Results of a national survey of the current use of steroids in newborns in 1993 showed that 95% of the neonatologists in the United States have used dexamethasone for neonates at risk for chronic lung disease. Dexamethasone therapy for a period of a week or longer is associated with suppression of the hypothalamic-pituitary-adrenal axis (HPAA) in a substantial number of premature infants. A review of our current understanding of the biochemical tests evaluating HPAA function in premature infants and suggested guidelines for HPAA evaluation and management following dexamethasone therapy are presented.

Increased risk of central venous line thrombosis in tiny premature infants occurs because the size of the catheter relative to the cross-sectional area of the vessel is large, decreased plasma levels of plasminogen and antithrombin III, and relative low flow of the infusate through the catheter, in comparison with larger infants. A potentially fatal complication of central venous catheters is an intracardiac thrombus. The yield of detecting right atrial thrombi by routine echocardiographic monitoring is very low. Persistent positive blood cultures in infants with central venous lines, in spite of appropriate antibiotic therapy, or signs of catheter occlusion, may increase the yield of echocardiographic detection of intracardiac thrombi. Surgical removal of intracardiac thrombi in infants weighing less than 1500 gm carries a high mortality rate because of the need to use cardiopulmonary bypass with total circulatory arrest and profound hypothermia during surgery. It is in these infants that thrombolysis with urokinase should be considered. A successful therapy with urokinase of a complete occlusion of the right pulmonary artery by an embolus originating from the right atrium is described in a premature infant. For thrombolysis, a loading dose of urokinase of 4400 U/kg followed by 4400 to 8800 U/kg/hr for a few days was used. The thrombolytic effect was manifested by decreased thrombus echogenicity followed by its disappearance, by increased fibrinogen split products, and by decreased plasma fibrinogen. Urokinase therapy may cause massive bleeding, dislodge an intracardiac thrombus causing obstruction of cardiac valves or main vessels or causing embolization to the pulmonary or systemic circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

No abstract

Xanthines are frequently being used in the management of premature babies. Studies in adult subjects have demonstrated a diuretic effect of aminophylline due to the inhibition of solute reabsorption in various segments of the nephron. We evaluated the effects of aminophylline on the developing kidney. Nineteen premature infants, with a mean +/- SD gestational age of 31.1 +/- 2.8 weeks and mean birth weight of 1481 +/- 454 g were studied at mean age of 4.5 +/- 4.0 days before and after a 20-minute loading infusion of 6 mg/kg aminophylline, followed by maintenance therapy at a dose of 2 mg/kg every 12 hours. A marked diuresis occurred immediately after the loading dose, the ratio of urinary output to water intake increased from 0.58 +/- 0.36 to 1.19 +/- 0.65. Concomitantly, the fractional excretion of sodium increased from 2.7 +/- 2.6% to 5.7 +/- 4.4% and that of potassium rose from 21 +/- 19% to 31 +/- 21%. Urinary calcium and uric acid excretion were also enhanced: calcium to creatinine ratio rose from 0.31 +/- 0.29 to 0.60 +/- 0.54 and uric acid to creatinine ratio increased from 2.5 +/- 1.5 to 3.8 +/- 2.0. Tubular reabsorption of phosphorus (TRP) was not affected. Most of the effects were no longer evident after 24 hours, despite continuing aminophylline maintenance therapy. In premature infants the aminophylline loading dose, but not maintenance therapy, affected renal functions. Because heart rate, blood pressure, and creatinine clearance did not change, it appears that aminophylline acts directly on tubular reabsorptive functions.