Visceral trauma to the liver, spleen, or adrenal gland occurs in macrosomic infants and in extremely premature infants, with or without breech or vaginal delivery. Rupture of the liver with subcapsular hematoma formation may lead to anemia, hypovolemia, shock, hemoperitoneum, and disseminated intravascular coagulation. Infants with anemia and shock who are suspected to have an intraventricular hemorrhage but with a normal head ultrasound examination should be evaluated for hepatic or splenic rupture. Adrenal hemorrhage may be asymptomatic, detected only by finding calcified adrenal glands in normal infants. Infants with severe adrenal hemorrhage may exhibit a flank mass, jaundice, and hematuria, with or without shock.
After birth, a newborn remains covered by amniotic fluid and situated in a cold environment (20° C to 25° C). An infant’s skin temperature may decrease 0.3° C/min, and the core temperature may decrease 0.1º C/min in the delivery room. In the absence of an external heat source, the infant must increase metabolism substantially to maintain body temperature.
Heat loss occurs through four basic mechanisms. In the cold delivery room, the wet infant loses heat predominantly by evaporation (cutaneous and respiratory loss when wet or in low humidity), radiation (loss to nearby cold, solid surfaces), and convection (loss to air current). When the infant is dry, radiation, convection, and conduction (loss to object in direct contact with infant) are important causes of heat loss. After birth, all high-risk infants should be dried immediately to eliminate evaporative heat losses. A radiant or convective heat source should be provided for these high-risk infants. Normal term infants should be dried and wrapped in a blanket.
The ideal environmental temperature is the neutral thermal environment, the ambient temperature that results in the lowest rate of heat being produced by the infant and maintains normal body temperature. The neutral thermal environmental temperature decreases with increasing gestational and postnatal age. Ambient temperatures less than the neutral thermal environment result in increasing rates of oxygen consumption for heat production, which is designed to maintain normal body temperature. If the ambient temperature decreases further or if oxygen consumption cannot increase sufficiently (due to hypoxia, hypoglycemia, or drugs), the core body temperature decreases.
Heat production by a newborn is created predominantly by nonshivering thermogenesis in specialized areas of tissue containing brown adipose tissue. Brown fat is highly vascular, contains many mitochondria per cell, and is situated around large blood vessels, resulting in rapid heat transfer to the circulation. The vessels of the neck, thorax, and interscapular region are common locations of brown fat. These tissues also are innervated by the sympathetic nervous system, which serves as a primary stimulus for heat production by brown adipose cells. Shivering does not occur in newborns.
Severe cold injury in an infant is manifested by acidosis, hypoxia, hypoglycemia, apnea, bradycardia, pulmonary hemorrhage, and a pink skin color. The color is caused by trapping of oxygenated hemoglobin in the cutaneous capillaries. Many of these infants appear dead, but most respond to treatment and recover. Milder degrees of cold injury in the delivery room may contribute to metabolic acidosis and hypoxia after birth. Conversely, hypoxia delays heat generation in cold-stressed infants.
Treatment of severe hypothermia should involve resuscitation and rapid warming of core (e.g., lung and stomach) and external surfaces. Fluid resuscitation also is needed to treat hypovolemia seen in many of these infants. Reduced core temperature (32° C to 35° C) in the immediate newborn period often requires only external warming with a radiant warmer, incubator, or both.