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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Respiratory distress, apnea, and chronic pulmonary disease since birth were identified in 14 infants who also had symptomatic gastroesophageal reflux. Birth weights varied from 760 to 4,540 gm. All infants had radiographic changes similar to those in bronchopulmonary dysplasia. Cessation of apnea and improvement of pulmonary disease occurred only after medical (8) or surgical (6) control of gastroesophageal reflux. Simultaneous tracings of esophageal pH, heart rate, impedance pneumography, and nasal air flow in five infants demonstrated that reflux preceded apnea. Apnea could be induced by instillation of dilute acid, but not water or formula, into the esophagus. Prolonged monitoring of esophageal pH more than two hours after feeding in 14 other infants less than 6 weeks of age (birth weight 780 to 3,350 gm) without a history of recent vomiting indicated that reflux was not greater than in normal older children.
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PMID:Gastroesophageal reflux causing respiratory distress and apnea in newborn infants. 3 84

One hundred ten infants with congenital diaphragmatic hernia (CDH) developed life-threatening respiratory distress in the first 6 hours of life. Associated anomalies were present in 33%. Twenty-eight of 65 infants (43%) treated before 1987 (pre-extracorporeal membrane oxygenation [ECMO] era) survived after immediate CDH repair, and mechanical ventilation with or without pharmacologic support. Only two of 16 (12.5%) infants requiring a prosthetic diaphragmatic patch survived. Since 1987, 31 of 46 (67.4%) infants with birth weight, gestational age, and severity of illness similar to the pre-1987 group survived. All patients were immediately intubated and ventilated. Seven (four with lethal chromosomal anomalies) infants died before treatment, and 30 stabilized (partial pressure of carbon dioxide [PCO2] < 50; partial pressure of oxygen [PO2] > 100; pH > 7.3) and underwent delayed CDH repair at 5 to 72 hours. Fifteen did well on conventional support and survived. Fifteen infants deteriorated after operation: 11 were placed on ECMO with eight survivors, and four infants were not considered ECMO candidates. Nine babies failed to stabilize initially and were placed on ECMO before CDH repair (alveolar-arterial gradient > 600 and oxygenation index > 40), and seven survived. The overall survival rate was 80% at 3 months in this ECMO-treated group. Early mortality was due to inability to wean from ECMO (one), intracranial hemorrhage (one), liver injury (one), and pulmonary hypoplasia (one). Nine of 11 babies requiring a prosthetic patch in the post-1987 ECMO group survived (81.8%). There were three late post-ECMO deaths (3 to 18 months) of right heart failure (two) and sepsis (one). Symptomatic gastroesophageal reflux occurred in nine cases, six requiring a fundoplication in the bypass babies. Recurrent diaphragmatic hernia occurred in nine cases (five ECMO). The overall survival rate was significantly improved in the delayed repair/ECMO group (67% versus 43%; p < 0.05) and was most noticeable in infants requiring a prosthetic diaphragm (81.2% versus 12.5%; p < 0.005). These data indicate that early stabilization, delayed repair, and ECMO improve survival in high-risk CDH. Early deaths are related to pulmonary hypertension and can be reversed by ECMO.
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PMID:Delayed surgical repair and ECMO improves survival in congenital diaphragmatic hernia. 141 95

From 1977 to 1991, 136 neonates have had corrective surgery for diaphragmatic hernia at Children's Hospital of Los Angeles. A retrospective study was performed to determine how many of the 136 neonates had defects large enough to require the use of a prosthetic patch to repair the defect. Twelve were found. All 12 were symptomatic at birth for respiratory distress. Mean arterial blood gas values at birth were pH 6.95, PCO2 94.8, and PO2 47.2. The mean oxygen index (n = 10) was 61.8. Six of these patients were repaired without extracorporeal membrane oxygenation (ECMO) support while the other six received ECMO bypass perioperatively. All six of the patients who did not receive ECMO support died despite successful diaphragmatic repair. Five of six patients who received ECMO perioperatively survived (83%). These surviving infants are now between 1 month and 4 years of age. In the survivors, four of five required subsequent repair and patch enlargement for a recurrent diaphragmatic hernia. Gastroesophageal reflux, requiring a Nissen fundoplication in two infants, complicated the course of three survivors. Four survivors were discharged with supplemental oxygen therapy lasting less than 13 months. Patch disruption is predicted to occur at approximately 18 months of age in all patients, especially if little or no muscle was available at primary repair for prosthetic attachment. These children should be followed closely for feeding or respiratory symptoms. Diagnosis of patch disruption can be made by chest x-rays and confirmed by contrast studies. Patch expansion by laparotomy and careful search for additional musculature for patch attachment is recommended when reherniation occurs.
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PMID:ECMO and the management of congenital diaphragmatic hernia with large diaphragmatic defects requiring a prosthetic patch. 150 Oct 39

Anatomical and physiological considerations specific to newborn infants with congenital thoracic abnormalities directly affect the timing and nature of surgical intervention during the neonatal period. This paper uses oesophageal atresia as an example of a common neonatal thoracic condition to highlight the way in which these considerations have influenced the approach to their surgical management. The type of surgical approach employed during thoracotomy determines the likelihood of subsequent chest wall deformity: an intercostal approach is preferable to rib resection. Multiple thoracotomies adversely affect the chest wall appearance and lung function. In premature infants with respiratory distress syndrome early surgical closure of the tracheo-oesophageal fistula is advantageous, and gastrostomy alone often prolongs the ventilatory difficulties. The upper oesophagus can be extensively mobilized with little danger to its blood supply, whereas the lower oesophagus, because it receives a segmental supply, is more vulnerable to ischaemia. The severity and distribution of tracheomalacia is reflected in its symptomatology. Tracheomalacia often coexists with gastro-oesophageal reflux, which should be corrected by a fundoplication if respiratory symptoms persist or an oesophageal stricture develops. The numerous factors producing heat loss in the newborn during thoracotomy are discussed. It is clear that an understanding of the anatomy and physiological changes which occur in the neonate is required if these infants are to be treated effectively and safely.
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PMID:Influence of anatomy and physiology on the management of oesophageal atresia. 190 89

In order to study the effect of cisapride on gastric stasis and to evaluate the possible risk of cholestasis, 20 premature neonates born in the hospital during one year were orally treated with cisapride 0.15 mg/kg q.i.d., over a mean period of 38 days. The gestational age ranged from 26 to 34 weeks and the mean age at the start of the cisapride treatment was 18 days. All patients were ventilated, 13 had a respiratory distress syndrome (hyaline membrane disease), and 9 had gastro-oesophageal reflux (GOR). All patients were given a semielementary formula by means of a continuous nasogastric infusion. The gastric residue was studied during three days: 24 hour baseline and 48 hours under cisapride treatment. The mean residue decreased (p less than 0.0001) from 50.6% during the last 6 baseline hours to 12.1% during the last 6-hours of the cisapride period. The mean feeding volume increased from 24.2 ml to 34.2 ml (p less than 0.001). A group of four patients had reversible cholestasis against the background of an outbreak of Candida, three before and one during cisapride treatment. Therefore, it could not be demonstrated that cisapride plays a role in the development of cholestasis. Because of the risks of GOR and the drawbacks of delayed enteral feeding, it is concluded that the use of cisapride is justified in premature neonates with gastric stasis.
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PMID:Long-term use of cisapride (Prepulsid) in premature neonates. 209 83

Dysphagia due to cricopharyngeal dysfunction is well known; however, there have been no previous data indicating an association between cricopharyngeal dysfunction and COPD. After observing marked cricopharyngeal dysfunction with aspiration in three patients who had frequent and severe exacerbations of COPD, we performed pharyngoesophageal examinations with videotaping in another 22 nonrandomized patients. Cineradiography or videofluoroscopic recording with capabilities of slow-motion and freeze-frame playback is mandatory, since the transit time of the bolus through the pharynx is rapid. Severe cricopharyngeal dysfunction was observed in 17 elderly patients with COPD. Deglutition disorders were elicited by careful questioning in 15 of these. In eight subjects, cricopharyngeal myotomy resulted in improvement of swallowing and complete or partial relief of acute exacerbations of respiratory distress. In one subject, myotomy relieved only the swallowing problem. The mechanism of cricopharyngeal dysfunction in elderly patients with COPD is unknown at this time, but may be related to gastroesophageal reflux, therapeutic agents, and/or alterations in pharyngoesophageal anatomic structures. We conclude that investigations for swallowing disorders should be considered in patients with COPD who have frequent acute exacerbations of respiratory distress.
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PMID:Cricopharyngeal dysfunction in chronic obstructive pulmonary disease. 229 59

We report 30 patients with exogenous lipoid pneumonia due to vegetal oil. This was employed in most of the cases during the first month of life for digestive tube symptomatology; clinical manifestations began three months following administrations, as a pneumonia or bronchopneumonia with a respiratory distress syndrome of variable severity. 60% of the thorax x-ray studies were abnormal, the main finding was opacity. One patient has alterations of the mechanics of deglutition; seven had gastroesophageal reflux. Arterial gasometry showed hypoxaemia and increase of alveolo-arterial gradient of oxygen in all. Ten patients died and all the survivors were reevaluated in september, 1988; 18 had normal physical findings. Thorax x-ray studies in 13 patients had right reticulate infiltration and 6 right apical opacity; ECG showed right ventricular hypertrophy in 3. Perfusion pulmonary gamagram with technetium 99 was abnormal in 5. Gastroesophageal reflux was evident in 2. Five were under treatment for several causes. Diagnosis and treatment is discussed.
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PMID:[Exogenous lipoid pneumonia]. 260 74

Gastroesophageal reflux (GER) is a well-recognized problem in infants and children. Only scant mention of the premature infant with GER can be found in the literature. Of 760 preterm infants admitted to the NICU between 1980 and 1984, 22 had documented GER. These infants all underwent medical management including upright positioning, small frequent feeds, and often, nasojejunal feedings. Seventeen babies did not respond to medical management and underwent surgical therapy to control the reflux. Of the 17 babies requiring fundoplication, 15 had been initially intubated for treatment of respiratory distress syndrome. Eight of these 15 were extubated in less than 25 days and were improving until they exhibited sudden episodes of deteriorating pulmonary status requiring reintubation. The other seven intubated patients developed striking bronchopulmonary dysplasia (BPD) in the first month and required prolonged ventilatory support. Pulmonary deterioration, failure to grow, and refusal to eat became the herald of GER in these infants. Fundoplication dramatically improved the pulmonary status in all but one infant. Three late deaths can be attributed to cor pulmonale and pulmonary failure. BPD was striking predisposing factor for severe GER in these premature infants. In the total premature population without BDP only 8 of 684 (1.2%) had GER with five responding to medical management and three others undergoing fundoplication for apnea-bradycardia spells. Fourteen of the 76 infants with BPD (18.4%) had significant GER and all required surgical management for control of symptoms. Premature infants who develop deteriorating pulmonary function, poor growth, and/or refusal to eat should be evaluated for GER.
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PMID:Gastroesophageal reflux and the premature infant. 309 Feb 24

Enteral nutrition is a safe technique but complications may arise. Mechanical problems can occur as a result of tube malposition: regurgitation can induce respiratory distress. Esophagitis is rare and does not seem to be related to acid gastro-oesophageal reflux. Diarrhea, the main gastro-intestinal side effect, has a complex etiology; management requires knowledge of gastro-intestinal physiology during enteral nutrition. Many of the problems encountered with enteral feeding can be avoided by using a fine bore tube, administering the feed by continuous infusion, and careful monitoring of patients for metabolic abnormalities.
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PMID:[Digestive and respiratory complications in enteral nutrition]. 314 96

The case of a 3-week-old male infant is described. After receiving an iatrogenic overdose of metoclopramide (1.0 mg/kg every six hours) throughout a 36-hour period for the treatment of suspected gastroesophageal reflux, he became cyanotic, lethargic, and irritable, he fed poorly, and he had diarrhea and respiratory distress. Methemoglobinemia (20.5%) and reduced oxyhemoglobin saturation (79%) were identified. The patient had an excellent clinical response following a single IV dose of methylene blue. Subsequently, methemoglobin reductase activity was normal and there was no measurable hemoglobin M. The diagnosis of methemoglobinemia should be considered in any infant receiving large doses of metoclopramide who has clinical findings of cyanosis, ashen color, or a history of lethargy and/or motor restlessness.
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PMID:Metoclopramide-induced methemoglobinemia. 340 65


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