Review
RenalColic: Emergency Evaluation and Management JASON C. ABBER,
MD, JACK W. McANINCH,
Renal colic, the excruciating pain caused by an acute obstruction of the ureter (usually from a urinary calculus), is one of the most common urological problems encountered in the emergency department. This is especially true in the southwest, northwest, and southeast United States where urolithiasis is more common.i*2 The peak incidence of urinary stones occurs during the months of July, August and September, immediately following the periods when mean temperatures are highest.3q4 A national study revealed that 7.1 of every 1,000 general hospital admissions (and up to 15.0 in the southeast) were for urinary calculi.2 However, most patients with symptomatic urolithiasis do not require hospital admission for treatment. The symptomatic complex from a ureteral stone is unequivocal, and in the majority of cases the clinical diagnosis is straightforward. As a result, most journal articles and some urological textbooks deal only briefly with the acute management of renal colic, while delving more deeply into the metabolic and pharmacological aspects of diagnosing and treating urolithiasis. In this article, we review the characteristics of renal colic, explain when and what radiographic studies are necessary, discuss emergency department treatment of calculi, enumerate the indications for hospital admission, and outline the instructions a patient with renal colic should receive on discharge from the emergency department. Table 1 summarizes the evaluation and management of renal colic. PATHOPHYSIOLOGY The onset of renal colic is abrupt and frequently occurs in the middle of the night or early in the From the Department of Urology, University of California School of Medicine and San Francisco General Hospital, San Francisco, California. Manuscript received October 11, 1983; revision 28, 1984; revision accepted May 2, 1984.
received
Address reprint requests to Dr. McAninch: Urology, versity of California, San Francisco, CA 94143. Key Words: emergency, excretory teral obstruction, urolithiasis. 56
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ure-
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morning while the patient is sedentary. The pain is sharp and severe, with paroxysms lasting several minutes. There are two mechanisms responsible for renal colic: complete or partial urinary obstruction leading to increased renal capsular pressure, which causes a constant flank ache; and hyperperistalsis of smooth muscle in the ureter, pelvis, and calyces, which accounts for the sharp radiating pain. Mere passage of the urinary stone without obstruction does not cause renal colic. There are five regions of narrowing in the urinary system where a stone is most likely to become impacted: in a renal calyx; at the ureteropelvic junction; at the point where the ureter crosses over the iliac vessels at the pelvic brim; in the posterior pelvis in female patients, where the ureter is crossed anteriorly by the pelvic vessels and broad ligament; and the ureterovesical junction (the most constricted region). A calculus in the upper urinary tract (above the fourth lumbar vertebral body) produces excruciating flank pain that courses laterally around the abdomen and usually radiates to the ipsilateral testicle or labia majora. The autonomic nerve fibers that serve both the kidney and genital region account for this radiation of pain. These fibers originate very near where the renal artery branches off the aorta: some then travel down the gonadal artery to the site of referred pain. An obstruction at mid-ureter usually causes pain at the lateral flank and abdomen, where the local irritation is greatest. If ureteral impaction occurs in the distal ureter, severe renal colic is produced with radiation to the scrotum or vulva, and urinary urgency with dysuria is often reported (Fig. I). Because the celiac ganglion supplies the kidneys, stomach, and small intestine, gastrointestinal symptoms frequently accompany renal colic. Nearly 50% of patients with renal colic experience nausea and vomiting, which may even, on occasion, be the presenting complaint.5 Furthermore, abdominal distention from a paralytic ileus is not unusual. Backache related to local ureteral irritation is a common symptom (in about a third of cases). Gross hematuria is also reported in approximately a third of
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the cases of ureteral stones5 and frequently precedes or accompanies the pain. The differential diagnosis of gross hematuria should include trauma, hematological abnormalities, urinary tract infection, tumor, and tuberculosis. PHYSICAL SIGNS Restlessness and “continuous moving about” are characteristic of a patient with renal colic. The pain does not allow the patient to be comfortable in any position. A temperature above 100°F is rare unless there is superimposed kidney infection. The pulse rate and blood pressure are generally normal or mildly elevated because of anxiety. The skin may be cold and clammy, as in mild shock, because of the pain induced by alpha-adrenergic stimulation. The abdomen is generally moderately tender on deep palpation over the location of the calculus. In cases where prolonged ureteral impaction causes inflammatory changes and peritoneal irritation, rebound tenderness may be present. Bowel sounds are often absent or decreased because of a paralytic ileus. One can expect to palpate marked tenderness at the costovertebral angle and flank. Spasms of the abdominal and back muscles on the affected side are not unusual. URINALYSIS AND BLOOD TESTS Urinalysis is very relevant to the evaluation of a patient with renal colic. Although gross or microscopic hematuria is common, the blood loss is rarely sufficient to cause a decrease in hematocrit value. In up to 25% of the patients with ureteral calculi, neither gross nor microscopic hematuria is observed.6 This is especially true if the calculus has caused complete obstruction . A small to moderate number of leukocytes in the urine is not unusual in patients with stones, even in patients without infected urine. However, if there are more than ten to 12 leukocytes per high-power microscopic field, the examining physician should be alerted to the possibility of a urinary infection proximal to urinary obstruction; a urine specimen should be sent to the laboratory for culture and sensitivity testing. Urinary pH can be significant and should be noted. Cystine and uric-acid calculi usually occur in an acidic urine. Alkaline urine @H > 8.0) suggests infection stones from urea-splitting organisms that include Proteus, Pseudomonas and Klebsiella species. A careful microscopic urinary analysis may demonstrate crystals indicating the nature of the stone (Fig. 2). “Maltese cross” calcium oxalate crystals or long, thin, rectangular calcium phosphate crystals strongly suggest calcium stone formation. Uric acid crystals appear as small broken panes of glass, whereas triple
TABLE 1.
Renal Colic:
& McANlNCH
Evaluation
n RENAL COLIC
and Management
Symptoms Upper urinary tract obstruction-excruciating flank pain with radiation to the ipsilateral testicle or labia majora Mid-ureter obstruction-flank pain with lower quadrant abdominal pain Ureterovesical junction obstruction-flank pain with radiation to scrotum or vulva; urinary urgency Associated symptoms-nausea and vomiting, gross hematuria, backache Physical Signs General-restlessness and concomitant irritation Vital signs-fever rare unless infection is present; pulse and blood pressure normal or mildly elevated Abdominal examination-absent or decreased bowel sounds; moderate tenderness over site of ureteral obstruction; occasional rebound tenderness Back-marked costovertebral tenderness; muscle spasm Laboratory Tests Urinalysis necessary-pH helpful; gross or microscopic hematuria usual finding Less than 10 WBCs per high power field-not uncommon More than 10 WBCs per high power field-obtain urine culture and sensitivity Routine blood tests not necessary unless a hospital admission is expected Differential Diagnosis intrinsic ureteral obstruction-tumor, blood clot, papillary necrosis, congenital ureteropelvic junction narrowing Extrinsic ureteral obstruction-carcinomatous lymph node Nonurinary causes of pain-acute appendicitis, cholecystitis, gastroenteritis, small bowel obstruction, abdominal aortic aneurysm Radiographic Tests Plain film (KUB)-recommended IVP-should be done if infection is in doubt
(oblique films optional) is suspected or if diagnosis
Early Management and Treatment Morphine (lo-15 mg) or meperidine cularly Hydroxyzine (50 mg) or promethazine for nausea and vomiting
(75-150
mg) intramus-
(25 mg) intramuscularly
Indications for Admission Protracted vomiting Intractable pain Evidence of infectious process proximal to urinary obstruction (Relative indications-solitary kidney, stone size >5 mm, and decreased renal function) Emergency Department Discharge Instructions Strain all voided urine (in emergency department as well) Pain medicine as needed Follow-up by a urologist within 24 hours Return to emergency department if fever develops
phosphate crystals composing infection stones may look like low, flat-topped pyramids. Routine blood tests in the emergency department are usually neither helpful nor necessary for the acute management of renal colic. One would expect the leukocyte count to be mildly to moderately elevated 57
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Flank paln
Veshcal irrltablllty
FIGURE 1. Radiation of pain with various types of ureteral stones. Lefr, ureteropelvic stone. Severe costovertebral angle pain results from capsular and pelvic distention; acute renal and ureteral pain results from hyperperistalsis of smooth muscle of calyces. pelvis, and ureter, with pain radiating along the course of the ureter (and into the testicle. as the nerve supply to the kidney and testis is the same). The testis is hypersensitive. Middle, midureteral stone causes the same symptoms as with ureteropelvic stone. but with more pain in the lower abdominal quadrant. Righf. low ureteral stone, again causing the same symptoms. with pain radiating into bladder. vulva, or scrotum. The scrotal wall is hyperesthetic. and testicular sensitivity is absent. When the stone approaches the bladder. urgency. frequency. and burning on urination result from inflammation of the bladder wall around the ureteral orifice. (From Smith DR. Urinary stones. In Smith DR [ed]. General Urology, 10th edition. Los Altos. California: Lange Medical Publications, 1981:~ 234).
(lO,OOO- 16,000/mm3) because of the demargination associated with extreme stress. Furthermore, if the patient has vomited repeatedly, a state of dehydration may artificially increase the leukocyte count. In patients with a fever, the leukocyte count may be more significant, especially if the differential leukocyte count indicates a systemic infection. This would suggest pyelonephritis or another severe intra-abdominal infection (for example, inflamed or ruptured appendix). For septic patients, a urine culture must be done, as well as other tests to be discussed later, as a kidney infection proximal to an obstructing calculus requires an emergency operation. Blood urea nitrogen (BUN) and serum creatinine levels, as well as metabolic screening tests, are rarely important in the acute management of renal colic and need not be ordered in uncomplicated cases. DIFFERENTIAL DIAGNOSIS Renal colic is usually caused by a stone obstructing urinary drainage; however, the signs and symptoms observed can also be those of functional or anatomical ureteral obstruction secondary to pathological conditions other than urolithiasis. Large abdominal aortic aneurysm in an elderly patient, acute appendicitis, and 58
small bowel obstruction are nonurinary causes of colic-like pain that should always be considered, as they require prompt surgical evaluation. Other nonurinary causes of pain that may be confused with renal colic include cholecystitis, acute pancreatitis, and gastroenteritis. Clinical acumen and a complete diagnostic work-up will distinguish these processes from urolithiasis. A tumor or blood clot in the kidney or ureter may mimic the symptoms of an acutely obstructing stone. Papillary necrosis caused by analgesic abuse, or as a complication of diabetes mellitus or sickle cell anemia,7 may also cause renal colic. Congenital narrowing at the ureteropelvic junction can produce periodic hydronephrosis and renal colic. These symptoms frequently follow a marked diuresis such as that occurring after excessive fluid consumption. Finally, extra-ureteral compression, from a carcinomatous lymph node for instance, may also create severe recurrent pain, which may be confused with the symptoms of urinary stone. Appropriate questions about the patient’s medical history may provide further clues in establishing the diagnosis of urolithiasis. At least 67% of patients with urinary stones develop recurrent calculi.8 Thus, a previous diagnosis of calculi or a history of “passing
ABBER 8 McANlNCH n RENAL COLIC
Tyrosine needles
ACID
Leucine
spheres
REACTION
.:,_. .r:_<;;_ I
A&wphous
3
+&
J
Am&&ium
phosphate
-s
$ urate _ & 1 crysfals _I
ALKALINE
REACTION
FIGURE 2. Identification of urinary crystals indicating the nature of a calculus. Crystals precipitate out of solution in distinct pH environments. (Smith DR. Uroloe;ic laboratory examination. In Smith DR [ed]. General Urology, 10th edition. Los Altos, California: Lange Medical Publications, 1981:~ 45.) -
gravel” in the urine is important. It should be determined whether the renal colic was preceded by dehydration, inasmuch as urinary calculi are more likely to develop in concentrated urine.9 Finally, a family history of urolithiasis is helpful as a genetic predisposition has been demonstrated. 1o.11 RADIOLOGICALCONSIDERATIONS Urography is the method of choice to verify the presence of a urinary stone. With the exception of uric acid and xanthine stones, urinary calculi are of high density, and 90-95% of all stones are radiopaque.‘2 A supine, plain radiograph including the kidneys, ureter, and bladder (KUB) should routinely be obtained for all patients with renal colic. An opaque calculus must be at least 2 mm in its longest dimension to be visualized on a good quality radiograph.‘* If a calculus is suspected on KUB radiographic examination, oblique films and an intravenous pyelogram (IVP) will frequently be helpful in verifying the presence and location of a stone. Familiarity with the anatomy of the urinary tract is necessary in stone localization on a KUB film. The ureters generally lie along the transverse processes of
the lumbar vertebrae and then turn somewhat laterally as they cross over the pelvic brim into the true pelvis (Fig. 3). Larger calculi (longest diameter > 1 cm) tend to obstruct the upper or mid-ureter. Small calculi (longest diameter < 0.5 cm) most commonly impact in the distal third of the ureter. Sandegard’st3 study of 541 cases of ureteral stones indicated that fewer than 1% of the large stones (width > 6 mm) in the upper half of the ureter passed spontaneously; in contradistinction, 93% of the small stones (width < 4 mm) in the lower half and 81% in the upper half of the ureter passed spontaneously. A careful review of the radiographs, along with full consideration of the clinical data, should allow a reasonably high percentage of ureteral stones to be located (Fig. 4). Carstensen and Hansen’s14 study of 346 cases of stones in the ureter demonstrated that 253 (73%) were visible on plain film of the urinary tract. EXCRETORYUROGRAM An IVP demonstrates the ureters, bladder, and urethra along with the renal parenchyma and pelvicalyteal system. It is the most reliable method to confirm both the presence and the degree of an obstruction in 59
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FIGURE 3. A normal retrograde pyelogram and cystogram that illustrate the usual course of the ureters where one would find symptomatic calculi.
the urinary system. The question of when to obtain an emergency IVP is frequently controversial. The emergency department physician must obtain an IVP if renal infection is suspected proximal to an obstruction, as emergency drainage (by ureteral catheterization or percutaneous nephrostomy)t5,“j is required to relieve the obstruction. As mentioned earlier, a temperature greater than 100°F (37.8”(Z), leukocytosis with many immature polymorphs, and marked pyuria and bacteriuria are all important clues that may indicate an obstructing stone. Many urologists would recommend parenteral antibiotics before the IVP if this situation is suspected, as the increased pressure in the renal collecting system from the contrast diuresis may cause extravasation of infected urine into the perinephric tissues. When the diagnosis of urolithiasis is in doubt or if renal colic is severe enough to necessitate hospitalization, an IVP should also be performed on an emergency basis. A patient with a solitary kidney and pos60
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sible obstruction also requires an emergency IVP. Other possible candidates include the unreliable patient or one whose socioeconomic status or distance from the hospital would prevent him or her from obtaining an IVP within 24 hours. If more than one day passes after the attack of renal colic, findings on pyelography will be negative in more than 50% of patients.t7 With the exception of the cases mentioned above, an IVP to assess renal colic need not be done on an emergency basis, provided that it can be obtained within 24 hours. This gives time to perform a bowel preparation and to schedule the IVP during regular working hours, both of which contribute to an examination of optimal quality. Before ordering an IVP for a patient with renal colic, some thought should be given to the possible risks associated with injection of contrast medium. Idiosyncratic allergic reactions and renal toxicity both warrant discussion. Approximately 8% of patients experience a mild transient reaction characterized by mild urticaria, nausea and vomiting, arm pain, or a flushing sensation. About one in 2,000 patients experiences a moderate reaction to contrast materials, including marked urticaria, sneezing, prolonged nausea and vomiting, and headache.18 Approximately one in 14,000 patients will develop a serious reaction requiring cardiopulmonary resuscitation. Finally, despite all measures taken, about one in 40,000 patients will die from causes directly attributable to the administration of contrast material. 19.*0 An increased risk of acute oliguric renal failure after intravenous contrast injection exists for patients with multiple myeloma,21 as well as those with diabetes mellitus accompanied by some degree of renal insufficiency.22*23 Dehydration appears to be the main predisposing factor to acute oliguric renal failure in these patients. Individuals with elevated serum uric acid or hyperuricosuria may also be at increased risk for developing renal failure following injection of contrast material,t8 and in these patients dehydration is also a predisposing factor in the development of renal failure. In this high-risk group, fluids should be allowed ad libitum before the IVP to ensure satisfactory hydration. Although the possibility of a history of renal insufficiency should be elicited before an IVP, screening BUN and serum creatinine are not necessary in the emergency department unless anuria accompanies renal colic. Decreased renal function or renal failure alone has not been shown to increase the patient’s risk of developing renal failure.24*25 If the emergency department physician is concerned that the patient is at risk for developing acute renal failure, he should empirically encourage hydration. Although dehydration is usually recommended by radiologists to improve the
ABBER
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FIGURE 4. Plain abdominal films demonstrating urinary stones. A (above, lefr), left ureteropelvic junction (notice pelvic phleboliths); B (above, righr), left mid-ureter overlying a lumbar spine transverse process; C (right), left lower ureter.
quality of imaging of an IVP, the improvement is only slight.*‘j It is certainly not warranted in patients at risk for developing renal failure. In patients who report a severe reaction to previous injection of contrast medium, periprocedural hydro-
cortisone may be given before IVP, or a retrograde pyelogram can be used to demonstrate ureteral obstruction. Ultrasonography of the urinary tract27 and radioisotope renography are alternative methods for detecting gross hydronephrosis and ureteral obstruc61
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tion in patients who are at significant risk from intravenous contrast medium. EARLY MANAGEMENT AND TREATMENT Adequate pain relief should be of high priority when patients present to the emergency department with severe renal colic. Intramuscular injections of naloxonereversible narcotics such as morphine (lo-15 mg) or meperidine (75-150 mg) usually are effective. Narcotics may be administered intravenously in smaller doses and will provide faster pain relief. In many cases there is no recurrence of colic after the initial relief of pain. However, multiple analgesic doses should be given as necessary to control persistent discomfort. To control narcotic-induced or exacerbated nausea and vomiting, hydroxyzine (50 mg) or promethazine (25 mg) can be administered intramuscularly every four to six hours. A second benefit is the potentiation of the analgesic effects of the narcotics. The use of the antispasmodic medications atropine and methantheline bromide (Banthinea) along with narcotics has not been shown to be effective. Furthermore, those medications subject the patient to unpleasant side effects (decreased salivary secretions, blurred vision, etc.) associated with anticholinergic drugs. Fluid management for patients with acute renal colic from partial or complete ureteral obstruction is controversial. It is thought that increasing fluid intake produces a diuresis that mechanically flushes out the stone and may also decrease the peristalsis contributing to urinary colic.8 However, if the urinary system is totally obstructed, excessive fluid administration may increase flank pain and hydronephrosis, leading to rupture of the renal fornices or possible renal damage. We do not recommend hydration beyond maintenance requirements in euvolemic patients while renal colic persists. If the patient has had severe nausea and emesis, intravenous fluid replacement will be necessary. INDICATIONS FOR HOSPITALIZATION In most cases, renal colic can be managed in the emergency department, and the patient can be instructed and sent home. However, there are times when a patient with renal colic must be admitted to the hospital. Indications include: 1) protracted vomiting; 2) intractable pain; or 3) evidence of a renal infection behind the obstruction. The need to admit a patient to the hospital is defined by the patient’s having extraordinary renal colic. An IVP should be performed, as well as a complete blood count with differential leukocyte count, serum electrolytes, 62
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BUN, creatinine and uric acid, calcium, and phosphate levels. Relative indications for hospitalization, which may be considered on an individual basis, include the socio-economic status and occupation of the patient, an obstructed solitary kidney, stone size >5 mm, and decreased renal function. INSTRUCTIONS FOR HOME CARE When the patient is discharged from the emergency department, he will require analgesic tablets. Usually codeine with aspirin or acetaminophen is adequate. The patient should collect and strain all urine, especially that voided in the emergency department. If an IVP is obtained as part of the evaluation, urine voided in the radiology suite should also be strained. Recovery and analysis of the calculus provides information necessary for a urologist to advise the patient. Although several funnel-like straining devices are marketed. it is probably easier and cheaper to dispense several packages of cotton gauze 4 x 4 dressings (not tissue meshed “Topper” dressings) through which the patient can strain his urine. The patient should be scheduled to see a urologist within the 24 hours following the episode of renal colic for appropriate follow-up. If instructions are given for a pre-IVP bowel preparation on discharge from the emergency department, good hydration should be emphasized, as dehydration predisposes to further crystal precipitation.9 Because of the danger of developing an infection proximal to a ureteral obstruction, the patient should be instructed to return to the emergency department or to a urologist’s office if fever develops. The authors
thank
Dr. Paul Auerbach
for editorial
advice
REFERENCES 1. Burkland CE, Rosenberg M. Survey of urolithiasis in the United States. J Urol 1955;73:198-207. 2. Boyce WH, Strawcutter HE. Incidence of urinary calculi among patients admitted to General Hospitals, 19481952. JAMA 1956;161:1437-1442. 3. Prince CL, Scardino PL. A statistical analysis of ureteral calculi. J Urol 1960;83:561-565. 4. Prince CL, Scardino PL, Wolan TC. The effect of temperature, humidity, and dehydration in the formation of renal calculi. J Urol 1956;75:209-215. 5. Kretschmer HL. Stone in the ureter-Clinical data based on 500 cases. Surg Gynecol Obstet 1942;74:1065-1077. 6. Straffon RA, Higgins CC. Urolithiasis. In Campbell MF, Harrison JH (eds). Campbell’s Urology, 3rd Edition. Philadelphia: WB Saunders, 1970:667-765. 7. Pandya KK, Koshy M, Brown N, et al. Renal papillary necrosis in sickle cell hemoglobinopathies. J Urol 1976;115:497-501. 8. Drach GW. Urinary lithiasis. In Harrison JH, Gittes RF, Perlmutter AD, et al (eds). Campbell’s Urology, 4th Edition. Philadelphia: WB Saunders, 1979:779-878.
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9. Pak CYC, Sakhaee K, Crowther C, et al. Evidence justifying a high fluid intake in treatment of nephrolithiasis. Ann Intern Med 1980;93:36-39. 10. Resnick M, Pridgen DB, Goodman, HO. Genetic predisposition to formation of calcium oxalate renal calculi. N Engl J Med 1968;278:1313-1318. 11. McGeown MG. Heredity in renal stone disease. Clin Sci 1960;19:465-471. 12. Thornbury JR, Parker TW. Ureteral calculi. Semin Roentgenol 1982;17:133-159. 13. Sandegard E. Prognosis of stone in the ureter. Acta Chir Stand (suppl) 1956;219:1-67. 14. Carstensen HE, Hansen TS. Stones in the ureter. Acta Chir Stand (suppl) 1973;433:66-71. 15. Perinetti E, Catalona WJ, Manley CB, et al. Percutaneous nephrostomy: Indications, complications and clinical usefulness. J Urol 1978;120:156-158. 16. Stables DP, Ginsberg NJ, Johnson ML. Percutaneous nephrostomy: A series and review of the literature. Am J Roentgen01 1978;130:75-82. 17. Walsh A. Renal colic. In Kaufman JJ (ed). Current Urologic Therapy. Philadelphia: WB Saunders, 1980. 18. Broderick TW. Contrast material reaction. In Friedland GW, Filly R, Goris ML, et al (eds). Uroradiology, An Integrated Approach, Volume 1. New York: Churchill Livingstone, 1983.
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19. Witten DM, Hirsch FD, Hartman GW. Acute reactions to urographic contrast medium: Incidence, clinical characteristics and relationship to history of hypersensitivity states. Am J Roentgen01 1973;119:832-840. 20. Ansell G. Adverse reactions to contrast agents: Scope of problem. Invest Radio1 1970;5:374-384. 21. Myers GH Jr, Witten DM. Acute renal failure after excretory urography in multiple myeloma. Am J Roentgen01 1971;113:583-588. 22. Bergman LA, Ellison MR, Dunea G. Acute renal failure after drip-infusion pyelography. N Engl J Med 1968;279:1277. 23. Barshay ME, Kaye JH, Goldman R, et al. Acute renal failure in diabetic patients after intravenous infusion pyelography. Clin Nephrol 1973;1:35-39. 24. Grainger RG. Renal toxicity of radiological contrast media. Br Med Bull 1972;28:191-195. 25. Talner LB. Urographic contrast media in uremia: Physiology and pharmacology. Radio1 Clin North Am 1972;10:421432. 26. Benness GT, Evil1 CA. Urographic physiology and contrast materials. In Friedland GW, Filly R, Goris ML, et al (eds). Uroradiology, An Integrated Approach, Volume 1. New York: Churchill Livingstone, 1983. 27. Ellenbogen PH, Scheible FW, Talner LB, et al. Sensitivity of gray scale ultrasound in detecting urinary tract obstruction. Am J Roentgen01 1978;130:731-733.
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