Postobstructive Diuresis

Etiology

Risk factors associated with POD include similar lower urinary tract symptoms, diabetes, a history of multiple urethral catheterizations, prostatic hyperplasia, fecal impaction, and the use of anticholinergic medications.

The exact etiology is unclear, but it 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
• A decline in glomerular filtration rate (GFR) leads to ischemia and damage to juxtamedullary nephrons
• Diminished response to antidiuretic hormone.

Causes of urinary obstruction encompass a variety of factors including phimosis, prostatic hyperplasia, meatal stenosis, urinary stones, posterior urethral valves, ureteropelvic junction obstruction, blocked Foley catheters, urological malignancies such as prostate cancer,[5] fecal impaction,[6] diabetes, neurogenic disorders such as spinal cord disorders and multiple sclerosis, and preputial calculus.[7]

Patients with bilateral hydronephrosis on ultrasound or CT and bladder distension should be presumed to have urinary retention until proven otherwise.[8][9]

Epidemiology

The incidence of POD is unclear, but estimates state 0.5% to 52% of patients experience the condition following relief of obstruction.[10] Around 10% of men in their 70s and 30% of men in their 80s will have at least 1 episode of urinary retention. POD 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 POD following the alleviation of urinary retention is unclear but is reported to be up to 50% in some literature.[8] POD has also been reported in pediatric cases after the repair of ureteropelvic junction obstructions. This is sometimes, but not always, associated with renal tubular acidosis.[3] POD has occurred in the presence of a normal contralateral kidney.[4]

Pathophysiology

POD typically occurs after larger amounts of urine drainage from the bladder, 1500 mL or more. While diuresis is the expected response to any relief of urinary obstruction, typically, this is limited to the period necessary to normalize the fluid volume and excess solutes that may have accumulated when obstructed. This temporary condition, physiological diuresis, is generally self-limited to 24 hours or less. When the obligatory loss of salt and water continues beyond a homeostatic state, the POD is dangerous and typically lasts 48 hours or longer.[8]

A few clues help identify which patients with physiological POD will progress to the more dangerous pathological type. No strict correlation is apparent between serum creatinine, electrolyte levels, creatinine clearance, or hypertension and the eventual development of POD. However, some association is apparent 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 POD, with patients being at higher risk if the immediate residual urine is 1500 mL or more.[4]

The pathophysiology of POD is complex to understand as it varies due to the evolution of different physiological, hormonal, biochemical, and immunological processes. Three main factors are generally implicated:

• Tubulopathy
• Physiopathological state caused by acute renal failure
• Biochemical and immunological mechanisms

Tubulopathy is characterized by impaired dilution, concentration capacity, and a decline in sodium reabsorption.[11] Potassium, magnesium, and phosphate leakage in prolonged obstruction are potential risks.[12] Alteration of urine acidification capacity, such as reduced H+ secretion, is also possible when the obstruction persists for over 24 hours.[13] In cases of acute renal failure, increased levels of nitrogenous compounds, such as urea and creatinine, are seen. Other abnormalities like hyperkalemia, hyponatremia, and metabolic acidosis are also noted.

Regarding biochemical and immunological mechanisms, various mediators play a role in the pathophysiology of POD, such as the atrial natriuretic peptide, prostacyclins, prostaglandins, thromboxane A2, and endothelins.[14] Immunological mechanisms also contribute if macrophage infiltrates, platelet activation factor (PAF) elevation, and cytokines are visualized.[15]

History and Physical

The most common presentation is acute urinary retention (suprapubic pain associated with a total inability to void), typically 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. Suprapubic distension or fullness is expected, but bladder ultrasound or catheter confirmation is required.[16] When the urinary obstruction is relieved, it results in a physiological response of diuresis. As discussed above, when this diuresis exceeds a certain limit, it becomes pathological.

In such cases, patients may present with symptoms that include excessive and uncontrolled urine production, excessive thirst, dehydration, red or pink-colored urine indicating hematuria,[17] diaphoresis, generalized weakness, leg cramps, altered mentation, and collapse or syncope.

The initial examination allows the clinicians to assess the patient’s hydration status by measuring simple parameters, such as weight and, in particular, the change in weight concerning the previous weight. Signs of dehydration, such as loss of skin turgor, tachycardia, and postural hypotension, could be picked up on examination.[18] Conversely, biochemical changes could also result in weight gain, high blood pressure, and edema of the lower limbs. In addition, the Glasgow Coma Scale (GCS) can help establish the extent of altered consciousness in patients with metabolic encephalopathy.

Evaluation

POD is a clinical diagnosis based on urine output after decompressing an obstructed bladder or ureter. The measurement of the post-void residual urine is necessary to establish a baseline level of bladder distension or over-distension. The greater the amount of residual urine and the longer it has been present, the greater the chance of a prolonged POD. No test or method is recognized to predict which patients will develop POD following the release of urinary tract obstruction. Hamdi et al reported that initial high serum creatinine levels, sodium bicarbonate, and urinary retention were independent risk factors for developing POD after decompression.[19] However, some reports claim that renal insufficiency, dizziness, heart failure, and central nervous system depression put the patient at risk of developing substantial POD.

Diagnostic criteria include identifying patients with the above-mentioned risk factors. It is recommended that the patient's overall fluid status, urine output, and electrolyte levels be monitored. Clinicians should also hourly monitor urine volume and urinary osmolality, sodium, and urea. Weight measurement should be carried out every 8 hours, and blood tests should be repeated every 24 hours.

Patients who are at risk of developing POD may need admission to the hospital for 24 hours. Such patients should have their urine output measured every 2 hours and vital signs checked every 6 to 8 hours. Furthermore, their serum sodium, potassium, phosphate, magnesium, urea, and creatinine should be measured every 12 to 24 hours and managed accordingly.[20] Suppose their urine output exceeds 200 mL/h for 2 consecutive hours or exceeds 3 L in 24 hours. This diagnostic of physiologic POD requires close monitoring for conversion to pathologic POD. Urinary sodium and potassium levels and urinary osmolality help determine whether it is a urea or salt type of diuresis.[21] Urea diuresis is often self-limiting; salt diuresis may convert to pathologic POD, requiring closer monitoring of serum electrolytes and hydration status. Spot urinary sodium of more than 40 mEq/L suggests renal tubular injury and can result in pathologic POD if prolonged.

Measuring the specific gravity of urine is helpful. For example, a specific gravity of 1.020 indicates that the urine is concentrated and POD has settled or nearly settled. In contrast, a specific gravity of 1.000 indicates the body's inability to concentrate the urine, consistent with pathologic salt-wasting POD. Again, this should alert the interprofessional team to monitor the patient closely.

Treatment / Management

It was thought that large bladder volumes needed to be drained slowly or by intermittent clamping of the catheter to prevent hematuria, vasovagal response, POD, 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.[22] Those patients with a higher risk of developing pathologic POD 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. Daily weights are helpful. Urine samples can be collected to measure urinary osmolality, sodium, and potassium.[23](A1)

Intravenous (IV) fluid support should be tailored to the type of POD, and normal saline should be used. The recommendation is to administer no more than 75% of the prior 1 to 2-hour urine production to avoid stimulation of further diuresis. Excess fluid administration should be avoided as it may exacerbate diuresis. Patients with intact cognition should continue oral hydration. However, those with impaired cognition should have 0.45% saline IV.

Pathological POD 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.[8][10] The patient should be discharged once the condition improves and lab parameters settle. A follow-up appointment with a urologist is recommended for the later management of obstructive uropathy.

Differential Diagnosis

Patients with excessive urine production following decompression of their urinary bladder should undergo evaluation for various underlying reasons. The differentials to consider when suspecting POD in a patient include Cushing syndrome, primary hyperaldosteronism, diabetes insipidus, drugs such as diuretics, caffeine, acetazolamide, and lithium, early renal failure, excess IV fluids, high fluid intake, hypercalcemia, hyperglycemia, hypokalemia, inability to concentrate urine (eg, chronic pyelonephritis, sickle cell disease, and amyloidosis), mannitol, osmotic diuresis, POD, and psychogenic polydipsia.

Prognosis

Renal recovery following relief of obstruction varies according to certain factors, such as duration of obstruction, degree of obstruction, unilateral or bilateral obstruction, and the presence of concomitant infection.

Relief of urinary tract obstruction could result in excessive diuresis, needing a meticulous management plan with appropriate fluid and electrolyte replacement. Generally, the prognosis of pathological POD is favorable, except for situations where a patient develops any of the abovementioned complications.

Complications

The complications that may arise in patients with POD include volume depletion, hyponatremia or hypernatremia, hypokalemia, hypomagnesemia,[24] metabolic acidosis, hypovolemic shock, and death.