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Newborn presenting with firm, erythematous rash
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An infant was born at 39-weeks gestation. The pregnancy was complicated by gestational diabetes, maternal hypothyroidism and group B strep colonization.
Vice Chair for Education at The Children’s Hospital at Scott
and White and Associate Professor of Pediatrics at Texas A&M University,
College of Medicine, Temple, Texas.
e-mail:jhbrien@aol.com
Preeclampsia developed, prompting induction of labor. Due to fetal decelerations, an emergent cesarean section was performed. At delivery, the infant was noted to be large for gestational age, limp and cyanotic, and had no heart rate, no respiratory effort, and required chest compressions and mechanical ventilation. She was transferred to our neonatal ICU for further management. Abnormal writhing movements and decerebrate posturing occurred; an electroencephalograph was abnormal, consistent with diffuse encephalopathy. Due to concerns of hypoxic/ischemic encephalopathy, her head was placed into a head cooling blanket. The infant received treatment with antibiotics and supportive care; blood cultures showed no growth. During the first week of life, ventilatory support was no longer required, feeds were started and head cooling was discontinued.
On day 8, an erythematous, tender, raised, firm rash was noticed at the posterior aspect of the neck. Within 24 hours, the area had spread to include the posterior occipital region of the skull, and two-thirds of the upper back (Figure 1). The peripheral white blood cell count was 18.5 × 103 cells/mL with 1% bands, 71% segmented neutrophils, 23% lymphocytes and 5% monocytes. Platelet count was 185 × 103 cells/mL; serum electrolytes and calcium were normal. The infant was tolerating feedings and had no fever or temperature instability. Antibiotics were restarted after a blood culture was obtained. After 3 days, the physical examination and clinical status were unchanged, with sterile blood culture.
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Figure 1: On day 8, an erythematous, tender,
raised, firm rash was noticed at the posterior aspect of the neck. Within 24
hours, the area had spread to include the posterior occipital region of the
skull, and two-thirds of the upper back. |
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Figure 2: The differential diagnosis can
include: hemangioma, sclerema neonatorum, and bacterial infection/cellulitis or
erysipelas. |
What’s Your Diagnosis?
- Cellulitis
- Hemangioma
- Subcutaneous fat necrosis
- Sclerema neonatorum
CASE DISCUSSION:
This infant had subcutaneous fat necrosis (SFN). This relatively rare condition usually affects term or post-term newborns in the first few weeks of life, often following perinatal complications such as meconium aspiration syndrome, birth asphyxia/hypoxia, newborn failure to thrive, perinatal complications, hypothermia or forceps delivery. Other risk factors include Rh factor incompatibility, gestational diabetes, pre-eclampsia, neonatal cardiac surgery, maternal cocaine abuse, meconium aspiration, placenta previa, local pressure trauma, exposure to active or passive smoking during pregnancy, macrosomia, and maternal, paternal or newborn risk factors for thrombosis.
SFN is a lobular panniculitis likely the result of antecedent trauma and/or ischemia to adipose tissue. Typical lesions include smooth, erythematous, subcutaneous nodules or plaques; these commonly develop on the cheeks, buttocks, back and limbs, often over boney prominences, 1 to 4 weeks after birth. The anterior trunk tends to be spared. The lesions may become fluctuant as fat liquefies; some may become calcified. Resolution of SFN usually occurs within 1 to 2 months, occasionally taking up to 6 months, if lesions become calcified.
The pathogenesis of SFN is likely due to the primary defect in fat metabolism of the neonate. Neonatal fat contains more saturated fatty acids that have a higher melting point. Once the temperature of the skin drops below the melting point of the fat, crystallization occurs, leading to formation of the granulomatous infiltrate. As a result, nonrenal absorption of calcium increases, occasionally leading to hypercalcemia.
If biopsied, the histologic appearance is a granulomatous reaction in the fat, with foreign body giant cells, lymphocytes, histiocytes and fibroblasts. Needle-shaped clefts are seen within the histiocytes, and giant cell and fibrosis may develop as the lesions resolve.
The differential diagnosis to be considered when evaluating a newborn for SCN include: hemangioma, sclerema neonatorum, and bacterial infection/cellulitis or erysipelas (Figure 2). As with SFN, most of these conditions are unlikely to be present at birth, with the exception of a large hemangioma. However, such a lesion would not enlarge so rapidly within the first week of life. Sclerema neonatorum, which appears in the first months after birth, is characterized by diffuse, wax-like hardening of the subcutaneous adipose tissue, in which the skin is bound to the underlying muscle and bone. The infant often has respiratory distress and feeding difficulties from flexion contractures. There is minimal subcutaneous inflammation, prominent thickening of the trabeculae supporting the subcutaneous adipose tissue, and an absence of fat necrosis. Infants with sclerema neonatorum, in contrast to SFN, are often preterm and severely ill, with a poor prognosis. A neonate with such an extensive bacterial cellulitis would be expected to be ill, with bacteremia, and demonstrate response to antimicrobial agents.
Complications that occur with SFN are hypercalcemia, thrombocytopenia and hypoglycemia; the frequency is uncertain. Infants with SFN and hypercalcemia may have irritability, anorexia, constipation and failure to thrive as well as renal failure. Sequestration of platelets within the subcutaneous tissue as the mechanism for thrombocytopenia has been proposed.
The panniculitis of SFN resolves spontaneously in 6 to 8 weeks. Infants should be closely monitored for the development of hypercalcemia. In the infant in this case, antibiotics were discontinued after the diagnosis of subcutaneous fat necrosis was made. A biopsy was not indicated. Platelet and calcium levels remained normal. She was discharged home within several days. It is unclear the role that head cooling played in the development of SFN in this infant.
Columnist comments
I would like to thank our guest columnists from the West Virginia University College of Medicine for contributing this very interesting case. Kathryn Moffett, MD received her medical degree at Penn State College of Medicine in Hershey; Pediatric Residency and Chief Resident at Children’s Hospital Medical Center of Akron; Pediatric Infectious Diseases Fellowship at Emory University in Atlanta. She joined the staff at WVU in 1998, where she is the director of the Cystic Fibrosis Center.
Alison Ardito, MD, received her medical degree from the University of Tennessee College of Medicine. After completing her pediatric residency last June, she joined the section of pulmonary medicine at WVU.
Robyn Schultz, MD, received her medical degree from Temple University in Philadelphia. She is currently a PL-3 at WVU and plans to practice general pediatrics in a rural setting.
Please remember our troops during this holiday season, especially those deployed far from home. The image below is the 41st Combat Support Hospital as it appeared in Iraq in 1991. Imagine spending your favorite holiday in a place like this. It can be fairly depressing and demoralizing. Care packages can make a huge difference and can be sent via any local military post or base, or a donation can be made to the USO by going online here. They do a great job of bringing little things to soldiers that can make a big difference, as well as providing a place for traveling military personnel to rest at airports.
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The 41st Combat Support Hospital as it appeared
in Iraq in 1991. |
The Brien family wishes you all a fun and safe holiday season.
All images courtesy of: Brien JH