The renal factor in the post-traumatic "fluid overload" syndrome.

Hypervolemia with hypertension often occurs 36-72 hours following massive blood and fluid replacement for hypovolemic shock. This syndrome of "fluid overload" has been attributed to the rapid intravascular flux of previously sequestered fluid in patients with impaired diuresis. This hypothesis was tested in 35 injured patients who received a mean of 9.3 L of blood and 17.4 L of salt during resucitation. The renal parameters measured soon after resuscitation included: 1) renal clearance of inulin (GFR), para-amino hippurate (ERPF), milliosmoles, sodium, and free water; 2) inulin space, renal vascular resistance (RVR), O2 consumption, renin, renal blood flow (RBF), and response to furosemide. Eighteen patients developed hypertension, hypervolemia, and respiratory insufficiency. When compared to the 17 normovolemic, non-hypertensive patients, the 18 hypervolemic patients had significantly increased RVR, with a significant decrease in RBF despite an increase in plasma volume and cardiac output. Furosemide produced less diuresis and natriuresis in the hypertensive patients. The balance between hypovolemia and "fluid overload" seemed percarious in the hypertensive patients. Peripheral renin and catecholamine levels were normal in both groups. Patients with post-traumatic "fluid overload" appear to have a combination of hypervolemia, respiratory insufficiency, hypertension, increased cardiac output, decreased extracellular fluid space, and decreased renal perfusion. These findings suggest that decreased interstitial fluid space compliance rather than "fluid overload" is the underlying factor leading to respiratory insufficiency. The therapeutic aspects of these findings are discussed.

Renal hemodynamic response to furosemide in septic and injured patients.

Furosemide frequently is advocated as a prophylaxis against renal failure in septic and injured patients; this effect is thought to be secondary to an increase in renal blood flow. This postulate was tested within 72 hours of admission in 22 previously healthy patients with acute pancreatitis (two), massive trauma (ten), or severe sepsis (ten). Renal clearances of inulin (GFR), para-amino hippurate (ERPF), sodium (CNA), osmoles (COsm), and free water (CH2O) were measured in milliliters per minute before and after the intravenous infusion of furosemide (0.5 mg. per kilogram of body weight). Renal vein PAH levels (EPAH) in eight patients were used to calculate true renal plasma flow (TRPF), true renal blood flow (TRBF), and renal vascular resistance (RVR). Furosemide caused a significant increase in urine volume, CNa, and COsm; there were no significant changes in GFR, ERPF, RVR, TRBF, and EPAH. These findings also were observed when the patients were subgrouped according to elevated, normal, or low renal plasma flow and elevated renal vascular resistance. No significant changes were seen in EPAH, thus making a redistribution of renal blood flow unlikely. These studies indicate that furosemide has only a diuretic effect and no hemodynamic effect in the kidney; it has the potential of seriously reducing the circulatory volume and causing renal failure in critical patients.