Obstructive Uropathy: A Clinical Update
Authors: Harrison Alter, MS, MD, Chief Resident, Department of Emergency Medicine, Alameda County Medical Center, Highland Campus, Oakland, CA.
Eric Snoey, MD Associate Residency Director, Department ofEmergency Medicine, Alameda County Medical Center, Highland Campus, Oakland, CA.
Peer Reviewers: Norman E. Peterson, MD, Chief, Division of Urology, Denver Health Medical Center, Professor of Urology and Surgery, University of Colorado Health Sciences Center, Denver, CO.
Marshall Salkin, MD, JD, FACEP,FCLM, Attending Physician, Emergency Department of Northwest Community Hospital, Arlington Heights, IL.
Urinary tract obstruction is a relatively common but potentially serious clinical phenomenon, and optimal clinical approaches may be elusive to the emergency physician. Because obstructive processes can range from congenital posterior urethral valves, to urolithiasis, to the normal condition of pregnancy, effective management requires accurate diagnosis. Autopsy-based studies estimate incidences of obstruction to be 3% in adults and 2% in children.1 The most common causes in males occur at the extremes of ageboys with congenital anatomic abnormalities and older men with prostatism. Among females, physiological ureteral obstruction occurs in up to 65% of pregnancies.1
This review will focus primarily on urolithiasis and its importance in the practice of emergency medicine. We will briefly touch upon the renal pathophysiology of obstructive uropathy, as well as review other causes of urinary obstruction.
The Editor
Epidemiology. Kidney stones occur frequently in the ED population. An annual incidence of 16 per 10,000 population in the United States was cited in an extrapolation of 1974 hospital discharge data, though this figure may be conservative.2
Urolithiasis affects males more commonly by a ratio 2:1 to 4:1, peaking in the fourth to sixth decades. Whites are more commonly affected than blacks at a ratio of about 3:1. The risk of developing urolithiasis in middle-aged white men, a high-risk group, is approximately 1% per year.
The incidence of renal calculi exhibits geographic and seasonal variability as well. Australians are more commonly affected than North Americans, while within North America, inhabitants of the Southeast are at highest risk. Seasonal peak incidence appears to lag about two months behind peak local temperature, which may parallel peak intake of high-oxalate content foods. Earlier theories relating geographic patterns of stone formation to dehydration have been largely discredited.3
Pathogenesis. Composition. Figure 1 displays the distribution of chemical constituents of ureteral calculi.4 It is interesting to note that 80% of all stones contain calcium. The majority of the remaining 20% comprise struvite and uric acid stones, which develop in alkaline and acid urine, respectively. Cystine stones account for fewer than 1%.4
Anatomy. Kidney stones arise within the collecting ducts and grow in the renal pelvis, only resulting in symptoms as they obstruct the ureteropelvic junction or proceed down the ureter. Some stones never make it beyond the renal pelvis, being too large to pass the ureteropelvic junction. If a stone is to move on, however, the first likely point of obstruction is at the ureteropelvic junction, the "headwaters" of the drainage. Internal diameter there can be as small as 2-3 mm. Common stones are unlikely to fix in the next segment, the abdominal spindle, which can pass a 10 mm ureterolith. The ureter narrows to about 4 mm as it passes into the pelvis crossing over the iliac vasculature, and it narrows again in the posterior pelvis as it crosses under the hypogastric vessels. The last obstacle for a passing stone is the ureterovesicular junction, where the lumen may be as narrow as 1 mm. Figure 2 illustrates these anatomic relationships within the urinary tract.5
Pathophysiology. The end product of the complex process of glomerular filtration and tubular excretion/reabsorption is supersaturated filtrate urine. Any alterations in the degree of supersaturation of calcium, oxalate, ammonium, uric acid, or citrate, may predispose urine to crystal formation, as will the availability of a ready nidus for crystal growth, known as a nucleus.6
A low urine-output state, once thought to account for a significant proportion of stone disease, is now believed to account for fewer than 5-15% of stones but may be a co-factor in up to 50% of calcium-containing stones.7,8 High dietary calcium, also thought to contribute significantly to stone formation, may actually be inversely related to stone risk.9 In contrast, a rise in dietary oxalate results in disproportionate increases in urinary oxalate excretion and appears to play a major role in the formation of calcium oxalate stones, the most common calculi in the United States.10 Oxalate-rich diets are heavy in coffee, tea, cola, and beer, as well as chocolate, nuts, citrus, and spinach. Some authors theorize that the seasonal and geographic variations in incidence are merely reflective of similar variations in diet. For example, a high rate of disease in the South after the summer months correlates with a high rate of iced tea consumption. High urinary oxalate concentrations can also be found in patients with Crohn’s disease, short gut syndrome, and other functional disturbances in absorption.
Urinary citrate inhibits stone formation in two important ways: formation of a soluble citrate-calcium compound that leaves less free calcium to form crystals; and direct inhibition of calcium crystallization. Therefore, low urinary citrate, occurring idiopathically or in Type 4 renal tubular acidosis and chronic diarrheal syndromes, may be an important etiologic factor implicated in about 30% of stone formers.7 Primary hyperparathyroidism, an uncommon cause of hypercalciuria and stones, must be considered since it may be amenable to surgical correction. Idiopathic stone formation, the largest category of disease, is thought to arise as a result of abnormalities contributing to increased enteric absorption of calcium.
Uric acid stones are largely a phenomenon associated with hyperuricemia and only rarely occur in the absence of clinical gout. Hyperuricemia unassociated with clinical gout can provide a nidus for calcium crystallization and may occur in up to 25% of calcium oxalate stones.
Cystine stones result from a hereditary defect in the renal tubular reabsorption of cystine, ornithine, lysine, and arginine, generally found in younger patients. Lastly, struvite stones, which can propagate into the "staghorn"-type calculi, are formed in a urinary environment created by the presence of urea-splitting bacteria. These organisms, which include Proteus, Klebsiella, Pseudomonas, Entercoccus, and Morganella species yet notably exclude Escherichiae, create an alkaline environment. Cleaving urea promotes the availability of free ammonium that compounds rapidly with magnesium and phosphate to form the struvite stone. Ureteral obstruction that involves struvite stones suggests a high-risk patient due to the implied associated urinary tract infection, though true staghorn calculi rarely obstruct.
The pathophysiological model of unilateral obstruction primarily addresses stone disease, although ureteral impingement from a pelvic cancer and post-operative ureteral injury are also common mechanisms. There is a widely cited belief that the uninfected kidney can tolerate one week of complete obstruction without serious sequelae. This belief appears to be based upon small dog studies in the 1950s and 1970s that demonstrated complete recovery of GFR after seven days of ureteral ligation. The degree of recovery after this window was found to be proportional to the duration of ligation up to 40 days. After 40 days, recovery of renal function was unlikely in the animals.11-13 The dog data are supplemented by a handful of case reports describing recovery of renal function in humans following presumed obstruction of 28-150 days’ duration.14
Despite the suggestion of reversibility, there is evidence suggesting renal injury during the period of obstruction, beginning after the first 24 hours.15,16 There is significant dropout of functioning nephrons, down to about 40% of normal after the first day of complete obstruction. Florid renal macrophage infiltration progresses, both as a function of cytokine transmission and as a direct result of mechanical obstruction, resulting in renal scarring. What is not currently known is the degree to which such renal insufficiency places the affected kidney at risk for further insult, including insult from IV contrast, NSAIDs, or infection. Therefore, it seems wise not to depend upon the theoretic one-week window and instead to recommend urgent specialty referral in patients with persistently obstructing stones.
Diagnosis. History and Physical Examination. There is legitimate controversy among practicing emergency physicians as to whether a firm diagnosis of urolithiasis must be established in the ED or if a presumptive diagnosis is adequate with close referral. Indeed, since the vast majority of patients with stones have an uncomplicated course, the emergency physician may choose to accept a presumptive diagnosis of calculus disease while ruling out infection and eliminating other items on the differential diagnosis, including leaking abdominal aortic aneurysm, appendicitis, renovascular occlusion, and acute tubular necrosis. (See Table 1.)
As with many common problems facing the emergency physician, an accurate history is critical in the diagnosis of urolithiasis. A presumptive diagnosis will rely heavily upon the presence of a clinical triad: unilateral costovertebral angle pain, abrupt in onset, associated with hematuria. (See Figure 3.) The patient who presents with this scenario has a 90% probability of having a stone.17 Radiation of pain to the abdomen and groin may also be a helpful historical feature, present in up to 70% of patients.17 Ureteropelvic junction stones produce aching back pain related to distention. Pain from a stone in the distal ureter may radiate to the testes or ovaries, as a result of their common embryologic origin and shared autonomic innervation. Stones in the ureterovesicular junction can create urinary tenesmus.
The character of the pain may provide another clue to the diagnosis. The patient with calculus disease seems unable to find a comfortable position, an observation that weighs against intra-abdominal processes that result in peritoneal irritation. The term renal colic may be a misnomer, since the pain is only colicky in nature if the stone lodges, dislodges, and lodges again in the ureter. More typically, the pain rises to a crescendo over 15-30 minutes and persists until the stone lodges or passes to a wider portion of the ureter. Associated symptoms are largely nonspecific. Nausea and vomiting, found in 50-80% of patients, and dysuria, present in 25%, predominate.17
Both calcium-containing stones and cystine stones may be associated with a positive family history. A history of prior stone is important, since the recurrence rate is high 50% within five years.19
The physical exam is primarily helpful in excluding other potential causes of the patient’s presenting complaint. Hypertension and tachycardia may occur in response to the pain. Temperature greater than 100.5°F is important in that it occurs in only 5% of patients with uncomplicated ureteral calculi; fever should alert the clinician to the possibility of proximal infection.17 Point or rebound abdominal tenderness does not rule out the diagnosis of urolithiasis, but it is not part of the classical presentation. Costovertebral angle tenderness may suggest a proximal stone but is also worrisome for the presence of infection. Symptomatic abdominal aortic aneurysm is of particular concern in older patients; the emergency physician should attempt to palpate the abdominal aorta and both femoral pulses.
Laboratory. Microscopic urinalysis is the linchpin of the laboratory evaluation of urolithiasis. Microscopic hematuria is present in 70-80% of patients, and is part of the classical triad of acute onset costovertebral angle pain with hematuria.5 Absence of hematuria suggests either a 100% ureteral occlusion, lab error, or a chance event.17 Low-grade pyuria can exist in uncomplicated urolithiasis, but more than 3 WBC/hpf in the presence of bactiuria indicates a possible infection.
Urine pH is also worth noting. Acid urine suggests uric acid calculi, though they may act only as the nucleus for a calcium-containing stone. Acid urine also rules out renal tubular acidosis as a cause for the stone. Alkaline urine raises the suspicion of urease-producing organisms and the presence of infection.
Other laboratory evaluation rarely affects management decisions. A complete blood count may demonstrate an elevated WBC count, which, in the moderate range, can be attributed to the stress response. Hypokalemia in the presence of low bicarbonate may be useful in diagnosing renal tubular acidosis. A serum creatinine establishes normal renal function prior to the use of intravenous contrast material. Further laboratory evaluation, including uric acid, serum calcium, and analysis of a passed stone is best undertaken during the follow-up phase of care.
Radiographic. The ideal radiographic study in patients with urolithiasis provides diagnostic, anatomic, and functional information.
Historically, physicians have relied upon the "KUB" (kidneys, ureters, bladder) plain film as the study of choice in urolithiasis. This modality, which provides only anatomic data, has been supplanted by more effective imaging techniques. The frequently cited claim that 90% of stones are visible on KUB is based upon data from the early part of the century that has never been reproduced in the modern era.
Several studies from the 1980s demonstrate that the sensitivity and specificity of KUB varies between 50% and 85%, with a negative predictive valueits ability to rule out urolithiasisas low as 22%. KUB is equally unreliable when interpreted by radiologists or emergency physicians.17,20-22 While many clinicians continue to use KUBs to influence their decision to proceed to IVP, this strategy has been shown not to be cost-effective and to add little information to the decision-making process.22 One study reported that a positive KUB in the setting of the classic triad improved sensitivity from 90% to 98%. However, the authors made no comment on the impact of a negative KUB, an important consideration in a test known to have a high false-negative rate.17 In the contemporary era, the only role for KUB may be as an adjunct to ultrasonography, since it may serve the operator as a roadmap for identifying a stone. KUB actually increases the sensitivity of the ultrasound.23 Some urologists may also use KUB to follow a stone expectantly.
The intravenous pyelogram (IVP) remains the urologists’ study of choice, both out of custom and for the functional data it may convey. Classic IVP findings supporting the presence of a stone include a dense nephrogram with delayed excretion on the affected side and interruption of the dye column. A delayed nephrogram, usually of more than two hours, suggests clinically important obstructive nephropathy. Extravasation of contrast, a rare finding, may be seen in ureteral "blowout" and necessitates prompt urological consultation.
Convention aside, however, the IVP may not be optimal for the ED evaluation of ureteral calculi. Most of the studies demonstrating its efficacy were performed with patients referred for the study who had presumably undergone adequate bowel preparation. Even in ideal conditions, there is a 10-15% false-negative rate, usually due to non-occlusive stones that are also radiolucent (typically uric acid) or stones obscured by the urographic medium.24 In ED patients, who typically have poor bowel preparation, the study can be even more difficult to interpret. False-positive results may be incurred in the setting of acute tubular necrosis when sloughed cells may obstruct the ureter. Ureteral thrombus and transitional cell carcinoma may create a similar appearance. These conditions mimic an obstructive radiolucent stone.
Although claims of the health risks of IVP may be overstated, it is not an entirely benign procedure. Most recent estimates of the risk of a contrast reaction place the incidence in the 1:75,000 range, with contrast nephropathy occurring in 1.5-15% of patients.25 Although pre-existing renal insufficiency is the only clearly established risk factor for contrast nephropathy, other conditions, including diabetes, dehydration, multiple myeloma, congestive heart failure, and peripheral vascular disease have all been cited as posing increased risk in contrast administration.25 In addition, excretory urography can be very time-consuming, occasionally requiring up to 24 hours before definitive results are obtained, thereby extending a patient’s stay in the ED.
One of the newer proposed modalities for evaluation of ureteral calculi is ultrasound. In experienced hands, ultrasound is excellent at detecting intracalyceal stones, very proximal stones larger than 5 mm, and, when performed with a full bladder, distal stones stuck at the ureterovesicular junction.27 Ultrasound can also detect hydronephrosis, which correlates with the degree of obstruction in a manner similar to IVP. When performed in conjunction with KUB, ultrasound demonstrates a favorable receiver operating characteristic (ROC) curve in comparison to IVP.23 However, in another recent study, this method missed three cases out of 18 diagnosed by CT.28 Furthermore, the emergency physician who relies upon ultrasound should be aware of a series of reports demonstrating nondilated obstructive uropathy, including cases of obstructive urolithiasis.26,29,30
The more recent addition of Doppler to the ultrasound exam can add important functional information. Doppler can assess both intrarenal pressures and distal ureterovesicular jets, a further clue to the degree of obstruction.31 Although not widely available, non-ionic intravenous sonographic contrast materials promise to greatly enhance the effectiveness of ultrasound in this setting.
In 1995, Smith and Rosenfield et al published a landmark article which established the use of non-contrast helical CT (NCHCT) in imaging urolithiasis. The authors found NCHCT to be more sensitive than IVP, since even radiolucent stones lit up, and equally specific.32 While the urine flow component of kidney function cannot be assessed, the obstructive component (e.g., hydronephrosis or hydroureter) is reliably evident. Furthermore, in an estimated 10% of cases, NCHCT identified an extra-urologic source for a patient’s complaint.
Findings on NCHCT characteristic of urolithiasis include: perinephric stranding consistent with hydronephrosis, dilatation of the collecting system, and the presence of a brightly opaque density in the kidney or ureter. Even non-calcium-containing stones will give this rather dramatic presentation. In the initial study, most patients were scanned with 10 mm cuts (although some centers currently use 7 mm sections) with acquisition time averaging about one second per segment. Radiation exposure per unit of tissue is small, as the scanner operates in a corkscrew fashion, and there is no need for IV or PO contrast material.
One of the criticisms of this technique has been its increased cost. This is an imprecise allegation; it is actually an increased charge. In fact, in many centers, radiology groups elect to set their charge for the use of NCHCT for evaluation of flank pain with hematuria at a pace with IVP to promote appropriate use of their imaging services.
Urologists have been slow to embrace NCHCT for two reasons: CT cannot provide data about concentrating function within the kidney, and it offers a nontraditional axial perspective on the anatomy rather than the more familiar coronal image of IVP. With the latter obstacle in mind, new CT software permits curved planar reformatting, a coronal reconstitution of the kidneys, ureters, and bladder. In one recent study, this system outperformed axial images by defining calculi in three cases in which the axial images were equivocal.28
Despite its advantages, helical CT scanning is currently available only at larger institutions, and ultrasound is highly operator-dependent. Therefore, the IVP remains a popular study with many ED physicians, and its flaws do not obviate its usefulness in the radiographic evaluation of renal colic.
Differential Diagnosis. The panoply of imaging options for suspected ureteral calculi begs the question: Why bother? If the clinical presentation is 90% sensitive, and more than half of all stones pass spontaneously, what is the value of ED diagnosis, assuming infected obstruction has been ruled out?33,34 This debate exists on many levels; for the emergency physician, the matter of differential diagnosis is paramount.
Table 1 depicts the main points of the differential diagnosis. There are a few entities, such as aortic aneurysm or appendicitis, in which missing the diagnosis could lead to significant morbidity or mortality. This suggests one approach to the patient with suspected stone disease: make it a diagnosis of exclusion, and study all the catastrophic alternatives instead. However, in a disease entity so common and so easy to definitively diagnose, this approach seems wasteful.
And why proceed in the setting of "clinical certainty"? While the clinical and laboratory diagnosis is 90% sensitive, its specificity is not known. With a high sensitivity and unknown specificity, we are at risk for treating and referring as stones many cases that are not stones. Contemporary medicine demands appropriate use of subspecialty referral; in the case of kidney stones, imaging may be required. Finally, definitive diagnosis is also relevant in the ED because patients in distress look to their physician for some degree of reassurance, and definitive prognosis regarding stone passage or the need for surgery requires an imaging study.
One common management strategy is to defer the ultimate diagnosis to the follow-up clinician. Based upon the patient’s response to therapy, the need for imaging or other ancillary testing can be more selectively applied, with substantial cost savings. This approach, however, begs the question of whether an ED imaging study results in an important change in management. A recent study specifically addressing the use of IVP argues for a more liberal use of ED imaging.35 The author studied emergency physicians caring for patients with suspected ureteral colic over a one-year period and assessed the degree to which obtaining the IVP changed management. In nearly a quarter of the patients, the study forced consideration of an alternative diagnosis, and 40% of the studies yielded an unexpected result. Nearly two-thirds of the studies changed management based on pre- and post-IVP questionnaires. The use of routine imaging resulted in hospitalization of some patients who would otherwise have been sent home and allowed discharge of some who had been marked for admission. The author did not offer data on outcomes, or compare the strategy of emergency department IVP to outpatient referral. However, the results are compelling.
Given the inconclusive state of research on the subject, however, the practicing emergency physician remains well within the standard of care in electing to make a presumptive diagnosis in the setting of the classic presentation of renal colic.
Treatment. The patient’s foremost preoccupations are pain and, by extension, pain control. The options available include non-steroidal anti-inflammatory medications, narcotics, or both.
The proposed mechanism of NSAID efficacy relates to their anti-prostaglandin effects. Even partial obstruction of the urinary tract results in increased pressure in the renal pelvis, stimulating renal prostaglandin release, especially PGE2. This substance has a vasodilatory effect on the afferent arteriole, leading to further increased pressure. Prostaglandins also mediate the phasic and tonic contractile activity of ureteric smooth muscle.38 Therefore, the three effects that promote painpressure, spasm, and the local inflammatory responseall are potentially remediable by the action of an NSAID. Two studies demonstrate the efficacy of ketorolac for renal colic, one of them head-to-head with meperidine.36,37 If ketorolac is unavailable, rectal indomethacin also has been demonstrated efficacious in comparison with narcotic analgesia.38 However, some patients may require the addition of a potent parenteral narcotic, such as IV morphine, when NSAIDs are not enough, and the ED physician is certainly within the standard of care in relying upon narcotics alone.
Hydration remains the standard of care despite some controversy. The theory challenging its use centers on the problem of increased flow leading to increased intrarenal back-pressure and worsening compression of nephrons. This question requires more study before reversal of this common practice can be recommended. Glucagon, diuretics, and antispasmodics have all been tried without success, and none is indicated in the acute setting, although the osmotic diuresis from IVP dye has been reported to promote stone passage. One recent study using nifedipine and methylprednisolone in combination showed promise in hastening stone passage.33
Hospital admission is occasionally warranted. It should be reserved for those patients with a proximal infection, a solitary kidney, intractable pain, or dehydration. Some authors advocate hospitalizing patients with complete obstruction as well.5 All patients with ureteral calculi will require follow-up to ensure resolution of symptoms and to initiate stone analysis and consideration for a metabolic work-up, the results of which may dictate long-term therapy. The necessity for subspecialty follow-up may depend on the radiographic findings. Signs of obstruction and large stones unlikely to pass spontaneously suggest prompt referral within 72 hours. Patients with smaller, distal stones can be deferred for up to two weeks, with instructions to return sooner if their pain persists. Those physicians who elect to make the definitive diagnosis outside the department by scheduling an outpatient imaging study with urologic follow-up must ensure that the referral will be prompt.
At discharge, patients are given a set of strainers, with instructions to use them with every void. Oral NSAIDs are typically adequate for outpatient pain control but may be supplemented with oral narcotics and anti-emetics. Patients should make an effort to remain well-hydrated, although some authors question the utility of such a strategy since agents that inhibit crystallization are diluted out at the same rate as those that promote stone formation.3,39 Common recommendations for hydration include drinking two glasses of liquid every two hours, half of it as water, or drinking until the urine is clear. Alternatively, the patient can be discharged with dipsticks and instructions to keep the urine specific gravity at about 1.010.40 Obvious caveats apply regarding return to the ED, and include fever, chills, and dysuria (worrisome symptoms of infection), or worsening pain.
Long-Term Treatment. Surgical. Table 2 demonstrates the relationship between size of stones and likelihood of passage, allowing the surgeon and patient together to balance the risks and benefits of surgical treatment.34 Asymptomatic stones are rarely treated, regardless of location; the classic exception is an airline pilot, who can little afford a sudden bout of renal colic.
Once it is determined that some intervention is required, the strategy depends upon the location and size of the stone. Calculi trapped within the kidney may be treated with extracorporeal shock-wave lithotripsy (ESWL) alone or with percutaneous nephrolithotomy. Among patients with stones within the kidney less than 2 cm in size, ESWL will be definitive in 80%; stones greater than 2 cm require nephrostomy drainage as well. A stone lodged in the proximal ureter may be pushed back into the kidney ureteroscopically to a position more amenable to ESWL or treated in situ. Ureteral stenting may facilitate drainage of the fragments after ESWL and can also be used to provide temporary urine outflow during the course of ESWL therapy. The most common stone requiring intervention is the distal stone, and this is removed ureteroscopically, sometimes with the assistance of a basket or balloon. Cystine stones are, in general, not amenable to fragmentation by ESWL and must be removed directly by one of the approaches described above or by open lithotomy.
The predominant adverse effects of ESWL are pain and hematuria; more serious complications are rare. The procedure is generally performed with anaesthesia, although newer-generation machines may focus energy more effectively and reduce trauma to surrounding tissue.
Medical. Long-term medical therapy is directed primarily at prevention of recurrence and is dictated by the composition of the stone.42 The most common combination of findings in the metabolic workup is idiopathic hypercalciuria, elevated urinary uric acid, and low urinary citrate. Patients with this panel are placed on thiazide diuretics, which increase calcium reabsorption at the distal nephron and reduce intestinal absorption, and potassium phosphate, which lowers renal calcium excretion. Potassium alkali salts, which are metabolized and excreted as citrate, may also be used independently.
Infection. Any patient with fever or pyuria in the setting of suspected urolithiasis should be assumed to have a proximal upper tract infection. Nephric abscess and sepsis are potential complications. After obtaining blood and urine cultures, the treating physician should start parenteral antibiotics (ticarcillin/clavulanate or an anti-pseudomonal third-generation cephalosporin is recommended) and obtain urologic consultation for urgent drainage.43
Other Causes of Obstructive Uropathy
Intrinsic Processes. Intrinsic causes of urinary obstruction refer to those disease processes, systemic or local, that arise from the urinary system itself. Intrarenal pathologies include nephrocalcinosis, primarily seen in patients receiving alkylating chemotherapy agents. The disease process relates to the high serum uric acid levels associated with necrosis of some tumors, mainly lymphomas and leukemias. Similar phenomena are seen in patients given high-dose sulfadiazine or acyclovir therapy in the primary treatment of HIV-related illnesses. In multiple myeloma, the accumulation of Bence-Jones proteins can lead to precipitation in the renal tubules resulting in complete obstruction and renal failure. Urgent urologic referral for percutaneous nephrostomy drainage offers the best hope of promoting the recovery of renal function. Nevertheless, the incidence of irreversible renal damage is high among patients with multiple myeloma, and renal failure continues to be the leading cause of death in these patients.1
Papillary necrosis is an acute process seen in a variety of systemic diseases, including sickle cell disease, anti-inflammatory agent overuse, amyloid, pyelonephritis, and diabetes. Necrotic renal papillae slough into the collecting system, where they may easily be mistaken for a radiolucent obstructing stone on IVP. Similarly, in the setting of severe hematuria (hemophilia, polycystic kidney disease), thrombus may obstruct the ureter. Percutaneous drainage may also be tried here, although stenting the ureter is a common therapeutic modality, especially in distal obstruction.
Bladder dysfunction resulting in urinary obstruction is an important source of morbidity for a variety of disease processes and medications. The "neurogenic" bladder associated with diabetes, multiple sclerosis, or Parkinsonism may either be flaccid or spastic, depending on the prevailing etiology. The bladder dysfunction associated with spinal cord lesions similarly depends on the level involved. Lesions above S4 commonly result in a spastic bladder that can be treated without catheterization, whereas low sacral lesions produce a flaccid bladder and lead to dependency on catheter drainage. Anticholinergic medications can cause functional obstruction due to bladder hypotonia, whereas the anti-Parkinsonian drug levodopa results in sphincter spasm through alpha-adrenergic stimulation.
The most common cause of urinary obstruction worldwidethough rare in the United Statesis ureteral and bladder fibrosis from bilharziasis, caused by chronic infection with Schistosoma haematobium. Ten to 40% of the 100 million people with schistosomiasis develop these uropathic complications. Other microbial infections, most prominently tuberculosis, aspergillosis, and candidiasis, may cause physical obstruction of the urinary tract.
Ureteral strictures develop in the setting of radiation therapy for pelvic cancers and are most commonly treated with a simple stent. Urethral strictures arise as a result of urethral trauma, including surgery or chronic infection, such as gonorrhea, and present fairly often to the ED. Urethral strictures resulting in urinary retention can often be treated with simple Foley drainage,but may require more advanced drainage techniques, such as Coude catheter placement or an "over-the-wire" technique using a fine filiform catheter. Filiforms are designed to reduce the incidence of false passage in the male urethra, a common complication of attempted drainage in the setting of urethral stricture.44 If the treating physician is unfamiliar with the use of such devices, and urologic consultation is remote, percutaneous suprapubic drainage is a simple and low-morbidity alternative.45 In the setting of prior suprapubic procedures, however, the percutaneous approach becomes more dangerous, and surgical consultation is advisable.
Extrinsic Processes. Urologic Causes. The most common etiologies of urinary obstruction in the United States relate to compression of the urinary outflow tract by adjacent structures. Of these, benign prostatic hyperplasia (BPH) is the largest single cause. It is estimated that 75% of men over age 70 experience symptoms of outflow obstruction, and, in 1990, over 300,000 men underwent transurethral resection of the prostate (TURP) at an estimated cost of $2.2 billion.46
The classic presentation of BPH includes decreased force of the urinary stream, difficulty initiating the stream, and nocturia. The digital rectal examination (DRE) will reveal an enlarged gland with a firm consistency similar to that of the tip of the nose, although the exam can be unreliable. Objective evidence may include an increased post-void residual. Greater than 100 cc is suggestive of outlet obstruction. In fact, an older man who is unable to void and requires catheter drainage is a well-recognized presentation of BPH to the ED. Transrectal ultrasound (TRUS) has also been used to estimate gland size and stratify patients for therapy, although the great variability in its positive predictive value limits this modality to an ancillary role at present. 47
Therapy for BPH ranges from temporizing measures such as transurethral or suprapubic catheterization, to medical management with alpha-1-adrenergic antagonists and 5-alpha-reductase inhibitors, to more definitive surgical procedures like the TURP or open prostatectomy. The indications and timing of intervention are generally dictated by the patient’s symptom complex. But when the Agency for Health Care Policy and Research (AHCPR) issued its 1994 clinical practice guidelines for the evaluation and treatment of BPH, the vagaries of this approach were somewhat rectified. Relative indications for operative intervention were based, in part, upon a large longitudinal study demonstrating the four factors that most closely correlated with the eventual need for surgery: age of the patient, change in size or force of the urine stream, sensation of incomplete voiding, and enlarged prostate on DRE.48 Incontinence was negatively correlated to the need for subsequent surgery, and hesitancy, still a part of the guidelines, did not survive multivariate analysis as a predictor of surgery.
Absolute indications for surgery, based on the AHCPR guidelines, include refractory urinary retention, recurrent UTIs, recurrent or persistent gross hematuria, bladder stones or evidence of renal failure. Relative indications are based on the degree to which the disease impacts upon the patients’ daily activities.46
The clinical complications of BPH are limited to its effects on renal function, either as a consequence of recurrent infection or direct obstructive nephropathy. The incidence of renal dysfunction in BPH, based on IVP data, is estimated at 5-15%. However, more sensitive nuclear medicine testing demonstrates reduced glomerular filtration rates in as many as 54% of patients.15 In the ED, evidence of outlet obstruction should be addressed with urgent drainage via transurethral or suprapubic catheter. Assuming no acute renal failure, the patient may be referred with a leg bag to a urologist for outpatient evaluation.
A major concern in the setting of bladder obstruction in a male patient is the possibility of carcinoma of the prostate, second only to lung cancer as a cause of cancer death in American men. This diagnosis should be suspected when DRE reveals a hard nodule or asymmetric prostate. Definitive evaluation involves a needle biopsy. The use of the prostate-specific antigen assay as a screening device is best left to the discretion of the treating physician.47 Bladder cancer also may cause obstruction and should be suspected in the setting of obstructive uropathy associated with constitutional symptoms.
Gynecologic and Obstetric Causes. The only malignancy more likely than bladder cancer to cause urinary obstruction is cervical cancer.15 Due to the anatomic proximity to the bladder neck, obstruction will complicate about 30% of cases of cervical cancer. It is a serious complication associated with shortened median survival and reduced five-year survival rates in all pelvic cancers.49 Patients likely to benefit from urinary diversion are those for whom further treatment options for the malignancy exist. Other groups fare more poorly because the diversion procedures carry significant morbidity and do not themselves prolong life, even in acute renal failure.50 Clearly, emergent referral is useful in this setting, allowing the specialist the widest window in which to consult with the patient facing a difficult decision.
Uterine fibroid tumors, particularly in the cervical distribution or large posterior fibroids in the retroflexed uterus, may cause bladder neck obstruction. Endometriosis may also cause obstruction and represents a true diagnostic challenge. By contrast, uterine prolapse and subsequent compression of the ureters by the uterine vascular supply is rarely a subtle presentation. Lastly, more than 50% of postoperative cases of inadvertent ureteral injury result from gynecologic surgery.1
Hydronephrosis and hydroureter are common during pregnancy and should not be considered pathologic. These usually occur around the 20th week and affect two-thirds of patients.1 Although the pathophysiology has classically been attributed to direct compression by the uterus, some authors propose that the smooth-muscle-relaxant effect of progesterone better explains the timing of the phenomenon, which is relatively early in the ascent of the fundus. Regardless of the mechanism, the importance of the finding is that it can mask pathological obstruction of another cause. Thus, recurrent urinary tract complaints in the pregnant patient must be viewed with special attentiveness to obstructive nephropathy. Ultrasound indices to account for acceptable degrees of obstruction have been well-described.
The pregnant patient who complains of sudden-onset abdominal pain and oliguria should raise the suspicion for incarcerated uterus. This occurs at about week 12, as the gravid uterus outgrows the pelvis. The anatomically retroflexed uterus may become "wedged" within the pelvis and compress anteriorly on the bladder neck. Generally, bimanual reduction by the obstetrician is effective.
Miscellaneous Causes. There are numerous other causes of obstructive uropathy extrinsic to the urinary tract. Of particular interest to the emergency physician are:
• Pelvic fractures and hematoma, compressing the ureter;51,52
• Retroperitoneal fibrosis involving the ureter, associated with a wide variety of conditions, including abdominal aortic aneurysm, scarring from appendiceal or diverticular abscess, gonorrhea, and Henoch-Schönlein purpura;
• Congenital abnormalities, such as congenital ureteropelvic junction obstruction; a hyperplastic condition; ureteral folds, valves, and strictures; and posterior urethral valves in boys.
The degree to which the kidney tolerates obstruction depends first upon whether the insult is unilateral or bilateral and then upon the degree and the duration of obstruction. In no case is the science of obstructive uropathy conclusive, and many mysteries remain.
The pathophysiology of unilateral obstruction is discussed above, and the mechanisms of bilateral disease appear to be similar. Although injury appears to be slower in onset, the consequences of bilateral obstruction (i.e., post-renal azotemia and renal failure) are much more severe.15 In many cases, the clinician can undertake a temporizing procedure in the ED and relieve the obstruction. Sometimes, however, as with a pelvic mass compressing both ureters, bladder catheterization is not helpful, and emergent consultation is indicated. Timely treatment is paramount, however, because the duration of obstructionas with urolithiasisis inversely related to the degree of renal recovery.53
If temporizing measures are undertaken in the ED, the clinician must be aware of the risk of post-obstructive diuresis. This phenomenon occurs in the relief of longstanding bilateral obstruction, and probably relates to abnormal salt retention. Onset may be immediate or delayed for several hours; output ranges between 8 and 20 L per day. Treatment involves close monitoring of vital signs, urine output, and electrolytes. Since the output has a sodium concentration of approximately 80 mEq/L, replacement with half-normal saline is recommended until the syndrome subsides, usually within a week.15
Obstructive uropathy is most commonly associated with calculus disease. The chief priorities in approaching the patient with renal colic are pain control, ruling-out infection, and establishing the correct diagnosis. Pain control is best achieved with parenteral NSAIDs, although narcotics are also acceptable. Infection should also be suspected in patients with fever or pyuria, and this constitutes a true emergency in the presence of obstruction. Once infection has been excluded, the ultimate diagnosis can be confirmed either in the ED or as an outpatient. The best diagnostic study is non-contrast CT, although IVP and ultrasound are widely used as well. Patients with suspected obstructive stones should be seen well before one week lapses. Although no human data exist, it is believed that the uninfected kidney can tolerate at least one week of complete obstruction without irreversible damage, requiring that these patients receive expedited follow-up. Other causes of urinary tract obstruction are numerous, but prostatic hypertrophy and cancer should be prominent in the clinician’s mind.
References
1. Curhan GC, Zeidel ML. Urinary tract obstruction. In: Brenner BM, ed. The Kidney. 5th ed. Philadelphia: WB Saunders; 1996:1936-1958.
2. Sierakowski R, Finlayson B, Landes RR, et al. The frequency of urolithiasis in hospital discharge diagnoses in the United States. Invest Urol 1978;16:438-441.
3. Ljunghall S, Fellstrom B, Johansson G. Prevention of renal stones by a high fluid intake? Eur Urol 1988;14:381-385.
4. Wilson DM. Clinical and laboratory approaches for evaluation of urolithiasis. J Urol 1989;141:770-774.
5. Stewart C. Urolithiasis. Emerg Med Clin North Am 1988;6:617-630.
6. Coe FL, Parks JH, Asplin JR. The pathogenesis and treatment of kidney stones. N Engl J Med 1992;327:1141-1152.
7. Levy FL, Adams-Huet B, Pak CYC. Ambulatory evaluation of urolithiasis: An update of a 1980 protocol. Am J Med 1995;98:50-59.
8. Preminger GM. The metabolic evaluation of patients with recurrent urolithiasis: A review of comprehensive and simplified approaches. J Urol 1989;141:760-763.
9. Curhan GC, Willett WC, Rimm EB, et al. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993;328:833-838.
10. Yendt ER, Cohanim M. Clinical and laboratory approaches for evaluation of urolithiasis. J Urol 1989;141:764-769.
11. Kerr WS. Effects of complete ureteral obstruction in dogs on kidney function. Am J Physiol 1956;521-526.
12. Widén T. Restitution of kidney function after induced urinary stasis of varying duration. Acta Chir Scand 1957;113:507-510.
13. Vaughan ED, Jr, Gillenwalter JY. Recovery following complete chronic unilateral ureteral occlusion: Functional, radiographic and pathologic alterations. J Urol 1971;106:27-34.
14. Shapiro SR, Bennett AH. Recovery of renal function after prolonged unilateral ureteral obstruction. J Urol 1976;115:136-140.
15. Yarger WE. Urinary tract obstruction. In: Brenner BM, Rector F, ed. The Kidney. 4th ed. Philadelphia: WB Saunders; 1991:1768-1808.
16. Diamond JR. Macrophages and progressive renal disease in experimental hydronephrosis. Am J Kid Dis 1995;26:133-140.
17. Elton TJ, Roth CS, Berquist TH, et al. A clinical prediction rule for the diagnosis of ureteral calculi in emergency departments. J Gen Intern Med 1993;8:57-62.
18. Jenkins AD. Calculus formation. In: Gillenwalter J, et al, eds. Adult and Pediatric Urology. 3rd ed. St. Louis: Mosby-Year Book; 1996:461-486.
19. Coe FL, Keck J, Norton ER. The natural history of calcium urolithiasis. JAMA 1977;238:1519-1523.
20. Roth CS, Bowyer BA, Berquist TH. Utility of the plain abdominal radiograph for diagnosing ureteral calculi. Ann Emerg Med 1985;14:311-315.
21. Zangerle KF, Iserson KV, Bjelland JC. Usefulness of abdominal flat plate radiographs in patients with suspected ureteral calculi. Ann Emerg Med 1985;14:316-319.
22. Mutgi A, Williams JW, Nettleman M. Renal colic: Utility of the plain abdominal Roentgenogram. Arch Intern Med 1991;151:1589-1592.
23. Haddad MC, Sharif HS, Shahed MS, et al. Renal colic: Diagnosis and outcome. Radiology 1992;184:83-88.
24. LeRoy AJ. Diagnosis and treatment of urolithiasis: Current perspectives. Am J Roentgenol 1994;163:1309-1313.
25. Pollack HM, Banner MP. Current status of excretory urography: A premature epitaph. Urol Clin North Am 1985;12:585-601.
26. Haddad MC, Sharif HS, Abomelha MS, et al. Management of renal colic: Redefining the role of the urogram. Radiology 1992;184:35-36.
27. Vritska TJ, Hattery RR, King BF, et al. Role of ultrasound in medical management of patients with renal stone disease. Urol Radiol 1992;14:131-138.
28. Sommer FG, Jeffrey RB, Jr, Rubin GD, et al. Detection of ureteral calculi in patients with suspected renal colic: Value of reformatted noncontrast helical CT. Am J Roentgenol 1995;165:509-513.
29. Spital A, Valvo JR, Segal AJ. Nondilated obstructive uropathy. Urology 1988;31:478-482.
30. Spital A, Spataro R. Nondilated obstructive uropathy due to a ureteral calculus. Am J Med 1995;98:509-511.
31. Burge H, Middleton WD, McClennan BL, et al. Ureteral jets in healthy subjects and in patients with unilateral ureteral calculi: Comparison with color Doppler US. Radiology 1991;180:437-442.
32. Smith RC, Rosenfeld AT, Choe KA, et al. Acute flank pain: Comparison of non-contrast-enhanced CT and intravenous urography. Radiology 1995;194:789-794.
33. Borghi L, Meschi T, Amato F, et al. Nifedipine and methylprednisolone in facilitating ureteral stone passage: A randomized, double-blind, placebo-controlled study. J Urol 1994;152:1095-1098.
34. Morse RM, Resnick MI. Ureteral calculi: Natural history and treatment in an era of advanced technology. J Urol 1991;145:263-265.
35. Wrenn K. Emergency intravenous pyelography in the setting of possible renal colic: Is it indicated? Ann Emerg Med 1995;26:304-307.
36. Oosterlinck W, Philips NH, Charig C, et al. A double-blind single-dose comparison of intramuscular ketorolac tromethamine and pethidine in the treatment of renal colic. J Clin Pharmacol 1990;30:336-341.
37. Larsen LS, Miller A, Allegra JR. The use of intravenous ketorolac for the treatment of renal colic in the emergency department. Am J Emerg Med 1993;11:197-199.
38. Cordell WH, Larson TA, Lingeman JE, et al. Indomethacin suppositories versus intravenously titrated morphine for the treatment of ureteral colic. Ann Emerg Med 1994;23:262-269.
39. Pak CYC, Sakhee K, Crowther C, et al. Evidence justifying a high fluid intake in treatment of urolithiasis. Ann Intern Med 1980;93:36-39.
40. McCormack M, Dessureault J, Guitard M. The urine specific gravity dipstick: A useful tool to increase fluid intake in stone forming patients. J Urol 1991;146:1475-1477.
41. O’Brien WM, Rotolo JE, Pahira JJ. New approaches in the treatment of renal calculi. Am Fam Physician 1987:36:181-194.
42. Preminger GM. Renal calculi: Pathogenesis, diagnosis and medical therapy. Sem Nephrol 1992;12:200-216.
43. Sanford JP, Gilbert DN, Sande MA. The Sanford Guide to Antimicrobial Therapy. 26th ed. Dallas: Antimicrobial Therapy, Inc; 1996:23.
44. Heyman AM, Kogler P, Vogel M, et al. Slipover urethral instrument system. J Urol 1982;128:759.
45. Zbaraschuk I, Berger RE, Hedges JR. Genitourinary procedures. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Emergency Medicine, 2nd ed. Philadelphia: WB Saunders; 1991:867-889.
46. Jacobsen SJ, Girman CJ, Guess HA, et al. New diagnostic and treatment guidelines for benign prostatic hyperplasia: Potential impact in the United States. Arch Intern Med 1995;155:477-481.
47. Hostetler RM, Mandel IG, Marshburn J. Prostate cancer screening. Med Clin North Am 1996;80:83-98.
48. Arrighi HM, Guess HA, Metter, EJ, et al. Symptoms and signs of prostatism as risk factors for prostatectomy. Prostate 1990;16:253-261.
49. Lau MWM, Temperley DE, Mehta S, et al. Urinary tract obstruction and nephrostomy drainage in pelvic malignant disease. Br J Urol 1995;76:565-569.
50. Harrington KJ, Pandha HS, Kelley SA, et al. Palliation of obstructive nephropathy due to malignancy. Br J Urol 1995;76:101-107.
51. Flint P, Allen CF. Pelvic fracture complicated by bilateral ureteral obstruction: Case report. J Trauma 1994;36:285-287.
52. Kluger Y, Altman GT, Deshmukh R, et al. Acute obstructive uropathy secondary to pelvic hematoma compressing the bladder: Report of two cases. J Trauma 1993;35:477-478.
53. Thadhani R, Pascual M, Bonventre JV. Acute renal failure. N Engl J Med 1996;334:1448-1460.
Physician CME Questions
9. A high urinary pH in a patient with renal colic should alert the physician to:
A. the presence of renal tubular acidosis.
B. a higher risk of infection.
C. laboratory error necessitating repeat lab tests.
10. The smallest caliber of the urinary outflow tract can be found at:
A. the ureteropelvic junction.
B. the ureterovesicular junction.
C. the abdominal spindle.
11. All of the following are correct regarding imaging in renal colic except:
A. Non-contrast helical CT of the abdomen is more sensitive than IVP in calculus disease and is equally specific.
B. KUB can reliably and cost-effectively be used to screen for patients who may require IVP.
C. No role has yet been established for MRI in renal colic.
D. Imaging in the ED may be indicated if the clinical diagnosis is in doubt, if prognostic information is desired, or to avoid inappropriate referral.
12. The factor most predictive of renal injury in unilateral obstruction is:
A. duration of obstruction greater than one week.
B. location of the obstruction at the ureteropelvic junction.
C. presence of a "staghorn" calculus.
D. presence of a lymphocytic infiltration in the renal parenchyma.
13. All of the following are true regarding the diagnosis of ureteral calculi except:
A. radiations of the pain to the groin is seen in 70% of patients.
B. hematuria is not part of the classic triad.
C. calcium-containing stones and cystine stones may be associated with a positive family history.
D. leukocytosis may be present in the absence of infection.
14. Regarding the use of KUB in patients with urolithiasis:
A. KUB increases the sensitivity of ultrasound.
B. KUB has no role in following a stone expectantly.
C. the negative predictive value is very high.
D. A negative KUB obviates the need for IVP.
15. All of the following factors may contribute to kidney stone formation except:
A. a family history of stone disease.
B. a diet high in calcium.
C. a diet high in oxalate.
16. Non-steroidal anti-inflammatory agents:
A. have no role in treating the pain of renal colic
B. are effective pain relievers due to their prostaglandin effects.
C. should never be used in conjunction with narcotics.
D. may relieve urinary tract spasm in patients with renal colic.
You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
- Award-winning Medical Content
- Latest Advances & Development in Medicine
- Unbiased Content