1214J Med Assoc Thai Vol. 90 No. 6 2007
Correspondence to : Singalavanija S, Dermatology Unit, Queen
Sirikit National Institute of Child Health, 420/8 Rajvithi Rd,
Bangkok 10400, Thailand. Phone: 0-2354-8439, E-mail:
Subcutaneous Fat Necrosis of the Newborn
Srisupalak Singalavanija MD*,
Wanida Limponsanurak MD*, Titaporn Wannaprasert MD*
* Dermatology Unit, Queen Sirikit National Institute of Child Health, Department of Medical Service,
Ministry of Public Health, College of Medicine, Rangsit University
Subcutaneous fat necrosis of the newborn (SCFN) is an uncommon disorder in full term infants who
have a perinatal condition. The authors reported seven cases of subcutaneous fat necrosis of the newborn at
Queen Sirikit National Institute of Child Health from 2002 to 2005. All cases were term babies with four male
cases, and three female cases. Five cases (70%) had perinatal asphyxia. The mean age of onset was 14 days
(range 3-42 days).The locations of SCFN were back (3 cases), shoulder (2cases), arm (2 cases), buttock (1
case), and neck (1 case). Skin biopsy was performed in three cases and was compatible with subcutaneous fat
necrosis. The treatment was supportive with close monitoring of serum calcium. Hypercalcemia was seen in
five cases (70%) and three cases were treated with oral prednisolone. Cutaneous lesions of all cases resolved
In conclusion, infants with subcutaneous fat necrosis should have serial serum calcium determina-
tions and should be observed closely for signs and symptoms of hypercalcemia such as irritability, anorexia,
constipation, and failure to thrive.
Keywords: Subcutaneous fat necrosis of the newborn, Hypercalcemia
Subcutaneous fat necrosis of the newborn
(SCFN) is an uncommon, benign process in full term
infants who experienced perinatal distress. It is cha-
racterized by indurated, erythematous nodules or
plaques over bony prominences such as the back,
arms, buttocks, thighs, and face. The condition may be
associated with maternal disorders such as diabetes,
preeclampsia, or perinatal complications such as birth
asphyxia, cord accidents, meconium aspiration, cold
injury, hypothermia, hypoxemia, and hypoglycemia(1-6).
It is a temporary, self-limited condition of unknown
pathophysiology. Hypercalcemia is a rare complication,
which can be life threatening if not treated adequately(7).
There have been few case reports of SCFN
and mainly single case reports(8-12).The authors herein
report a series of seven cases of SCFN seen at Queen
Sirikit National Institute of Child Health during 2002-
The patient was a full term infant girl, born by
caesarian section due to thick meconium stain amniotic
fluid with a birth weight of 3180 grams. Her Apgar scores
were 5 and 7at 1 and 5 minutes. She developed respira-
tory distress with meconium aspiration syndrome
and left pneumothorax requiring 4 days of ventilatory
support. On the 7th day of life, a painful subcutaneous
mass measuring 5 x 5 cm was noticed at the left upper
thigh and another 3 x 3 cm mass was seen at the right
shoulder with some inflammation and fluctuation. Skin
biopsy from the upper thigh was done and showed
normal epidermis and dermis, scattered patchy areas of
fat necrosis with crystallization of fat, forming needle-
shaped clefts in a radial arrangement in the macro-
phages and lipocytes (Fig. 1, 2). Subcutaneous fat
necrosis of the newborn with secondary bacterial
infection was diagnosed. The patient was treated with
cloxacillin and gentamicin intravenously for 7 days.
Serum ionized calcium was monitored. The level was
1.21 mmol/L (normal 1.18-1.3 mmol/L) which increased
J Med Assoc Thai 2007; 90 (6): 1214-20
Full text. e-Journal: http://www.medassocthai.org/journal
J Med Assoc Thai Vol. 90 No. 6 2007 1215
to 1.24 mmol/L on the 14th day of life. At the age of 27
days, serum calcium increased to 1.41 mmol/L with
clinical symptoms of irritability. Oral prednisolone at
the dose of 1 mg/kg/day was given for 2 weeks. Follow
up serum calcium levels were normal after predniso-
lone treatment 2 weeks. The lesions resolved in 4
months without scarring.
The patient was a full term infant boy, born by
emergency cesarean section due to fetal distress with
a birth weight of 3640 grams. His Apgar scores were
1 and 1 at 1 and 5 minutes. Cardiopulmonary resus-
citation was performed for 10 minutes. The infant
developed respiratory distress requiring ventilatory
support for 2 days. Ampicillin and cefotaxime were given
for 18 days due to clinical sepsis. On the 20th day of
life, multiple painless firm subcutaneous plaques were
noticed on the left arm. A clinical diagnosis of subcuta-
neous fat necrosis was made. Skin biopsy from the left
arm revealed lobular panniculitis with needle-shaped
cleft in fat cells. His serum calcium levels were slightly
elevated at 1.41 mmol/L (normal 1.18-1.30 mMol/L).
Serum phosphate, BUN, creatinine, parathyroid hor-
mone, urine calcium/creatinine, and film of the long
bone were normal. The infant developed signs of irrita-
bility and poor feeding so he was treated with oral
prednisolone at the dose of 1mg/kg/day for 2 weeks
and weaned off in 3 months. The infant was kept in the
hospital for 6 weeks. His serum calcium was closely
monitored and was unremarkable when he was 3
months old. The lesions resolved without scarring at
age 5 months but he developed spastic cerebral palsy
due to severe perinatal asphyxia.
The third patient was a full term infant boy, born by
cesarean section due to primibreech presentation with
a birth weight of 3335 grams. His Apgar scores were 8
and 10 at 1 and 5 minutes. During the perinatal period,
he developed hypoglycemia and hyperbilirubinemia.
On the third day of life, a single, non-tender, firm 3x5 cm
subcutaneous nodule was noticed at the upper back.
His serum calcium was slightly elevated at 1.34 mmol/L
(normal 1.18-1.30 mmol/L). His mother refused a skin
biopsy. Serial serum calcium levels were monitored and
were within normal limits. He was closely observed
without prednisolone treatment. At the age of 1 month,
the lesion disappeared completely without any skin
The fourth patient was an infant girl with
Down’s syndrome, born via caesarean section due to
previous caesarian section, from a hepatitis B antigen
positive mother, with a birth weight of 3790 grams.
Her Apgar scores were 5 and 6 at 1 and 5 minutes. The
infant developed respiratory distress requiring venti-
latory support for 3 days. During the perinatal period,
she developed transient hypoglycemia, dyspnea and
tachypnea. Cardiac examination showed systolic
murmur grade II at left lower parasternal border. Echo-
cardiogram showed atrium septal defect secondum. She
was also diagnosed with congenital hypothyroidism
and was treated with eltroxin. The infant was discharged
home after 1 month of hospitalization. On the 42nd day
Biopsy from the subcutaneous tissue showed the
pathology in the subcutaneous tissue (Low power)
A high power view showed inflammatory cells with
the characteristic needle-shaped clefts
1216J Med Assoc Thai Vol. 90 No. 6 2007
of life, the infant developed two non-tender, firm sub-
cutaneous nodules with diameter of 1x1 cm and 2 x 2 cm
at the left shoulder. A clinical diagnosis of subcuta-
neous fat necrosis was made. The baby’s mother
refused a skin biopsy. Serum ionized calcium was moni-
tored and revealed 1.33 mmol/L (normal 1.18-1.30 mmol/
L). Serum phosphate level was normal. The infant was
closely monitored for serial serum calcium and revealed
normal levels. The baby was closely observed because
she had no signs and symptoms of hypercalcemia.
At the age of 4 months, the subcutaneous nodules
decreased in size and had completely disappeared at
the age of 7 months without specific treatment.
The fifth patient was a 22-day-old term boy,
born by cesarean section due to fetal distress at a
private hospital, with a birth weight of 3,330 grams. His
Apgar scores were 1, and 1 at 1 and 5 minutes. The
patient was intubated at birth because of bradycardia
and poor respiratory effort. He was diagnosed with
severe birth asphyxia with sepsis and he was treated
with intravenous cefotaxime and amikin. On the fifth
day of life, multiple subcutaneous plaques were ob-
served on his back and left arm. The baby was dis-
charged from the hospital on the 18th day of life without
treatment. When he was 22 days old, his mother brought
him to Queen Sirikit National Institute of Child Health
for evaluation of his skin lesions. Physical examination
revealed multiple violaceous, firm, well-circumscribed,
subcutaneous plaques involving left upper arm and
upper back. His ionized serum calcium level was 1.44
mmol/L (normal 1.18-1.30mmol/L). Histopathology from
the subcutaneous plaques showed focal lobular pan-
niculitis with needle-shaped cleft in fat cells. Treat-
ment was observation for signs and symptoms of hy-
percalcemia and the skin lesions resolved in 2 months
without specific treatment.
The sixth patient was a full term infant boy,
born by forcep extraction due to thick meconium stain
amniotic fluid and fetal distress. His Apgar scores were
3 and 7 at 1 and 5 minutes. He developed mild meco-
nium aspiration syndrome and required oxygen therapy.
On the 4th day of life, a subcutaneous mass diameter
0.5x3.5 cm was noticed on the left neck. Serum ionized
calcium was 1.41mmol/L (normal 1.18-1.30 mmol/L) but
the patient had no signs and symptoms of hypercalce-
mia. At age 1 month, the skin lesion disappeared with-
out specific treatment.
The seventh patient was a full term infant girl,
born by caesarian section due to large omphalocele
and fetal distress with a birth weight of 2900 grams.
Her Apgar scores were 1 and 3 at 1 and 5 minutes. On
the 5th day of life, large subcutaneous plaques were
noticed on her back and both buttocks. Her serum
ionized calcium was 1.77 mmol/L (normal 1.18-1.30
mmol/L). Prednisolone at the dose of 1 mg/kg/day was
given for 2 weeks due to signs of irritability and serum
ionized calcium was normal after two weeks of treat-
ment. The lesions were resolved in 1 month.
The details of clinical manifestations and
treatments of the presented cases are summarized in
Subcutaneous fat necrosis of the newborn
was first described by Cruise in 1875 and initially was
called scleroderma of the newborn infant(13). It is an
uncommon transient condition seen in term to post
term neonates who experience perinatal complications
in the first few weeks of life.
The etiology for SCFN is unknown, but may
be initiated by ischemic injury, hypoxia and hypother-
mia(1-6). Perinatal asphyxia or difficulty at labor may be
associated with SCFN. The most frequently recognized
possible etiologic factors in this series was birth as-
phyxia in 5 of 7 cases (70%) and meconium aspiration
syndrome in 2 of 7cases (28%).
The main clinical differential diagnosis of
SFCN is sclerema neonatorum (SN). These two entities
may be distinguished from each other based on history
and physical examination(14). When the clinical diag-
nosis is not typical, the skin biopsy is helpful. Skin
biopsy of SCFN demonstrated necrosis of fat, abundant
histiocytes, multinucleated giant cells with granuloma
formation and lipocytes with characteristic radically
arranged needle shaped clefts in comparisons with
SN that showed adipocytes with scattered small clefts
and in older lesions with thickened fibrotic septate and
calcifications(14). In the present study, the authors did
skin biopsies in three cases and were compatible with
subcutaneous fat necrosis.
Subcutaneous fat necrosis of the newborn
generally follows an uncomplicated course with
spontaneous resolution over several weeks to several
months(15,16). The treatment was aimed at prevention
and management of complications. Some lesions become
calcified or fluctuant with liquefied fat. Mild atrophy of
the skin may be noticed after resolution(10).
J Med Assoc Thai Vol. 90 No. 6 20071217
Table 1. Demographic data of SCFN of the term newborn
calcium (normal =
C/S due thick
Patchy areas of fat
- Meconium aspiration
necrosis with needle-
C/S due to
- Respiratory distress
C/S due to
C/S due to
- Down’s syndrome
C/S due to
F/E due to
- Mild meconium
C/S due to
- Rupture omphalocele
C/S = caesarian section, F/E = forceps extraction, ND = not done
1218J Med Assoc Thai Vol. 90 No. 6 2007
cutaneous lesions resolved without sequelae.
1. Chen TH, Shewmake SW, Hansen DD, Lacey HL.
Subcutaneous fat necrosis of the newborn. A case
report. Arch Dermatol 1981; 117: 36-7.
2. Glover MT, Catterall MD, Atherton DJ. Subcu-
taneous fat necrosis in two infants after hypo-
thermic cardiac surgery. Pediatr Dermatol 1991; 8:
3. Chuang SD, Chiu HC, Chang CC. Subcutaneous
fat necrosis of the newborn complicating hypo-
thermic cardiac surgery. Br J Dermatol 1995; 132:
4. Wiadrowski TP, Marshman G. Subcutaneous fat
necrosis of the newborn following hypothermia
and complicated by pain and hypercalcaemia.
Australas J Dermatol 2001; 42: 207-10.
5. Silverman AK, Michels EH, Rasmussen JE. Subcu-
taneous fat necrosis in an infant, occurring after
hypothermic cardiac surgery. Case report and
analysis of etiologic factors. J Am Acad Dermatol
1986; 15(2 Pt 2): 331-6.
6. Katz DA, Huerter C, Bogard P, Braddock SW.
Subcutaneous fat necrosis of the newborn. Arch
Dermatol 1984; 120: 1517-8.
7. Cunningham K, Paes BA. Subcutaneous fat
necrosis of the newborn with hypercalcemia: a
review. Neonatal Netw 1991; 10: 7-14.
8. Fenniche S, Daoud L, Benmously R, Ben Ammar F,
Khelifa I, Chaabane S, et al. Subcutaneous fat
necrosis: report of two cases. Dermatol Online J
2004; 10: 12.
9. Kaya Z, Ergenekon E, Erol I, Poyraz A, Koc E,
Atalay Y. Subcutaneous fat necrosis. Indian J
Pediatr 2004; 71: 1041.
10. Burden AD, Krafchik BR. Subcutaneous fat
necrosis of the newborn: a review of 11 cases.
Pediatr Dermatol 1999; 16: 384-7.
11. Caple JI, Reyes S. Subcutaneous fat necrosis of
the newborn: a case presentation. J Perinatol
1996; 16: 140-1.
12. Klaiudom C. Subcutaneous fat necrosis of the new-
born (SCFN): a case report. Nopparat Rajathanee
Hosp Med J 1999; 10: 56-60.
13. Crus P. Ein fall von sclerodermie (sogenannt
sclerodermis adulotorum bei saighing. St
Peterburg) Zeitichrify 1875: 5: 306.
14. Fretzin DF, Arias AM. Sclerema neonatorum and
subcutaneous fat necrosis of the newborn. Pediatr
Dermatol 1987; 4: 112-22.
The most important complication of SCFN,
which all the patients should be regularly monitored
for, is hypercalcemia. Other complications are throm-
bocytopenia, hypoglycemia, and hypertriglyceride-
Hypercalcemia usually occurs between 2 to
16 weeks, most commonly at 6-8 weeks(17-22). The hy-
percalcemia is often mild and asymptomatic but can be
symptomatic. Clinically, the most common feature of
hypercalcemia is failure to thrive, vomiting, feeding
difficulties, irritability, hypotonia, and constipation.
Seizures, cardiac arrest, and renal failure are serious
sequelae of prolong hypercalcemia. Mortality rate from
untreated hypercalcemia complicating SCFN has been
estimated at 15%(19).
The pathogenesis of hypercalcemia follow-
ing SCFN is not well understood. Suggested mecha-
nisms include elevated prostaglandin E and elevated
parathyroid hormone levels(21,23). Other proposed the
elevated 1, 25 (OH)2D3 from the fat tissue stimulates
intestinal calcium uptake(24,25).
Management of hypercalcemia in SCFN
depends on the clinical and level of serum inonized
calcium. If the patient has symptoms of hypercalcemia
such as lethargy or irritability, aggressive management
is indicated. Treatment of SCFN with hypercalcemia
may include adequate hydration, vitamin D restriction,
a low calcium diet, and a calcium wasting diuretic such
as furosemide(26-28). Oral prednisone effectively lowers
serum calcium levels by interfering with metabolism of
vitamin D to the active form 1, 25-dihydroxyvitamin D.
Prednisone may also inhibit production of this meta-
bolite by macrophages involved in the granulomatous
inflammatory process. Etidronate, which is a member
of the bisphosphanate group, is known to decrease
bone resorption. It has been reported to be successful
in controlling severe hypercalcemia in cases of resis-
In the present study, all cases were closely
monitored for hypercalcemia and five cases (70%)
developed hypercalcemia. Three cases (case 1, 2, and
7) developed symptoms of hypercalcemia such as irri-
tability and were treated with oral prednisolone. Serum
calcium returned to normal after treatment ranged
from 2 weeks to 3 months. Another two cases with
hypercalcemia (case 5 and case 6) were asymptomatic
so treatment is only observation.
In summary, the indurated skin lesions and
clinical course of the presented patients were typical
of SCFN with compatible skin biopsy in three cases.
Hypercalcemia developed in five cases (70%). All sub-
J Med Assoc Thai Vol. 90 No. 6 20071219
15. Anderson DR, Narla LD, Dunn NL. Subcutaneous
fat necrosis of the newborn. Pediatr Radiol 1999;
16. Tran JT, Sheth AP. Complications of subcuta-
neous fat necrosis of the newborn: a case report
and review of the literature. Pediatr Dermatol
2003; 20: 257-61.
17. Lewis A, Cowen P, Rodda C, Dyall-Smith D. Sub-
cutaneous fat necrosis of the newborn compli-
cated by hypercalcaemia and thrombocytopenia.
Australas J Dermatol 1992; 33: 141-4.
18. Hicks MJ, Levy ML, Alexander J, Flaitz CM.
Subcutaneous fat necrosis of the newborn and
hypercalcemia: case report and review of the
literature. Pediatr Dermatol 1993; 10: 271-6.
19. Norwood-Galloway A, Lebwohl M, Phelps RG,
Raucher H. Subcutaneous fat necrosis of the
newborn with hypercalcemia. J Am Acad Dermatol
1987; 16(2 Pt 2): 435-9.
20. Puzenat E, Aubin F, Zyka F, Fromentin C, Humbert
P. Subcutaneous fat necrosis of the newborn with
hypercalcemia. Ann Dermatol Venereol 2000; 127:
21. Thomsen RJ. Subcutaneous fat necrosis of the
newborn and idiopathic hypercalcemia. Report of
a case. Arch Dermatol 1980; 116: 1155-8.
22. Liu FT, Dobry MM, Shames BS, Goltz RW. Subcu-
taneous nodules and hypercalcemia in an infant.
Subcutaneous fat necrosis of the newborn. Arch
Dermatol 1993; 129: 898-2.
23. Sharata H, Postellon DC, Hashimoto K. Subcuta-
neous fat necrosis, hypercalcemia, and prostag-
landin E. Pediatr Dermatol 1995; 12: 43-7.
24. Finne PH, Sanderud J, Aksnes L, Bratlid D, Aarskog
D. Hypercalcemia with increased and unregulated
1,25-dihydroxyvitamin D production in a neonate
with subcutaneous fat necrosis. J Pediatr 1988;
24. Metz SA, Hassal E. PGE, hypercalcemia, and sub-
cutaneous fat necrosis. J Pediatr 1980; 97: 336.
25. Kruse K, Irle U, Uhlig R. Elevated 1,25-dihydroxy-
vitamin D serum concentrations in infants with
subcutaneous fat necrosis. J Pediatr 1993; 122:
26. Dudink J, Walther FJ, Beekman RP. Subcutaneous
fat necrosis of the newborn: hypercalcaemia with
hepatic and atrial myocardial calcification. Arch
Dis Child Fetal Neonatal Ed 2003; 88: F343-5.
27. Ghirri P, Bottone U, Coccoli L, Bernardini M,
Vuerich M, Cuttano A, et al. Symptomatic hyper-
calcemia in the first months of life: calcium-regu-
lating hormones and treatment. J Endocrinol
Invest 1999; 22: 349-53.
28. Rice AM, Rivkees SA. Etidronate therapy for
hypercalcemia in subcutaneous fat necrosis of
the newborn. J Pediatr 1999; 134: 349-51.
1220 J Med Assoc Thai Vol. 90 No. 6 2007 Download full-text
ศรีศุภลักษณ์ สิงคาลวณิช, วนิดา ลิ้มพงศานุรักษ์, ฐิตาภรณ์ วรรณประเสริฐ
การตายของไขมันใต้ผิวหนังในทารกแรกเกิด พบได้ไม่บ่อย มักพบในทารกแรกเกิดคลอดครบกำหนด
ที่มีปัญหาระหว่างคลอด ผู้รายงานได้รายงานทารกแรกเกิดที่มีการตายของไขมันใต้ผิวหนังจำนวน 7 ราย ที่มารับ
การรักษาที่สถาบันสุขภาพเด็กแห่งชาติมหาราชินี ตั้งแต่ปี พ.ศ. 2545 - พ.ศ.2548
ผลการศึกษา: ทุกรายเป็นทารกคลอดครบกำหนด เพศชาย 4 ราย เพศหญิง 3 ราย อายุที่มีอาการทางผิวหนังตั้งแต่
3 วันถึง 42 วัน ( เฉลี่ย14 วัน ) ตำแหน่งที่พบบ่อย ได้แก่ หลัง 3 ราย ไหล่ 2 ราย แขน 2 ราย ก้น 1 ราย คอ 1 ราย
พบว่าปัจจัยเสี่ยงในการเกิดการตายของไขมันใต้ผิวหนัง ได้แก่ ภาวะหายใจลำบากระหว่างคลอด 5 ราย (ร้อยละ 70)
ได้ทำการตัดชิ้นเนื้อเพื่อตรวจทางพยาธิวิทยา 3 ราย ผลการตรวจทุกรายเข้าได้กับการตายของไขมันใต้ผิวหนัง
การรักษาเป็นการรักษาตามอาการและเฝ้าระวังภาวะแคลเซียมสูงในเลือด การศึกษานี้พบแคลเซียมสูงในเลือด 5 ราย
(ร้อยละ 70) ซึ่งต้องให้ยาเพร็ดนิโสโลนกิน 3 ราย ทุกรายอาการทางผิวหนังหายเป็นปกติ
สรุป: ทารกแรกเกิดทุกรายที่มีการตายของไขมันใต้ผิวหนัง ควรตรวจหาระดับแคลเซียมในเลือดเป็นระยะเพื่อเฝ้าระวัง
ภาวะแคลเซียมสูงในเลือดได้แก่ อาเจียน ร้องกวน เลี้ยงไม่โต