Post-obstructive diuresis
Post-obstructive diuresis (diuresis means passing more urine) is a rise in urine output after an obstruction (a blockage to urine flow) is relieved.
Remember
After long-standing obstruction is relieved, the injured tubules (the small tubes that take sodium and water back into the blood) do this poorly, so a large volume of dilute urine can be passed and fluid input and output need monitoring.
Take a patient with long-standing urinary retention (being unable to empty the bladder) whose bladder is drained by a catheter. Once urine can flow again, the output may rise markedly. This is post-obstructive diuresis.
It starts as a physiological response, meaning a normal one. While urine could not drain, salt and water accumulated in the body, and now the kidneys get rid of them. Urea that built up during the obstruction is cleared at the same time.
The tubules add to the volume. They reabsorb (take back into the blood) most of the sodium and water that the kidney filters, but the raised pressure behind a long-standing blockage injures them. Once the obstruction is lifted, they reabsorb sodium and water poorly and respond poorly to antidiuretic hormone (ADH, the hormone that normally makes the kidney hold on to water). The kidney also cannot concentrate its urine well, so a large volume of dilute urine is passed until the tubules recover.
In a few patients the diuresis becomes excessive and severe, causing dehydration and an electrolyte imbalance (abnormal blood salt levels). Careful monitoring of fluid input and output is usually enough, with oral fluids to replace the loss, although some patients need intravenous fluids. Patients with acute-on-chronic retention (a sudden blockage on top of long-standing retention) are at particular risk.
One definition is at least 200 mL of urine an hour for two consecutive hours, or over 3 litres in 24 hours.
Key facts
- What it is
- a rise in urine output after relief of an obstruction such as urinary retention.
- How it starts
- as a physiological response, as accumulated salt and water are removed from the body.
- What adds to the volume
- injured tubules reabsorb sodium and water poorly and respond poorly to ADH, so dilute urine is passed.
- Risks
- dehydration and electrolyte imbalance if the diuresis becomes excessive.
- Management
- monitor fluid input and output; oral fluids are usually enough, but some patients need intravenous fluids.
- One definition
- at least 200 mL of urine an hour for two consecutive hours, or over 3 litres in 24 hours.
- Higher risk
- long-standing or acute-on-chronic retention.
Exam traps
- An improving serum creatinine does not show that the diuresis has ended, because ongoing salt and water losses can still cause dehydration, so fluid balance monitoring continues.
- Treating the diuresis as abnormal and giving intravenous fluids at once overstates it, because it starts as a normal clearing of retained salt and water, and careful monitoring with oral fluids is usually enough. Some patients do need intravenous fluids, when the output becomes excessive or dehydration develops.
- Reduced antidiuretic hormone release, as in cranial diabetes insipidus (where the hormone fails to be released, so large volumes of dilute urine are passed), looks similar but is not the mechanism, because after obstruction the fault is in the kidney: the tubules respond poorly to the hormone.
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