Augmented renal clearance in traumatic brain injury
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KeywordsNorepinephrine Traumatic Brain Injury Active Management Central Venous Pressure Fluid Balance
Use of hypertonic saline and/or vasopressor infusion to achieve a desired cerebral perfusion pressure (CPP) in traumatic brain injury (TBI) is common. We hypothesised that the use of such therapies would significantly augment creatinine clearances (CrCl) in this population.
Head-injured patients requiring hyperosmolar therapy using 3% or 20% saline solutions and/or norepinephrine infusion for the maintenance of a CPP >60 mmHg were recruited into the study. Additional management was consistent with local practice and in line with the Brain Trauma Foundation guidelines . An 8-hour CrCl, physiological variables, fluid balance, and medications were recorded daily during active management of CPP. A further CrCl was collected just prior to discharge (off CPP therapy), and if this was elevated, was repeated on the ward. Augmented renal clearance (ARC) was defined as a CrCl >160 ml/minute/1.73 m2 for males and >150 ml/minute/1.73 m2 for females .
Twenty consecutive patients were enrolled. The average ICU length of stay was 15 days (CI 95% 11 to 18), and time to study entry averaged 2.3 days (CI 95% 1.7 to 2.8). All patients received norepinephrine (n = 20), 85% (n = 17) received hypertonic saline, and therapy lasted on average 7.6 days (CI 95% 5.6 to 9.5). ARC was demonstrated in 17 (85%) patients at any point during active management of CPP. The mean maximum CrCl was 179 ml/minute/1.73 m2 while on CPP therapy (CI 95% 159 to 198) returning to a mean CrCl of 111 ml/minute/1.73 m2 (CI 95% 91 to 131, P < 0.001) when measured in the ward. The mean CrCl in the ICU while not receiving CPP therapy was 150 ml/minute/1.73 m2 (CI 95% 134 to 167, P = 0.03). The mean time to reach peak CrCl while on active treatment was 4.7 days (CI 95% 3.0 to 6.4). Norepinephrine use, saline loading, mean arterial pressure, and central venous pressure, predicted CrCl on the day of measurement.
ARC is common in head-injured patients receiving active management of CPP and persists even after ceasing such therapy. This has significant implications for appropriate dosing of renally excreted drugs in this setting.