Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0019270 (hernia)
15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the pre-antibiotic era a herniation of brain tissue into the mastoid was a fairly frequent event following the transmastoid drainage of brain abscesses. Since the introduction of antibiotics and refinement of operative techniques a brain hernia into the mastoid has nowadays become very rare. Two almost identical cases of brain hernia in a radical mastoidectomy cavity were recently observed by the author. The surgical management is presented and the literature discussed.
HNO 1988 Jan
PMID:[Mastoid brain herniation following a cholesteatoma operation]. 245 Aug 57

Treatment of congenital diaphragmatic hernia (CDH) has undergone a revolutionary change in philosophy, from previous urgent repair to the present practice of stabilization and delayed repair. However, when extracorporeal membrane oxygenation (ECMO) is required, many people believe that the risk of postoperative pulmonary hypertension (PPHN) mandates hernia repair while on ECMO. This report details the experience in two ECMO centers with stabilization, ECMO if required, and CDH repair post-ECMO. All CDH patients symptomatic in the first hour of life with a gestational age of at least 34 weeks during the period were reviewed retrospectively. Standard criteria were used to select patients for ECMO. High-frequency jet or oscillating ventilators and nitric oxide were not routinely available throughout the study period, but were used in some of the more recent patients. A total of 60 patients presented to the two centers; 24 cases were stabilized with conventional management, repair of the CDH was done elective, and survival was 100%. Eight patients were referred after having repair elsewhere; six survived (75%). The two deaths were attributable to associated lethal lesions--complex cyanotic heart disease and alveolar capillary dysplasia. Eight patients who required ECMO were managed with the intention of repairing the defect on ECMO. Four survived (50%). Two patients died before repair. Twenty patients were managed with ECMO, with the intention of repairing the defect after decannulation. Overall survival was 13 (65%), deaths were caused by pre-ECMO hypoxia, pulmonary insufficiency, and associated cardiac disease. No patient had recurrent pulmonary hypertension after late repair.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Timing of repair of congenital diaphragmatic hernia requiring extracorporeal membrane oxygenation support. 747 78

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.
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PMID: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. 753 41

In acute hypoxemic respiratory failure of term and near-term neonates, extra- and intrapulmonary right-to-left shunting contribute to refractory hypoxemia. Inhaled nitric oxide (NO) decreases pulmonary arterial pressure and improves ventilation-perfusion mismatch in a variety of animal models and selected human patients. We report on 10 consecutive term and near-term newborns with severe acute hypoxemic respiratory failure due to diaphragmatic hernia, meconium aspiration syndrome, group B streptococcus sepsis, pneumonia or acute respiratory distress syndrome, who received increasing doses of inhaled NO (up to 80 ppm) to improve the arterial partial pressure of oxygen (PaO2). The response to NO and the optimum NO concentration which improved PaO2 varied considerably between patients. Improvement of PaO2 was absent or poor (less than 10 mm Hg) in the 4 newborns with meconium aspiration syndrome and in 1 patient with congenital diaphragmatic hernia, while in the other 5 patients inhaled NO increased the mean (+/- SE) PaO2 from 41 +/- 6 to 57 +/- 9 mm Hg (P < 0.05). Optimum NO concentrations determined by dose-response measurements performed during the first 8 hr of NO inhalation were 8-16 ppm except for 2 newborns with congenital diaphragmatic hernia who required 32 ppm to effectively increase PaO2. Four of the 5 patients in whom the PaO2 rose by more than 10 mm Hg received inhaled NO for extended periods of time (5 to 23 days) with no signs of tachyphylaxis. The optimum NO concentration dropped to less than 3 ppm after prolonged mechanical ventilation or when intravenous prostacyclin was given concomitantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-response to inhaled nitric oxide in acute hypoxemic respiratory failure of newborn infants: a preliminary report. 756 4

Nitric oxide (NO) produced by the enzyme nitric oxide synthase (NOS) is critically involved in the cardiopulmonary transition from fetal to neonatal life. In congenital diaphragmatic hernia (CDH) this transition often does not occur normally, resulting in persistent pulmonary hypertension of the newborn (PPHN). We sought to determine if pulmonary NOS expression is altered in a rat model of CDH induced by maternal ingestion of the herbicide 2,4-dichlorophenyl-p-nitrophenyl ether (Nitrofen) on day 9 of gestation (term = 22 days). Sixty-three percent of Nitrofen-exposed fetuses developed CDH. Endothelial NOS (eNOS) and neuronal NOS (nNOS) protein expression were assessed in ipsilateral CDH lungs and in control lungs (Nitrofen-treated, no hernia) at 20 d gestation using immunoblot analyses. eNOS and nNOS have been immunohistochemically localized to rat pulmonary endothelium and bronchiolar epithelium, respectively, and we have previously demonstrated that their expression normally increases during late gestation to be maximal near term. eNOS protein expression was decreased in CDH versus control lung (58 +/- 6 versus 100 +/- 6% of control, n = 5). In contrast, nNOS protein abundance was similar. Factor VIII-associated antigen expression was comparable in CDH and control lung, indicating that the change in eNOS is not related to differences in endothelial cell density. eNOS mRNA abundance was evaluated in semiquantitative reverse transcription-polymerase chain reaction assays. Paralleling the decline in eNOS protein expression, eNOS mRNA was decreased in CDH versus control lung (22 +/- 8 versus 100 +/- 31% of control, n = 4).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulmonary endothelial nitric oxide synthase gene expression is decreased in a rat model of congenital diaphragmatic hernia. 757 5

Nitric oxide (NO) represents a new therapeutic modality for treating neonatal pulmonary hypertension and may obviate the need for extracorporeal membrane oxygenation (ECMO) in a number of cases of neonatal respiratory failure. Recently, the authors treated an infant with a congenital diaphragmatic hernia and pulmonary hypertension with NO on two separate occassions. During the initial period of stabilization, NO failed to reverse the pulmonary hypertension and prevent the development of progressive respiratory failure. After a successful course of ECMO, recurrent pulmonary hypertension developed that was successfully treated with continuous low-dose NO therapy for over 1 month. Prolonged administration of NO in varying doses titrated to clinical and echocardiographic parameters was well tolerated by the infant and prevented the need for a second run of ECMO.
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PMID:Nitric oxide reversal of recurrent pulmonary hypertension and respiratory failure in an infant with CDH after successful ECMO therapy. 870 25

A newborn with right diaphragmatic hernia suffered myocardial stunning and suprasystemic pulmonary hypertension secondary to postpartal asphyxia. In addition to conventional therapy, norepinephrine, enoximone, and inhalational nitric oxide were successfully used. Norepinephrine improved myocardial perfusion pressure; the addition of enoximone, a phosphodiesterase-inhibitor, to beta-adrenergic agents increased cardiac performance. with decreasing concentrations of inhalational nitric oxide, severe pulmonary hypertension resolved after a few days, suggesting that transient endothelial dysfunction was partially responsible for pulmonary vasoconstriction in the newborn with congenital diaphragmatic hernia.
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PMID:Norepinephrine, enoximone, and nitric oxide for treatment of myocardial stunning and pulmonary hypertension in a newborn with diaphragmatic hernia. 766 10

Congenital diaphragmatic hernia (CDH) still has a mortality risk of around 40%. The concomitant pulmonary hypoplasia and the persistent pulmonary hypertension are of major prognostic importance. The use of a selective pulmonary vasodilator may revert this vicious circle that is fatal to many children. Inhalation of nitric oxide (NO) has been suggested as a rational treatment of this condition. The authors report three cases of high-risk infants with CDH where NO was used successfully. It is concluded that hypoxemia in CDH can be treated successfully with NO inhalation when conventional treatment fails, and it may in some cases prove to be an alternative to ECMO.
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PMID:Inhalation of nitric oxide as a treatment of pulmonary hypertension in congenital diaphragmatic hernia. 766 21

The pathophysiology of the lamb model of congenital diaphragmatic hernia (CDH) involves pulmonary hypoplasia, pulmonary hypertension, and surfactant deficiency. Inhaled nitric oxide (NO) is a highly selective pulmonary vasodilator. The aim of this study was to determine the effects of inhaled NO on pulmonary gas exchange, acid-base balance, and pulmonary pressures in a lamb model of CDH with or without exogenous surfactant therapy. At the gestational age of 78 days (full term, 145 days) 11 lamb fetuses had a diaphragmatic hernia created via a left thoracotomy and then were allowed to continue development in utero. After cesarean section, performed at term, six lambs received exogenous surfactant therapy (50 mg/kg, Infasurf) and five served as controls. All animals were pressure-ventilated for 30 minutes and then received 80 ppm of inhaled NO at an F1O2 of .9 for a 10-minute interval. Compared with the control lambs, the lambs with exogenous surfactant therapy had higher pH (7.17 +/- .06 v 6.96 +/- .07; P < .05), lower PCO2 (73 +/- 8 v 122 +/- 20, p < .05), and higher PO2 (153 +/- 38 v 50 +/- 23; P < .05). In control CDH lambs (without surfactant), inhaled NO did not improve pH, PCO2, or PO2, or decrease pulmonary artery pressure. In CDH lambs given exogenous surfactant, NO decreased pulmonary artery pressures (42 +/- 4 v 53 +/- 5; P < .005) and further improved PCO2 and PO2. NO also made the difference between pulmonary and systemic artery pressures more negative in the surfactant-treated lambs (-15 +/- 4 v -2.3 +/- 2.4; P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of congenital diaphragmatic hernia. VIII: Inhaled nitric oxide requires exogenous surfactant therapy in the lamb model of congenital diaphragmatic hernia. 772 7

Acute respiratory failure (ARF) secondary to congenital diaphragmatic hernia (CDH), unresponsive to maximal medical management, has traditionally been treated with venoarterial (VA) extracorporeal membrane oxygenation (ECMO). Venovenous (VV) ECMO offers several benefits over VA ECMO including preserved pulmonary blood flow, preservation of the carotid artery, and pulsatile flow. However, use of the VV modality has not been widespread because of concerns of the cardiac instability during bypass, and because only one double-lumen (DL) catheter size is available in the United States. The authors hypothesize that VV ECMO is a safe and effective treatment for CDH, symptomatic at birth, and report a single institution experience of preferential VV use for CDH. Over an 18-month period, 14 patients with CDH were placed on ECMO after maximal medical management failed, including high-frequency ventilation and nitric oxide in some cases. Ability to place the 14 Fr DL catheter was the sole criteria for VA or VV selection. Nine patients were successfully placed on VV and 5 on VA; no VV patient required conversion to VA. The two groups of patients were similar with respect to degree of illness, birth weight, EGA, time on and age at start of ECMO. Overall survival for this series was 64%: 66% in the VV group and 60% in the VA group. Two patients in the VV group were found to have congenital heart disease incompatible with life, were withdrawn from therapy and allowed to die, and are listed as treatment failures. The authors conclude that CDH patients receive adequate oxygenation and show hemodynamic stability on VV ECMO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preferential use of venovenous extracorporeal membrane oxygenation for congenital diaphragmatic hernia. 776 Feb 33


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