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Infant respiratory distress syndrome

Infant respiratory distress syndrome ("RDS", also called "Respiratory distress syndrome of newborn", previously called hyaline membrane disease), is a syndrome caused by developmental lack of surfactant and structural immaturity in the lungs of premature infants. RDS affects about 1% of newborn infants. The incidence decreases with advancing gestational age (length of pregnancy), from about 50% in babies born at 26-28 weeks, to about 25% at 30-31 weeks. The syndrome is more frequent in infants of diabetic mothers and in the second born of premature twins. more...

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Clinical course

Respiratory distress begins shortly after birth, and is manifest by a whining noise, flaring of the nostrils and "sucking in" of the chest wall during breathing efforts. The baby may become cyanotic ("blue") from lack of oxygen in the blood. As the disease progresses, the baby may have respiratory failure, and prolonged cessations of breathing ("apnea"). If untreated, the baby's condition may worsen, and death may ensue. Complications include metabolic exhaustion (acidosis, low blood sugar), patent ductus arteriosus, low blood pressure, chronic lung changes, and intracranial hemorrhage.


The characteristic pathology seen in babies who die from RDS was the source of the name "hyaline membrane disease". These waxy-appearing layers line the collapsed tiny air sacs ("alveoli") of the lung. In addition, the lungs show bleeding, over-distention of airways and damage to the lining cells.


The lungs are developmentally deficient in a material called surfactant, which allows the alveoli to remain open throughout the normal cycle of inhalation and exhalation. Surfactant is a complex system of lipids, proteins and glycoproteins which are produced in specialized lung cells called Type II cells. The surfactant is packaged by the cell in structures called lamellar bodies, and extruded into the alveoli. The lamellar bodies then unfold into a complex lining of the alveoli. This layer serves the purpose of reducing the surface tension which would tend to cause the alveoli to collapse in the presence of gas. Without adequate amounts of surfactant, the alveoli collapse and are very difficult to expand. Microscopically, it is characterized by collapsed alveoli alternating with hyperaerated alveoli, vascular congestion and hyaline membranes (resulted from fibrin, cellular debris, red blood cells, rare neutrophils and macrophages). Hyaline membranes appear like an eosinophilic (pink), amorphous material, lining or filling the alveolar spaces and blocking the gases exchange . The blood (which normally receives oxygen from the alveolar gas and unloads carbon dioxide into the alveoli) passes through the lungs without this vital exchange. Blood oxygen levels fall, and carbon dioxide rises, resulting in rising blood acid levels. Structural immaturity, as manifest by low numbers of alveoli, also contributes to the disease process. It is also clear that the oxygen and breathing treatments used, while life-saving, can also damage the lung. The diagnosis is made by the clinical picture and the chest xray, which has a "ground-glass" appearance.


Most cases of hyaline membrane disease can be prevented if mothers who are about to deliver prematurely can be given a hormone-like substance called glucocorticoid. This speeds the maturation of the lungs and surfactant system. For very premature deliveries, glucocorticoid is given without testing the fetal lung maturity. In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of lipid in the amniotic fluid, obtained by inserting a needle through the mother's abdomen and uterus. The maturity level is expressed as the lecithin-sphingomyelin (or "L/S") ratio. If this ratio is less than 2, the fetal lungs are probably immature, and glucocorticoid is given.


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Adult respiratory distress syndrome complicating recurrent antepartum pyelonephritis
From Journal of Family Practice, 7/1/90 by David A. Yost

Acute pyelonephritis is estimated to occur in 1 % to 2% of all pregnancies., Prompt antimicrobial therapy is essential to prevent the well-described hemodynamic, hematologic, and renal complications of urosepsis. Recently, a series of case reports have shown adult respiratory distress syndrome (ARDS) to be an additional potential complication of antepartum pyelonephritis. The background to this complication is presented along with the first reported case of ARDS associated with recurrent pyelonephritis.


A 16-year-old primigravida presented to the University of Arizona College of Medicine Family Practice Office at 31 weeks' gestation with flank pain, pyuria, and a temperature of 40.1 [degrees] (104 [degrees] F). Her pregnancy had been complicated only by a prior admission at 22 weeks' gestation for pyelonephritis caused by infection with Escherichia coli. She was successfully treated with cefazolin on that occasion and had normal findings on follow-up urine studies. Her managing physicians had decided against ongoing suppression therapy with antibiotics.

The patient was admitted and begun on intravenous cefazolin and maintenance fluids. She was assessed not to be significantly dehydrated. Her renal function tests at admission were normal, and her white cell count was 16.4 x 10[.sup.9]/L.

Approximately 39 hours after admission, she reported the rapid onset of dyspnea. Her hematocrit had fallen to 0.29 from an admission value of 0.36, and an arterial blood gas on room air revealed a PO[.sub.2] of 7.1 kPa (53 mm Hg), PCO[.sub.2] of 2.7 kPa (20 mm Hg), oxygen saturation of 0.90, bicarbonate of 2.7 kPa (18 mm Hg), and a pH of 7.42. A chest radiograph showed findings consistent with pulmonary edema. She was transferred to the intensive care unit (ICU), where hemodynamic monitoring revealed a pulmonary capillary wedge pressure of 1.6 kPa (12 mm Hg). A fractional inspired flow of oxygen of 60% was required for the first 24 hours; however, she was subsequently weaned to room air and transferred out of the ICU after 48 hours. Her urine grew E coli sensitive to cefazolin, but blood cultures were negative. She was discharged home on the 8th day of her hospitalization.

Suppression therapy with nitrofurantoin was begun at discharge, and she was followed for the remainder of her pregnancy without further problems. She subsequently had an uncomplicated vaginal delivery of a normal full-term infant.


Cunningham et al (2) initially reported respiratory insufficiency complicating antepartum pyelonephritis in 1984. In a 1987 review of 75,000 deliveries over a 7-year period, (3) they noted respiratory distress to affect approximately one in every 50 pregnant women admitted for pyelonephritis. Fifteen ARDS patients were presented in this latter review, but unlike the case presented here, none was stated to have had more than one episode of pyelonephritis.

Several similarities are noted between this case and those reported by Cunningham and others. (2-5) Respiratory distress complicating pyelonephritis often occurs around 30 weeks' gestation, with the mean gestational age in the largest series being 28.7 weeks ([+ or -] 5.6 weeks). (3) Onset of dyspnea in all cases was seen within 48 hours after admission, with a mean of approximately 30 hours. Eighty-five percent of reported cases have had parities of one or none, with the majority being nulliparous. E coli has been the primary bacterial organism in most cases; however, 25% of these patients grew Klebsiella pneumoniae. Additionally, the hematocrit levels of all but one patient were less than 0.30 when respiratory distress was apparent, and evidence of hemolysis was commonly seen. Unlike this case, severe morbidity has been reported, with three women requiting mechanical ventilation, and one death from sepsis recorded. (3)

Iatrogenic causes of pulmonary edema, such as fluid overload, have been ruled out in this and other cases. Proposed mechanisms of pathogenesis in these patients have centered on the role of endotoxins. Nonpulmonary evidence of endotoxin-induced organ dysfunction has been manifested in these patients in the form of thrombocytopenia, hemolytic anemia, and transient renal dysfunction. (3) The case illustrated here may also provide evidence of a progressive, pregnancy-enhanced susceptibility to endotoxins, as this patient endured a second-trimester episode of pyelonephtitis without difficulty, then later experienced ARDS with a third-trimester infection.


Since pyelonephritis is so common during pregnancy, it is important that family physicians providing prenatal care be aware of this serious complication. Prompt recognition and aggressive therapy of ARDS are essential to avoiding further morbidity or mortality.


1 .McNeeley SG: Treatment of urinary tract infections during pregnancy. Clin Obstet Gynecol 1988; 31:480-487

2. Cunningham FG, Leveno KJ, Hankins G, Whalley PJ: Respiratory insufficiency associated with pyelonephhtis during pregnancy. Obstet Gynecol 1984; 63:121-125

3. Cunningham FG, Lucas MJ, Hankins G: Pulmonary injury complicating antepartum pyelonephhtis. Am J Obstet Gynecol 1987; 156: 797-807

4. Pruett K, Faro S: Pyelonephritis associated with respiratory distress. Obstet Gynecol 1987; 69:444-446

5. Elkington KW, Greb LC: Adult respiratory distress syndrome as a complication of acute pyelonephritis during pregnancy: Case report and discussion. Obstet Gynecol 1986; 67:18S-20S

COPYRIGHT 1990 Dowden Health Media, Inc.
COPYRIGHT 2004 Gale Group

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