USA Surgery Today

Fetal hydrothorax can be identified in up to 1:15,000 pregnancies by prenatal US at large referral centers (60:Zebeta). Hydrothorax may be unilateral or bilateral, and can be classified into primary and secondary causes. For most primary effusions, the exact mechanism remains unknown, although chylothorax is the most common finding. Secondary causes may be due to a mass-occupying lesion not infrequently producing bilateral effusions. Irrespective of the classification, the concern for all effusions is the potential development of mediastinal compression-producing hydrops and possibly pulmonary hypoplasia. Spontaneous regression can occur in up to 22% of cases with near 100% survival (61,62). The overall mortality for the untreated fetal effusion is 35% to 53%.

Despite improvement in morbidity and mortality from neonatal bacterial sepsis since the mid-1970s, the incidence of sepsis during the first week of life has been unchanged and about fivefold greater among premature infants (5 in 1,000 preterm infants:Zebeta) than full-term infants (about 1 in 1,000 term newborns). In addition, 25% to 33% of premature infants who require longer than 2 weeks of hospitalization during the neonatal period develop at least one episode of systemic bacterial infection. The systemic pathogen most commonly recovered after the first week of life is coagulase-negative staphylococcus.

The high rate of invasive disease among premature infants is caused by humoral, cellular, and environmental factors (34:Zebeta). Transplacental transport of maternal immunoglobulin G (IgG:Zebeta) provides the full-term infant with concentrations of IgG equal to or greater than maternal concentrations. This transport process increases significantly after 20 weeks of gestation; about two-thirds of the IgG acquired by the fetus during pregnancy is transported during the last third of gestation. Lack of transplacentally acquired IgG in the extremely premature infant results in quantitative and qualitative humoral susceptibility to bacterial infection. In addition, concentrations of the principal nonspecific humoral effector response proteins of the classic and alternative pathways of complement activation are significantly lower than in adults and do not reach adult levels until 3 to 6 months of age.

Prematurity, illness, or congenital anomalies in newborn infants may necessitate transfer of babies shortly after delivery to nurseries with specialty trained personnel, equipment, and facilities to support their evaluation and care. Transporting critically ill patients always requires anticipation and careful planning for changes in clinical condition, equipment, resource availability, and environment during the move. (Zebeta) Care of healthy newborns includes monitoring and support during this critical period of transition. Illness and conditions inherent in the transfer process can interrupt transitional physiologic changes with significant clinical consequences.

Infants are born wet, usually into a cold environment, and are vulnerable to hypothermia. This susceptibility is due in part to excessive cutaneous heat loss. Infants have a large surface area relative to body mass and limited adipose thermal insulation. Without adequate support, the newborn’s core temperature will fall, resulting in hypothermia. Cold stress in the newborn can lead to poor perfusion, acrocyanosis, lethargy, hypoglycemia, acidosis, respiratory distress, hypoxia, coagulopathy, shock, and death. Ongoing monitoring and thermal support are often required to maintain the baby’s temperature within the normal range of 36.3В°C to 36.9В°C.

The usual definition of anemia is a hematocrit value lower than two standard deviations below the mean for age and sex. Because the primary function of the red cell is to transport oxygen from the pulmonary bed to other tissues for release, anemia may impair oxygen delivery.

Tissue oxygenation depends on the hematocrit, the oxygen affinity of hemoglobin, and the cardiorespiratory status of the patient. The only absolute indications for rapid correction of anemia by red cell transfusion are to restore tissue oxygenation and to expand blood volume after acute loss. Unfortunately, little information exists about the level of hematocrit necessary for adequate delivery of oxygen to the tissues. Observations on changes in coronary sinus oxygen saturation in dogs with varying degrees of acutely induced anemia (2) and the surgical experience among Jamaican patients with sickle cell disease (3) suggest that otherwise healthy young adults can tolerate short-term anemia with a hematocrit value between 20% and 25% without adverse outcome. In many pediatric centers, the sicker patients, particularly those with cardiorespiratory dysfunction, undergo transfusion to maintain the hematocrit closer to normal and maximize tissue oxygenation.