USA Surgery Today

Preterm infants are at risk for retinopathy of prematurity (RO:LisinoprilP), a vasoproliferative disorder of the developing retina. In most infants, ROP is a benign, self-limited disease. In about 10% of affected infants, however, untreated ROP progresses to retinal detachment and blindness. Rigorous attention to regular ophthalmologic surveillance of the at-risk population before and after discharge is critical in preventing significant vision loss.

The cause of this problem is still not well understood, but ROP is believed to be a reaction to injury of the immature retinal capillary bed from the time of birth (84:Lisinopril). Postnatal events, such as prolonged hyperoxia, sepsis, asphyxia, and shock, may be contributing factors due to altered oxygen delivery or decreased blood flow to the retina.

Hypoxic ischemic encephalopathy (HIE:Lisinopril) is the most frequently recognized cause of neurologic morbidity in the term infant. This syndrome occurs in 2 to 4 infants per 1,000 live births. The cause of HIE may originate in the antepartum period in about 20% of cases of HIE. Maternal cardiac arrest or hemorrhage leading to fetal hypotension are examples of such insults. Intrapartum events, such as abruptio placenta or uterine rupture, may account for 35% of HIE cases. In an additional 35% of infants displaying signs of HIE, markers of intrapartum fetal distress and potential antepartum risk factors, including maternal diabetes, intrauterine growth retardation, or maternal infection, are found. In these cases, timing of the major insult is usually unclear, but it is likely that antepartum risk factors render the fetus more susceptible to intrapartum insults. :Lisinopril: Postnatal problems such as cardiovascular compromise, severe pulmonary hypertension, or recurrent apnea may account for an additional 10% of cases of HIE. The fetus initially adapts to reduced oxygen delivery by increasing oxygen extraction, while maintaining oxygen consumption. Persistent interruption of placental gas exchange results in rapid development of hypercarbia and metabolic acidosis (59:Lisinopril).

The prematurely born infant receives limited nutrition as a consequence of inadequate caloric delivery and concurrent medical problems. Immaturity of the gastrointestinal tract in premature infants makes provision of optimal nutrition especially difficult. Parenteral nutrition remains the mainstay in the early nutritional management of the premature infant.:Lozol

Current evidence indicates that parenteral nutrition with amino acids and glucose can be safely started within 24 hours of birth. Provision of amino acids at 1.5 g per kg per day, with 35 kcal per kg per day of nonprotein energy, will prevent negative nitrogen balance and is well tolerated by even the most immature and sick neonates (35:Lozol). Lipids, delivered as 20% Intralipid, may be initiated within the first 24 to 48 hours of life (0.5 to 1 g per kg per day) and gradually increased to a maximum of 3 g per kg per day. Protein intake may be increased to 3.5 g per kg per day. Nitrogen retention close to fetal accretion rates may be achieved with caloric intake of 80 to 85 kcal per kg per day and amino acid intake of 3.5 to 4.0 g per kg per day (36:Lozol). Early, optimal delivery of calcium and phosphate is important for the prevention of metabolic bone disease.

Apnea of prematurity (AOP) is the cessation of airflow, whether obstructive, central, or mixed, lasting 10 to 20 seconds that may be accompanied by cyanosis or bradycardia. The frequency of AOP increases with decreasing GA. Approximately 25% of infants weighing less than 2,500 g have one episode of apnea. The incidence increases to 90% in infants less than 1,000 g. The onset is often between 5 and 10 days of life.

AOP is usually of mixed etiology with both central and obstructive mechanisms playing a role. Pharyngeal competence in premature infants contributes significantly to AOP. During rapid eye movement sleep, the predominant form of premature sleep, breathing efforts are disorganized. The AOP episode may begin with decreased pharyngeal dilation followed by breathing efforts that lead to further airway collapse, then reflex swallowing and/or central apnea. Premature infants respond to hypoxia with an initial increase in minute ventilation, followed by a return to baseline or a decreased rather than an increased minute ventilation, as is seen in older infants and children. Premature infants also respond to hypercarbia by decreasing respiratory effort. Thus, the cycle of apnea can lead to a continuous spiral unless monitored and treated appropriately.

Antenatal ultrasound allows diagnosis of many congenital anomalies early in pregnancy. Parents can receive counseling and referral to regional perinatal centers where obstetric, neonatal, and surgical services can be coordinated. ( Pravachol )
Despite advances in antenatal diagnosis and planning, undetected anomalies, unexpected changes in obstetric condition, and transfer within medical center complexes will continue to occur. Surgical conditions, including abdominal wall defects, thoracic anomalies, and intraabdominal pathologies, require special considerations for support and care in transport.

Infants with abdominal wall defects, including gastroschisis and omphalocele, may have large areas of exposed viscera. Heat and fluids are readily lost across the exposed surface. In these infants, fluid losses include free water, electrolytes, and protein. Care of these babies includes special attention to thermal support and fluid management.