Real-time urinary electrolyte monitoring after furosemide administration in surgical ICU patients with normal renal function

Background: Although the loop-diuretic furosemide is widely employed in critically ill patients with known long-term effects on plasma electrolytes, accurate data describing its acute effects on renal electrolyte handling and the generation of plasma electrolyte alterations are lacking. We hypothesized that the long-term effects of furosemide on plasma electrolytes and acid-base depend on its immediate effects on electrolyte excretion rate and patient clinical baseline characteristics. By monitoring urinary electrolytes quasi-continuously, we aimed to verify this hypothesis in a cohort of surgical ICU patients with normal renal function. Methods: We retrospectively enrolled 39 consecutive patients admitted to a postoperative ICU after major surgery, and receiving single low-dose intravenous administration of furosemide. Urinary output, pH, sodium [Na+], potassium [K+], chloride [Cl-] and ammonium [NH4+] concentrations were measured every 10 min for three to 8 h. Urinary anion gap (AG), electrolyte excretion rate, fractional excretion (Fe) and time constant of urinary [Na+] variation (tau Na+) were calculated. Results: Ten minutes after furosemide administration (12 +/- 5 mg), urinary [Na+] and [Cl-], and their excretion rates, increased to similar levels (P < 0.001). After the first hour, urinary [Cl-] decreased less rapidly than [Na+], leading to a reduction in urinary AG and pH and an increment in urinary [NH4+] (P < 0.001). Median urinary [Cl-] over the first 3-h period was higher than baseline urinary and plasmatic [Cl-] (P < 0.001). During the first 2 h, difference between FeCl- and FeNa+ increased (P < 0.05). Baseline higher values of central venous pressure and FeNa+ were associated with greater increases in FeNa+ after furosemide (P = 0.03 and P = 0.007), whereas higher values of mean arterial and central venous pressures were associated with a longer tau Na+ (P < 0.05). In patients receiving multiple administrations (n = 11), arterial pH, base excess and strong ion difference increased, due to a decrease in plasmatic [Cl-]. Conclusions: Low-dose furosemide administration immediately modifies urinary electrolyte excretion rates, likely in relation to the ongoing proximal tubular activity, unveiled by its inhibitory action on Henle's loop. Such effects, when cumulative, found the bases for the long-term alterations observed. Real-time urinary electrolyte monitoring may help in tailoring patient diuretic and hemodynamic therapies.