Urinary Tract Obstruction Management in the ED

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.

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 tract 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 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 tract obstruction is most common in men secondary to prostatic hypertrophy; prostate cancer accounts for occasional cases.

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.[6]

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.

Patients often present to the emergency department with acute urinary tract disorders manifesting as flank pain. Because laboratory and clinical findings (eg, hematuria) are neither sensitive nor specific for identifying the cause of the flank pain, imaging is important for both diagnosis and management.[7]

By contrast, pathologic 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.

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

In a study of 56 patients (42 boys, 14 girls) younger than 18 years who presented to the emergency department with acute urinary retention, causes of urinary retention were mechanical obstruction in 14 patients (25%), infection or inflammation in 10 (18%), fecal impaction in 7 (13%), neurologic disorders in 6 (11%), gynecologic disorders in 4 (7%), and behavioral processes in 3 (5%); 12 patients (21%) were idiopathic.  All patients with mechanical obstruction were boys, 5 of whom had a pelvic tumor. Fifteen children underwent surgery, and 3 children required continuous catheterization during follow-up.[8]

Lower urinary tract obstruction caused by polyps of the urethra has been reported.[9]

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) ^[10]

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)

As with any renal disease, initial workup should begin with a urinalysis and examination of sediment by an experienced examiner. Whenever an unremarkable urinalysis is observed in a patient with renal failure, obstruction should be considered. In a completely obstructed system, no distal urine flow occurs. A benign urinalysis may be seen with calculi or tumor.

Microscopic hematuria can be found with a calculus or tumor. Pyuria should suggest the possibility of UTI. Crystalluria may be found in nephrolithiasis or intratubular crystal formation. Proteinuria and casts rarely are found in acute obstruction.

Urinary diagnostic indices

Urine sodium, creatinine, and osmolality often are difficult to interpret in the face of obstruction.

Early in the course of obstruction, prior to severe renal impairment, prerenal indices commonly are observed where urine sodium is depressed, osmolality is elevated, and fractional excretion of sodium is less than 1%.

With progressive obstruction and renal failure, indices consistent with acute tubular necrosis are observed, with elevated urine sodium, depressed osmolality, and fractional excretion of sodium greater than 1%.

Serum electrolytes

Serum electrolytes (sodium, potassium, chloride, bicarbonate, BUN, creatinine), as well as calcium, phosphate, magnesium, uric acid, and albumin, should be measured.

A hyperkalemic nonanion gap metabolic acidosis (type IV RTA) may be an important clue to urinary obstruction.

Elevations of BUN and creatinine may be caused by renal failure secondary to obstruction.

Complete blood count

Elevated white blood cell (WBC) count may be consistent with UTI or hematologic malignancy.

Polycythemia can be a complication of obstruction; anemia commonly is described in chronic renal failure.

Goals of any imaging study are to distinguish anatomic etiologies from functional forms of collecting system dilation and to identify the site of blockage. Once the decision is made to use an imaging study, the patient's condition (eg, pregnancy and radiation risks, renal failure and radiocontrast risks) must be taken into consideration.[1, 2, 3, 4]  Imaging plays a significant role in the initial diagnosis of UTO, with ultrasonography and non-contrast CT being used to screen for dilation of the urinary collecting system. If necessary,, multiphase contrast-enhanced CT urography or dynamic contrast-enhanced MR urography, along with direct ureteroscopic evaluation, may be performed to identify the cause.[1]  

Dilation of urinary tract - Obstruction versus functional

Dilation without obstruction (functional) - Vesicoureteral reflux and one of the following:

• Chronic massive diuresis
• Extrarenal pelvis
• Calyceal diverticula
• Congenital megacalyces
• Ileal conduits

Obstruction without dilation - Intermittent obstruction with one of the following:

• Partial obstructions
• Intrarenal crystals
• Nephrocalcinosis
• Staghorn calculi
• Retroperitoneal obstruction

CT scan

Compared with ultrasonography, CT scan is particularly adept at diagnosing obstruction at the ureteric level. A dilated urinary collecting system is well visualized even without the use of intravenous dye. CT scan can identify calcified and noncalcified calculi.

Ionizing radiation and the nephrotoxicity of radiocontrast dye are of particular importance in patients with chronic renal failure, diabetes mellitus, or multiple myeloma.

Helical CT scan (especially without contrast) rapidly is replacing kidneys, ureter, bladder (KUB) x-rays as the first step in the radiologic evaluation of the urinary system. Although this technique is sensitive for diagnosing hydronephrosis, its real utility may be in delineating the anatomy of obstruction when ultrasonography and intravenous pyelography (IVP) fail to identify an etiology. CT scanning may replace invasive pyelography as the secondary procedure of choice to define the anatomy of obstruction after ultrasonography and IVP.

Singh et al studied  dual-eneergy CT (DECT) to determine the morphologic and chemical characterization of ureteric calculi, along with prediction of the grade of urinary obstruction. The sensitivity of DECT for hydroxyapatite, uric acid, cysteine, oxalic acid, and mixed types were 89.6%, 82.6%, 86.7%, 80%, and  88.9%, respectively; and specificity for hydroxyapatite, uric acid, cysteine, oxalic acid, and mixed types were 88.5%, 97.5%, 96.5%,  98.9%, and 98.9%, respectively.  The sensitivity and specificity of DECT for a high-grade obstruction were 94.3% and 86.2%.[2]

MRI

Advantages of MRI include the following:

• Sensitivity of 100% and specificity of 96% for urinary obstruction
• No ionizing radiation
• Paramagnetic contrast agents - Allow renal functional assessment without risks of iodinated contrast materials
• Can identify calcified and noncalcified calculi
• Can differentiate acute from chronic obstruction by demonstrating perinephric fluid accumulation, which is correlated highly with acute obstruction

MRI can identify only obstruction with dilation and cannot differentiate functional dilation from anatomic obstruction.

Where available, MRI quickly is becoming the imaging study of choice for urinary obstruction.

Intravenous pyelography

IVP provides detailed morphology of the obstruction, and it is well accepted and easily accessible.

Nephrotoxicity of radiocontrast dye is of particular importance in patients with chronic renal failure, diabetes mellitus, or multiple myeloma. In patients with low GFR, excretion of the dye may take 12-24 hours after injection. Moreover, this technique cannot differentiate urinary dilation due to functional obstruction from that due to anatomic obstruction.

IVP is the procedure of choice for defining the extent and anatomy of obstruction.

Invasive pyelography

Invasive pyelography provides the same information as IVP without dependence upon renal function and does not expose the patient to nephrotoxicity from intravenous dye.

It cannot differentiate urinary dilation from functional versus anatomic obstruction, and the invasive techniques have the added risk of infection.

This technique can be used when the risks of IVP are considered too great; dye can be injected directly into the renal pelvis (antegrade) or cystoscopically into the ureters (retrograde).

Ultrasonography

Sensitivity of ultrasonography is higher than that of IVP; sensitivity for detecting hydronephrosis is 90%. Ultrasonography is particularly useful in identifying hydronephrosis in patients with low GFR. Patients are not exposed to ionizing radiation or intravenous dye (ie, no nephrotoxicity), and cost is low. Additionally, bladder wall thickness, bladder weight, and prostate size may aid in diagnosing bladder outlet obstruction.

Urolithiasis guidelines from the European Association of Urology (EAU) recommends ultrasound for initial assessment when there is concern for an acute symptomatic stone, followed by non–contrast-enhanced computed tomography to confirm stone diagnosis.[11]

The study's effectiveness is operator dependent; false-positive rate is as high as 20%; ureters cannot be visualized. Reliability of bladder wall thickness index and variable anatomic sites needs to be confirmed in larger studies.

Ultrasonography is the procedure of choice to determine the presence of hydronephrosis.

Electrocardiography (ECG) should be completed rapidly to identify the effects of hyperkalemia, a common complication of obstructive nephropathy.

A postvoid residual (PVR) urine volume test can provide important information if bladder outlet obstruction is suspected. Perform the test by placing a urinary catheter after a voiding attempt. Urologists often observe the voiding attempt, looking for signs of bladder outlet obstruction, as follows: hesitancy, stream strength, and need to double void. PVR urine volume greater than 125 mL is abnormally large and may indicate obstruction.

Radionucleotide scan

Radionucleotide scanning has high sensitivity (90% for detecting hydronephrosis) and involves no exposure to intravenous dye (ie, no nephrotoxicity). It lacks the resolution of IVP to adequately define the exact site of anatomic obstruction.

Injection of a diuretic agent during the study helps in differentiation of functional and anatomic obstruction. Increased postdiuretic radionucleotide excretion points to a functional cause rather than an obstructive cause. Renal blood flow measurement by radionucleotide scan is becoming the technique of choice to assess the potential for renal recovery after relief of obstruction.

Nonvisualization of the kidney does not conclusively rule out the potential for recovery after relief of obstruction.

In pediatric patients with dilated urinary tract or suspected vesicoureteral reflux (VUR), perform voiding cystourethrography. Alternative imaging study methods include CT, MRI, and echo-enhanced cystosonography.

Initial management and catheterization

Partial obstruction can cause significant defects in salt and water retention, resulting in hypovolemia, which responds to standard fluid administration protocols. Before addressing the specific therapy for obstruction, the ED physician must investigate and begin treatment of the life-threatening complications of obstructive uropathy (eg, pulmonary edema, hypovolemia, urosepsis, hyperkalemia). Pulmonary edema as a consequence of renal failure from complete urinary tract obstruction should be treated conventionally. 

The overriding goal in the treatment of urinary obstruction is the reestablishment of urinary flow. As stated previously, the longer the obstruction exists, the lower the rate of renal recovery and the lower the GFR if any recovery occurs.

Once urinary obstruction is entertained in the differential diagnosis, a transurethral bladder catheter should be placed. A properly positioned Foley catheter can be diagnostic as well as therapeutic for obstruction below the level of the bladder. If no urine is obtained, the proper placement of the Foley should be tested by catheter irrigation. If 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 such as radiography and ultrasonography also may be used to establish proper Foley placement.

If a large PVR volume is noted, obstruction below the bladder should be investigated. Catheter drainage should then be maintained until the etiology of the obstruction is treated appropriately. Intermittent clamping of the Foley is recommended to prevent symptoms of hypotension and hematuria often ascribed to rapid bladder decompression.

Hypotension after bladder decompression is thought to be due to a vagolytic response from a rapid change in bladder-wall tension.

In a series of patients with obstruction, Christensen et al found a 50% decrease in intravesical pressure after only the first 100 mL of urine was removed.[12] Since the major drop in bladder pressure occurred with the early removal of relatively small amounts of urine, they concluded that fractionating urine removal in bladder obstruction was unjustified.

Hematuria and bladder spasm is another well-known complication of bladder decompression. Gould et al compared the incidence of hematuria in rapidly emptied and gradually emptied obstructed dog bladders.[13] They found that hematuria was correlated strongly with the degree of bladder wall damage prior to relief of obstruction and was not correlated with the rate of emptying.

Urine should be drained completely and rapidly from an obstructed bladder. Prolonged urine stasis only predisposes the patient to UTI, urosepsis, and renal failure.

Consult a urologist when a transurethral catheter cannot provide adequate bladder drainage. Filiform catheters or a suprapubic cystotomy may be required to drain the bladder completely. Invasive pyelography for higher-level obstructions can be diagnostic and therapeutic.

Consult a nephrologist to provide emergent hemodialysis if necessary.

Calculi

Calculi are the most common causes of unilateral ureteral obstruction. More than 90% of renal calculi less than 5.0-7.0 mm in size pass spontaneously. Obstruction in these cases can be treated conservatively with intravenous fluids and analgesia. Surgical drainage is necessary only for patients with unrelenting pain, UTI, or persistent obstruction.

Acute renal colic due to ureteral stone obstruction is an emergency that requires immediate pain management. Medical expulsive therapy (MET), usually with α-receptor antagonists, can facilitate stone passage and reduce the need for analgesia.[14]

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.

Location of obstruction

Bilateral obstruction of the ureters is almost always an asymmetric process. Generally, whatever the etiology of ureteral obstruction, one ureter is obstructed slowly and asymptomatically over a long period of time. Not until the second ureter is obstructed are symptoms of renal failure, hyperkalemia, or acidosis observed. In this condition, radionucleotide scanning can be helpful in identifying the most viable kidney for drainage.

For midureteral or proximal ureteral obstruction, percutaneous nephrostomy tube placement is indicated.

For distal obstruction, cystoscopic placement of a ureteral stent can be attempted.

Cases of renal recovery have been detected by radionucleotide scan in kidneys without renal blood flow.

In case of suspected urosepsis from bilateral ureteral obstruction, bilateral percutaneous nephrostomy tubes must be placed to ensure that both potentially infected systems are drained.

Intrarenal obstruction secondary to crystals or protein casts is not amenable to surgical drainage. Maintenance of adequate hydration to promote high rates of urine output to dilute crystals and casts is the main treatment.

Postobstructive diuresis is an uncommon but clinically significant complication following the release of urinary obstruction. It is characterized by a marked natruresis and diuresis with excretion of large amounts of sodium and water.

In addition to the potential for severe volume depletion, electrolyte disorders such as hypokalemia, hyponatremia, hypernatremia, and hypomagnesemia may occur. The etiology of this massive diuresis and electrolyte loss is multifactorial. It is related to fluid and urea overloads during obstruction and acquired tubular resistance to antidiuretic hormone and aldosterone.

Treatment of postobstructive diuresis consists of judicious fluid replacement with 0.45% saline (at a rate slightly less than urine output) and replacement of electrolytes. Urinary tract infections may occur due to urinary stasis. Additionally, instrumentation may also introduce contamination. Antibiotic selection depends on the age, sex, and comorbid conditions of the patient. Additionally, minimizing drug interactions, such as patients on anticoagulation, should also guide antibiotic selection.

Acute urinary retention has been reported following photoselective vaporization (PVP) to treat benign prostatic obstruction. Risk factors for this complication include adenoma volume lower than 40 mL, lower lasting time, international prostate symptoms score (IPSS) ≥19, and previous treatment with 5-alpha-reductase inhibitors.[15]

Medical therapy for benign prostate hypertrophy (BPH) has provided a very successful alternative to surgical therapy, whose risks include anesthesia, infection, impotence, incontinence, consistent failure to restore normal flow, and frequent necessity for retreatment.

Medical therapy should not be offered to individuals presenting with absolute indications for surgical intervention.

Indications for surgical prostatectomy are recurrent urinary retention, recurrent UTIs, renal insufficiency, bladder calculi, and recurrent gross hematuria.

Class Summary

The rationale for alpha-blockers in the treatment of BPH is based on the fact that smooth muscle accounts for 40% of the hypertrophied prostatic mass. The basal tone of prostatic smooth muscle is increased significantly by stimulation of alpha1-adrenergic receptors. Alpha-blockers relieve bladder obstruction from BPH by decreasing tonic contraction of prostatic smooth muscle.

Recent molecular studies have identified 3 subtypes of alpha1 receptors. The alpha1-AR subtype is specific for prostatic smooth muscle. Tamsulosin is a selective alpha1-AR antagonist. Recently, a new alpha1-AR antagonist, silodosin (Rapaflo), was approved.

Prazosin (Minipress)

Treats prostatic hypertrophy. Improves urine flow rates by relaxing smooth muscle. This relaxation produced by blocking alpha1-adrenoceptors in bladder neck and prostate. When increasing dosages, give first dose of each increment at bedtime to reduce syncopal episodes. Although doses >20 mg/d usually do not increase efficacy, some patients may benefit from doses as high as 40 mg/d.

Terazosin (Hytrin)

Quinazoline compound that counteracts alpha1-induced adrenergic contractions of bladder neck, facilitating urinary flow in presence of BPH.

Tamsulosin (Flomax)

Selective alpha1-antagonist for treatment of BPH.

Alfuzosin (UroXatral)

Alpha1-adrenoceptors blocker in the prostate. Blockade of adrenoceptors may cause smooth muscles in bladder neck and prostate to relax, resulting in improvement in urine flow rate and reduction in symptoms of BPH.

Silodosin (Rapaflo)

Selectively antagonizes postsynaptic alpha1-adrenergic receptors in prostate, bladder base, prostatic capsule, and prostatic urethra. This action induces smooth muscle relaxation and improves urine flow. Indicated for signs and symptoms of benign prostatic hyperplasia.