eMedicine Specialties > Emergency Medicine > Genitourinary

Urinary Obstruction

Author: Michael A Policastro, MD, Assistant Professor of Emergency Medicine, Fellow in Medical Toxicology, Department of Emergency Medicine, University of Cincinnati; Consulting Staff, Department of Emergency Medicine, Jewish Hospital, Health Alliance
Coauthor(s): Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center; Pilar Guerrero, MD, Assistant Professor, Department of Emergency Medicine, John H Stroger Jr Hospital, Cook County Hospital
Contributor Information and Disclosures

Updated: Jan 29, 2009

Introduction

Background

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.

Pathophysiology

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.

Frequency

United States

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.

Mortality/Morbidity

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.

Sex

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.

Age

  • 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.

Clinical

History

Most acute obstructive uropathies are associated with significant pain or the abrupt diminution of urine flow that alerts the clinician to the need for further evaluation and treatment. However, the insidious nature of chronic urinary obstruction requires a careful history and a high index of suspicion, which prompt an appropriate evaluation that may confirm or rule out the presence of obstruction. A large (933 patients) prospective study by de la Rosette et al failed to correlate a wide range of symptoms of lower urinary tract obstruction with bladder outflow studies.1

  • Pain secondary to stretching of the urinary collecting system is the most common symptom in acute obstruction.
    • Prevalence of pain is related more to acuity of obstruction than degree of distention.
    • Acute obstruction of the ureter by a calculus commonly results in an excruciating pain, commonly referred to as renal colic. This pain is described as unrelenting, radiating from the flank to lower abdomen and testicles or labia on the affected side.
    • By contrast, pathological processes that slowly obstruct, such as retroperitoneal tumors, are relatively pain free. Prostatic hypertrophy also may be associated with an obstructive uropathy that is relatively painless. It usually is identified when a superimposed acute obstruction occurs with the inability to void effectively; the resultant painful, distended bladder prompts a visit to an emergency physician.
  • Alterations in patterns of micturition often associated with more distal obstructions are early but frequently missed symptoms.
    • Although anuria is dramatic and specific for obstruction, nocturia and polyuria are much more common presenting symptoms associated with renal concentrating defects due to partial obstruction.
    • Bladder outlet obstruction leads to the symptoms of prostatism (eg, frequency, urgency, hesitancy, dribbling, decrease in voiding stream, the need to double void).
  • Acute and chronic renal failures are common complications of urinary obstruction. Obstructive nephropathy should be considered especially in uremic patients without a previous history of renal disease, hypertension, or diabetes.
  • Gross or microscopic hematuria often is associated with renal calculi, papillary necrosis, and tumors, all of which can cause obstruction.
  • Recurrent UTIs should always lead to an investigation for urinary obstruction.
  • New-onset or poorly controlled hypertension secondary to obstruction and increased renin-angiotensin has been reported.
  • Polycythemia secondary to increased erythropoietin production in the hydronephrotic kidney also has been reported.
  • History of recent gynecologic or abdominal surgery can give important clues to the etiology of urinary obstruction.
  • Pediatric patients may present with recurrent infections. Symptoms of voiding dysfunction such as enuresis, incontinence, or urgency should be sought.
  • A thorough medication history should be elicited. A variety of drugs and toxins affect renal function. Bladder dysfunction is seen with a variety of xenobiotic drugs with antimuscarinic anticholinergic activity such as antihistamines, antipsychotics, and antidepressants. A variety of xenobiotics such as ethylene glycol, indinavir, methotrexate, phenylbutazone, or sulfonamides will induce crystal deposition throughout the tubulointerstium obstructing urine output. Additionally, drug-induced retroperitoneal fibrosis may obstruct ureteral function such as methysergide or other natural-occurring ergotamines.
  • In cases of both acute and chronic obstructive uropathy, occupational exposure history may be beneficial. For example, in textile manufactures, shipyard workers, roofers, or asbestos miners, retroperitoneal fibrosis due to asbestos-induced mesothelioma should be considered. Bladder cancer–induced outlet obstruction may occur in textile workers, rubber manufacturing workers, leather workers, painters, hairdressers, or drill press workers exposed to alpha- or beta-naphthylamine, 4-aminobiphenyl, benzidine, chlornaphazine, 4-chlor-o-toluidine, 2-chloroaniline, phenacetin compounds, benzidine azo dyes, or methylenedianiline.

Physical

  • Signs of dehydration and intravascular volume depletion can be seen as a result of urinary concentrating defects associated with partial obstruction. Peripheral edema, hypertension, and signs of congestive heart failure from fluid overload may be observed in obstruction from renal failure.
  • Palpable kidney or bladder provides direct evidence of a dilated urinary collection system.
  • Rectal and/or pelvic examination is essential in determining whether enlargement of pelvic organs (eg, prostate, uterus) is a possible source of urinary obstruction.
  • Examination of the external urethra may disclose phimosis or meatal stenosis.

Causes

  • Infants and children
    • Urethral and bladder outlet obstruction may be associated with the following:
      • Urethral atresia
      • Phimosis
      • Meatal stenosis
      • Anterior and posterior urethral valves (males)
      • Calculus (Southeast Asia)
      • Blood clot
      • Neurogenic bladder (meningomyelocele)
      • Ureterocele
    • Ureteral obstruction may be associated with the following:
      • Vesicoureteral reflux (female preponderance)
      • Ureterovesical junction narrowing or obstruction
      • Ureterocele
      • Retrocaval ureter
      • Retroperitoneal tumor
      • Megaureter -Prune belly syndrome
      • Blood clot
      • Ureteropelvic junction narrowing or obstruction
  • Adults
    • Urethral and bladder outlet obstruction may be associated with the following:
      • Phimosis
      • Stricture (male preponderance)
      • Sexually transmitted diseases (STDs), particularly in women with severe genital herpes involving the urethral orifice, occasionally in males with significant prostatitis or purulent urethritis
      • Trauma
      • Blood clot
      • Calculi
      • Benign prostate hypertrophy (BPH)
      • Cancer of prostate or bladder
      • Carcinoma of cervix or colon
      • Neurogenic bladder (diabetes mellitus, spinal cord disease, multiple sclerosis, Parkinson disease, anticholinergic drugs, alpha-adrenergic antagonists, calcium channel blockers, opioids, sedative-hypnotics)
    • Ureteral obstruction may be associated with the following:
      • Vesicoureteral reflux (female preponderance)
      • Calculi
      • Uric acid crystals
      • Blood clot
      • Trauma
      • Papillary necrosis (sickle cell disease, diabetes mellitus, pyelonephritis)
      • Inflammatory bowel disease
      • Pregnant uterus
      • Aortic aneurysm
      • Carcinoma of ureter, uterus, prostate, bladder, colon, or rectum
      • Retroperitoneal fibrosis
      • Idiopathic tumors (cervix, uterus, prostate, colon)
      • Tuberculosis
      • Sarcoidosis
      • Chronic UTI (methysergide, propranolol)
      • Retroperitoneal lymphoma
      • Uterine leiomyomata
      • Stricture (tuberculosis, radiation, schistosomiasis, nonsteroidal anti-inflammatory drugs [NSAIDs])
      • Accidental surgical ligation
    • Intrarenal obstruction may be associated with the following:
      • Crystals (uric acid, sulfonamide, acyclovir)
      • Protein casts (multiple myeloma, amyloidosis)

More on Urinary Obstruction

Overview: Urinary Obstruction
Differential Diagnoses & Workup: Urinary Obstruction
Treatment & Medication: Urinary Obstruction
Follow-up: Urinary Obstruction
References

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Further Reading

Keywords

urinary obstruction, obstruction of the urinary tract, blocked urine flow, renal failure, kidney failure, renal dysfunction, kidney dysfunction, renal insufficiency, renal calculi, urinary tract infection, UTI, renal tubular acidosis, RTA, hyperkalemia, hypomagnesia, hypophosphatemia

Contributor Information and Disclosures

Author

Michael A Policastro, MD, Assistant Professor of Emergency Medicine, Fellow in Medical Toxicology, Department of Emergency Medicine, University of Cincinnati; 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, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and 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.

Medical Editor

David S Howes, MD, Residency Program Director, Professor of Medicine, Section of Emergency Medicine, University of Chicago/Pritzker School of Medicine
David S Howes, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Richard H Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: eMedicine.com, Inc. Consulting fee Consulting

 
 
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