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  • Eighty-five percent of renal blood flow perfuses the outer cortical glomeruli, whereas the remaining 15% perfuses the juxtamedullary glomeruli.

  • The final concentration and volume of urine vary with plasma volume, serum osmolality, release of antidiuretic hormone (ADH), and other factors.

  • Renal failure is classified by the RIFLE (Risk, Injury, Failure, Loss, and End Stage), AKIN (Acute Kidney Injury Network), or KDIGO (Kidney Disease: Improving Global Outcomes) systems.

  • The incidence of renal failure after trauma is 3% to 9%.

  • Causes of renal failure after trauma include hemorrhage, hypovolemia, functional prerenal renal failure, toxins (eg, antibiotics), contrast nephropathy, sepsis, and rhabdomyolysis.

  • Current KDIGO guidelines promote the use of isotonic crystalloid solutions over colloids for the initial volume resuscitation in patients at risk for or with acute kidney injury.

  • Overall energy use is not affected by renal failure alone, and calorie repletion should not be increased based solely on this finding.

  • Much as with patients with chronic kidney disease, indications for acute renal replacement therapy include hyperkalemia resistant to usual therapy, acidosis, uremia, and severe volume overload.


Fluid is distributed in the human body through three separate compartments: the intracellular fluid (ICF), and the extracellular fluid (ECF), which is itself broken down into the interstitial and intravascular compartments. The majority of the fluid, roughly two-thirds, is in the intracellular compartment. The extracellular one-third is itself divided such that roughly one-third to one-fourth of the fluid is in the intravascular space as the solute portion of plasma and the remaining two-thirds to three-quarters is interstitial fluid. There is a relatively volumetrically insignificant volume of fluid in the transcellular space, which is to say secretions, cerebrospinal fluid, and ocular fluid.1,2

Fluid and some small molecules move in and out of the intravascular space, both in normal and pathologic states. In normal cases, fluid outside of the vasculature distributes between the interstitial and intracellular compartments and can return to the vascular compartment. Vascular endothelial injury leads to vascular leak, with escape of larger molecules and proteins that would normally stay within the vasculature. This extravascular fluid accumulates and becomes edema when more fluid that can be reabsorbed through the lymphatic system is lost into the interstitial space.1 Functionally, this space, when pathologically engaged, is the so-called “third space.”2 This fluid is trapped and is essentially nonfunctional, or unable to participate in the essential functions of intravascular volume expansion.

In the setting of direct injury, such as traumatic swelling, this can be well circumscribed and have a negligible volume. In critical pathologic states, especially sepsis, this is a widespread process that makes volume estimation and replacement a complex process. There is no clear measure of “third-space” losses, only surrogates, such as ultrasound, physical exam, or patient weight. When this extravascular fluid accumulation happens in organ tissues, this can also contribute to organ dysfunction, as seen ...

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