Subcutaneous Fat Necrosis in Neonates after Therapeutic …

Szpecht D, Bagnosz-Magnuszewska A, Szymankiewicz M, Gadzinowski J. Subcutaneous fat necrosis in neonates after therapeutic hypothermia – report of two cases. Postepy Dermatol Alergol. 2016;33(2):152-154. doi:10.5114/ada.2016.59164

Subcutaneous fat necrosis (SCFN) is a rare, transient and self-limiting complication of birth asphyxia [1]. It is characterized by painless nodules developing on the back, limbs and buttocks, which move freely over muscle and bone. The overlying skin may be of normal color or with erythematous discoloration. These lesions disappear spontaneously without scarring, but there may be systemic complications associated with SCFN. The most serious potential complication is hypercalcemia, which carries with it serious risks to the child’s health and life [1].

Both neonates diagnosed with SCFN following therapeutic hypothermia were born with indicators of serious birth asphyxia in the Clinical Hospital of Gynecology and Obstetrics at Poznan University of Medical Sciences.

A female newborn weighing 4340 γ was delivered by cesarean section (indication: fetal life-threatening symptoms) at 37 weeks of pregnancy complicated by type C diabetes and Hashimoto’s thyroid deficiency. She was born with an Apgar score of 0 at 1 min, and then 0, 0, 1 and 4 at 3, 5, 10 and 15 min, respectively. Umbilical cord pH (artery and vein) was measured immediately after birth at 6.71 (BE –21.2 mEq/l) and 6.78 (–21.0 mEq/l). The child was resuscitated at birth, with heart action returning at 10 min. Artificial ventilation (initially by the synchronized intermittent mechanical ventilation (SIMV) method and then with non-invasive ventilation support) in the Neonatal

Intensive Care Unit (NICU) was continued until day 10 of her life. Due to clinical symptoms of hypoxic ischemic encephalopathy whole-body cooling was initiated at 4 h, and continued for the next 3 days of life.

In the first cranial ultrasound scan performed within the initial 24 h of the infant’s life, no hypoxic-ischemic areas were detected. Abnormal values of pulsatility index (PI) of 3.4, resistive index (RI) of 0.93, end-diastolic velocity (EDV) of 3.5 cm/s and peak systolic velocity (PSV) of 50.5 cm/s were detected in the middle cerebral artery. Subsequent cranial ultrasound scans done at weekly intervals revealed minor ischemic areas around cerebral ventricles, also confirmed by cranial magnetic resonance imaging in week 5 of the patient’s life.

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