John J. Pahira, MD
BASICS
DESCRIPTION
• Postobstructive diuresis is excessive polyuria resulting from the relief of bilateral ureteral obstruction or obstruction of a solitary kidney, bladder outlet obstruction
• More likely with chronic rather than acute obstruction
• After relief of obstruction, >3 L over 24 hr or >200 mL/hr over each of 2 consecutive hr is diagnostic of polyuria found with POD
EPIDEMIOLOGY
Incidence
• Peak incidence in men 70–90, due to increased obstruction from BPH and prostatic cancer
• Peak incidence in women 40–60, due to obstruction from pregnancy and carcinoma of the cervix and uterus
Prevalence
N/A
RISK FACTORS
• Urinary tract obstruction is caused by a number of processes, grouped into extrinsic and intrinsic causes:
– Intrinsic: Nephrolithiasis, blood clot, ureteral strictures, urethral strictures, neurogenic bladder, anticholinergic agents, levodopa
– Extrinsic: BPH, prostate cancer, tubo-ovarian abscess, ovarian tumor or cyst, endometriosis, arterial aneurysms, tumors of the kidney, ureter, bladder, and urethra and their corresponding lymphatic and metastatic spread
• Obstructed patients most likely to have POD
– Chronic obstruction
– Edema
– Congestive heart failure
– HTN
– Weight gain
– Azotemia
– Uremic encephalopathy
Genetics
N/A
PATHOPHYSIOLOGY
• Retained urea, sodium, and water; impaired sodium reabsorption and concentrating ability of the renal tubule; and circulating hormones all contribute:
– Increased sodium, potassium, and magnesium losses result in increased water excretion
– Accumulated urea acts as an osmotic agent, bringing fluid with it as it is cleared, thereby increasing diuresis
– Impaired concentrating ability of the renal tubule leads to continuing fluid losses and hypovolemia
• ANP, which causes vasodilation, natriuresis, and diuresis, has been found to be elevated in patients with ureteral obstruction (1)[B]
ASSOCIATED CONDITIONS
• BPH
• Malignancies (bladder or prostate cancer)
• Urolithiasis
• Any cause of chronic obstruction with hydronephrosis
GENERAL PREVENTION
Treat and repair the cause of obstruction to prevent recurrence
DIAGNOSIS
HISTORY
• Obstruction:
– Asymptomatic but often associated with flank pain radiating to groin and/or ipsilateral thigh, nausea, vomiting, fevers, chills
– Resulting uremia may cause mental status changes, tremors, and GI bleeding (2)[A]
• Diuresis:
– Increase in urine output out of proportion to fluid intake, usually >200 mL/hr
• Chronic obstruction:
– Weight gain, malaise, fatigue, shortness of breath
• Acute obstruction
– Flank pain associated with forced diuresis (consumption of coffee, tea, or alcohol), nausea, vomiting, hematuria, anuria
PHYSICAL EXAM
• Chronic obstruction:
– Pulmonary congestion, pitting edema of lower extremities, HTN
• Acute obstruction:
– Abdominal mass, suprapubic tenderness, flank tenderness
DIAGNOSTIC TESTS & INTERPRETATION
Lab
• CBC, urine culture and sensitivity:
– Infection in the setting of obstruction requires emergent evaluation and treatment
• SMA-7
– BUN and creatinine are typically elevated and are monitored after relief of obstruction
– POD may cause profound hypokalemia
• Magnesium and calcium may need preplacement
• Urine osmolality:
– Evaluate the kidney’s ability to concentrate urine; typically impaired concentrating ability
Imaging
• US is the screening test of choice to evaluate obstruction:
– Avoid risk of contrast agents
– Without hydronephrosis, diagnosis of POD should be questioned
Diagnostic Procedures/Surgery
Monitor urine output
Pathologic Findings
N/A
DIFFERENTIAL DIAGNOSIS
• Causes of polyuria:
– Medications:
Lithium carbonate, methoxyflurane, demethylchlortetracycline, amphotericin B, mannitol, glycerol, diuretics, ethanol, opiate antagonist, phenytoin
– Diabetes insipidus, diabetes mellitus
– Renal disease: Diuretic phase of ATN
– Physiologic diuresis from fluid excess
TREATMENT
GENERAL MEASURES
• After the obstruction is relieved, admit the patient to the hospital to closely monitor hemodynamic status and electrolytes, I/O’s and daily weights
• Monitor urine output q2h and replace with oral fluids or if oral intake is not keeping up then with IV fluids (0.5–1.0 mL of 1/2 NS/mL of urine output) in addition to PO fluids
– If urine output decreases to <250 mL/hr replace fluids volume <50 mL of the urine output per hour. Adjust accordingly as the diuresis resolves
• If patient at risk of congestive heart failure or has pulmonary edema, replace at a slower rate
• Check serum sodium and potassium q6–12h and replace as needed
• Follow BUN and creatinine values until normal:
• Replace sodium, potassium, magnesium, and bicarbonate as needed
• Diuresis is usually self-limiting and typically lasts <48 hr
• If diuresis lasts >48 hr, usually due to impaired proximal tubular reabsorption of sodium causing a salt diuresis
– If outputs remain elevated, obtain a follow-up renal US to rule out hydronephrosis
ALERT
If there is persistent hydronephrosis, consider persistent obstruction of ureter(s) above the level of the bladder or a nonfunctioning stent/percutaneous tube (3)[A].
MEDICATION
First Line
None needed beyond replacement of fluid and electrolyte losses as noted above
Second Line
N/A
SURGERY/OTHER PROCEDURES
N/A
ADDITIONAL TREATMENT
Radiation Therapy
N/A
Additional Therapies
Management of any renal insufficiency
Complementary & Alternative Therapies
N/A
ONGOING CARE
PROGNOSIS
• The rate of recovery is largely determined by the duration and severity of obstructive disease.
• Extent of recovery can be estimated by the improvement in renal function within 7–14 days after the obstruction has been relieved:
– Some patients may require short-term treatment with dialysis, until their renal function recovers.
COMPLICATIONS
• Uremic death
• Hypovolemic circulatory collapse
• Bladder mucosal bleeding secondary to vein rupture resulting from rapid bladder decompression
• Arrhythmia secondary to electrolyte abnormalities
FOLLOW-UP
Patient Monitoring
Serial (weekly to monthly) renal function testing (creatinine, BUN), renal US imaging if lab values do not return to normal range
Patient Resources
N/A
REFERENCES
1. Li C, Wang W, Kwon TH, et al. Downregulation of AQP1, -2, and -3 after ureteral obstruction is associated with a long term urine concentrating defect. Am J Physiol Renal Physiol. 2001;281:F163–F171.
2. Pais VM, Strandhoy JW, Assimos DG. Pathophysiology of urinary tract obstruction. In: Wein AJ, ed. Campbell-Walsh Urology. 9th ed. St. Louis, MO: WB Saunders; 2007.
3. Gulmi FA, Felson D, Vaughan ED. Management of post-obstructive diuresis. AUA Update Series. Lesson 23. 1998;27:177–183.
ADDITIONAL READING
Nyman MA, Schwenk NM, Silverstein MD. Management of urinary retention: Rapid versus gradual decompression and risk of complications. Mayo Clin Proc. 1997;72(10):951–956.
See Also (Topic, Algorithm, Media)
• Hydronephrosis/Hydroureteronephrosis, (Dilated Ureter/Renal Pelvis), Adult
• Polyuria
• Urinary Retention, General
CODES
ICD9
• 592.0 Calculus of kidney
• 599.60 Urinary obstruction, unspecified
• 788.42 Polyuria
ICD10
• N13.9 Obstructive and reflux uropathy, unspecified
• N20.0 Calculus of kidney
• R35.8 Other polyuria
CLINICAL/SURGICAL PEARLS
• Maintain a high degree of suspicion for the potential for postobstructive diuresis when relieving chronic obstruction of the urinary tract.
• Diuresis is usually self-limiting and typically lasts <48 hr.