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Renal response and acid-base balance alterations during furosemide administration
Critical Care volume 17, Article number: P415 (2013)
Furosemide is one of the most employed diuretics in the ICU for its ability to induce negative water balance. However, one common side effect is metabolic alkalosis . We aimed to describe the time course of urinary excretion and changes in plasmatic acid-base balance in response to the administration of furosemide.
We connected the urinary catheter of 39 ICU patients to a quasi-continuous urine analyzer (Kidney INstant monitorinG®), allowing measurement of pH (pHU), sodium, chloride, potassium and ammonium concentrations (Na+U, Cl-U, K+U, NH4+U) every 10 minutes. The study period lasted 3 hours after a single intravenous bolus of furosemide (time 0). In 13 patients receiving two or more administrations over a longer period (46 (26 to 49) hours), according to clinical needs, we reviewed data on fluid therapy, hemodynamics and acid-base balance from the beginning to the end of the observation.
Ten minutes after furosemide administration, Na+U and Cl-U rose from 65 ± 6 to 140 ± 5 and from 109 ± 6 to 150 ± 5 mEq/l respectively, while K+U fell from 60 ± 5 to 39 ± 4 mEq/l (P 0.001 for all electrolytes vs. time 0) with a consequent increase in urinary anion gap (AGU = Na+U + Cl-U - K+U). Urinary output increased from 10 (5 to 19) to 53 (29 to 71) ml/10 minutes (P 0.05). After the first hour Cl-U remained higher than Na+U, which progressively decreased, leading to a reduction in AGU and pHU over time. In parallel, a progressive increment in NH4+U was observed. In patients receiving more than one administration we observed an increase in arterial base excess (1.8 ± 0.8 vs. 5.0 ± 0.6 mmol/l, P 0.001) and plasmatic strong ion difference (SIDpl) (31 (30 to 33) vs. 35 (34 to 36) mEq/l, P = 0.01) during the study period. These changes were due to a decrease in plasmatic Cl- concentration (109.0 ± 1.1 vs. 106.6 ± 0.9 mEq/l, P = 0.009). Plasmatic sodium and potassium concentrations did not change. In these patients, considering the total amount of administered fluids and urine, a negative water and chloride balance was observed (-460 ± 403 ml and -48 ± 48 mEq, respectively).
Furosemide acts immediately after administration, causing a rise in urinary output, Na+U and Cl-U concentrations. Loop-diuretic-induced metabolic alkalosis may be due to an increased urinary chloride loss and the associated increase in SIDpl.
Wilcox CS: Metabolic and adverse effects of diuretics. Semin Nephrol 1999, 19: 557-568.
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Zazzeron, L., Ottolina, D., Scotti, E. et al. Renal response and acid-base balance alterations during furosemide administration. Crit Care 17, P415 (2013). https://doi.org/10.1186/cc12353
- Metabolic Alkalosis
- Negative Water
- Arterial Base
- Single Intravenous Bolus