Subcutaneous fat necrosis of the newborn with hypercalcemia

Norwood-Galloway, Anne; Lebwohl, Mark; Phelps, Robert; Raucher, Harold S.

doi:10.1016/s0190-9622(87)70056-5

Cited by 70 publications

(43 citation statements)

References 19 publications

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“…In a case series of 15 patients, Norwood-Galloway et al reported three deaths as a result of hypercalcaemia [10]. The hypercalcaemic infant may present with lethargy, irritability, failure to thrive, weight loss, hypotonia, vomiting, and constipation.…”

Section: Discussionmentioning

confidence: 99%

“…All neonates with subcutaneous fat necrosis should have their serum calcium level monitored regularly during the episode and also during follow-up. Hypercalcaemia usually develops when the subcutaneous fat necrosis begin to resolve, but the onset of hypercalcaemia can be delayed up to 6 months after the development of skin manifestations [10], which emphasizes the importance of prolonged follow-up.…”

Section: Discussionmentioning

confidence: 99%

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Subcutaneous fat necrosis in newborn—an unusual case and review of literature

2011

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Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon, self-limiting panniculitis mostly occurring within the first few weeks after birth. SCFN has been described mostly in term or post-term newborn infants in literature. We report a preterm infant developing extensive subcutaneous fat necrosis within the first week of life after significant perinatal hypoxic injury. The infant was conservatively managed for subcutaneous fat necrosis but developed hypercalcaemia and required prolonged medical treatment. Hypercalcaemia is a rare but serious complication of subcutaneous fat necrosis and needs prolonged follow-up. The etiopathogenesis of both subcutaneous fat necrosis in newborn and the resultant hypercalcaemia are poorly understood. Conclusion: Significant subcutaneous fat necrosis can develop in both preterm and term infants, and preterm infants also develop significant complications including hypercalcaemia.Keywords Subcutaneous fat necrosis of newborn . Hypercalcaemia . Perinatal hypoxia . Hypoglycaemia Case reportA male preterm infant weighing 2,300 g was born after a crash Caesarean section at a gestational age of 33+6 weeks. His mother presented with a foetal heart of 30/min and a history of reduced foetal movements for 24 h. The infant was born in poor condition (blue, floppy with no respiratory effort) and no heart rate was noted at birth. The infant needed full cardiopulmonary resuscitation till 4 min of age. First heart rate was detected at 2 min of age, and first gasping effort was noted at 9 min of age, The infant needed continued ventilatory support in view of poor respiratory effort. Apgar scores were 1 at 1 min and 5 at 5 min. Cord blood gases reflected severe combined respiratory and metabolic acidosis. He was ventilated for the first 24 h of life.He suffered from severe hypoxic ischaemic encephalopathy, and abnormal movements of both the upper extremities were noted from 11 h of age. In view of his prematurity, therapeutic hypothermia was not considered appropriate. He was treated with phenobarbitone for the first 6 days of life. He developed abnormal liver and renal functions and also developed severe hypoglycaemia requiring high concentration of dextrose infusion (25% dextrose) to maintain normoglycaemia (total fluid intake was restricted initially in view of severe hypoxic ischaemic encephalopathy (HIE)). Generalised hypertonia was noted very early in life. He developed large bilateral intraventricular haemorrhages which subsequently resulted in bilateral posthaemorrhagic hydrocephalus.He developed an erythematous rash over the dorsum of the chest, abdomen, and right arm which felt warm in comparison to the rest of the body on the third day of life. This developed into a sclerematous appearance by day 5. A punch biopsy of skin confirmed subcutaneous fat necrosis

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Subcutaneous fat necrosis in newborn—an unusual case and review of literature

2011

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“…The skin lesions disappear within 3–6 months without treatment. The incidence of hypercalcemia as a complication seems to be low and usually, hypercalcemia appears between 1 and 6 weeks following the onset of skin lesions [10]. The hypercalcemia may cause irritability or lethargy, dehydration with failure to thrive and secondary calcifications [11].…”

Section: Discussionmentioning

confidence: 99%

Pamidronate: Treatment for Severe Hypercalcemia in Neonatal Subcutaneous Fat Necrosis

Alos¹,

Eugène²,

Fillion³

et al. 2006

Horm Res Paediatr

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Background: Subcutaneous fat necrosis (SCFN) of the newborn is an uncommon disorder that occurs in the first weeks of life after foetal distress. It can be complicated by potentially life-threatening hypercalcemia. Treatments of hypercalcemia have included hydration, furosemide and corticosteroids. Only one report has described the use of intravenous bisphosphonates for this condition. We propose that pamidronate could be the first line therapy for severe hypercalcemia in SCFN. Patients and Results: Four newborns presented between 2001 and 2004 with SCFN complicated by severe hypercalcemia. At diagnosis, ionized calcium levels were higher than 1.4 mmol/l and were associated with high urinary calcium/creatinine ratios and high 1,25-dihydroxyvitamin D levels. Despite treatment with IV fluids, low calcium diet and furosemide, calcium levels remained high. The patients were given 3–4 doses (0.25–0.50 mg/kg/dose) of pamidronate. Urinary calcium/creatinine ratios and calcium levels decreased within 48–96 h. 1,25-dihydroxyvitamin D levels normalized with resolution of the skin lesions. No persistent nephrocalcinosis was observed. Conclusion: Pamidronate is effective, well-tolerated in the short-term and obviates the need for prolonged treatment with furosemide and corticosteroids. To prevent nephrocalcinosis, pamidronate might be considered as first line treatment for severe hypercalcemia in SCFN.

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“…Electron microscopy reveals short, rectangular crystals that are irregularly arranged, and long, needle-shaped crystals that are parallel or radial. 3 The cause of the disease is unknown. Trauma, hypothermia, asphyxia, and intrauterine circulatory defects are thought to be the cause,7 but the pathophysiology is not fully understood.…”

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confidence: 99%