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Unlabelled: The influence of dexamethasone on diuresis in preterm infants has not been well studied. We examined 15 preterm infants at risk for chronic lung disease with gestational ages ranging from 26 to 29 wk (median 27.6 wk) and birthweights ranging from 700 to 1485 g (median 965 g). Urine output, blood glucose, serum urea, serum creatinine, serum sodium and serum potassium, as well as systolic, diastolic and mean arterial pressure were measured on the day before, and on 4 consecutive days after starting treatment with dexamethasone (0.25 mg kg-1 i.v., twice daily). We found an increase of diuresis of 30 ml kg -1 d-1, 48-96 h after starting dexamethasone treatment. This coincided with a gradual but significant increase of serum urea levels and arterial pressure. During the study period, fluid and protein intake remained constant. Blood glucose and serum creatinine levels did not change. Our findings suggest that the increased urine output following dexamethasone treatment might be caused by two factors: (1) pressure diuresis induced by the increase of arterial pressure and (2) an increase of the osmolar load to the kidney due to an increase of serum urea.Conclusions: This study demonstrates that a significant increase of diuresis occurs in preterm infants, 48-96 h after starting dexamethasone. A careful monitoring of fluid balance during the first days of dexamethasone treatment is recommended. [ABSTRACT FROM AUTHOR]

The article reports on the study on the effects of icodextrin dialysis solution on the peritoneal membrane in Amsterdam, Netherlands. Researchers found that the solution is effective in inducing fluid and removing it from the body during long dwells, compared to low-molecular-weight osmotic agents. Despite its efficacy, they cannot assess its impact on peritoneal membrane because it is not used as a monotherapy.

Background and Objective: Mild therapeutic hypothermia (MTH) is used after out-of-hospital cardiac arrest (OHCA) to minimize cerebral damage. Induced hypothermia may further interfere with cardiac function and influence haemodynamics after OHCA., Methods: This was a prospective study of haemodynamic variables in 50 consecutive patients with OHCA treated with MTH. Patients were cooled to a core body temperature of 32.5 degrees C for 24 h. Induction and maintenance of cooling was accomplished via infusion of 2 l of cold isotonic saline (4 degrees C) and a cooling blanket. Rewarming was performed to 36 degrees C at a rate of 0.3 degrees C per hour. Haemodynamic data were analysed and compared in individual patients during different temperature phases., Results: Heart rate dropped from a mean of 85 to 60 beats per min (P=0.001) during hypothermia. Mean arterial pressure dropped from 79 to 72 mmHg, despite a rise in vasopressors and inotropes. Lactate levels were elevated throughout the induction (mean+/-SD) and maintenance phase (mean+/-SD); however, this did not correlate with a decrease in SVO2. Pulmonary artery pressures decreased during induction of hypothermia despite rapid infusion., Conclusion: MTH after OHCA lowered the heart rate. Despite induction of hypothermia with cold fluids, filling pressures decreased. Lower mean arterial pressure and cardiac output were observed during MTH, without deleterious effect on ScVO2. Lactate levels were elevated during MTH; however, levels did not correlate with outcome. Although the need for vasopressors and inotropes increases, this hypothermia-induced metabolic beta-blocker-like effect seems to have no negative effect on oxygen consumption and only temporarily affects anaerobic metabolism. No association of haemodynamic changes during MTH with outcome was found.