The authors studied the predictive value of detailed fetal sonographic parameters on outcome for 55 patients with prenatally diagnosed congenital diaphragmatic hernia managed at an ECMO center. Their ...sonographic assessment included gestational age at time of diagnosis, polyhydramnios (largest amniotic fluid pocket diameter), presence of liver and/or stomach herniation, and abdominal circumference at the level of the umbilical cord. They measured the right lung two-dimensional area at the level of the atria as an estimate of lung size and mediastinal shift. The ratio of right lung area to head circumference (LHR) was calculated to minimize lung size differences owing to gestational age. The principal outcome variable was survival. The overall survival rate was 65%. If the diagnosis was made after 25 weeks' gestation, the survival rate was 100% (12 of 12); the rate was 56% if the diagnosis was made at or before 25 weeks (
P < .005). All five neonates with an LHR of less than 0.6 died; the survival rate was 100% for those whose LHR was greater than 1.35; and those with an LHR between 0.6 and 1.35 had a 61% survival rate (
P < .001). The survival rate for those whose liver was not herniated was 100% (10 of 10); herniation of the liver decreased the survival rate to 56% (
P < .05). Stomach position, polyhydramnios, and abdominal circumference were not found to be useful survival predictors. No prenatal sonographic parameter was absolutely predictive of postnatal death except very small right lung size, which was present in only 5 of the 55 patients. Survival is highly likely if the liver is not herniated into the thorax and/or the right lung is large.
The cost of medical care in the United States is under close scrutiny. Birth defects have surpassed prematurity as the leading cause of infant mortality in the United States and contribute ...significantly to infant morbidity. Few estimates have been made of the costs of individual birth defects. The authors sought to determine the cost of initial hospitalization for an infant with a congenital diaphragmatic hernia (CDH). They analyzed hospital bills and professional fees from all 35 cases of infants who underwent postnatal CDH repair at their institution between January 1990 and December 1993. The cost averaged $137,000 per patient, and ECMO dramatically increased the cost. The cost per survivor was $98,000 in the non-ECMO group and $365,000 in the ECMO group. The estimated cost of CDH per year in the United States is more than $230 million. This study suggests several strategies for cost reduction, provides data for future cost comparisons, and serves as a cost comparison for evaluating new therapeutic strategies for CDH.
We sought to delineate contributions of nitric oxide (NO) and other mechanisms to impairment of contraction and endothelium-dependent relaxation following prolonged
in vitro incubation, endotoxin and ...interleukin-1 exposure in isolated rat aorta. Responses from freshly-dissected (control) rings ±endothelium were compared with those from rings incubated in sterile, antibiotic containing medium ±
E. Coli endotoxin (LPS, 100 μg/ml) ± interleukin-1 (IL-1, 40 ng/ml) at 37° C for 20–24 h. In some experiments, medium included dexamethasone (DEX, 1 μg/ml), cycloheximide (10 μg/ml), or N
G-nitro-L-arginine (NNLA, 10
−4M). After incubation, medium nitrite was measured. Incubation alone, without addition of inflammatory mediators, impaired contraction in an agonist-specific manner, by both NO-dependent and NO-independent mechanisms. Either LPS or IL-1 diminished contraction further, in a similarly heterogeneous manner. For example, contractions were changed in LPS-incubated endothelium-intact rings (vs. fresh controls) by −85%, +115%, −15%, −96%, and −37% for phenylephrine (PE), serotonin, prostaglandin F
2α, angiotensin II, and U46619, respectively. NO synthase inhibition with NNLA either following, or during LPS incubation only partially normalized subsequent PE contractions, an effect which was smaller than that of DEX. Nitrite accumulation was inversely proportional to PE response, even though NO was not the sole mediator of LPS-impaired contraction. LPS and IL-1 nearly abolished ACh-induced relaxation, which was only mildly impaired by incubation alone. We conclude that prolonged incubation impaired vasoconstriction via
both NO synthase induction and NO-independent mechanisms. LPS or IL-1 incubation impaired vasoconstriction further, primarily by NO-independent mechanisms. Moreover, vasoconstrictor responses following LPS varied with the agonist's ability to modulate endothelial NO release. These results are in accord with the failure of NO synthase inhibition to fully restore systemic vascular resistance indices in experimental endotoxemia or in hyperdynamic septic patients.
