Use of diuretics in shock: Temporal trends and clinical impacts in a propensity-matched cohort study.

OBJECTIVE: Fluid overload is common among critically ill patients and is associated with worse outcomes. We aimed to assess the effect of diuretics on urine output, vasopressor dose, acute kidney injury (AKI) incidence, and need for renal replacement therapies (RRT) among patients who receive vasopressors. PATIENTS AND METHODS: This is a single-center retrospective study of all adult patients admitted to the intensive care unit between January 2006 and December 2016 and received >6 hours of vasopressor therapy and at least one concomitant dose of diuretic. We excluded patients from cardiac care units. Hourly urine output and vasopressor dose for 6 hours before and after the first dose of diuretic therapy was compared. Rates of AKI development and RRT initiation were assessed with a propensity-matched cohort of patients who received vasopressors but did not receive diuretics. RESULTS: There was an increasing trend of prescribing diuretics in patients receiving vasopressors over the course of the study. We included 939 patients with median (IQR) age of 68(57, 78) years old and 400 (43%) female. The average hourly urine output during the first six hours following time zero in comparison with average hourly urine output during the six hours prior to time zero was significantly higher in diuretic group in comparison with patients who did not receive diuretics [81 (95% CI 73-89) ml/h vs. 42 (95% CI 39-45) ml/h, respectively; p<0.001]. After propensity matching, the rate of AKI within 7 days of exposure and the need for RRT were similar between the study and matched control patients (66 (15.6%) vs. 83 (19.6%), p = 0.11, and 34 (8.0%) vs. 37 (8.7%), p = 0.69, respectively). Mortality, however, was higher in the group that received diuretics. Ninety-day mortality was 191 (45.2%) in the exposed group VS 156 (36.9%) p = .009. CONCLUSIONS: While the use of diuretic therapy in critically ill patients receiving vasopressor infusions augmented urine output, it was not associated with higher vasopressor requirements, AKI incidence, and need for renal replacement therapy.

Hypertonic saline dextran produces early (8-12 hrs) fluid sparing in burn resuscitation: a 24-hr prospective, double-blind study in sheep.

OBJECTIVE: Resuscitation of large burn injuries must quickly restore and maintain cardiovascular function and fluid balance while minimizing secondary edema-related damage. We tested the hypothesis that two 4-mL x kg(-1) doses of hypertonic saline dextran (HSD; 7.5% NaCl/6% dextran-70) can produce prolonged reduction in fluid requirements after burn injury. DESIGN: Prospective, pseudo randomized, double-blind study. SETTING: Animal research laboratory. SUBJECTS: Female adult Merino sheep (n = 12). INTERVENTIONS: Sheep were given a 40% total body surface area full-thickness flame burn under halothane anesthesia. One hour after the burn, the conscious animals received an initial dose of 4 mL x kg(-1) HSD (n = 6) or normal saline (NS; NaCl 0.9%) (n = 6) intravenously during 30 mins. This was followed by lactated Ringer's solution, infused to a target urine output of 1 mL x kg(-1) x hr(-1) throughout the 24-hr study. A second 4-mL x kg(-1) dose of HSD or NS was started at 12 hrs, and infused during 5 hrs. MEASUREMENTS AND MAIN RESULTS: Hourly urine output measurements were used to guide the infusion rate of the lactated Ringer's. The initial infusion of HSD 1 hr after the burn injury promptly restored cardiac index, promoted diuresis, and reduced fluid requirements compared with the NS controls (73% reduction for HSD relative to NS at 8 hrs). Subsequent rebound fluid accumulation resulted in similar net fluid balances in both groups within 12 hrs after the burn. The second dose of HSD, given at 12 hrs, was without effect on hemodynamics and fluid balance. CONCLUSIONS: We conclude a considerable initial, but not sustained fluid-sparing effect of early HSD, and no effect of a late, slowly infused HSD dose in this two-dose regimen.

Effect of voluntary exercise on urinary excretion of catecholamines after traumatic shock in rats.

Thirteen rats were kept in cages equipped with running wheels for 10 months (exercise group), and 12 rats were kept in cages without running wheels during the same period (control group). Rats in both groups were subjected to a Noble-Collip drum trauma (40 rpm, 350 revolutions in total) after the 10-month conditioning period. Urine output, urinary epinephrine (E), and norepinephrine (NE) were measured until the seventh day after the trauma. Urine output decreased after the trauma in both groups to the same extent, but the recovery of urine output after trauma was accomplished faster in the exercise group than in the control group, and diuresis after trauma was seen only in the exercise group. Urinary E increased in both groups within 24 hours after trauma, but the increase in the exercise group was significantly less than in the control group. The amount of NE excreted depended somewhat on the urine volume, but there was no significant difference in changes in urinary NE after trauma between the groups. These results suggest that rats bred in an active condition suffered less severe traumatic shock accompanied by a reduced sympathoadrenal activity as compared with rats bred in a relatively sedentary condition.

Hypochloruria associated with hypovolemia.

Hypochloruria is proposed as an indicator of hypovolemia in ICU non cardiac patients. Twelve of 13 patients presenting with Clu less than or equal to 20 mmol X l-1 and Nau greater than or equal to 20 mmol X l-1 or twice the Clu value had a CVP less than or equal to 0 mmHg. This pattern occurred in those with a metabolic alkalosis or acidosis, renal insufficiency or normal renal function, in the presence or absence of dopamine and/or diuretic administration and with or without controlled ventilation. Hypochloruria may be a better indicator of hypovolemia than a low urinary Na in ICU patients.