Controlled trial of furosemide therapy in infants with chronic lung disease

McCann, Ellen M.; Lewis, Kathleen; Deming, Douglas; Donovan, Margaret J.; Brady, June P.

doi:10.1016/s0022-3476(85)80252-3

Cited by 96 publications

(36 citation statements)

References 23 publications

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“…This water was derived primarily from the interstitial space, presumably including lung IW. We postulate that the mobilization of IW observed in this study accounts, at least partly, for the acute effects of furosemide on lung function observed by other investigators (2)(3)(4).…”

Section: Discussionsupporting

confidence: 77%

Effects of Furosemide on Body Water Compartments in Infants with Bronchopulmonary Dysplasia

O'donovan

Bell

1989

Pediatr Res

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ABSTRACT. We studied the effects of a single dose ofStudies in adults with pulmonary edema (5-7) have shown intravenous furosemide on the body water compartments variable effects of furosemide on plasma volume. Davidor et al.of nine infants with bronchopulmonary dysplasia. We (5) measured plasma vol in patients with refractory edema 2 h measured total body water, extracellular water, and plasma after an intravenous dose of furosemide. These patients had a volume using deuterium oxide, sodium bromide, and Evans mean decrease of 25% in plasma volume. Figueros and Weil(6) blue dye, respectively. From the results of these measure-found that the plasma volume of adults with acute cardiogenic ments, we calculated cell water, interstitial water, red cell pulmonary edema was lower than normal before therapy but volume, and total blood volume. We performed these meas-rose after treatment with furosemide, oxygen, and morphine.urements on the first day of the study and again 28 h later, Schuster et al. (7) measured blood volume in 2 1 patients with 4 h after an intravenous dose of furosemide (1 mglkg). All pulmonary edema who had either normal or decreased renal infants had a brisk diuresis in the first hour after the dose, function. The patients who had normal renal function, as indibut urine output was no greater during the 24-h period cated by a good diuresis, had no change in plasma volume 4 to after the dose than during the preceding 24-h period. Total 6 h after a single intravenous dose of furosemide. Patients who body water, extracellular water, and interstitial water were did not have a good diuresis had a rise in plasma volume. significantly decreased 4 h after furosemide. There was no There have been no similar studies in infants. Infants with change in plasma volume, red cell volume, or total blood BPD are often fluid restricted with the hope that this will reduce volume (Pediatr Res 26: 121-124, 1989) pulmonary edema. It would be of practical value to know whether furosemide causes a decrease in plasma volume in these Abbreviations infants, because hypovolumeemia might compromise organ perfusion and activate the compensatory mechanisms that stimulate BPD, bronchopulmonary dysplasia water and sodium retention. Our study was undertaken to assess TBW, total body water the effects of a single intravenous dose of furosemide on the IW, interstitial water plasma volume and other body water compartments of infants ECW, extracellular water with BPD. PV, plasma volume CBS, corrected bromide space Br, bromide MATERIALS AND METHODS

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Section: Discussionsupporting

confidence: 77%

Effects of Furosemide on Body Water Compartments in Infants with Bronchopulmonary Dysplasia

O'donovan

Bell

1989

Pediatr Res

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“…The improved survival rate among oxygen, calcium and phosphate supplementations, and a high incidence of hypercalciuria has been found [4,5]. In addition, furosemide is often used to reduce pulmonary edema and to improve pulmonary gas exchange in pre term infants with lung disease [6,7], Prolonged use of furosemide has been reported to further aggravate hyper calciuria and lead to renal calcification [8. 9], Other fac tors that may cause hypercalciuria and play a role in the development of renal calcification, such as decreased urine output, alkaline urine, acidosis, presence or absence of inhibitors of crystal formation and immobilization, have not been well studied in very low birth weight infants.…”

Section: Introductionmentioning

confidence: 99%

Renal Calcification in Very Low Birth Weight Infants

et al. 1993

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Between January 1990 and December 1991, serial real-time ultrasound examinations and analyses of urine were performed on a total of 50 infants with birth weights less than 1,500 g to assess the incidence of renal calcification. Five infants (10%) developed renal calcification at a mean age of 48.8 ± 14.1 days. These 5 infants with renal calcification had significantly shorter gestations (28.2 ± 0.8 vs. 30.1 ± 1.7 weeks, p < 0.0005) and lower birth weights (934 ± 45 vs. 1,311 ± 188 g, p < 0.0005) when compared with infants without renal calcification. None of the affected infants were treated with furosemide. Affected infants had a mean urine volume of 85.8 ± 11.3 ml/kg/24 h, mean urine calcium level of 5.07 ± 1.18 mg/kg/24 h, mean urine calcium to creatinine (mg/mg) ratio of 0.67 ± 0.09, and a mean urine N-acetyl-β-D-glu-cosaminidase (NAG) to creatinine (U/g) ratio of 259 ± 133. Urinalyses showed that affected infants had significantly higher urine pH values and hematuria. Alkaline phosphatase concentrations and initial parathyroid hormone levels were not different among the two groups. In summary, renal calcification occurred in 10% of very low birth weight infants and multiple risk factors seem to be contributory. The smaller, sicker and more immature infants appear to have increased risk for developing renal calcification. For earlier detection and treatment of renal calcification, follow-up screening by serial ultrasound examinations and assay of urinary excretion of calcium, creatinine and NAG are useful, and a meticulous search for the causes of renal calcification is mandatory.

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“…2 The correlation between PaCO2 and PETCO2 was good in infants with healthy lungs, 2 though the correlation was not good in infants who are critically ill. 3,4 McCann 'et al, however, used successfully (a-ET) PCO2 difference, where PETCO2 was sampled from nasal cavity, as a trend monitor to evaluate the improvement of pulmonary functions following therapy in critically ill infants with RDS. 3 Second, Campbell et al confirmed that negative (a-ET) PCO2 gradients occurred in children and may not be due to experimental errors. The incidence of negative (a-ET) PCO 2 gradients is 12% in healthy adults, s whereas the incidence may be higher (50%) in pregnant patients, 6.7 and children.…”

Section: Negative Arterial To End-tidal C02 Gradients In Childrenmentioning

confidence: 97%

Negative arterial to end-tidal CO2 gradients in children

Bhavani-Shankar

1994

Can J Anaesth

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Controlled trial of furosemide therapy in infants with chronic lung disease

Cited by 96 publications

References 23 publications

Effects of Furosemide on Body Water Compartments in Infants with Bronchopulmonary Dysplasia

Effects of Furosemide on Body Water Compartments in Infants with Bronchopulmonary Dysplasia

Renal Calcification in Very Low Birth Weight Infants

Negative arterial to end-tidal CO2 gradients in children

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