Monitoring urine output is an easy way to assess a patient’s fluid status. Often
after surgery or trauma, a Foley catheter is placed in the bladder to measure urine
output accurately. Decreasing urine output may be because of hypovolemia or
injury to the urinary tract system. In this case, the decreased urine output probably
was secondary to hypovolemia, because the patient also has hypotension
and tachycardia. The blood pressure remained relatively normal initially because
of the renin-angiotensin system, which sensed the decreased blood flow to the
renal artery, and the sympathetic nervous system, which sensed the decreased
blood volume and pressure. The decreased blood flow through the renal artery
will stimulate renin to be released, with the subsequent generation of angiotensin
II, leading to increased systemic blood pressure and total peripheral resistance.
Decreased blood volume and pressure will be sensed by volume and pressure
receptors, leading to modest vasoconstriction and increased systemic blood pressure.
With excessive blood loss (hypovolemic shock), the action of the autonomic
(sympathetic) nervous system causes pronounced vasoconstriction of the
renal arteries with shunting of blood to vital organs (brain, heart, lungs) and is
seen clinically with decreased urine output. Replacement with crystalloid fluids
and blood is necessary to maintain kidney perfusion and prevent acute tubular
necrosis. If a patient is in shock and urine output is not responding to IV fluids
and blood, low-dose dopamine often is used to cause renal artery dilation and
increased renal blood flow. In any case, the source of bleeding must be addressed
and intravascular volume must be replaced