Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The histopathologic pattern in the Central Nervous System in 12 out of 21 new-borns and young infants, below 2 months of age, operated for various congenital heart defects, is that of recent necroses in the deep and subcortical white matter of the pallium, seen from a few hours to 8 days following completion of surgery. Type and location of these lesions of ischemic coagulative necrosis, resembling findings in the perinatal respiratory distress syndrome, seem to depend on shock-like states, the low output syndrome of the left heart with hypovolemia and hypotension. The cause of death in all these infants was cardio-respiratory failure. The question to what extent glial scars replacing necroses within the mostly non-myelinated fiber systems of the pallium will lead to defective maturation of the brain in later infancy and childhood remains a challenge for neurologic and psychological investigation, even if the heart defect has been successfully repaired by the surgeon. Post-mortem data of the CNS in 24 older infants and children below 9 years of age in association with cardia surgery include thrombembolic infarctions, also, after catheterization alone, diffuse or segmental cortical necroses, and cortical scars, especially in children older than 1 year, confirming data recently reported from this laboratory.
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PMID:Brain changes in newborns, infants and children with congenital heart disease in association with cardiac surgery. Additional observations. 5 75

In a retrospective analysis of infants born with meconium staining over an 18-month period at Cook County Hospital, 32 infants met two of the three criteria for the diagnosis of meconium aspiration syndrome: (1) history of meconium in the oropharynx or trachea; (2) clinical evidence of respiratory distress; and (3) x-ray evidence of aspiration pneumonia. Seventeen infants developed respiratory failure; nine of these infants died. One infant without respiratory failure died of sepsis. Analysis of sequential arterial blood pH and gas tension showed that nonsurviving infants had persistently high PCO2 and A-a gradient in spite of initiation of assisted ventilation. These changes seem to be related to severe right-to-left shunting and ventilation perfusion abnormalities. The data further suggest that asphyxia and acidosis occur well before the infant is born and that intrapartum monitoring to recognize fetal asphyxia may help in improving morbidity and mortality from meconium aspiration syndrome.
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PMID:Assisted ventilation in infants with meconium aspiration syndrome. 24 Jan 48

We recently utilized continuous infusion intravenous isoproterenol in the treatment of respiratory failure in an 18-yr-old steroid-dependent asthmatic female. Aminophylline, hydrocortisone, aerosolized isoetharine, and oxygen were also administrered. The patient responded to this therapy, with PaCO2 falling from 70 torr to 33 torr in 18 hr. The maximum isoproterenol dosage administered was 0.32 microgram/kg/min. Thirty-six hours following the institution of therapy, while the isoproterenol was being tapered, the patient experienced an increase in respiratory distress followed by cardiac arrest. Postmortem examination revealed multiple small areas of myocardial necrosis. These findings, unusual in asthma, probably were related to the effects of isoproterenol or the combination of isoproterenol and aminophylline on the stressed myocardium. The vulnerability of the hypoxic myocardium to the effects of isoproterenol suggests that careful cardiac monitoring is essential in the management of patients receiving this medication for treatment of respiratory failure secondary to severe asthma.
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PMID:Fatal myocardial toxicity during continuous infusion intravenous isoproterenol therapy of asthma. 44 42

Death in the late stage of Duchenne muscular dystrophy is most frequently a consequence of respiratory failure. Since muscles of ventilation become weakened the bellows mechanism fails insidiously. Patients exhibit symptoms of ventilatory insufficiency, the first to be noticed are those associated with CO2 retention: dyspnea, nightmares, increased heart rate, and increased blood pressure. Ten patients with late stage Duchenne muscular dystrophy have been supplied with mechanical aid for ventilatory assistance. The age of onset of respiratory distress needing mechanical assistance varied from 10 to 20 years. Meaningful survival after allegedly reaching the end stage has been from 2 to 7.5 years with an average of 3.4 years. With a caring family, these patients can have a meaningful life, even though they require continuous mechanical ventilatory aid.
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PMID:Mechanical ventilation of patients with late stage Duchenne muscular dystrophy: management in the home. 45 24

The occurrence of unilateral phrenic nerve injury with the resultant hemidiaphragm paralysis or paresis can cause significant respiratory distress or respiratory failure in infants and children. An early bedside diagnosis of this problem will allow appropriate therapy and prevent needless diagnostic procedures. With the patient in the lateral decubitus position and the paralyzed side up, accentuated paradoxical inspiratory inward epigastric motion ipsilateral to the paralyzed hemidiaphragm can be seen. With the paralyzed hemidiaphragm down, abdominal motion appears to be normal as if the paralyzed hemidiaphragm were plicated. Thus, ventilation may be improved by changing body position as well as instituting ventilatory support while the potential for phrenic nerve recovery is evaluated.
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PMID:A physiological approach to hemidiaphragm paralysis. 50 71

Posterolateral diaphragmatic hernias and cystic hamartomatous malformations of the lung can cause actue respiratory distress in the immediate postnatal period. The clinical and radiological features of these two conditions can be similar. Owing to misdiagnosis, the surgical approach was inappropriate in 2 of 26 patients diagnosed as having posterolateral diaphragmatic hernias on admission. During the same period, 5 cases of congenital cystic lung disease were treated surgically. Three of these patients were admitted in severe respiratory failure within 48 hours of birth, and in 2 of these cases the wrong diagnosis was made. The clinical features of these two easily confused congenital anomalies are discussed, and the main differentiating points on the chest radiographs are presented.
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PMID:Cystic pulmonary hamartoma simulating posterolateral diaphragmatic hernia. 51 76

The morphology and sequential evolution of the pulmonary lesions in respiratory distress syndrome have been reviewed. Reasons have been presented to support the conclusion that these lesions are in the main produced by toxic effects of oxygen rather than the underlying disease process which initiated the episode of respiratory failure. The mechanism of oxygen toxicity has been briefly reviewed. The implication of these considerations is that in any patient with acute respiratory impairment, oxygen should be used as therapy only if it is required to prevent death from hypoxia and should be used in the lowest possible effective dose. As the patient improves and arterial oxygen tension rises this dose should be promptly reduced.
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PMID:Pathology of adult respiratory distress syndrome. 74 13

Thirty-one neonates with early onset of serious group B streptococcal infections were observed in a four-year period. The mortality was 52%. Premature infants with clinical signs of respiratory distress syndrome were at highest risk of death; clinical signs of RDS were typical until apnea, shock, respiratory failure, and worsening of the radiographic pattern unexpectedly intervened. Pathologic material from infants with radiographic evidence either of RDS or of pneumonia showed both typical hyaline membrane disease and pneumonia in most instances. Factors which may be helpful in recognizing premature infants at risk for GBS disease in the much larger group of premature infants with uncomplicated RDS include: history of artificial, premature, or prolonged rupture of membranes; localized pulmonary infiltrates on chest roentgenogram; low absolute neutrophil count; and an unusually rapid progression of RDS.
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PMID:Early onset group B streptococcal disease: clinical, roentgenographic, and pathologic features. 78 Dec 1

A retrospective study involving all admissions to two neonatal intensive care centers over a 4-year period was carried out to assess the protective effect, or lack of it, of prolonged rupture of membranes (ROM) on the prevalence of idiopathic respiratory distress syndrome (IRDS) in premature infants. Significantly fewer cases of IRDS were found in patients in all gestational age groups when ROM was greater than 24 hours as compared with those with ROM of less than 12 hours' duration. However, prolonged ROM was not consistently associated with a difference in prevalence of respiratory failure accompanying IRDS, or in the prevalence of sepsis or neonatal mortality in this patient population. It is concluded that benefit to a premature infant in the form of reduced risk of developing IRDS is possible if the mother is allowed 24 hours after ROM before the delivery is initiated.
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PMID:Association of premature rupture of membranes with idiopathic respiratory distress syndrome. 83 98

An acute respiratory distress syndrome in 10 adult dogs was usually preceded by vomiting, anorexia and lethargy followed, after a short interval, by dyspnoea. The dyspnoea became increasingly severe, despite oxygen therapy, and cyanotic respiratory failure ensued. All 10 dogs died or were killed after illnesses lasting between one and eight days. Necropsies revealed pulmonary congestion, oedema, collapse and haemorrhage with loss of alveolar epithelial cells. Early alveolar fibrosis was also found. Paraquat was identified in post mortem samples from four of the 10 dogs.
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PMID:Acute respiratory distress in the dog associated with paraquat poisoning. 86 Mar 82


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