerbate this defect and
increase the susceptibility to subcutaneous fat necrosis of the newborn.
The fat of neonates is composed of saturated fatty acids (stearic and
palmitic acids) with a relatively high melting point. Neonatal stress
resulting in hypothermia may induce fat to undergo crystallization
leading to necrosis.
Local pressure induced trauma during delivery from macrosomia,
forceps, or prolonged trauma may play a role in the induction of necrosis.
Subcutaneous fat necrosis of the newborn has been reported in children
delivered by cesarean section, suggesting that pressure necrosis cannot be
the only cause.
CASE STUDY:.A 3.5kg term male baby was delivered to a primi gravida
mother, with uneventful antenatal period, by normal vaginal delivery. There was
no history suggestive of perinatal asphyxia. Child was on exclusive breast
feeding with no complaints during early neonatal period. On 10th.day of life,
child presented to out patient department with complaint of excessive cry since
two days. On examination child was having a large 6x5 cm plaque with
irregular margin, raised above the surrounding area, on the back of the chest,
which was noticed by mother two days back. Skin over plaque was smooth,
reddish purple in color with irregular borders, indurated and was not mobile.
Tenderness was present .Other systemic examination was normal. Child was
kept on exclusive breast feeding. Total serum calcium value was found to be
11.2mg/dl. Sepsis screen was negative. Child was followed up with monthly
serum calcium which came back to normal value and swelling gradually
resolved.
Discussion: SCFN is a rare, benign, inflammatory disorder of the adipose
tissue, which resolves spontaneously in a few weeks time. Its exact prevalence
and etiopathogenesis are yet unknown. Several etiological factors have been
associated with SCFN. However, in many cases the past history of the patient is
negative [3, 4]. Complications of SCFN include hypercalcemia, pain,
dyslipidemia, renal failure, and late subcutaneous atrophy [8]. Hypercalcaemia
is a rare complication of SCFN with a high mortality rate up to 15%. Its
pathogenesis remains obscure while possible mechanisms include enhanced
bone resorption (as a result of prostaglandin E2 action), increased vitamin D
sensitivity, calcium release from calcified necrotic subcutaneous fat and,
mainly, extra renal unregulated production of calcitriol from the macrophages
at the site of the granulomatous inflammatory process.[3,6] Owing to the
severe sequelae of hypercalcaemia, it is recommended that serum calcium
levels be checked periodically in infants with SCFN[3,5,6]as it was performed in
the present case. The main clinical differential diagnosis is sclerema
neonatorum (SN). Although the association of SN and SCFN has been reported
in a neonate, several features distinguish between SCFN and SN, such as early
onset, the wide distribution and extent of lesions, and a poor general status of
the baby in latter condition. [7].
SCFN is a complication that should come to mind in newborns with perinatal
asphyxia, and the presence of hypothermia and polycythemia may accelerate
the pathogenic process. In neonates hospitalized for perinatal asphyxia, special
care should be taken to avoid hypothermia unless absolutely indicated for
prevention of hypoxic ischemic encephalopathy. It is needed to stress the
importance of nursing care of avoiding pressure induced trauma to prevent the
development of SCFN.
REFERENCES:
[1] Howard Pride, MD; Chief Editor: William D James, M, medscape reference
[2]Mahe E, Girszyn N, Hadj-Rabia S, Bodemer C, Hamel-Teillac D, De Prost Y.
Subcutaneous fat necrosis of the newborn: a systematic evaluation of risk factors, clinical
manifestations, complications and outcome of 16 children. Br J Dermatol. Apr
2007;156(4):709-15. [Medline].
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and hypercalcemia: Case report and review of the literature. Pediatr Dermatol 1993; 10: 271–
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Subcutaneous fat necrosis of the newborn: a systematic evaluation of risk factors, clinical
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