Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We hypothesized that enteral doxapram would effectively treat apnea of prematurity without the appearance of major side effects. Of 16 infants, 10 (BW 1,520 +/- 102 g) received doxapram alone and 6 (BW 1,020 +/- 35 g) received doxapram plus theophylline. Apneas decreased from 16.7 +/- 1.9 to 2.1 +/- 0.6 in infants receiving doxapram alone, and from 38.2 +/- 4.4 to 7.9 +/- 2.2 apneas/24 h in those receiving doxapram plus theophylline. This was associated with an increase in alveolar ventilation, a shift of the ventilatory response to CO2 to the left, and no change in the immediate ventilatory response to 100% oxygen. Side effects included premature teeth buds corresponding to the lower central incisors, prevalence of occult blood in stool and necrotizing enterocolitis. The findings suggest that doxapram effectively controls apnea when given enterally, but should be used cautiously because of potentially harmful side effects.
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PMID:Clinical and physiological responses to prolonged nasogastric administration of doxapram for apnea of prematurity. 207 20

The relationship between periodic breathing and idiopathic apnea of prematurity was investigated. We recorded respiratory impedance, heart rate, pulse oximetry and end-tidal CO2 from 68 untreated infants of less than or equal to 34 wk gestation with a diagnosis of idiopathic apnea of prematurity. Mean birth wt was 1476 g (SD 420) and mean gestational age was 29.9 wk (SD 2.6). Apneas of more than 15 s duration that were associated with hypoxemia or bradycardia were identified by semiautomated analysis of computerized records. A total of 1116 significant apneic spells were identified, only one of which occurred during an epoch of periodic breathing, five others occurred within 2 min of the end of an epoch of periodic breathing. Less than 0.6% of significant apneic spells occur within 2 min of periodic breathing. In all of the 12 infants that were monitored starting in the first 12 h of life, significant apneic spells were identified before 36 h of age and no precipitating factors were identified. Periodic breathing did not occur during the first 48 h of life, a finding that supports the concept that the peripheral chemoreceptor is inactive in the first 48 h of life. Periodic breathing in the premature infant is not a precursor to significant apnea.
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PMID:Periodic breathing and apnea in preterm infants. 231 39

To determine the incidence of long-term sequelae after meconium aspiration syndrome (MAS), we studied 11 children who had MAS at age 8.2 +/- 0.2 years (mean +/- SD) and nine healthy control subjects with pulmonary function and exercise stress tests. The MAS children had evidence of mild airway obstruction, hyperinflation, and increased closing volumes in comparison with control values. During graded exercise stress tests on a treadmill, MAS children achieved normal maximal oxygen consumption and anaerobic threshold without a significant fall in arterial oxygen saturation or increase in CO2 tension. Exercise-induced bronchospasm occurred in four (36%) MAS subjects but in none of the control subjects. We conclude that children surviving MAS have long-term pulmonary sequelae, including airway obstruction, hyperinflation, elevated closing volumes, and airway hyperreactivity; yet they achieve normal aerobic capacity. These findings are similar, although less severe, than those after prematurity and bronchopulmonary dysplasia.
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PMID:Long-term pulmonary sequelae of meconium aspiration syndrome. 275 72

In an effort to establish the minimum effective dose of theophylline in the treatment of idiopathic apnea of prematurity, a prospective trial of 22 infants with at least 0.33 episodes of apnea per hour were studied. Apnea was diagnosed exclusively by continuous recording of heart rate, respiratory impedance, end-tidal CO2, and either or both transcutaneous oxygen and pulse oximetry. Four discrete serum concentrations of theophylline (23 mumol/l or 4.2 mg/L, 47 mumol/L or 8.5 mg/L, 70 mumol/L or 12.7 mg/L, and 84 mumol/L or 15.3 mg/L) were attained by using repeated loading doses of 4 mg/kg and increasing the maintenance dose from 1 to 1.5 mg/kg to 2 to 2.5 mg/kg, given every 8 hours. Before treatment and 24 hours after each loading dose, airway occlusions and measures of tidal volume, minute ventilation, and respiratory timing were performed. The effectiveness of therapy was assessed by either a continuous computer data-acquisition system or paper recording for the duration of the study. Of the 22 infants, three responded at level 1, three at level 2, and 10 at level 3. One of the four infants loaded to the fourth level had a sustained response for a total cumulative response of 77%. The five remaining infants required additional treatment with doxapram or continuous positive airway pressure. There was a significant increase in inspiratory pressure 100 msec after airway occlusion, maximum inspiratory pressure during airway occlusion, tidal volume, ratio of tidal volume to inspiratory time (mean inspiratory flow), and minute ventilation from the pretreatment measurements to those at the maximum dose of theophylline. The apnea response did not correlate with these improvements in ventilation measures.
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PMID:The dose response of theophylline in the treatment of apnea of prematurity. 327 63

The respiratory performance was studied after intraperitoneal administration of the adenosine agonists N6-phenyl-isopropyl-adenosine (PIA) and adenosine-5-ethylcarboxamide to preterm (gestational age 29-30 days) newborn halothane-anesthetized rabbits. Both agonists induced marked hypoventilation and irregular breathing by decreases in the breathing frequency as well as the tidal volume. Expiratory time was markedly prolonged, resulting in a decrease in the respiratory duty cycle (inspiratory time/total cycle duration). Analysis using the occluded-breath technique revealed that the adenosine analogues altered the time setting of the expiratory (inspiratory) neuronal circuits and lowered the inspiratory off-switch level, while inspiratory drive and the bulbopontine setting of the inspiratory phase were unaltered. The ventilatory response to CO2 was blunted after both adenosine analogues studied. Theophylline almost completely reversed the hypoventilation and irregular breathing seen after PIA injection. It is concluded that activation of central nervous adenosine receptors induced a marked respiratory depression in the preterm rabbit. Furthermore, our data imply that an overactivity of central adenosine mechanisms may have a pathophysiological significance for the irregular breathing or apnea of prematurity sometimes seen in the human neonate.
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PMID:Characterization of adenosine-induced respiratory depression in the preterm rabbit. 383 98

It has been suggested that apnea of prematurity may be caused by "immaturity" of central control of breathing. To test the validity of this hypothesis tidal volume (VT), alveolar ventilation (VA), alveolar Pco2 (Paco2), esophageal pressure change, and the slope of the CO2 response curve (delta Ve [minute ventilation]/delta Paco2) were determined in 18 infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 healthy newborns used as control subjects. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The results were as follows: Vt (4.4 +/- 1.0 mL/kg v 5.3 +/- 1.6 mL/kg), Va (96 +/- 21 mL/kg/min v 129 +/- 33 mL/kg/min), Paco2 (45.4 +/- 8.5 mm Hg v 35.6 +/- 4.7 mm Hg), esophageal pressure change (4.5 +/- 0.9 cm H2O v 6.0 +/- 1.8 cm H2O), delta Ve/delta Paco2 (20.2 +/- 10.6 mL/min/kg/mm Hg CO2 v 40.7 +/- 19.9 mL/min/kg/mm Hg CO2). There was a significant difference between infants with and without apnea for all measurements. The results indicate a decreased respiratory center output and a depressed ventilatory response to CO2 in infants with apnea. As there was no difference between the two groups in pulmonary mechanics or oxygenation, the findings support the hypothesis that a central disturbance in regulation of breathing is the cause of apnea in these infants.
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PMID:Apnea of prematurity: I. Lung function and regulation of breathing. 642 25

Prematurely born children have reduced peak VO2 compared with their peers, inferentially attributed to ventilatory limitation. The primary purpose of this study was to compare exercise ventilation and cardiac output in a sample of childhood survivors of lung disease of prematurity with those of a control group to elucidate reasons for lower peak VO2. A secondary aim was to describe and compare the ventilatory response to incremental exercise. Thirty-two children, aged 8-9 y, were recalled for lung function and progressive exercise tests. Fifteen of them also performed submaximal exercise with measurement of cardiac output (indirect [CO2] Fick) and physiologic dead space. Results were compared with those of term-born, age- and sex-matched, control children. Pulmonary function tests showed mild airflow limitation. Peak VO2 was lower in prematurely born children compared with control children, and was correlated with lean body mass. Their heart rate-VO2 relationship and stroke volume were similar to that of term-born control children. Children with a history of bronchopulmonary dysplasia and hyaline membrane disease as infants exhibited greater exercise hyperpnea than did healthy control children, because of higher breathing frequency, and maintained lower end-tidal PCO2 during submaximal exercise. Physiologic dead space normalized for body weight was similar in preterm and term-born children. Lower peak VO2 in this population is not caused by cardiopulmonary factors, but is best predicted by lean body mass. Ventilation did not limit exercise performance, although it appears that breathing during exercise is regulated differently in prematurely born children than in term-born children.
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PMID:Cardiopulmonary exercise performance in prematurely born children. 1081 92

Apnea of prematurity is common and none of the treatments being used are fully effective and free of significant adverse side effects. We hypothesized that low concentrations of CO2 (< or = 1.5%) may reduce apnea without causing discomfort from an increase in ventilation. We studied 10 preterm infants at a gestational age of 32+/-1 wk (mean +/- SEM) and birthweight 1.8+/-0.2 kg. After a control period of 1 hour, concentrations of CO2 were given (0.5%, 1%, and 1.5%) for 1 hour each, followed by a recovery period of 1 hour. Apnea number significantly decreased from 2.0+/-0.3 apneas/min during control to 1.0+/-0.1 apneas/min (0.5% CO2; P < .05), 1.1+/-0.2 (1% CO2; P < .05), and to 0.7+/-0.2 (1.5% CO2; P < .01). The apnea time significantly decreased from 14.2+/-2.5 s/min during control to 5.2+/-0.8 (0.5% CO2; P < .01), 5.8+/-0.7 (1% CO2; P < .01), and to 3.7+/-0.9 (1.5% CO2; P < .01). Minute ventilation significantly increased with CO2 without evidence of respiratory discomfort. TcPCO2 did not change and TcPO2 increased slightly. These findings suggest that inhalation of low concentrations of CO2 in preterm infants with apnea 1) decreases the number and time of apneas, 2) improves oxygenation, 3) increases ventilation, and 4) is effective even in such low concentrations as 0.5%. We speculate that inhalation of CO2 (< 1%) is more effective and safer than methylxanthines for the treatment of apnea of prematurity.
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PMID:Inhalation of low (0.5%-1.5%) CO2 as a potential treatment for apnea of prematurity. 1133 62

A 12-month-old child with a history of prematurity, severe respiratory compromise and failure to thrive required laser supraglottoplasty for severe laryngotracheobronchomalacia. Maintaining adequate oxygenation intraoperatively proved very difficult. Our usual technique with no endotracheal tube was not possible and CO2 lasering was commenced with a polyvinylchloride endotracheal tube in the operative field. The endotracheal tube was struck by the laser but did not ignite. Concern about the very serious morbidity from a laser-induced fire in the airway prompted a search for possible solutions. No commercially available laser-resistant tube is available in small enough diameter to use in an infant. An aluminium foil tape (3M #425) was evaluated and found to be potentially very useful to protect against an airway fire in this uncommon situation.
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PMID:Avoidance of laser ignition of endotracheal tubes by wrapping in aluminium foil tape. 1553 4

Great strides have been made in our understanding of developmental respiratory neurobiology. A clear picture is, therefore, emerging of the physiological mechanisms that underlie apnea of prematurity. The ventral surface of the medulla and adjacent areas play a key integrative function for central CO2 chemosensitivity and modulation of afferent inputs from peripheral chemoreceptors and laryngeal afferents. Maturational change in medullary neurotransmitter function appears to contribute to the physiological events that characterize apnea of prematurity. Despite this greater scientific insight, therapeutic strategies for neonatal apnea have changed little in 30 years. Xanthine therapy and continuous positive airway pressure remain the mainstay of therapy while other therapeutic approaches have been inadequately studied. Our understanding of a possible relationship between the triad of apnea, bradycardia and desaturation, and impaired neurodevelopmental outcome is also limited. These are all issues that need our attention if optimal therapy and outcome are to be provided for preterm infants with immature respiratory control.
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PMID:Control of breathing and neonatal apnea. 1598 51


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