Oliguria &  Volume Depletion




What causes a low urinary output (oliguria)?

On an average night on call in ICU you will receive multiple calls because patients are oliguric. Oliguria means “little urine” and is conventionally considered to be <400ml/day. In ICU “oliguria” means insufficient urinary output for that particular patient. As a rule of thumb, 0.5 ml per kilo per hour is a good limit. However, after major surgery or trauma, where large amounts of waste materials have been generated by tissue damage, an output of 1ml/kg/hour may be more appropriate. In other words, urinary output must be tailored to patient needs - an output of 200ml/hour may be required in rhabdomyolysis.
Oliguria is an important clinical sign: it is one of the best measures, for a number of reasons, of end organ perfusion and circulating volume.

Human beings are, essentially, big bags of water, the volume of which must be kept under tight control to prevent us from either drying out or drowning. The kidney is a sophisticated organ, which maintains circulating volume and excretes waste products in response to materials presented to it. Overall control of body fluid is via a complex set of reflexes in the vascular system and the brain. This is the extrinsic system of volume control. The kidney is partially independent of the circulation in that it is able to control it’s own blood flow and protect itself in the face of hypoxemia. This is the intrinsic system of control.

Oliguria may result from a number of causes, the conventional approach is:

  1. Outrule post-renal obstruction.
  2. Outrule renal hypoperfusion / hypotension (pre-renal).
  3. Outrule acute renal injury.

Oliguria is based firmly in physiology, either the kidney is making urine or it is not. If the kidney is making urine and none is flowing, then there is a blockage to flow. If the kidney is not making urine, is this because it has no substrate to work off (low filtered load) or because the renal tubules themselves are damaged. It is essential to understand the difference between acute renal success (renal self preservation) and acute renal failure (renal injury).

What is meant by volume depletion?

Volume depletion is a manifestation of abnormality of fluid distribution: the patient is either relatively (third space fluid loss such as capillary leak, or vasodilatation) or absolutely (hemorrhage, dehydration) hypovolemic. The endpoint is the same: the patient initially compensates (by the extrinsic system discussed below) to restore circulating volume. If the injury persists or is not corrected then decompensation occurs: decompensation = shock and tissue hypoperfusion. Oliguria is a sensitive indicator of volume depletion.

How does the extrinsic system work in a fluid depleted patient?

In a volume depleted patient, it is the purpose of the vascular system and kidneys to conserve salt and water and maintain blood flow to vital organs (the brain and heart).

Extrinsic Control

Hypovolemia, for any reason, reduces venous return to the heart, preload and atrial stretch, reducing the release of atrial natiuretic peptide: the brain produces more anti-diuretic hormone as a result – conserving water. Blood pressure falls due to lower stroke volume (Starling curve). The baroreceptors in the carotid sinus and aortic arch sense the fall in blood pressure, their output is reduced activating the vasomotor center and inhibiting the cardioinhibitory center, leading to increased sympathetic (and decreased parasympathetic) discharge -> increased heart rate, blood pressure, and cardiac output and peripheral vasoconstriction. Simultaneously, in the kidney, the combination of hypotension and sympathetic activation lead to reduced perfusion pressure in the afferent arteriole and a decrease in the GFR. A decrease in tubular NaCl (due to slower transit and increased reabsorption) is sensed by the macula densa in the distal convoluted tubule, and this causes the juxta-glomerular apparatus to release renin. Renin activates angiotensin, which is converted peripherally to angiotensin II.  This agent is a potent vasoconstrictor, it also acts on the adrenal cortex to produce aldosterone, which increases salt and water reabsorption in the kidney. Hypovolemia also decreases atrial stretch, reducing the release of atrial natiuretic peptide: the brain produces more anti-diuretic hormone as a result – conserving water.

Fluid overload is dealt with in an opposite manner. Baroreceptor output decreases, atrial natiuretic peptide release increases (which has diuretic effects and antagonizes ADH). Renal perfusion pressure increases, leading to higher GFR, and increased NaCl delivery to the distal tubule, with a resultant decrease in renin release. The overall effect is decreased sympathetic activity, increased vascular capacitance, and increased salt and water excretion from the kidneys.

Think of the kidney as being a little brain, if the kidney is not being perfused (oliguria), then neither is the brain?

Intrinsic Regulation

The kidney, like the brain, is able to control it’s own blood flow. This is essential because, in the course of an active day, systemic blood pressure may go up and down depending on factors such as sitting or standing, activity, anxiety etc. The kidney, in general, acts as a passive filter, so the amount filtered would vary enormously. This is inefficient. The kidney is able to control it’s own blood flow and filtration rate over a large range of blood pressures (e.g. a MAP of 80 to 180mmHg). The urinary flow rate is determined principally by renal perfusion pressure.

The kidney neither autoregulates or perfuses at low blood pressures; this appears to be a protective effect due to the fact that the medulla is relatively hypoxemic. Treatment for oliguria, under these circumstances, is to increase the renal perfusion pressure.

Oliguria, therefore, signals low renal perfusion, and the kidney protecting itself from ischemia.





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