Wilcox Dt

Partial liquid ventilation and nitric oxide in congenital diaphragmatic hernia

PURPOSE In congenital diaphragmatic hernia (CDH) there is immature lung development with a resulting clinical picture of pulmonary hypoplasia, surfactant deficiency, and pulmonary hypertension. Pulmonary hypoplasia and surfactant deficiency both have been successfully treated using partial liquid ventilation (PLV). Pulmonary hypertension associated with CDH has proven difficult to treat, but inhaled nitric oxide, which is a potent highly selective pulmonary vasodilator, may have potential. The aim of this study was to assess PLV in CDH and to document the effect of nitric oxide when administered through perfluorocarbon. METHODS This study using the lamb CDH model consisted of two groups; a conventional mechanically ventilated (CMV) group and a PLV group. At 1 and 3 hours, nitric oxide (80 ppm) was given for 15 minutes. Data collected included blood gases, pulmonary function tests, pulmonary and systemic blood pressure. RESULTS After 30 minutes of ventilation, blood gases in the PLV group were all significantly improved (P < .001): pH, CMV 6.92 +/- 0.15 versus PLV 7.24 +/- 0.11; P(CO2), CMV 139 +/- 26 mmHg versus PLV 52 +/- 11 mmHg; P(O2), CMV 26 +/- 15 mmHg versus PLV 184 +/- 60 mmHg. In addition, there was a significant increase in dynamic compliance and a reduction in pulmonary hypertension. Nitric oxide was only efficacious in the PLV group, causing a further increase in oxygenation and a decrease in pulmonary hypertension. These effects were reversed when the nitric oxide was stopped. CONCLUSION This study shows that PLV both improves gas exchange and pulmonary mechanics in CDH and allows the effective delivery of nitric oxide to reduce the pulmonary hypertension associated with CDH.

Pathophysiology of congenital diaphragmatic hernia X: Localization of nitric oxide synthase in the intima of pulmonary artery trunks of lambs with surgically created congenital diaphragmatic hernia

The pathophysiology of congenital diaphragmatic hernia (CDH) results from a combination of pulmonary hypoplasia, pulmonary hypertension, and surfactant deficiency. Previously we demonstrated that inhaled nitric oxide (NO), a known vasodilator, only improves oxygenation and decreases pulmonary artery pressures when the lamb model of CDH is pretreated with exogenous surfactant. Nitric oxide synthase (NOS) in endothelial cells is responsible for the production of NO, a mediator of smooth muscle cell relaxation. Pulmonary hypertension in CDH may result from a defect in the endogenous production of NO. Our aim was to determine whether the main pulmonary artery trunks in CDH lambs have NOS immunoreactivity. Cryostat sections of paraformaldehyde-fixed specimens of pulmonary artery and aortic rings from 10 CDH lambs and five control lambs were processed for NADPH-diaphorase activity. Immunolocalization of NOS was studied in paraformaldehyde-fixed sections and compared with serially cut specimens from identical rings that were tested for NADPH-diaphorase activity. Intense NADPH-diaphorase staining was present in the intimal layer (endothelial lining) of the pulmonary artery and aortic rings of both the CDH and control lambs. This activity colocalized with NOS immunoreactivity in all specimens. Both NOS immunoreactivity and NADPH-diaphorase staining were lacking in cartilage, which were used as negative controls. NOS is present in the main pulmonary artery trunks of CDH lambs. To our knowledge, this is the first report of NOS immunoreactivity in CDH. We can only speculate whether this activity is preserved in other areas of the vascular tree in CDH, ie, pulmonary capillaries and veins. Perhaps the pulmonary hypertension in CDH is not caused by an NOS deficiency.

Toothbrush ingestion by bulimics may require laparotomy

Two girls accidentally swallowed their toothbrush while inducing emesis; both had bulimia. Early removal of the brush is advised to prevent complications. Endoscopic removal is the preferred method, but because of the toothbrushs geometric qualities, surgical retrieval is often required.

Pathophysiology of congenital diaphragmatic hernia IX: Correlation of surfactant maturation with fetal cortisol and triiodothyronine concentration

In addition to pulmonary hypoplasia and an altered pulmonary vascular bed, the abnormal lung development caused by congenital diaphragmatic hernia (CDH) is associated with an impairment in the pulmonary surfactant system. The aim of this study was to correlate fetal serum cortisol and triiodothyronine (T3) levels, known indicators of surfactant development, with maturation of the surfactant system in the lamb CDH model. Analysis of the products of bronchoalveolar lavage in CDH showed decreased phospholipid (P < .01) and increased protein concentration (P < .02) per gram of lung tissue when compared with controls, but cortisol and T3 concentrations did not differ significantly between the two groups. These results suggest that the surfactant deficiency in CDH is not related to an alteration in cortisol or T3 levels but may be directly related to the mechanical effects of the intrathoracic bowel.

Care of the fetus/newborn with congenital diaphragmatic hernia

Congenital diaphragmatic hernia (CDH) is a simple anatomical defect. The reported incidence is between 1:2000 and 1:5000 live births, with the majority affecting the left side. A defect in the diaphragm allows abdominal viscera to herniate into and stay within the thoracic cavity during crucial stages of lung development. This results in pulmonary hypoplasia, a reduction in pulmonary vascular branching and an alteration in the surfactant system.