From the Guidelines
Fat necrosis in neonates causes hypercalcemia through the release of calcium from damaged adipose tissue, and management includes hydration, loop diuretics, and in severe cases, glucocorticoids or bisphosphonates. This condition typically occurs following birth trauma, such as forceps delivery, or in infants with subcutaneous fat necrosis of the newborn (SCFN) 1. When fat cells are damaged, they release calcium that was previously bound within the tissue. Additionally, there is increased production of 1,25-dihydroxyvitamin D by macrophages in the areas of inflammation, which enhances intestinal calcium absorption, as noted in the context of calcium homeostasis and bone mineralization 1. Granulomatous inflammation in the necrotic areas may also contribute to calcium release. The hypercalcemia usually develops 2-16 weeks after the appearance of skin lesions and can be severe, with calcium levels sometimes exceeding 15 mg/dL.
Key Considerations
- The release of calcium from damaged adipose tissue is a critical factor in the development of hypercalcemia in neonates with fat necrosis 1.
- Increased production of 1,25-dihydroxyvitamin D by macrophages in areas of inflammation enhances intestinal calcium absorption, further contributing to hypercalcemia 1.
- Management of hypercalcemia in neonates with fat necrosis includes hydration with normal saline, loop diuretics like furosemide (1-2 mg/kg/dose), and in severe cases, glucocorticoids (prednisolone 1-2 mg/kg/day) or bisphosphonates (pamidronate 0.5-1 mg/kg/dose).
- Regular monitoring of serum calcium levels is essential until resolution, which typically occurs within weeks to months as the fat necrosis resolves.
Clinical Implications
- Early recognition and management of hypercalcemia are crucial to prevent long-term complications, such as nephrocalcinosis and impaired bone mineralization 1.
- A multidisciplinary approach, including pediatricians, nephrologists, and endocrinologists, may be necessary for the management of persistent hypercalcemia or hypercalciuria in neonates with fat necrosis 1.
From the Research
Mechanism of Hypercalcemia in Neonates with Fat Necrosis
- Fat necrosis in neonates can lead to hypercalcemia due to aberrant 1,25-dihydroxyvitamin D synthesis in the necrotic tissue, increasing intestinal absorption of calcium 2
- The mechanism of hypercalcemia is usually related to the increased levels of 1,25-dihydroxyvitamin D, which enhances calcium absorption in the intestine 3, 2
Clinical Presentation and Treatment
- Hypercalcemia in neonates with fat necrosis can be asymptomatic, but severe cases can cause symptoms such as irritability, vomiting, and seizures 4, 5
- Treatment options for hypercalcemia in neonates with fat necrosis include hydration, furosemide, corticosteroids, and intravenous bisphosphonates like pamidronate 3, 6, 5
- Pamidronate has been shown to be effective in treating severe hypercalcemia in neonates with fat necrosis, with a faster resolution of hypercalcemia compared to other treatments 6
Complications and Outcomes
- Nephrocalcinosis is a common complication of hypercalcemia in neonates with fat necrosis, and can persist even after treatment 6, 4, 5
- Despite the risk of nephrocalcinosis, outcomes are generally good with routine surveillance and interventions, and a multidisciplinary team approach is recommended 2, 5