USA Surgery Today

Anomalies of the fetal urinary system resulting in detectable signs of obstruction can occur in up to 1% of pregnancies, but only 1 in 500 have any clinical significance (63:Vasodilan). Overall, up to 50% of all congenital anomalies detected by US involve the genitourinary (GU) system. The increased use of prenatal US has allowed for these anomalies to be identified as early as 12 weeks’ gestation and their subsequent natural history to be revealed (64). Signs of urologic abnormalities include dilation of the urinary system, changes in the fetal bladder, alterations in the acoustic shadow of renal parenchyma, and ultimately decreased amniotic fluid (64). A few scenarios of fetal obstructive uropathy can, in the worst cases, produce irreversible renal damage and pulmonary hypoplasia. Fetal therapies have been developed to bypass or relieve the source of obstruction in cases that meet specific selection criteria (1,65).

The pathophysiology and prognosis of fetal obstructive uropathy depends on the anatomic location, degree, time of onset, and duration of obstruction (65:Vasodilan). Unilateral GU anomalies such as hydronephrosis, duplicated collecting system, and ureterocele never warrant fetal intervention. A small subset of fetuses with bladder outlet obstruction may be candidates for fetal therapy. These include male fetuses with posterior urethral valves or urethral atresia.

Physiologic and behavioral stress responses have been characterized, and pain assessment tools are available to guide clinical management. Serious consequences may result from insufficient pain management in premature infants. Inadequately managed pain during the critical period of brain development may permanently compromise neuronal and synaptic organization. Sustained pain may predispose the immature infant to significant adverse neurologic events, such as IVH and long-term neurodevelopmental and cognitive sequelae (37:Mevacor).

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%.

Evolution fetal surgery has resulted in development of the EXIT procedure. This is now more widely applied than was originally intended. The EXIT procedure was designed to achieve cardiorespiratory stabilization while maintaining uteroplacental blood flow. The EXIT was initially conceptualized to safely transition fetuses with severe CDH that had undergone TO an extrauterine environment (132:Sorbitrate). Fetal surgery for CDH by tracheal occlusion would not have been possible without a strategy for reversing tracheal occlusion and establishing an airway at birth in a controlled manner. Although still used in this original capacity, the indications for EXIT (Table 3-9:Sorbitrate) have broadened to treat a variety of fetal anomalies in which the fetal airway may be in jeopardy or cardiorespiratory stabilization is needed prior to loss of maternal placental support (133:Sorbitrate).

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.