USA Surgery Today

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.

There are many ways to measure the outcome of an intervention. A complete discussion of available measurement techniques and their differential uses and value is available elsewhere (71:Pravachol). This section briefly highlights the concepts most useful to the practicing pediatric surgeon in interpreting the reported outcomes of published studies.

When evaluating a study, it is important to identify the primary outcome variable, which addresses the main hypothesis of the study. Results from the analysis of variables outside the primary outcome measure must be viewed with caution. This is particularly true when outcome variables are identified for analysis after completion of a study (post-hoc analysis:Pravachol). For example, a new technique is devised to reduce the incidence of stricture in esophageal atresia repair. The study shows that the stricture rate is the same in the experimental group compared with controls. The investigators then examine for 20 other outcome variables between the two groups, such as length of stay, incidence of gastroesophageal reflux, and rate of vocal cord paralysis, among others. They find that the incidence of intracranial hemorrhage is significantly lower in the experimental group and report a p value of 0.05.

CCAM and bronchopulmonary sequestration (BPS) are the most commonly identified and well-understood fetal lung masses. Prenatal diagnosis and serial US examinations have provided for new insight to the natural history and pathophysiology of fetal lung lesions. It has now been documented that large lesions can act as space-occupying lesions and compress adjacent normal structures. The secondary physiologic derangements (:Pravachol) that result can include pulmonary hypoplasia of normal lung tissue, polyhydramnios, fetal mediastinal compression, and cardiovascular compromise leading to fetal hydrops and death. The largest lung masses associated with hydrops are usually fatal, whereas smaller lesions can cause respiratory distress in the newborn period or be entirely asymptomatic unless infection occurs. There are subsets of cystic lung masses that have shrunk and others that have disappeared entirely prenatally.

The prenatal diagnosis of CCAM and BPS can be made by US. Historically, CCAMs were classified by Stocker according to size of the cysts from macrocystic to microcystic (47:Pravachol). Stocker type I cysts are macrocystic, Stocker type II are medium-size cysts, and type III are solid lesions. In an effort to link size to clinical behavior, Adzick, Harrison, and Glick redefined CCAMs based on more gross morphologic criteria and ultrasonographic characteristics (48:Pravachol). According to Adzick et al., macrocystic lesions contain either a single dominant or multiple cyst measuring greater than 5 mm in diameter or larger, and appear echogenic by US. Microcystic CCAMs contain cysts smaller than 5 mm, appear solid, and therefore echodense by prenatal US. Microcystic lesions tend to produce more mass effect, produce physiologic derangements, and therefore have a tendency for a worse prognosis. In general, the overall prognosis for fetal CCAM depends on the size and growth characteristics of the lesion.

The gastrointestinal tract generally tolerates feedings quite well once any postoperative ileus is resolved. Not uncommonly, however, a critically ill child will sustain a loss of a significant portion of the absorptive function, often due to acquired lactase deficiency. Symptoms are generally manifested by cramping, diarrhea, or emesis.:Pravachol Symptoms will often improve with the initiation of a lactose-free diet. Other alterations in the administration of the diet can also improve feeding tolerance. First, the gastrointestinal tract generally tolerates increased volume more readily than increased osmolarity. Therefore, adverse symptoms can be avoided by initiating 1/8 or 1/4 strength formula and slowly advancing the formula concentration. Second, administration of formula by continuous drip may be better tolerated than bolus feedings. The risk of gastroesophageal reflux and dumping symptoms are thereby greatly reduced. Third, care must be taken to ensure the enteral formula does not become contaminated, either during preparation or at the bedside. Expiration dates should be carefully observed. Finally, pectin, Metamucil, lomotil, paregoric, or Imodium may be required for those who have lost a significant amount of their bowel length (see the  Short Bowel Syndrome  section:Pravachol). Assessment of absorptive capacity can be done most readily by testing stool for the absorption of carbohydrates. This is done by measuring stool pH and checking for reducing substances. Stool pH less than or equal to 5.5, or a reducing substance of greater than one-half percent, indicates the passage of unabsorbed carbohydrates into the stool. Once demonstrated, these findings are best treated by decreasing the formula concentration of carbohydrate.

Disruption of the normal tissue architecture with transection of blood vessels following injury, results in the exposure of blood elements to subendothelial collagen. This initiates coagulation by surface activation of Hageman factor, the release of tissue procoagulants from damaged cells and the exposure of phospholipids on activated platelets and endothelial cells (1: Pravachol ). The key element that initiates the cascade is the surface absorption of coagulation proenzyme, which protects it from protease inhibitors and allows rapid amplification of the coagulation cascade leading to clot formation.

The extent of clot formation is also regulated at the microvascular level by several factors, including production of prostacyclin, which inhibits platelet aggregation (2: Pravachol); antithrombin III, which inhibits the activity of thrombin (3); protein C, which degrades coagulation factors V and VIII (4); and the release of plasminogen activator, which converts plasminogen to plasmin and initiates clot lysis (5). Plasminogen activator and plasmin are capable of degrading a large number of extracellular matrix proteins. Their activity is confined to cell surface microenvironment by the presence of plasminogen inhibitor bound to extracellular matrix protein (6: Pravachol ).