Neonatal Hypothermia

A Method to Provide Neuroprotection After Hypoxic Ischemic Encephalopathy

Katherine M. Newnam, MS, RN, CPNP, NNP-BC; Donna L. DeLoach, MS, RN, CPNP, NNP-BC


NAINR. 2011;11(3):113-124. 

In This Article

Complications of the Integument System

The development of sclerema neonatorum has been reported secondary to birth asphyxia before the implementation of therapeutic hypothermia; this ultimately resolves.[36] However, sclerema is a disorder of the subcutaneous fat that appears first on the thighs and/or buttocks, then spreads to other body surface areas with the exception of the palms, soles, and genitalia. The skin is noted to be pale and waxy and cannot be pinched up because it is bound to the underlying tissue. The condition can lead to flexion contractures of the elbows, knees, and hips because mobility can be altered.[37]

The infant is also at risk for subcutaneous fat necrosis (SCFN) as a result of asphyxia, a phenomenon seen before cooling was instituted.[36] The condition is an inflammation of the subcutaneous fat tissue that typically develops during the first week of life.[38] Complications include pain, scarring, infection, the development of abscesses, subcutaneous atrophy, hypoglycemia, hypertriglyceridemia, and thrombocytopenia with hypercalcemia as late complication. The condition is best described as areas of "firm, mobile, circumscribed nodules and plaques overlying bony prominences and may be present on the trunk, extremities, buttocks, and cheeks."[38] The skin color may range from flesh colored to red, to a purple discoloration. The confirmation of SCFN often requires a punch or needle biopsy from the affected site and laboratory analysis.

This condition is the result of the physiologic protective mechanism commonly known as the "diving reflex," which typically occurs in response to profound hypoxemia. The body's blood is shunted away from the skin and splanchnic regions to preserve the brain, heart, and adrenal glands (see Fig 1). Decreased circulation to the subcutaneous tissue creates hypoxia and hypothermia, leading to the inflammation and necrosis of fat tissue.[38]

Uncomplicated cases of SCFN should resolve spontaneously; however, the infant remains at risk for hypercalcemia as mentioned above (see Table 4) because by-products of the SCFN is reabsorbed and liquefied. The parents should be instructed to report signs of failure to thrive; vomiting; and lethargy, which are known complications of hypercalcemia. Follow-up of infants with SCFN should include weekly calcium levels until the lesions completely resolve to identify those infants at risk.


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