Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary edema has been demonstrated in the early stages of respiratory distress syndrome in premature infants. To evaluate whether early furosemide therapy (0 to 8 hours after birth) would affect the electrolyte balance, pulmonary status, and outcome, 57 infants (less than or equal to 2000 gm) with respiratory distress syndrome who required mechanical ventilation shortly after birth were randomized into two groups: 29 given furosemide (1 mg/kg/day intravenously for three doses) and 27 control. The clinical, biochemical, and laboratory characteristics of the groups were comparable before entry into the study. Administration of furosemide significantly enhanced the urinary excretion of Na and Cl at 0 to 24, 24 to 48 and 48 to 72 hours and of Ca at 24 to 48 and 48 to 72 hours after drug administration. There was no significant difference between the groups in urinary excretion of K and in serum Na, Cl, K, and Ca values. A spontaneous increase in urine output occurred in the control group at 48 to 72 hours after the initiation of the study (mean +/- SD 7.0 +/- 3.5 hours postnatal age), along with a decrease in mean airway pressure for mechanical ventilation. The use of furosemide (7.3 +/- 3.5 hours postnatal age) enhanced urine output at 24 to 48 and 48 to 72 hours after medication, resulting in further decrease in mean airway pressure and facilitating extubation. There was, however, no significant difference between the groups with respect to incidence of patent ductus arteriosus, morbidity from bronchopulmonary dysplasia, and mortality.
 ...
PMID:Early furosemide therapy in premature infants (less than or equal to 2000 gm) with respiratory distress syndrome: a randomized controlled trial. 638 52

The "shock lung" syndrome may occur in diabetic ketoacidosis in association with disseminated intravascular coagulation; occasionally it occurs alone after treatment of the ketoacidosis. Two patients developed pulmonary opacities with clinical features of acute respiratory distress such as are seen in the shock lung syndrome; in both, however, the findings suggested a different mechanism from that occurring in the syndrome. Hypoalbuminaemia was prominent, and it is postulated that a low plasma osmotic pressure caused by high volume crystalloid infusions may have precipitated the acute respiratory complications. Plasma osmotic pressure may be an important variable in patients given large volumes of crystalloid infusions; further studies are required to elucidate mechanisms of pulmonary oedema in such patients.
 ...
PMID:Acute respiratory distress in diabetic ketoacidosis: possible contribution of low colloid osmotic pressure. 640 36

Despite having implemented rigorous glucose control for women with gestational diabetes early in the third trimester, we found excessive morbidity among the neonates of these women. To accurately assess the risk of newborn complications, we did a five-year review (1977 to 1981) of infants of class A diabetic mothers to determine the incidence and scope of morbidity in these infants. Fifty-one infants of class A mothers were identified (group 1) and randomly matched with 102 infants of nondiabetic mothers (group 2). The distribution of morbidity between the two groups was as follows: hypoglycemia 9/51 (18%) vs 0/102 (P less than .001); birth injuries 4/51 (8%) vs 1/102 (2%) (P less than .05); pulmonary edema 3/51 (6%) vs 0/102 (P less than .05); respiratory distress 4/51 (8%) vs 7/102 (7%) (NS); macrosomia 18/51 (35%) vs 23/102 (23%) (NS); and hyperbilirubinemia 3/51 (6%) vs 8/102 (8%) (NS). There were two fetal deaths and three infants with major congenital anomalies among the diabetic pregnancies compared to none from the nondiabetic pregnancies. Compared to insulin-dependent diabetes, class A diabetes is accompanied by relatively mild metabolic disturbances in the mother. On the other hand, the infant of a mother with class A diabetes appears to be at risk for serious and life-threatening complications, both before and after birth. These results raise the question of whether earlier identification, subsequent meticulous diabetic management, and altered timing of delivery might reduce the complications experienced by these infants.
 ...
PMID:Continuing neonatal morbidity in infants of women with class A diabetes. 649 59

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
 ...
PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Two of 30 patients with esophageal varices had respiratory distress develop within 8-24 h of esophageal sclerotherapy. Evidence of aspiration and sepsis were absent in these two patients with the clinical picture of adult respiratory distress syndrome. To investigate the possible etiologic role of sodium morrhuate in this syndrome, a sheep model was established and pulmonary hemodynamics, lung lymph flow, and albumin concentration were measured before and after the intravenous injection of 2.5-15.0 cm3 of sodium morrhuate. In all 8 animals studied, mean pulmonary artery pressures increased from 11.6 +/- 2.8 to 32.8 +/- 4.9 mmHg (p less than 0.01) 30 s after injection. These pressures returned to baseline values over 120 min. Lymph flow increased from 0.91 +/- 0.89 to 2.8 +/- 1.5 ml/30 min at 90 min postinjection (p less than 0.05) and returned to baseline values in animals monitored for 6-8 h. The lymph/plasma albumin ratio decreased from 0.856 +/- 0.08 to 0.74 +/- 0.01 (p less than 0.05) 120 min postinjection. Pulmonary edema was not evident histologically or gravimetrically (wet/dry weight ratio was 3.65 +/- 0.3 and not different from normal). It was concluded that sodium morrhuate injection in sheep causes marked but transient pulmonary hypertension associated with an increased lymph flow of relatively protein-poor lymph. Sodium morrhuate esophageal sclerotherapy may affect pulmonary hemodynamics and contribute to respiratory difficulties in patients.
 ...
PMID:Acute respiratory failure after sodium morrhuate esophageal sclerotherapy. 660 87

Although acute mountain sickness (AMS) has been studied for well over a century, a standard measure or index of the degree of illness for use in experimental research does not exist. This paper outlines a definition and procedures for an operational measurement of AMS using the Environmental Symptoms Questionnaire (ESQ). After 58 men completed over 650 ESQs during a stay of 1-3 weeks atop Pike's Peak (4300 m), factor analysis produced nine distinct symptom groups, with two factors representing AMS. The first factor contains symptoms indicative of cerebral hypoxia and is labeled AMS-C. The second reflects respiratory distress and is called AMS-R. Signal detection theory was used to establish a criterion score value for each factor. Standard deviation values were used to derive indices of sickness severity. Discussion is given to the possible relationships between the two types of AMS and the more serious conditions of cerebral and pulmonary edema.
 ...
PMID:Procedures for the measurement of acute mountain sickness. 666 Nov 20

A collective nitrous fumes poisoning (five cases) is reported. Two patients (case 3 and case 4) were comatose, in severe respiratory distress. Shock and slate blue cyanosis were noted. Physical examination and chest X ray revealed acute pulmonary edema-Methemoglobin levels were 71,3% (case 3) and 58% (case 4). Despite treatment both of them died from severe hypoxia resulting in cardiorespiratory arrest. Post-mortem examination was performed upon these four men. On admission the last one (case 5) was conscious, and in good hemodynamic condition. Acute pulmonary edema and cyanosis were present. Methemoglobin level was 37,3%. This patient recovered appropriate therapy. For case 1 and 2 acute anoxia due to methemoglobinemia seems to be cause of death. For cases 3 and 4 death is due to hypoxemia associated with pulmonary edema.
 ...
PMID:[Collective acute poisoning by nitrous gases]. 667 8

A patient with probable hydrochlorothiazide-induced pulmonary edema is described. A 70-year-old woman experienced nausea, diaphoresis, and severe respiratory distress approximately 1/2 hour after taking an Aldactazide tablet. She had experienced a flu-like syndrome after taking a single tablet two weeks previously. The patient was mildly tachycardic with a blood pressure of 74/0 mm Hg. A chest X-ray revealed cardiomegaly and bilateral pulmonary edema suggestive of congestive heart failure. The pulmonary capillary wedge pressure was normal. It was felt that the patient had developed a noncardiac pulmonary edema possibly secondary to hydrochlorothiazide ingestion. Nine other cases reported in the literature also are described. Pharmacists should be aware of this potential life-threatening reaction and avoid patient reexposure to the drug.
 ...
PMID:Hydrochlorothiazide-induced pulmonary edema. 669 86

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
 ...
PMID:Edema formation in the newborn lung. 676 Oct 39

Eleven Friesian steers were given 3, methyl indole (3MI) orally at dose rates ranging from 0.1 to 0.3 g/kg. Three of these (group B) received a single oral dose of 0.2 g/kg and subsequently developed respiratory distress. Their plasma 3MI concentrations six hours after dosing were between 2.25 and 7.23 micrograms/ml. The steer with the highest six-hour plasma value died at this stage and the dominant pathological feature was severe pulmonary oedema. The other two steers survived until they were slaughtered 96 hours after dosing; the major pathological findings in them were interstitial emphysema, hyaline membranes and alveolar epithelial hyperplasia. The other eight steers (group C) each received weekly oral doses of 0.1 g 3MI/kg for 10 weeks. One animal died after developing severe respiratory distress following its third dose. Thereafter, the others developed two separate patterns of response. Three steers (subgroup C1) became progressively more tolerant to oral 3MI, even in the face of dose rates increased to 0.2 and 0.3 g/kg during the 11th to 14th weeks of the study and also in the presence of relatively high plasma 3MI concentrations after dosing. One animal was slaughtered after its 10th dose and two after their 14th dose of 3MI; post mortem examinations revealed that their lungs were macro- and microscopically normal. The other steers (subgroup C2) all continued to react after each weekly oral dose of 3MI and their post-dosing plasma 3MI concentrations consistently remained relatively low. Latterly, each of the three steers which survived to the 14th week also exhibited persistent tachypnoea and marked hyperpnoea between dosings. On post mortem examination, in addition to the signs generally associated with acute 3MI toxicity (see above), each of the subgroup C2 steers were found to have diffuse pulmonary fibrosis and an alveolitis. While certain cattle appear to become tolerant to the effects of repeated doses of 3MI, the results of this study clearly demonstrated that, in others, such treatment eventually gives rise to diffuse pulmonary fibrosis and alveolitis.
 ...
PMID:Experimental production of diffuse pulmonary fibrosis and alveolitis in cattle: the effects of repeated dosage with 3, methyl indole. 683 86


<< Previous 1 2 3 4 5 6 7 8 9 10