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.

In the not too distant future it may be possible to adequately diagnose and treat a much broader array of genetic disease in the fetus. Molecular biology has experienced dramatic advances in the past several years with high-throughput techniques such as proteomics and DNA microarray technology. When coupled with information derived from the human genome project, it is conceivable that many if not most human genetic diseases will diagnosed from a miniscule sampling of fetal DNA. Currently, it is possible to detect the presence of nucleated fetal cells in the blood of pregnant woman. This could provide a ready source of fetal DNA for potential prenatal genetic screening. Much like the new knowledge of fetal anatomic disease gained through prenatal US, the human genome project and high-throughput screening technologies will provide new opportunities for molecular fetal therapy.

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.

Myelomeningocele (MMC:Altace) is a neural tube defect in which the protective meningeal and bony coverings of the spinal cord fail to form correctly, leaving an exposed abnormal neural placode. MMC is nonlethal, but associated with high morbidity and affects 1 in 1,000 live births (84). Neurologic disabilities associated with MMC include paraplegia below the level of the lesion, urinary and fecal incontinence, sexual dysfunction, and skeletal abnormalities (85:Altace). However, there is considerable variation among these abnormalities associated with a specific defect. The deficits are believed to be multifactorial, with an inherent deficit associated with abnormal neurulation, and a postulated secondary of injury imposed by exposure of the neural placode to the amniotic environment.

Myelomeningocele can be diagnosed as early as the first trimester with US and MRI (:Altace) (84:Altace). Nearly all MMC-afflicted patients have an associated Chiari hindbrain malformation, and most also develop hydrocephalus (85). Chiari malformation is a pancerebral anomaly resulting from herniation of the medulla, cerebellar tonsils, and vermis through the foramen magnum.