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Urinary Obstruction

  • Author: Michael A Policastro, MD; Chief Editor: Erik D Schraga, MD  more...
Updated: Feb 23, 2016

Practice Essentials

Urinary obstruction is a blockage of the flow of urine out of the body. It is a common cause of acute and chronic renal failure and may result from a wide variety of pathologic processes, intrinsic and extrinsic to the urinary system. Symptoms and signs of obstruction are often mild, occurring over long periods of time and requiring a high index of suspicion for diagnosis. Early recognition and treatment are the keys to preventing renal loss.

Signs and symptoms

Most acute obstructive uropathies are associated with significant pain or abrupt diminution of urine flow; however, chronic urinary obstruction is insidious and requires a careful history and a high index of suspicion. The following may be noted in urinary obstruction:

  • Pain (most common symptom in acute obstruction but typically absent with slowly obstructing conditions)
  • Altered patterns of micturition
  • Acute and chronic renal failure
  • Gross or microscopic hematuria
  • Recurrent urinary tract infection (UTI)
  • New-onset or poorly controlled hypertension secondary to obstruction and increased renin-angiotensin
  • Polycythemia secondary to increased erythropoietin production in the hydronephrotic kidney
  • History of recent gynecologic or abdominal surgery

See Clinical Presentation for more detail.


Physical exam

The physical examination should include the following:

  • Evaluation for signs of dehydration and intravascular volume depletion; peripheral edema, hypertension, and signs of congestive heart failure from fluid overload may be observed in obstruction from renal failure
  • Palpable kidney or bladder (indicative of a dilated urinary collection system)
  • Rectal or pelvic examination to help determine whether enlargement of pelvic organs is a possible source of urinary obstruction.
  • Examination of the external urethra for phimosis or meatal stenosis

Lab studies

Laboratory studies that may be helpful include the following:

  • Urinalysis and examination of sediment
  • Urinary diagnostic indices (eg, sodium, creatinine, osmolality)
  • Serum electrolytes (sodium, potassium, chloride, bicarbonate), as well as blood urea nitrogen (BUN), creatinine, calcium, phosphate, magnesium, uric acid, and albumin
  • Complete blood count (CBC)

Imaging studies

The goals of any imaging study are to distinguish anatomic etiologies from functional forms of collecting system dilation and to identify the site of blockage. Imaging studies that may be considered include the following:

  • CT – Helical CT (especially without contrast) rapidly is replacing kidneys-ureters-bladder (KUB) x-rays as the first step in the radiologic evaluation of the urinary system
  • MRI - Where available, MRI quickly is becoming the imaging study of choice for urinary obstruction
  • IV pyelography (IVP) – IVP is the procedure of choice for defining the extent and anatomy of obstruction
  • Invasive pyelography – This modality provides the same information as IVP without depending on renal function and can be used when the risks of IVP are considered too great
  • Ultrasonography – This is the procedure of choice for determining the presence of hydronephrosis

See Workup for more detail.


The overriding therapeutic goal is reestablishment of urinary flow. Before specific therapy for obstruction is initiated, the life-threatening complications of obstructive uropathy must be investigated and treatment started.

Once urinary obstruction is under consideration, a transurethral bladder catheter should be placed:

  • If the catheter is properly placed and fluid returns freely, the catheter tip is probably in the bladder, and obstruction above the bladder should be investigated; if a question still remains, imaging studies may be used to establish proper placement
  • If a large PVR volume is noted, obstruction below the bladder should be investigated; catheter drainage should be maintained until the etiology of the obstruction is treated appropriately
  • Urine should be drained completely and rapidly from an obstructed bladder; prolonged urine stasis only predisposes the patient to UTI, urosepsis, and renal failure
  • A urologist should be consulted when a transurethral catheter cannot provide adequate bladder drainage

Calculi are the most common causes of unilateral ureteral obstruction. The following considerations apply:

  • Most small renal calculi pass spontaneously; conservative treatment typically suffices
  • Surgical drainage is necessary only for patients with unrelenting pain, UTI, or persistent obstruction
  • The position of the stone in the ureter determines the preferred method of removal
  • Calculi in the renal pelvis and proximal ureter are amenable to nephroscopy and removal under direct visualization
  • Percutaneous nephrostomy drainage is used for midureteral stones
  • Distal ureter stones can be removed cystoscopically by the use of a loop or basket
  • Extracorporeal shock wave lithotripsy is another viable option for stones in any position in the ureter

Bilateral obstruction of the ureters is almost always asymmetric. The following considerations apply:

  • For midureteral or proximal ureteral obstruction, percutaneous nephrostomy tube placement is indicated
  • For distal obstruction, cystoscopic placement of a ureteral stent can be attempted
  • In case of suspected urosepsis from bilateral ureteral obstruction, bilateral percutaneous nephrostomy tubes must be placed

For obstruction of prostatic origin, medical therapy for benign prostate hypertrophy (BPH) has provided a very successful alternative to surgical therapy but should not be offered to individuals presenting with absolute indications for surgical intervention (eg, recurrent urinary retention, recurrent UTIs, renal insufficiency, bladder calculi, recurrent gross hematuria).[1]

See Treatment and Medication for more detail.



Urinary obstruction is a common cause of acute and chronic renal failure. A wide variety of pathological processes, intrinsic and extrinsic to the urinary system, can cause obstruction. Symptoms and signs of obstruction are often mild, occurring over long periods of time and requiring a high index of suspicion for diagnosis.

Because the degree and duration of obstruction are the chief determinants of renal dysfunction, early recognition and treatment are the keys to preventing renal loss. Urinary obstruction should be viewed as a potentially curable form of kidney disease.



Normal urine production in an adult is about 1.5-2 L/day. Urine flow depends on 3 factors—a pressure gradient from the glomerulus to the Bowman capsule, peristalsis of the renal pelvis and ureters, and the effects of gravity (ie, hydrostatic pressure).

Obstruction of the urinary tract at any level eventually results in elevation of intraluminal ureteral pressure. With prolonged obstruction, ureteral peristalsis is overcome and increased hydrostatic pressures are transmitted directly to the nephron tubules.

As pressures in the proximal tubule and Bowman space increase, glomerular filtration rate (GFR) falls. After 12-24 hours of complete obstruction, intratubular pressure decreases to preobstruction levels. If complete obstruction is not relieved, a depressed GFR is maintained by decreases in renal blood flow mediated by thromboxane A2 and angiotensin II (AII). With continued obstruction, renal blood flow progressively falls, resulting in ischemia and incremental nephron loss. Thus, obstructive uropathy may lead to obstructive nephropathy. Several phases of obstructive nephropathy may be seen, including an early hyperemia and a late vasoconstriction followed by regulation of GFR post obstruction. Recovery of GFR depends on the duration and level of obstruction, preobstruction blood flow, and coexisting medical illness or infection.



No data are available on incidence and prevalence of urinary obstruction in unselected populations. Most epidemiologic studies of obstruction are in selected populations or autopsy studies. In large surveys of elderly men for symptoms of urinary obstruction, a prevalence of 20-35% has been estimated. Most (60%) of the men surveyed with moderately severe to severe symptoms of prostatism did not consult their physicians with these symptoms. Postmortem examinations have found hydronephrosis in 3.8% of adults and 2.0% of children.



Urinary tract obstruction may lead to acute or chronic renal insufficiency or overt kidney failure. Obstruction may lead to a salt-losing nephropathy and urinary concentrating defects. Renal tubular acidosis (RTA) type IV, hyperkalemia, hypomagnesia, and hypophosphatemia are common sequelae of chronic obstruction. Although acute or chronic obstruction may cause urinary tract infection (UTI), other sequelae such as renal calculi, hypertension, and polycythemia are associated with a chronic setting. Ascites is a common sequela of neonatal obstruction syndrome. In cases of acute obstruction, a postobstructive diuresis following relief of the problem is well described.

In adults, incidence and etiology of urinary obstruction vary significantly with the age and sex of the patient. In young and middle-aged men, renal calculi are the most common cause of at least temporary urinary obstruction. Rare cases of obstructive uropathy due to seminal vesicle cyst and appendiceal mucocele have been reported. In young and middle-aged women, gynecologic surgery, pregnancy, and cancers of pelvic organs are important etiologies of obstruction.

Special considerations in pediatric patients include acquired or congential urethral stricture, congenital ureteropelvic junction (UPJ) or ureterovesical junction (UVJ) obstruction, vesicoureteral reflux, and urolithiasis.

After age 60 years, urinary obstruction is most common in men secondary to prostatic hypertrophy; prostate cancer accounts for occasional cases.

Contributor Information and Disclosures

Michael A Policastro, MD Assistant Professor of Emergency Medicine, Fellow in Medical Toxicology, Department of Emergency Medicine, University of Cincinnati College of Medicine; Consulting Staff, Department of Emergency Medicine, Jewish Hospital, Health Alliance

Michael A Policastro, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Wilderness Medical Society

Disclosure: Nothing to disclose.


Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Pilar Guerrero, MD Assistant Professor, Department of Emergency Medicine, John H Stroger Jr Hospital, Cook County Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Vice-Chair in Charge of Research, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

David S Howes, MD Professor of Medicine and Pediatrics, Residency Program Director Emeritus, Section of Emergency Medicine, University of Chicago, University of Chicago, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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