Postobstructive Diuresis
- Article Author:
- Stephen Leslie
- Article Author:
- Hussain Sajjad
- Article Editor:
- Sandeep Sharma
- Updated:
- 9/22/2020 8:51:35 AM
- For CME on this topic:
- Postobstructive Diuresis CME
- PubMed Link:
- Postobstructive Diuresis
Introduction
Urinary retention is a relatively common urological problem encountered in both inpatient and outpatient situations. It should be suspected in any patient with lower abdominal discomfort and any degree of urinary difficulty. Retention can be confirmed with a post-void residual determination either with a bladder ultrasound or a catheterization.
Post-obstructive diuresis is an abnormal condition of prolonged polyuria, involving both excessive salt and water loss, after the acute drainage and decompression of a distended bladder, typically from urinary retention.
Normal maximum bladder capacity is about 450 cc to 500 cc. Post obstructive diuresis is not typically an issue unless the residual urine is 1,500 cc or more. If the post-obstructive diuresis condition becomes pathologic, it can cause serious consequences such as dehydration, electrolyte abnormalities, hypotension, hypovolemic shock, and even result in death.[1][2]
Etiology
Risk factors associated with post-obstructive diuresis include the presence of other lower urinary tract symptoms, diabetes, history of multiple urethral catheterizations, prostatic hyperplasia, fecal impaction, and the use of anticholinergic medications.
The exact etiology is unclear, but it certainly involves several mechanisms such as the following:
- Progressive reduction in medullary concentrating ability due to vascular washout
- Down-regulation of the sodium transport mechanism in the thick, ascending loop of Henle
- Reduction in glomerular filtration rate (GFR) leading to ischemia and damage to juxtamedullary nephrons
- Diminished response to antidiuretic hormone.
Causes of urinary obstruction include phimosis, prostatic hyperplasia, meatal stenosis, urinary stones, posterior urethral valves, ureteropelvic junction obstruction, blocked Foley catheters, urological malignancies such as prostate cancer, fecal impaction, diabetes, and neurogenic disorders such as spinal cord disorders and multiple sclerosis.
Patients with bilateral hydronephrosis on ultrasound or CT and bladder distension should be presumed to have urinary retention until proven otherwise.[3][4]
Epidemiology
It has been estimated that 10% of men in their 70s and 30% of men in their 80s will have at least one episode of urinary retention. It is more common in men than women, and the incidence increases with age. Chronic retention may be either high pressure or low pressure. High pressure is potentially more dangerous as it can cause vesicoureteral reflux resulting in renal damage due to direct injury to the nephrons.
The incidence of post-obstructive diuresis following the alleviation of urinary retention is unclear but is reported to be up to 50% in some series.[3]
Post-obstructive diuresis has also been reported in pediatric cases after repair of ureteropelvic junction obstructions. This is sometimes, but not always, associated with renal tubular acidosis.[1] Post-obstructive diuresis has occurred even in the presence of a normal contralateral kidney.[2]
Pathophysiology
Post-obstructive diuresis typically occurs after drainage of larger amounts of urine from the bladder, typically 1,500 cc or more. While diuresis is the expected response to any relief of urinary obstruction, typically this is limited to the period necessary to normalize fluid volume and excess solutes that may have accumulated while obstructed. This temporary condition is known as physiological diuresis and is generally self-limited to 24 hours or less.
When the obligatory loss of salt and water continues long beyond a homeostatic state, the condition becomes pathologic post-obstructive diuresis which is far more dangerous and typically lasts 48 hours or longer.[3]
There are very few clues to help identify which patients with physiological post-obstructive diuresis will progress to the more dangerous pathological variety. There does not appear to be a strict correlation with serum creatinine, electrolyte levels, creatinine clearance or the presence of hypertension and the eventual development of post-obstructive diuresis. However, there is some association with renal failure or insufficiency, congestive heart failure, and volume overload. The degree or volume of immediate drainage is a reasonable predictor of the likelihood of a period of post-obstructive diuresis with patients being at higher risk if the immediate residuals are 1,500 cc or more. This is a good reason to record the residuals, especially when they are expected to be more than 1,000 cc, as this can provide some warning regarding the potential for an extended post-obstructive diuresis.[2]
History and Physical
The most common presentation is acute urinary retention (suprapubic pain associated with total inability to void) which typically is preceded by various urinary symptoms such as weak stream, hesitancy, and frequency. Chronic urinary retention can be more gradual in onset with no associated pain. Usually, it is found with relatively small amounts of voided urine and overflow incontinence. There may be obvious suprapubic distension or fullness, but confirmation with a bladder ultrasound or catheter is required.[5]
Evaluation
The measurement of the post-void residual urine is necessary to establish a baseline level of bladder distension or over-distension. In general, the greater the amount of residual urine and the longer it has been present, the greater the chance for a prolonged post-obstructive diuresis.
By definition, post-obstructive diuresis is the condition of prolonged urine production of at least 200 cc for at least two consecutive hours immediately following the relief of urinary retention or similar obstructive uropathy. It may also be defined as more than 3,000 cc over 24 hours.[6]
Treatment / Management
Once, it was thought that large bladder volumes needed to be drained slowly or by intermittent clamping of the catheter to prevent hematuria, vasovagal response, post-obstructive diuresis, and hypotension. However, recent studies have shown that immediate, complete drainage with an unrestricted Foley is safe and effective with no increase in these complications.
Those patients with a higher risk of developing pathologic post-obstructive diuresis should be considered for 24-hour hospitalization for close monitoring of urine output and electrolytes. Urine output should be monitored at least every 2 hours. Serum electrolytes including sodium, potassium, urea, creatinine, magnesium, and phosphate, should be checked every 12 hours initially. They are allowed unrestricted access to water for drinking. Daily weights are helpful. Urine samples can be collected for urinary measurements of osmolality, sodium, and potassium.[6]
Random urine sodium levels greater than 40 mEq/L are suggestive of possible renal tubular injury which can progress to pathologic post-obstructive diuresis.
Intravenous (IV) fluid support should be normal saline and limited to no more than 75% of the prior 1 to 2-hour urine production to avoid stimulation of further diuresis.
Urine osmolality can be estimated from the specific gravity. A specific gravity of 1.010 is roughly equivalent (iso-osmolar) to serum. This would indicate that the kidneys are not concentrating the urine which is most consistent with physiological post-obstructive diuresis. If the specific gravity is 1.020 or more, the kidneys are concentrating the urine and the period of diuresis is resolving. If the specific gravity is lower than 1.010, the kidneys are not concentrating the urine, or may not be able to, which would indicate pathological salt wasting post-obstructive diuresis.
Pathological post-obstructive diuresis puts the patient at risk for hypovolemia and hemodynamic instability as well as acid-base disturbances and electrolyte imbalances. Careful monitoring of fluid status, weight, serum electrolytes, and renal function is necessary to minimize the duration of the condition and facilitate recovery.[3][7]
Differential Diagnosis
- Cushing's syndrome, primary hyperaldosteronism
- Diabetes insipidus
- Drugs: diuretics, caffeine, acetazolamide, lithium
- Early renal failure
- Excess intravenous fluids
- High fluid intake
- Hypercalcemia
- Hyperglycemia
- Hypokalemia
- Inability to concentrate urine (e.g. chronic pyelonephritis, sickle cell disease, amyloidosis
- Mannitol
- Osmotic diuresis
- Post-obstructive diuresis
- Psychogenic polydipsia
Enhancing Healthcare Team Outcomes
Urinary retention is a common urological condition that will frequently be encountered by clinicians, nurses, and physician assistants. Pharmacists may be the first to discover it as a side effect of a medication. It is particularly common in those who treat the elderly. Recognizing post-obstructive diuresis is critical because the condition can occur in up to 50% of these patients and may progress to the potentially dangerous pathological form which can be life-threatening if not identified and treated properly. Resolution often requires a Foley catheter and an interprofessional team to provide insertion and care until the condition resolves. [Level V]