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NEPHROLITHIASIS
GENITOURINARY EMERGENCIES
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NEPHROLITHIASIS David E. Manthey, MD, FACEP, FAAEM, and Joel Teichman, MD, FRCSC
The evaluation and treatment of patients with nephrolithiasis is rapidly changing. New imaging modalities have emerged that have changed the way we evaluate patients with flank pain. Criteria previously used as indication for admission no longer apply, and many of these same patients are now managed as outpatients. This chapter will review the subject of nephrolithiasis as it pertains to emergency medicine physicians. When applicable, evidence-based medicine reviews of certain articles are included. EPIDEMIOLOGY
Approximately 3%-5% of the population will experience nephrolithiasis during their lifetime. Depending on the type of stone, up to 50% of these patients will have a recurrence within 10 years.lg Although several of the disorders that cause nephrolithiasis are hereditary (familial renal tubular acidosis, cystinuria), there has been no conclusive data to date that nephrolithiasis is hereditary. The incidence of stone disease is highest among whites, reportedly twice as high as that of Asians. It is relatively rare in African Americans and Native Americans. Age is an important consideration for stone disease with the peak incidence of stones between ages 20 and 50. It is relatively uncommon in patients less than age 15, and the male-to-female ratio remains about 3:1.19
From the Department of Emergency Medicine, Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina (DEM); and Department of Urology, University of Texas Health Science Center, San Antonio, Texas (JT)
EMERGENCY MEDICINE CLINICS OF NORTH AMERICA
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VOLUME 19 NUMBER 3 * AUGUST 2001
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With respect to geography, the prevalence is higher in Virginia, North Carolina, Georgia, Tennessee and Kentucky.17This does not translate into the Southeast, but does roughly approximate a "stone belt." In addition to geographic location, climate also appears to play a role in stone formation, with the peak months including July, August, and September.24This correlates with a time period that is 1 to 2 months after the maximum mean annual temperature for that assigned area.19 Many theories have been proposed to explain this phenomenon to include increased perspiration causing concentrated urine, increased exposure to sunlight causing increased production of vitamin D3 subsequently increasing urinary calcium excretion, and higher summer intake of oxalate-rich foods such as iced tea and fresh vegetables. Sedentary occupations carry a higher risk for the development of stones. Robertson et a1 showed that affluence and therefore the ability to buy animal protein increases the incidence of stone formation.27The increased consumption of foods with large amounts of calcium (cheese), oxalate (tea, Worcestershire sauce), and purines may also lead to increased stone formation. Water intake is an oft-debated topic within the subject of nephrolithiasis. It is believed that increased intake of water decreases the subsequent incidence of disease in those patients predisposed to nephrolithiasis.8 This relationship may occur because of the decreased dwell time of free crystals within the kidney and dilution of other necessary components for crystallization. It is important to remember that the amount of water ingested should surpass that lost by sweating and breathing, and that it should not contain large amounts of minerals that promote crystallization (sodium carbonate) or low amounts of inhibitory substances ( ~ i n c ) . ~ PATHOPHYSIOLOGY BEHIND STONE FORMATION
Stone formation occurs because of supersaturation of the urine with oxalate and calcium. As the amount of solute put into solution is increased, the solution goes through stages of saturation. When the amount of solute is below the thermodynamic solubility product, it dissolves into the solution (undersaturated). At some point, the addition of more solute will not dissolve into solution (saturated). After this point, the addition of more solute causes crystals to precipitate out of solution (thermodynamic solubility product) because the urine is now supersaturated with the solute. However, the process is more complicated in the urinary tract because more factors are at play. The solvent (urine) is in flux with respect to dwell time, dilution of other solutes, electrical ion interaction, and presence of inhibitory substances (citrate). Urinary supersaturation must occur, either intermittently or continuously, for crystallization to O C C U ~ . ' ~ Even after crystal formation, most individuals do not form stones because other low molecular weight compounds (pyrophosphate) and
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molecules prevent the formation. When these inhibitors are lacking, crystals may aggregate to form a stone. However, these crystals cannot aggregate into a stone large enough to occlude the collecting system as long as there is a free-flow of urine, which would transport crystals harmlessly to the bladder to be voided. This brings us to the last ingredient in the formation of stones. There must be some type of abnormality that allows for retention of these crystals at a rate at which they can form a larger stone. This may be caused by anatomic abnormalities such as medullary sponge kidney, intramedullary stasis, or abnormal tubular epithelium. More often, no anatomic abnormality is present, and crystals grow within the renal tubules or adhere to collecting ducts (Randall's plaques). There are numerous types of stones, but for the purpose of this monograph, only five basic categories will be reviewed. Calcium oxalate, struvite, uric acid, cystine, and miscellaneous causes. Calcium oxalate stones make up almost 80% of all stones. Of these patients, up to 60% have increased urinary calcium levels without elevation of serum calcium 1e~els.l~ Hypercalciuria may be caused by several mechanisms: (1) absorptive, because of increased intestinal absorption of calcium; (2) renal, caused by a primary loss of calcium through the kidney; and (3) resorptive, caused by increased demineralization of bone., Other causes include the subset of calcium oxalate stone-forming patients that have elevated serum calcium (hypercalcemia). Almost all hypercalcemic stone patients will have primary hyperparathyroidism. Other causes include hyperthyroidism and sarcoidosis.26 Hyperoxaluria also predisposes one to the formation of calcium oxalate stones. This occurs because of primary hyperoxaluria (a genetic defect), short bowel syndrome, malabsorption, and increased transport of oxalate by the red blood ~el1s.l~ Struvite stones make up the second most common category of stones, accounting for 2% to 20% of all They are responsible for the majority of staghorn calculi. They are also known as "triple-phosphate" stones because of their makeup of magnesium, ammonium, and phosphate. Struvite stones require two things for their formation-urine pH of 7.2 or above and the presence of ammonia in the urine. Urinary tract infections caused by urease-producing bacteria are the underlying cause of these "infection" stones. Urease splits one mole of urea into two moles of ammonia (NH,). NH, plus H' combine to form NH, (ammonium), and the consumption of H' causes a rise in urine pH. Ammonium is relatively insoluble. Although Proteus is the most common urea-splitting organism, KZebsieZZa, StuphyZococcus species, Providenciu, and Corynebacteriurn species may produce urease as well. Foreign body within the urinary tract and neurogenic bladder are also associated with this type of stone. The symptoms of a patient with struvite stones may follow the classic presentation of pain, hematuria, and fever. However, a significant subset of patients will present only with malaise or weakness. Treatment
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for this type of stone includes removal of the stone and prevention of urinary tract infections. Uric acid stones account for approximately 6% of all stones and occur because of the supersaturation of the urine with uric acid. This occurs because of excess uric acid secretion, excessively acidic urine, and decreased urinary volume. The incidence of uric acid stones in patients with gout is about 1% per year after the first gouty episode. Approximately 20% of the population with gout suffers from uric acid stones. Of note, uric acid stones are the most common radiolucent stone. Hydration, alkalization of the urine, allopurinol to treat gout, and modification of the diet make up the multifaceted treatment of this disease. Cystine stones account for approximately 1% of all stones. They occur only in patients with cystinuria, which is an autosomal recessively inherited genetic disorder. Cystine is less soluble at lower pH, so the goal is to raise the pH of the urine and the intake of substances containing cystine. Pharmacologic agents such as D-penicillamine or alphamercaptoproprionylglycine (MPG or Thiola) may bind cystine and form a urine soluble complex. Miscellaneous stones include dihydroxyadenine, xanthine, silicate, triamterene, indinavir, and silicate stones, among others. These will not be discussed further here. CLINICAL PRESENTATION
Patients with urolithiasis most commonly present to the emergency department (ED) with renal colic. They may also present secondary to infection or complications associated with the treatment of nephrolithiasis. Renal colic presents abruptly as a severe paroxysmal pain on the affected side. It usually does not resolve completely before the next wave of pain begins. This visceral type pain, caused by the distention of the ureter, is secondary to obstruction of the ureter or passage of the stone (or associated blood clot and debris). The paroxysmal component is caused by the peristaltic action of the ureter. The patient with renal colic will usually writhe in pain or move constantly to try to find a position of comfort. In contrast to patients with peritoneal inflammation, they do not lie still. Nausea and vomiting commonly occur with the pain. The location of the pain may give some information about the location of the stone. The pain can occur anywhere from the flank down to the ipsilateral groin. Stones near the kidney produce flank pain. As the stone moves down, the pain radiates around to the front of the abdomen into the lower quadrant. Referred pain often occurs in the ipsilateral groin, testicle, and labia as the stone reaches the ureterovesicular junction (WJ). Stones within the renal calyces may present with dull flank pain and/or hematuria. UVJ and bladder stones may present with hematuria, dysuria, or urgency. These symptoms may mimic a urinary tract infection (UTI). Conversely, a concomitant UTI may mask the presence of a
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UVJ stone. Stones may also move within the ureter without any associated resistance or obstruction causing painless hematuria. HISTORY
The history obtained from the patient with suspected renal colic can be divided into three realms. First, risk factors for the formation of stones should be elicited. These include previous episodes of renal colic, presence of previously asymptomatic renal calyx stone, as well as a family or personal history of any hereditary disorder that can cause nephrolithiasis (familial renal tubular acidosis, cystinuria, and idiopathic hypercalciuria). A history of recurrent or chronic UTIs may put the patient at risk for struvite stones or produce the anatomic abnormality needed for stone formation. Second, the history should delineate if the patient is at risk for complications from urolithiasis. This includes patients with UTIs, solitary functioning kidney, renal transplant, anatomic abnormalities of the renal system, and immunocompromised patients (diabetes, HIV, cancer, steroids, etc). Finally, the history should also help rule out other disease processes that mimic renal colic. These processes will be covered in detail in the section on differential diagnosis. PHYSICAL EXAMINATION
The physical examination of the patient with suspected renal colic confirm the diagnosis and rule out other conditions that mimic renal colic. Starting with the vital signs, the patient frequently has an adrenergic surge associated with pain, including tachycardia, hypertension (relative to the patient’s usual blood pressure), tachypnea, and diaphoresis. The presence of fever is usually not associated with this response and should suggest infection, an important finding since an obstructed, infected kidney requires emergent decompression. Hypotension uncommonly occurs in renal colic as a ”vasovagal” response to pain or after a patient has had prolonged vomiting leading to dehydration. Hypotension, however transient, should prompt an aggressive search for a rupturing abdominal aortic aneurysm or sepsis caused by infection before assuming that it was the result of a vasovagal episode. Flank or costovertebral flank tenderness may be present on the affected side. However, this finding is also associated with pyelonephritis. Mild-to-moderate abdominal tenderness may be present on the ipsilateral side. However, there should be no peritoneal signs such as involuntary guarding or rebound. Coughing, heel tap, or pelvic shake should not increase the pain. Attempt to determine whether the examination increases the pain that the patient is experiencing or simply identifies the area of pain without exacerbating it. Generally, in renal colic, you will be able to identify the area of pain but will not exacerbate it with your exam. Remember that renal colic is hollow viscus pain secondary
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to the dilation of the ureter, not peritonitis. Although pain may be referred to the testicle or labia, the testicle or labia itself should be nontender to palpation and otherwise normal to exam. Pelvic and rectal exams should be unremarkable in renal colic. Recalling that many diseases may mimic renal colic, one must expand the examination to include these organ systems. A cardiovascular exam is required to rule out etiologies for embolic disease. The abdominal examination should evaluate for vascular bruits, pulsatile masses, and symmetry of femoral pulses. The bladder should be examined for tenderness and evidence of retention. The pelvic exam should evaluate for the presence of cervical discharge, cervical motion tenderness, adnexal masses or tenderness, and pregnancy. DIFFERENTIAL DIAGNOSES
Although the differential diagnoses for patients presenting with symptoms consistent with renal colic are listed in List 1, some deserve special mention. It is essential that the physician rule out the presence of the potentially life-threatening diseases.
List 1. Differential Diagnoses
Abdominal aortic aneurysm Renal artery thrombosis/Embolism/Dissection Appendicitis Pyelonephritis Ectopic pregnancy Ovarian torsion Diverticulitis Musculoskeletal pain Peritonitis Ischemic bowel Acute myocardial infarction Bowel obstruction Henoch-Schonlein purpura Renal papillary necrosis Ovarian cyst Endometriosis Psoas abscess or hematoma Retroperitoneal mass Biliary colic Urinary retention Fitz-Hugh Curtis syndrome Sup. Mesenteric A. occlusion Internal hernia Malingering
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The most worrisome mimicker of renal colic is an expanding abdominal aortic aneurysm (AAA).In fact, when an AAA is misdiagnosed, it is most commonly misdiagnosed as renal colic.lSRecall that the peak incidence of stone disease is between ages 20 and 50. Therefore, anyone over the age of 50 presenting with renal colic should be evaluated for the presence of an AAA. Identify the presence of peripheral vascular disease, hypertension, and tobacco use. Evaluate the abdomen for pulsatile mass or abnormal pulses. Actively seek out this diagnosis in patients with any episode of hypotension. A rupturing AAA can cause both ureteral obstruction with hydronephrosis (because of compression) and hematuria (because of ureteral irritation). Renal artery thrombosis or dissection may be very difficult to differentiate from renal colic because it presents with acute onset of pain that is visceral in nature. It causes hematuria as well as nausea and vomiting. The intravenous pyelography (IVP) may show complete obstruction with delayed uptake of contrast. Doppler ultrasound or arteriogram may be needed to identify vascular flow to the kidney. Risk factors for embolic disease such as atrial fibrillation, peripheral vascular disease, and ventricular hypokinesis should be identified.I6 Although these are rare conditions, they should be considered if a stone is not visualized or the pain/vomiting are difficult to control. A noncontrast helical computerized tomography (CT) does not give a functional assessment of the kidney or its blood supply. Serum CPK is invariably elevated in renal embolus. When appendicitis occurs, it can mimic right-sided renal colic. Periappendiceal inflammation may cause hematuria as well as partial ureteral obstruction. Although fever and significant abdominal tenderness should suggest appendicitis, their absence does not exclude it. Renal colic should not cause peritoneal signs, although mild abdominal tenderness may be present because of a stone-induced ileus. Most renal colic patients will writhe in pain, whereas most patients with peritonitis will resist movement. Both can cause radiation of pain to the groin and leukocytosis. Consider a helical CT, which will look for both disease processes. Both pyelonephritis and cystitis can mimic renal colic, but more importantly they may mask an underlying stone. As ureteral obstruction with a concomitant UTI is considered a urologic emergency, one must be careful not to overlook an underlying stone. The onset and character of the patient’s pain and history of UTI symptoms should help with differentiation.
EVALUATION
Evaluation of a patient with nephrolithiasis in the ED can be divided into laboratory and imaging studies.
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LABORATORY STUDIES
Laboratory studies that should be considered include urinalysis, urine culture, pregnancy test, complete blood count with differential, electrolytes, blood urea nitrogen (BUN), and creatinine. All women of reproductive age should undergo a urine pregnancy test. The urinalysis reveals hematuria in 90% of patients with stones. However, approximately 10% of patients with renal colic do not have hematuria. As well, false positives on the dipstick occur secondary to myoglobin or povidone-iodine. Always check for red blood cells on the microscopic evaluation. Recall that there are multiple other causes of hematuria (covered elsewhere in this text). Most importantly, appendicitis or other localized inflammation may irritate the ureter, causing hematuria. An expanding aortic aneurysm that obliterates the renal artery can cause hematuria and flank pain. The urinalysis will also guide therapy by diagnosing a UTI. A dipstick positive for leukocyte esterase or nitrates suggests an infection. The microscopic evaluation should be reviewed for white blood cells, bacteria, and number of epithelial cells. An obstructed stone with associated infection is a urologic emergency and requires immediate decompression. However, a UTI in the presence of an unobstructed stone in the absence of systemic symptoms may be initially treated on an outpatient basis with close follow-up by the urologist. The urinalysis also provides various other pieces of information. The specific gravity will add to the assessment of the patient's hydration status. An elevated pH may help suggest a struvite stone or the presence of renal tubular acidosis. Crystalluria may indicate a stone but also occurs in patients without stones. Calcium oxalate crystals associated with an anion gap metabolic acidosis might indicate possible ethylene glycol ingestion. If a UTI is suspected by history or urinalysis, a urine culture should be sent. This will help guide future antibiotic therapy, diagnose some UTI's missed by the urinalysis, and aid in the diagnosis of a ureasplitting species associated with struvite stones. Electrolytes, creatinine, and BUN will be considered together because this is how they are most commonly ordered. The elevation of creatinine and BUN will occur in renal insufficiency and failure. However, this most likely is not caused by the stone because bilateral obstruction or a single kidney would have to be present to elevate the creatinine. Recall that the glomerular filtration rate of the unaffected kidney increases during obstruction. However, noting that the patient already has compromised renal function may alter your treatment. As well, this information is important to know before ordering a contrast study. The electrolytes will allow for the calculation of an anion gap. This would aid in the diagnosis of Type I renal tubular acidosis, which presents with a nonanion gap metabolic acidosis with concomitant hypokalemia. Although serum levels of calcium, magnesium, phosphorus, and uric acid will not alter the ED management, they may aid the urologic
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consultant in the diagnosis of the type of stone and can be done on an outpatient basis. The complete blood count with differential is important when infection is suspected. However, the whole blood count is a nonspecific test that may be elevated because of demargination secondary to the pain and stress of renal colic. A differential will provide information about a ”left shift” with a predominance of polymorphonuclear cells and the presence of band forms, both of which suggest infection. The whole blood count also allows a baseline value to follow while treating infection. If the patient arrives with a ”passed” stone or passes it while within the ED, it should be sent to the lab for evaluation. If no stone is passed in the ED, the patient should be instructed to keep any stone they pass at home. Urine strainers or paper coffee filters can be used to strain the urine. TO STUDY OR NOT TO STUDY
When faced with the patient who has symptoms consistent with acute renal colic, the physician must decide if the patient needs emergent imaging. Unfortunately, there is little consensus regarding which patients with renal colic need imaging, or whether they need it before leaving the ED. Some clinicians image only those patients presenting with an apparent first time stone. Others image all patients presenting with probable renal colic even if they have a history of stones. All patients with serious consideration of AAA in the differential require a study regardless of the previous stone history. Ultimately, the need for emergent imaging depends on the accuracy of the history and physical examination and the morbidity and mortality of missed diagnoses. Imaging has four functions: (1) it may confirm the expected diagnosis; (2) it may rule out other serious disorders that clinically mimic renal colic; (3) it may detect or rule out potentially serious complications of renal colic, such as obstruction and infarction; and 4) it may define the site of the stone. Therefore, we need to begin this discussion with a review of the clinician’s ability to determine which patients have renal colic. Two separate studies evaluated the added effect of IVP findings on the physician’s pretest clinical judgment.36,37 Surprisingly, both studies found out that even though these physicians had a high pre-test suspicion of a stone, 30% of those patients did not have a stone. From these studies, it appears that our ability to clinically diagnose renal colic is poor. Thus, a negative study allows the consideration of alternative diagnoses. The question remains whether there might be any significant renal or extra-renal disease missed when we misdiagnose patients as having renal colic without obtaining an imaging study. One study showed that in 8% of patients, the IVP resulted in admission or emergent consultation, but the reason for the change in
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care was not noted.37In a 1997 study, the noncontrast helical CT determined an apparent cause of the flank pain in 14 of the patients without a stone. These included renal cell carcinoma, papillary necrosis, and a ureteropelvic junction obstruction with a horseshoe kidney. Incidental extrarenal disease was identified in additional 11 patients (11%).7 These studies suggest that whether or not the diagnosis of renal colic is correct, both renal and extrarenal disease processes may be missed if no imaging study is done on the patient with suspected renal colic. However, it is not clear that it is necessary to find all those processes during the patient's ED stay. Clinicians must decide how confident they are in their diagnosis and rule out immediate life threats. This is especially true in the elderly, for whom the margin for error is slim. If a decision is made not to study a patient, close follow-up must be assured so that there is another opportunity to determine other pathology. This author (DEM) recommends imaging all patients with a history consistent with a first-time stone. IMAGING MODALITIES
Which imaging modality is best depends both on its accuracy in identifying ureteral stones and the presence of obstruction, as well as on its ability to identify disease that mimic renal colic. If renal infarction is included in the differential diagnosis, it is important that the imaging modality assess the functional status of the kidneys. Additionally, consideration must be given to the side effects of the tests. Five radiographic modalities can be used to evaluate patients with renal colic: plain abdominal radiography, ultrasound, IVP, helical CT, and magnetic resonance imaging (MRI) (Table 1). PLAIN ABDOMINAL RADIOGRAPHS
Many texts and articles tout the plain radiograph as being able to detect 90% of all renal stones.36This practice was challenged in a 1985 study whose results showed a sensitivity of 62% and a specificity of 67?'0.'~ Aside from its lack of accuracy in diagnosing renal stones, the plain film provides little information about other sources of flank pain and no information about the functional status of the kidney.= If the clinician plans to advance to another study, the utility of a KUB is even less within the ED. However, if the stone is radiopaque, the urologist may be able to follow its progression with KUB films. ULTRASOUND
A 1988 study prospectively evaluated 85 patients with the suspected diagnosis of renal colic with both ultrasound and IVP. Both the ultra-
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Table 1. COMPARISON OF IMAGING MODALITIES FOR RENAL STONES
Study
Functional Assessment
lVP Yes Helical CT No, unless contrast given Ultrasound No, unless ureteral jets Study
IVP
Pregnancy
Yes, but radiation dose
Helical CT No, radiation to fetus too high Ultrasound Preferred study
.
Detect Obstruction Detect With Hydronephrosis Hydronephrosis
Extrarenal Disease
Yes Yes
Yes Maybe
No Yes
Yes
No
No
Operator Dependent
Time
Contraindications
No
1 hour plus
No
15 min
Contrast allergy, dehydration renal insufficiency >1.5, diabetes, multiple myeloma Pregnancy
Yes
45 minplus
None
sound and IVP identified calculi in 44 patients (sensitivity of 64% and specificity of 100%). Ultrasound indirectly identified another 21% and IVP another 26%, by detecting hydronephrosis alone (respectivesensitivities of 85% and go%, specificities of 100% and 94%).This study suggests that ultrasound in experienced hands is as effective as IVP in diagnosing stones.32 The diagnosis of renal stones by both IVP and ultrasound must sometimes be made indirectly through the diagnosis of obstruction. Follow-up is, therefore, very important to ensure the obstruction is not caused by another cause.12However, an acutely obstructed kidney may have only mild hydronephrosis, which can easily be overlooked on ultrasound. Additionally, abdominal ultrasound may be difficult secondary to overlying pelvic structures. With this in mind, use of the transvaginal ultrasound has improved identification of stones at the UV junction. Use of ultrasonographic diagnosis of renal stones depends to a great extent upon the skill of the ultrasonographer as well as the extent of the disease. The examination may be negative because of incomplete or early complete obstruction or because of an inexperienced sonographer. If this is the case, examination by another modality may still be necessary. New developments with the use of doppler ultrasound to detect ureteral jets as well as resistive indexes may make this a more effective modality. A resistive index of > 0.70 is considered suggestive of acute obstruction, but it is not reliable.31Ureteral jets are compared for symmetry but are only useful if the patient has sufficient urinary output.
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Despite these limitations, ultrasound remains the study for pregnant women and perhaps children (see Fig. 1A and B). IVP
In the discussion of ultrasound versus the gold standard of IVP, the clinician must remember three pearls. Stones are irregularly shaped, often causing incomplete obstruction without hydronephrosis. Administration of contrast causes a brisk diuresis, which may accentuate the degree of dilation. Most importantly, the IVP evaluates renal function. The IVP has long been considered the gold standard in evaluating
Figure 1. Ultrasounds. A, Dilation of the ureter associated with obstruction. B, identifying a stone with shadowing.
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for urolithiasis. However, the helical CT in many institutions has recently supplanted it for the evaluation of acute renal colic in the ED. IVP remains an effective method for detecting urolithiasis and its complications. It can identify the stone or the obstruction related to it with a sensitivity approaching go%.* The IVP visualizes the entire urinary tract and assesses the functional status of the kidney. Relative contraindications to IVP include allergy to contrast agents, renal insufficiency with creatinine > 1.8 mg/dL, diabetes, multiple myeloma, and dehydration. The incidence of allergic reactions resulting from the IVP contrast is approximately 0.1% and may be highest in patients with iodine and shellfish allergies. Those with a questionable history of contrast allergy can receive intravenous steroids and antihistamines or undergo a helical CT. Patients with a known history of contrast allergy should avoid the use of contrast media. Patients with an iodine allergy may receive nonionic contrast. The IVP may show the position of the stone. A delayed nephrogram or hydronephrosis is associated with obstruction. Columnization may occur at the point of obstruction. It is important to obtain delayed films until the diagnosis is made. Because obstruction and delay are common, it is typical ED practice to take successive films at increasing time intervals until two successive films document columnization at the site of the stone. All of these patients should receive urologic follow-up. Extravasation may be due to rupture of a renal calyx or less commonly, the ureter (Fig. 2A). In the absence of infection, rupture typically does
Figure 2. IVPs. A, Extravasation of contrast within Gerota’s fascia. B, Complete obstruction. Note the lack of uptake in the left.
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not require any specific therapy. If the kidney shows no uptake at all, concern for complete obstruction or a renal infarction must be raised (Fig. 2B). An ultrasound or arteriogram can evaluate the latter. MRI
The new modality of MRI urography was evaluated for the assessment of ureteric obstruction in a recent study (Fig. 3). With the HASTE MRI urography, all 41 cases of acute and chronic obstruction were noted. The MRI was able to determine chronic versus acute obstruction by signals read as perirenal fluid surrounding 20 of the 23 acutely obstructed kidneysz5MRI is difficult to use in the ED setting for all the usual reasons (cost, access, presence of magnetically active implants, and patient monitoring), but it may be beneficial in the patient with renal failure or contrast dye allergies. It needs to be compared against the less expensive helical CT scan. One benefit is that the functional status of the kidneys can probably be assessed using gadolinium contrast while the patient is in the MRI.3 HELICAL CT SCANS
The advent of noncontrast helical CT scanning has added a new diagnostic modality to the evaluation of renal stones. A small 1995 study (20 patients) compared noncontrast helical CT to IVP in the evaluation
Figure 3. MRI image of kidneys, ureter, and bladder. This is a normal study.
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of acute flank pain. Of the 20 patients, 12 were shown to have obstruction. All 12 were identified by both IVP and noncontrast helical CT. The CT showed a stone as the presumptive cause of obstruction in 11, whereas the IVP identified the stone in only five patients. Also, CTdiagnosed torsion of a paratubal cyst as the cause of pain in one patient who did not subsequently undergo an IVP. This small study suggests that noncontrast CT scans are as effective as IVP in diagnosing obstruction and better delineated the position of the It also suggests that the helical CT can identify other sources of pain when a stone is not the cause. A 1997 study prospectively evaluated 100 patients who presented to the ED with acute flank pain using helical CT scanning. The results were compared with the gold standard of spontaneous passage, retrieval, or identification of the stone on retrograde pyelography. CT demonstrated a stone in 55 patients and no ureteral obstruction in the other 45. CT was able to determine an apparent cause of the flank pain in 14 of the patients without a stone. Incidental extra-renal disease was identified in 11 additional patients (11Y0).The results showed that 50 of the documented 51 stones were identified, and that 38 of the 38 patients without stones were appropriately identified: a sensitivity of 98%, specificity of loo%, positive predictive value of loo%, and negative predictive value of 97%. The authors mention that the spiral CT would not be expected to evaluate renal function or the urothelium without the additional step of giving c o n t r a ~ t . ~ In many institutions, the non-contrast helical CT has become the study of choice for suspected renal colic (Fig. 4). It is able to identify radiolucent and radiopaque stones and/or hydronephrosis. It can help diagnose other causes of flank pain such as AAA, ovarian cysts, and
Figure 4. CT scan showing left hydronephrosis with perinephric stranding.
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appendicitis. The helical CT does not, however, evaluate the functional status of the kidney. Another advantage of the helical CT scan is that the test is completed quickly, whereas an IVP may require hours of follow-up film. In the ED, this time advantage may be significant. In this author’s opinion (JT), the helical CT scan is the imaging modality of choice for renal colic in the ED. ED TREATMENT Hydration
Patients who have clinical dehydration secondary to vomiting and decreased oral intake should receive intravenous fluid hydration. The idea that aggressively hydrating the patient will cause a ”pressure head” that would help the stone migrate down the ureter is debatable. Previously mentioned studies show that glomerular filtration rate for the obstructed kidney decreases. As well, overly aggressive hydration may dilute the IVP contrast and produce a less than optimal study. Conversely, giving IVP contrast to a dehydrated obstructed kidney is not advisable. The prudent approach is gentle rehydration. Analgesia
Rapid and adequate pain control should be a top priority in the initial management of a patient with renal colic. Opiate analgesics with antiemetics have long been the standard. However, it has recently been shown that nonsteroidal anti-inflammatory drugs (NSAIDs) will not only decrease the pain, but also have anti-prostaglandin effects that decrease the subsequent inflammatory response, and may even promote relaxation of the ureteral smooth m ~ s c l e . ~ The only available parenteral NSAID is ketorolac. If the patient is not vomiting, the NSAID can be given orally. Ketorolac is safe in the majority of patients with renal colic, despite case reports to the contrary. However, NSAIDS should be avoided in patients with know peptic ulcer disease, renal insufficiency, and pregnancy. They should be used judiciously in elderly patients and patients with diabetes, hypertension, and dehydration. Ketorolac should be avoided in those patients with greater than 1 week of o b s t r ~ c t i o n . ~ ~ ADMISSION
Admission criteria vary from institution to institution (List 2). Regional variations should be learned. However, there are some frequently quoted absolute and relative indications for admission.
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List 2. Admission Criteria Absolute Indications Intractable vomiting Intractable pain Single kidney or transplanted kidney with obstruction Concomitant urinary tract infection with obstruction Hypercalcemic crisis Relative Indications Fever Stone larger than 6 mm Solitary kidney Kidney transplantation High grade obstruction Intrinsic renal disease Urinary extravasation Social issues
Patients with an obstructing stone and evidence of infection should be admitted for decompression and intravenous antibiotics. Patients with intractable vomiting and/or pain should be admitted for intravenous hydration and symptom control. A single functional kidney or history of transplantation with obstruction should be admitted. Febrile patients due to UTI with a stone should be admitted because this probably represents a subclinical pyelonephritis. Hypercalcemic crisis in a patient with stones should also be admitted. Relative indications for admission include a solitary kidney or transplantation without obstruction, an unobstructed stone with a concomitant UTI, patients with intrinsic renal disease, and social issues preventing proper outpatient management. Complete obstruction and/or extravasations were previously considered to be absolute indications for admission. However, most urologists feel that these patients require only close follow-up, because they are not going to intervene emergently. CONSULTATION
The urologic consultant is available to the emergency medicine physician for three issues: admission, request for consultation on patients with relative indications for admission, and clarification of care on a complicated case. The goal of this monograph is to clarify the care of a majority of patients with renal colic. OUTPATIENT CARE
Patients should be discharged with a combination of an NSAID and a narcotic analgesic. They should be encouraged to maintain adequate
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hydration to maintain clear urine. Patients should strain their urine until the stone passes. They should return for medical evaluation for a fever of greater than 100.4 F, uncontrollable pain or vomiting, or if they develop abdominal pain and tenderness. If they pass the stone, they should bring it in for analysis if the etiology of their stones has not been previously established. COMPLICATIONS Obstruction
Does the presence of obstruction cause any change in the treatment or disposition of a patient with renal colic? If obstruction occurs in the presence of an infection, the obstruction must be relieved emergentlypossible. However, if obstruction occurs in the absence of infection, how long does it take for irreversible damage to occur? Decreases in renal blood flow as well as in ureteral pressures in the obstructed kidney begin 5-18 hours after obstruction. The degree of the reversibility of this process is not clear.20A decrease in both the glomerular filtration rate and renal plasma flow has been noted in both partially and completely obstructed kidneys.", l5 Hypertrophy of the ureteral musculature occurs after as little as three days of obstru~tion.~ Scar formation was noted if the obstruction continued for 2 weeks. One 1954 study evaluated the effect of 1 week of complete ureteral obstruction on kidney function. Within 1 hour of release, the obstructed kidney functioned at only 25% of its preobstructed glomerular filtration rate. However, the contralateral kidney was functioning at 165% its baseline glomerular filtration rate. The function of the obstructed kidney continued to improve for up to 2 months but stabilized at a level below its pre-morbid ~0ndition.l~ In contrast, a more recent 1997 study reviewed the role of renal resistive indexes in stages of obstruction and release. After relief of obstruction, the previous decrease in effective renal plasma flow and increase in the renal resistive index returned to near baseline levels.31 Despite the conflicting studies, a prominent urologic textbook states that "detectable renal damage does not occur in previously normal kidneys until complete obstruction has been present for 4 weeks."19 Although the studies reviewed would suggest that some damage may occur, urologists concur that obstruction in the absence of infection does not need to be acutely treated as long as there is a functioning contralateral kidney. Infection
A UTI in the presence of an obstructed stone is a urologic emergency. Obstruction causes increased renal pelvic pressure. Hydrostatic
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pressure represents the net difference between the renal capillary and Bowman’s space. Thus, obstruction reduces hydrostatic pressure and reduces glomerular filtration. Antibiotics cannot be excreted unless obstruction is decompressed. Intravenous antibiotics (Floroquinones, Gentamycin) to cover for the usual organisms should be administered. A urologist should be consulted for decompression of the obstruction as it effectively causes an abscess. UTIs in the patient with ureteral stones without obstruction can often be treated with oral antibiotics and close follow-up (24 hours). Renal Stents The care of patients with renal stents in patients with renal stones is covered elsewhere in this text under the chapter ”Infections in Patients with Indwelling Devices.” Patients with stents that complain of increasing pain or bleeding should be evaluated for migration of the stints as well as for obstruction. This can be done with a KUB and ultrasound or a helical CT. The urologist should be consulted as to the disposition and continued care of this patient. SPECIAL CONCERNS Pregnancy Issues The evaluation for a possible kidney stone in a pregnant patient arises in two unique problems: the dose of radiation to the fetus and the normal physiologic dilation of the ureters.35Ionizing irradiation of the fetus may increase the risk of teratogenicity, childhood cancer, or mental retardation. For these reasons, the dose of ionizing radiation should be minimized in pregnant women, especially those at less than 16 weeks gestation. The upper urinary tract begins to dilate in the first trimester and progresses until delivery. Involvement is greatest on the right. Ultrasound may be able to distinguish between physiologic dilation and calculus and does not carry the risk of radiation. With improvements in ultrasound diagnosis as well as the use of transvaginal ultrasound, the ability to detect a stone is increasing.lO, Ultrasound should therefore be the modality of choice in the evaluation of a possible renal stone in pregnant patients. If it is negative, the IVP may be performed if the benefit outweighs the risk to the fetus. A limited IVP ( 3 4 films) is relatively contraindicated after the first 16 weeks of pregnancy (Fig. 5) because this yields a radiation dose of less than 2 rads. A dose of approximately 20 rads in the first trimester is considered teratogenic. Consultation with an obstetrician/gynecologist and the urologist should be made to determine the best approach for women less than 16 weeks pregnant, or if more extensive testing is needed.
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Figure 5. IVP during pregnancy showing hydronephrosis.
Pediatric
Stone disease is uncommon in children. Therefore, one must maintain a high level of suspicion to be able to diagnose these patients. Of note, unusual dietary patterns, such as the ketogenic diet for intractable seizures, have been associated with stone formation. As well, these patients should be referred for a metabolic work-up for the etiology of their stone formation. Some authors suggest that ultrasound is the study of choice for children because of the radiation exposure and/or use of contrast.34The indications for admission remain the same. All children with urinary calculi need to be followed by a urologist, as there is a likelihood that they have metabolic stone disease. Thus, all pediatric stone formers eventually should be worked up for metabolic stone disease as outpatients. Geriatric
Remember that first-time stones do not usually first occur beyond the age of 50. Therefore, the differential diagnosis of diseases that mimic renal colic is very important in these patients. Acute abdominal aortic aneurysms and acute myocardial infarctions top this list. It is imperative to establish a diagnosis in these patients. This will invariably include imaging the patient with a helical CT to evaluate both the aorta and the renal system. Remember that without dye, the helical CT cannot diagnose an infarcted kidney. Finally, these patients do not tolerate narcotics or NSAIDS as well as the younger population. Concurrent medications and/or diseases may preclude their use.
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Pitfalls
1. Failure to image the elderly or first-time stone-patient to establish a definitive diagnosis. 2. Failure to consider stone disease in a patient with absence of hematuria. 3. Failure to diagnose infection with an obstructed stone. References 1. Begun FP, Foley WD, Peterson A, White B: Patient evaluation: Laboratory and imaging studies. Urologic Clin North Am 24:l-11, 1997 2. Balaji KC, Menon M Mechanism of stone formation. Urologic Clin North Am 24:l11, 1997 3. Choo SW, Kim SH, Jeong YG, et al: MR Imaging of segmental renal infarction: An experimental study. Clin Rad 52:6568,1997 4. Coe FL, Parks JH, Asplin Jr: The pathogensis and treatment of kidney stones. N Engl J Med 3271141-1152, 1992 5. Cordell WH, Wright SW, Wolfson AB: Comparison of intravenous ketorolac, meperidine, and both (balanced analgesia) for renal colic. Ann Emerg Med 28:151-158, 1996 6. Elliot JS, Eusebio E: Calcium oxalate solubility: The effects of trace metals. Invest Urol 4:428430, 1967 7. Fielding JR, Steele G, Fox LA, et al: Spiral computerized tomography in the evaluation of acute flank pain: A replacement for excretory urography. J Urol 1572071-2073, 1997 8. Finlayson B, Smith A: Stability of first dissociable proton of uric acid. J Chem Eng Data 19394-97, 1974 9. Gee WF, Kiviat M D Ureteral response to partial obstruction. Smooth muscle hyperplasia and connective tissue proliferation. Invest Urol 12:309-316, 1975 10. Gorton E, Whitfield H N Renal calculi in pregnancy. Br J Urol 8O(supp 1):4-9, 1997 11. Jones DA, Atherton JC, OReilly Ph, et al: Assessment of the nephron segments involved in post-obstructive diuresis in man, using lithium clearance. Br J Urol64:559563, 1989 12. Juul N, Brons J, Torp-Pedersen S, et a1 Ultrasound versus intravenous urography in the initial evaluation of patients with suspected obstructing urinary calculi. Scand J Urol Nephrol Supp113745-47,1991 13. Kerr WS Jr: Effect of complete ureteral obstruction for one week on kidney function. J Applied Physiol 6762-772, 1954 14. Labrecque M, Dostaler LP, Rousselle R. Efficacy of nonsteroidal anti-inflammatory drugs in the treatment of acute renal colic. Arch Int Med 1541381-1387, 1994 15. Lackner H, Barton LJ: Cortical blood flow in ureteral obstruction. Invest Urol 8:319323, 1970 et a1 Renal Artery embolism: Clinical features 16. Lessman RK, Johnson SF, Coburn JW, and long term follow-up of 17 cases. Ann Intern Med 89:477-482, 1978 17. Mandel NS, Mandel GS: Urinary tract stone disease in the United States veteran population: I. Geographical frequency of occurrence. J Urol 142:1513-1515,1989 18. Marston WA, Ahlquist R, Johnson G Jr, Meyer AA. Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg 16:17-22, 1992 19. Menon M, Parulkar BG, Drach G W Urinary lithiasis: Etiology, diagnosis, and medical management. In Walsh PC, Retik AB, Vaughan ED, Wein AJ (eds): Campbell’s Urology, ed 7. Philadelphia, WB Saunders, 1998, pp 2661-2705 20. Moody TE, Vaughan ED Jr, Gillenwater JY Relationship between renal blood flow and ureteral pressure during 18 hours of total unilateral ureteral occlusion. Invest Urol 13:246-251, 1975 21. Murthy LNS: Urinary tract obstruction during pregnancy: Recent developments in imaging. Br J Urol; 8O(suppl 1):l-3, 1997
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22. Mutgi A, Williams JW, Nettleman M Renal colic: Utility of the plain abdominal radiograph. Arch Intern Med 151:1589-1592, 1991 23. Perlmutter A, Miller L, Trimble LA, et al: Toradol, an NSAID used for renal colic, decreases renal perfusion and ureteral pressure in a canine model of unilateral ureteral obstruction. J Urol 149:92&930, 1993 24. Prince CL, Scardino PL, Wolan TC: The effect of temperature, humidity, and dehydration on the formation of renal calculi. J Urol 75:209, 1956 25. Regan F, Bohlman ME, Khazan R, et al: MR Urography Using HASTE Imaging in the Assessment of Ureteric Obstruction. AJR 167 1115-1120, 1996 26. Rizolli R, Bonjour JP: Management of disorders of calcium homeostasis. Baillieres Clin Endocrinol Metab 6129-142, 1992 27. Robertson WG, Peacock M The pattern of urinary stone disease in the United Kingdom in relation to animal protein intake during the period 1960-1980. Urol Int 373394-399, 1982 28. Roth CS, Bowyer BA, Berquist TH: Utility of the plain abdominal radiograph for diagnosing ureteral calculi. Ann Emerg Med 14311-315, 1985 29. Sharma RN, Shah I, Gupta S, et al: Thermogravimetric analysis of urinary tones. Br J Urol64:564566, 1989 30. Shokeir AA, Nijman RJ, El-Azab M, et al: Partial ureteral obstruction: Role of renal resistive index in stages of obstruction and release. Urology 49:52%535, 1997 31. Sinclair D, Wilson S, Toi A, et al: The evaluation of suspected renal colic: Ultrasound scan versus excretory urography. Ann Emerg Med 18:55&559, 1989 32. Smith RC, Rosenfield AT, Choe KA, et a1 Acute flank pain: Comparison of noncontrast-enhanced CT and intravenous urography. Radiology 194:789-794, 1995 33. Stapleton FB: Clinical approach to children with urolithiasis. Semin Nephrol 16:387397, 1996 34. Strothers L, Lee LM. Renal colic in pregnancy. J Urol 1483383-1387, 1992 35. Tasso SR, Shields CP, Rosenberg CR, et al: Effectiveness of selective use of intravenous pyelography in patients presenting to the emergency department with ureteral colic. Acad Emerg Med 4:780-785, 1997 36. Twinem FP: Some radiographic aspects of urinary calculi. Am J Surg 17389-394, 1932 37. Wrenn K. Emergency intravenous pyelography in the setting of possible renal colic: Is it indicated? Ann Emerg Med 26, 1995
Address reprint requests to David E. Manthey, MD, FACEP, FAAEM Department of Emergency Medicine Wake Forest University School of Medicine Medical Center Boulevard Winston-Salem, NC 27157
0733-8627/01 $15.00
+ .OO
NEPHROLITHIASIS David E. Manthey, MD, FACEP, FAAEM, and Joel Teichman, MD, FRCSC
The evaluation and treatment of patients with nephrolithiasis is rapidly changing. New imaging modalities have emerged that have changed the way we evaluate patients with flank pain. Criteria previously used as indication for admission no longer apply, and many of these same patients are now managed as outpatients. This chapter will review the subject of nephrolithiasis as it pertains to emergency medicine physicians. When applicable, evidence-based medicine reviews of certain articles are included. EPIDEMIOLOGY
Approximately 3%-5% of the population will experience nephrolithiasis during their lifetime. Depending on the type of stone, up to 50% of these patients will have a recurrence within 10 years.lg Although several of the disorders that cause nephrolithiasis are hereditary (familial renal tubular acidosis, cystinuria), there has been no conclusive data to date that nephrolithiasis is hereditary. The incidence of stone disease is highest among whites, reportedly twice as high as that of Asians. It is relatively rare in African Americans and Native Americans. Age is an important consideration for stone disease with the peak incidence of stones between ages 20 and 50. It is relatively uncommon in patients less than age 15, and the male-to-female ratio remains about 3:1.19
From the Department of Emergency Medicine, Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina (DEM); and Department of Urology, University of Texas Health Science Center, San Antonio, Texas (JT)
EMERGENCY MEDICINE CLINICS OF NORTH AMERICA
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With respect to geography, the prevalence is higher in Virginia, North Carolina, Georgia, Tennessee and Kentucky.17This does not translate into the Southeast, but does roughly approximate a "stone belt." In addition to geographic location, climate also appears to play a role in stone formation, with the peak months including July, August, and September.24This correlates with a time period that is 1 to 2 months after the maximum mean annual temperature for that assigned area.19 Many theories have been proposed to explain this phenomenon to include increased perspiration causing concentrated urine, increased exposure to sunlight causing increased production of vitamin D3 subsequently increasing urinary calcium excretion, and higher summer intake of oxalate-rich foods such as iced tea and fresh vegetables. Sedentary occupations carry a higher risk for the development of stones. Robertson et a1 showed that affluence and therefore the ability to buy animal protein increases the incidence of stone formation.27The increased consumption of foods with large amounts of calcium (cheese), oxalate (tea, Worcestershire sauce), and purines may also lead to increased stone formation. Water intake is an oft-debated topic within the subject of nephrolithiasis. It is believed that increased intake of water decreases the subsequent incidence of disease in those patients predisposed to nephrolithiasis.8 This relationship may occur because of the decreased dwell time of free crystals within the kidney and dilution of other necessary components for crystallization. It is important to remember that the amount of water ingested should surpass that lost by sweating and breathing, and that it should not contain large amounts of minerals that promote crystallization (sodium carbonate) or low amounts of inhibitory substances ( ~ i n c ) . ~ PATHOPHYSIOLOGY BEHIND STONE FORMATION
Stone formation occurs because of supersaturation of the urine with oxalate and calcium. As the amount of solute put into solution is increased, the solution goes through stages of saturation. When the amount of solute is below the thermodynamic solubility product, it dissolves into the solution (undersaturated). At some point, the addition of more solute will not dissolve into solution (saturated). After this point, the addition of more solute causes crystals to precipitate out of solution (thermodynamic solubility product) because the urine is now supersaturated with the solute. However, the process is more complicated in the urinary tract because more factors are at play. The solvent (urine) is in flux with respect to dwell time, dilution of other solutes, electrical ion interaction, and presence of inhibitory substances (citrate). Urinary supersaturation must occur, either intermittently or continuously, for crystallization to O C C U ~ . ' ~ Even after crystal formation, most individuals do not form stones because other low molecular weight compounds (pyrophosphate) and
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molecules prevent the formation. When these inhibitors are lacking, crystals may aggregate to form a stone. However, these crystals cannot aggregate into a stone large enough to occlude the collecting system as long as there is a free-flow of urine, which would transport crystals harmlessly to the bladder to be voided. This brings us to the last ingredient in the formation of stones. There must be some type of abnormality that allows for retention of these crystals at a rate at which they can form a larger stone. This may be caused by anatomic abnormalities such as medullary sponge kidney, intramedullary stasis, or abnormal tubular epithelium. More often, no anatomic abnormality is present, and crystals grow within the renal tubules or adhere to collecting ducts (Randall's plaques). There are numerous types of stones, but for the purpose of this monograph, only five basic categories will be reviewed. Calcium oxalate, struvite, uric acid, cystine, and miscellaneous causes. Calcium oxalate stones make up almost 80% of all stones. Of these patients, up to 60% have increased urinary calcium levels without elevation of serum calcium 1e~els.l~ Hypercalciuria may be caused by several mechanisms: (1) absorptive, because of increased intestinal absorption of calcium; (2) renal, caused by a primary loss of calcium through the kidney; and (3) resorptive, caused by increased demineralization of bone., Other causes include the subset of calcium oxalate stone-forming patients that have elevated serum calcium (hypercalcemia). Almost all hypercalcemic stone patients will have primary hyperparathyroidism. Other causes include hyperthyroidism and sarcoidosis.26 Hyperoxaluria also predisposes one to the formation of calcium oxalate stones. This occurs because of primary hyperoxaluria (a genetic defect), short bowel syndrome, malabsorption, and increased transport of oxalate by the red blood ~el1s.l~ Struvite stones make up the second most common category of stones, accounting for 2% to 20% of all They are responsible for the majority of staghorn calculi. They are also known as "triple-phosphate" stones because of their makeup of magnesium, ammonium, and phosphate. Struvite stones require two things for their formation-urine pH of 7.2 or above and the presence of ammonia in the urine. Urinary tract infections caused by urease-producing bacteria are the underlying cause of these "infection" stones. Urease splits one mole of urea into two moles of ammonia (NH,). NH, plus H' combine to form NH, (ammonium), and the consumption of H' causes a rise in urine pH. Ammonium is relatively insoluble. Although Proteus is the most common urea-splitting organism, KZebsieZZa, StuphyZococcus species, Providenciu, and Corynebacteriurn species may produce urease as well. Foreign body within the urinary tract and neurogenic bladder are also associated with this type of stone. The symptoms of a patient with struvite stones may follow the classic presentation of pain, hematuria, and fever. However, a significant subset of patients will present only with malaise or weakness. Treatment
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for this type of stone includes removal of the stone and prevention of urinary tract infections. Uric acid stones account for approximately 6% of all stones and occur because of the supersaturation of the urine with uric acid. This occurs because of excess uric acid secretion, excessively acidic urine, and decreased urinary volume. The incidence of uric acid stones in patients with gout is about 1% per year after the first gouty episode. Approximately 20% of the population with gout suffers from uric acid stones. Of note, uric acid stones are the most common radiolucent stone. Hydration, alkalization of the urine, allopurinol to treat gout, and modification of the diet make up the multifaceted treatment of this disease. Cystine stones account for approximately 1% of all stones. They occur only in patients with cystinuria, which is an autosomal recessively inherited genetic disorder. Cystine is less soluble at lower pH, so the goal is to raise the pH of the urine and the intake of substances containing cystine. Pharmacologic agents such as D-penicillamine or alphamercaptoproprionylglycine (MPG or Thiola) may bind cystine and form a urine soluble complex. Miscellaneous stones include dihydroxyadenine, xanthine, silicate, triamterene, indinavir, and silicate stones, among others. These will not be discussed further here. CLINICAL PRESENTATION
Patients with urolithiasis most commonly present to the emergency department (ED) with renal colic. They may also present secondary to infection or complications associated with the treatment of nephrolithiasis. Renal colic presents abruptly as a severe paroxysmal pain on the affected side. It usually does not resolve completely before the next wave of pain begins. This visceral type pain, caused by the distention of the ureter, is secondary to obstruction of the ureter or passage of the stone (or associated blood clot and debris). The paroxysmal component is caused by the peristaltic action of the ureter. The patient with renal colic will usually writhe in pain or move constantly to try to find a position of comfort. In contrast to patients with peritoneal inflammation, they do not lie still. Nausea and vomiting commonly occur with the pain. The location of the pain may give some information about the location of the stone. The pain can occur anywhere from the flank down to the ipsilateral groin. Stones near the kidney produce flank pain. As the stone moves down, the pain radiates around to the front of the abdomen into the lower quadrant. Referred pain often occurs in the ipsilateral groin, testicle, and labia as the stone reaches the ureterovesicular junction (WJ). Stones within the renal calyces may present with dull flank pain and/or hematuria. UVJ and bladder stones may present with hematuria, dysuria, or urgency. These symptoms may mimic a urinary tract infection (UTI). Conversely, a concomitant UTI may mask the presence of a
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UVJ stone. Stones may also move within the ureter without any associated resistance or obstruction causing painless hematuria. HISTORY
The history obtained from the patient with suspected renal colic can be divided into three realms. First, risk factors for the formation of stones should be elicited. These include previous episodes of renal colic, presence of previously asymptomatic renal calyx stone, as well as a family or personal history of any hereditary disorder that can cause nephrolithiasis (familial renal tubular acidosis, cystinuria, and idiopathic hypercalciuria). A history of recurrent or chronic UTIs may put the patient at risk for struvite stones or produce the anatomic abnormality needed for stone formation. Second, the history should delineate if the patient is at risk for complications from urolithiasis. This includes patients with UTIs, solitary functioning kidney, renal transplant, anatomic abnormalities of the renal system, and immunocompromised patients (diabetes, HIV, cancer, steroids, etc). Finally, the history should also help rule out other disease processes that mimic renal colic. These processes will be covered in detail in the section on differential diagnosis. PHYSICAL EXAMINATION
The physical examination of the patient with suspected renal colic confirm the diagnosis and rule out other conditions that mimic renal colic. Starting with the vital signs, the patient frequently has an adrenergic surge associated with pain, including tachycardia, hypertension (relative to the patient’s usual blood pressure), tachypnea, and diaphoresis. The presence of fever is usually not associated with this response and should suggest infection, an important finding since an obstructed, infected kidney requires emergent decompression. Hypotension uncommonly occurs in renal colic as a ”vasovagal” response to pain or after a patient has had prolonged vomiting leading to dehydration. Hypotension, however transient, should prompt an aggressive search for a rupturing abdominal aortic aneurysm or sepsis caused by infection before assuming that it was the result of a vasovagal episode. Flank or costovertebral flank tenderness may be present on the affected side. However, this finding is also associated with pyelonephritis. Mild-to-moderate abdominal tenderness may be present on the ipsilateral side. However, there should be no peritoneal signs such as involuntary guarding or rebound. Coughing, heel tap, or pelvic shake should not increase the pain. Attempt to determine whether the examination increases the pain that the patient is experiencing or simply identifies the area of pain without exacerbating it. Generally, in renal colic, you will be able to identify the area of pain but will not exacerbate it with your exam. Remember that renal colic is hollow viscus pain secondary
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to the dilation of the ureter, not peritonitis. Although pain may be referred to the testicle or labia, the testicle or labia itself should be nontender to palpation and otherwise normal to exam. Pelvic and rectal exams should be unremarkable in renal colic. Recalling that many diseases may mimic renal colic, one must expand the examination to include these organ systems. A cardiovascular exam is required to rule out etiologies for embolic disease. The abdominal examination should evaluate for vascular bruits, pulsatile masses, and symmetry of femoral pulses. The bladder should be examined for tenderness and evidence of retention. The pelvic exam should evaluate for the presence of cervical discharge, cervical motion tenderness, adnexal masses or tenderness, and pregnancy. DIFFERENTIAL DIAGNOSES
Although the differential diagnoses for patients presenting with symptoms consistent with renal colic are listed in List 1, some deserve special mention. It is essential that the physician rule out the presence of the potentially life-threatening diseases.
List 1. Differential Diagnoses
Abdominal aortic aneurysm Renal artery thrombosis/Embolism/Dissection Appendicitis Pyelonephritis Ectopic pregnancy Ovarian torsion Diverticulitis Musculoskeletal pain Peritonitis Ischemic bowel Acute myocardial infarction Bowel obstruction Henoch-Schonlein purpura Renal papillary necrosis Ovarian cyst Endometriosis Psoas abscess or hematoma Retroperitoneal mass Biliary colic Urinary retention Fitz-Hugh Curtis syndrome Sup. Mesenteric A. occlusion Internal hernia Malingering
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The most worrisome mimicker of renal colic is an expanding abdominal aortic aneurysm (AAA).In fact, when an AAA is misdiagnosed, it is most commonly misdiagnosed as renal colic.lSRecall that the peak incidence of stone disease is between ages 20 and 50. Therefore, anyone over the age of 50 presenting with renal colic should be evaluated for the presence of an AAA. Identify the presence of peripheral vascular disease, hypertension, and tobacco use. Evaluate the abdomen for pulsatile mass or abnormal pulses. Actively seek out this diagnosis in patients with any episode of hypotension. A rupturing AAA can cause both ureteral obstruction with hydronephrosis (because of compression) and hematuria (because of ureteral irritation). Renal artery thrombosis or dissection may be very difficult to differentiate from renal colic because it presents with acute onset of pain that is visceral in nature. It causes hematuria as well as nausea and vomiting. The intravenous pyelography (IVP) may show complete obstruction with delayed uptake of contrast. Doppler ultrasound or arteriogram may be needed to identify vascular flow to the kidney. Risk factors for embolic disease such as atrial fibrillation, peripheral vascular disease, and ventricular hypokinesis should be identified.I6 Although these are rare conditions, they should be considered if a stone is not visualized or the pain/vomiting are difficult to control. A noncontrast helical computerized tomography (CT) does not give a functional assessment of the kidney or its blood supply. Serum CPK is invariably elevated in renal embolus. When appendicitis occurs, it can mimic right-sided renal colic. Periappendiceal inflammation may cause hematuria as well as partial ureteral obstruction. Although fever and significant abdominal tenderness should suggest appendicitis, their absence does not exclude it. Renal colic should not cause peritoneal signs, although mild abdominal tenderness may be present because of a stone-induced ileus. Most renal colic patients will writhe in pain, whereas most patients with peritonitis will resist movement. Both can cause radiation of pain to the groin and leukocytosis. Consider a helical CT, which will look for both disease processes. Both pyelonephritis and cystitis can mimic renal colic, but more importantly they may mask an underlying stone. As ureteral obstruction with a concomitant UTI is considered a urologic emergency, one must be careful not to overlook an underlying stone. The onset and character of the patient’s pain and history of UTI symptoms should help with differentiation.
EVALUATION
Evaluation of a patient with nephrolithiasis in the ED can be divided into laboratory and imaging studies.
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LABORATORY STUDIES
Laboratory studies that should be considered include urinalysis, urine culture, pregnancy test, complete blood count with differential, electrolytes, blood urea nitrogen (BUN), and creatinine. All women of reproductive age should undergo a urine pregnancy test. The urinalysis reveals hematuria in 90% of patients with stones. However, approximately 10% of patients with renal colic do not have hematuria. As well, false positives on the dipstick occur secondary to myoglobin or povidone-iodine. Always check for red blood cells on the microscopic evaluation. Recall that there are multiple other causes of hematuria (covered elsewhere in this text). Most importantly, appendicitis or other localized inflammation may irritate the ureter, causing hematuria. An expanding aortic aneurysm that obliterates the renal artery can cause hematuria and flank pain. The urinalysis will also guide therapy by diagnosing a UTI. A dipstick positive for leukocyte esterase or nitrates suggests an infection. The microscopic evaluation should be reviewed for white blood cells, bacteria, and number of epithelial cells. An obstructed stone with associated infection is a urologic emergency and requires immediate decompression. However, a UTI in the presence of an unobstructed stone in the absence of systemic symptoms may be initially treated on an outpatient basis with close follow-up by the urologist. The urinalysis also provides various other pieces of information. The specific gravity will add to the assessment of the patient's hydration status. An elevated pH may help suggest a struvite stone or the presence of renal tubular acidosis. Crystalluria may indicate a stone but also occurs in patients without stones. Calcium oxalate crystals associated with an anion gap metabolic acidosis might indicate possible ethylene glycol ingestion. If a UTI is suspected by history or urinalysis, a urine culture should be sent. This will help guide future antibiotic therapy, diagnose some UTI's missed by the urinalysis, and aid in the diagnosis of a ureasplitting species associated with struvite stones. Electrolytes, creatinine, and BUN will be considered together because this is how they are most commonly ordered. The elevation of creatinine and BUN will occur in renal insufficiency and failure. However, this most likely is not caused by the stone because bilateral obstruction or a single kidney would have to be present to elevate the creatinine. Recall that the glomerular filtration rate of the unaffected kidney increases during obstruction. However, noting that the patient already has compromised renal function may alter your treatment. As well, this information is important to know before ordering a contrast study. The electrolytes will allow for the calculation of an anion gap. This would aid in the diagnosis of Type I renal tubular acidosis, which presents with a nonanion gap metabolic acidosis with concomitant hypokalemia. Although serum levels of calcium, magnesium, phosphorus, and uric acid will not alter the ED management, they may aid the urologic
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consultant in the diagnosis of the type of stone and can be done on an outpatient basis. The complete blood count with differential is important when infection is suspected. However, the whole blood count is a nonspecific test that may be elevated because of demargination secondary to the pain and stress of renal colic. A differential will provide information about a ”left shift” with a predominance of polymorphonuclear cells and the presence of band forms, both of which suggest infection. The whole blood count also allows a baseline value to follow while treating infection. If the patient arrives with a ”passed” stone or passes it while within the ED, it should be sent to the lab for evaluation. If no stone is passed in the ED, the patient should be instructed to keep any stone they pass at home. Urine strainers or paper coffee filters can be used to strain the urine. TO STUDY OR NOT TO STUDY
When faced with the patient who has symptoms consistent with acute renal colic, the physician must decide if the patient needs emergent imaging. Unfortunately, there is little consensus regarding which patients with renal colic need imaging, or whether they need it before leaving the ED. Some clinicians image only those patients presenting with an apparent first time stone. Others image all patients presenting with probable renal colic even if they have a history of stones. All patients with serious consideration of AAA in the differential require a study regardless of the previous stone history. Ultimately, the need for emergent imaging depends on the accuracy of the history and physical examination and the morbidity and mortality of missed diagnoses. Imaging has four functions: (1) it may confirm the expected diagnosis; (2) it may rule out other serious disorders that clinically mimic renal colic; (3) it may detect or rule out potentially serious complications of renal colic, such as obstruction and infarction; and 4) it may define the site of the stone. Therefore, we need to begin this discussion with a review of the clinician’s ability to determine which patients have renal colic. Two separate studies evaluated the added effect of IVP findings on the physician’s pretest clinical judgment.36,37 Surprisingly, both studies found out that even though these physicians had a high pre-test suspicion of a stone, 30% of those patients did not have a stone. From these studies, it appears that our ability to clinically diagnose renal colic is poor. Thus, a negative study allows the consideration of alternative diagnoses. The question remains whether there might be any significant renal or extra-renal disease missed when we misdiagnose patients as having renal colic without obtaining an imaging study. One study showed that in 8% of patients, the IVP resulted in admission or emergent consultation, but the reason for the change in
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care was not noted.37In a 1997 study, the noncontrast helical CT determined an apparent cause of the flank pain in 14 of the patients without a stone. These included renal cell carcinoma, papillary necrosis, and a ureteropelvic junction obstruction with a horseshoe kidney. Incidental extrarenal disease was identified in additional 11 patients (11%).7 These studies suggest that whether or not the diagnosis of renal colic is correct, both renal and extrarenal disease processes may be missed if no imaging study is done on the patient with suspected renal colic. However, it is not clear that it is necessary to find all those processes during the patient's ED stay. Clinicians must decide how confident they are in their diagnosis and rule out immediate life threats. This is especially true in the elderly, for whom the margin for error is slim. If a decision is made not to study a patient, close follow-up must be assured so that there is another opportunity to determine other pathology. This author (DEM) recommends imaging all patients with a history consistent with a first-time stone. IMAGING MODALITIES
Which imaging modality is best depends both on its accuracy in identifying ureteral stones and the presence of obstruction, as well as on its ability to identify disease that mimic renal colic. If renal infarction is included in the differential diagnosis, it is important that the imaging modality assess the functional status of the kidneys. Additionally, consideration must be given to the side effects of the tests. Five radiographic modalities can be used to evaluate patients with renal colic: plain abdominal radiography, ultrasound, IVP, helical CT, and magnetic resonance imaging (MRI) (Table 1). PLAIN ABDOMINAL RADIOGRAPHS
Many texts and articles tout the plain radiograph as being able to detect 90% of all renal stones.36This practice was challenged in a 1985 study whose results showed a sensitivity of 62% and a specificity of 67?'0.'~ Aside from its lack of accuracy in diagnosing renal stones, the plain film provides little information about other sources of flank pain and no information about the functional status of the kidney.= If the clinician plans to advance to another study, the utility of a KUB is even less within the ED. However, if the stone is radiopaque, the urologist may be able to follow its progression with KUB films. ULTRASOUND
A 1988 study prospectively evaluated 85 patients with the suspected diagnosis of renal colic with both ultrasound and IVP. Both the ultra-
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Table 1. COMPARISON OF IMAGING MODALITIES FOR RENAL STONES
Study
Functional Assessment
lVP Yes Helical CT No, unless contrast given Ultrasound No, unless ureteral jets Study
IVP
Pregnancy
Yes, but radiation dose
Helical CT No, radiation to fetus too high Ultrasound Preferred study
.
Detect Obstruction Detect With Hydronephrosis Hydronephrosis
Extrarenal Disease
Yes Yes
Yes Maybe
No Yes
Yes
No
No
Operator Dependent
Time
Contraindications
No
1 hour plus
No
15 min
Contrast allergy, dehydration renal insufficiency >1.5, diabetes, multiple myeloma Pregnancy
Yes
45 minplus
None
sound and IVP identified calculi in 44 patients (sensitivity of 64% and specificity of 100%). Ultrasound indirectly identified another 21% and IVP another 26%, by detecting hydronephrosis alone (respectivesensitivities of 85% and go%, specificities of 100% and 94%).This study suggests that ultrasound in experienced hands is as effective as IVP in diagnosing stones.32 The diagnosis of renal stones by both IVP and ultrasound must sometimes be made indirectly through the diagnosis of obstruction. Follow-up is, therefore, very important to ensure the obstruction is not caused by another cause.12However, an acutely obstructed kidney may have only mild hydronephrosis, which can easily be overlooked on ultrasound. Additionally, abdominal ultrasound may be difficult secondary to overlying pelvic structures. With this in mind, use of the transvaginal ultrasound has improved identification of stones at the UV junction. Use of ultrasonographic diagnosis of renal stones depends to a great extent upon the skill of the ultrasonographer as well as the extent of the disease. The examination may be negative because of incomplete or early complete obstruction or because of an inexperienced sonographer. If this is the case, examination by another modality may still be necessary. New developments with the use of doppler ultrasound to detect ureteral jets as well as resistive indexes may make this a more effective modality. A resistive index of > 0.70 is considered suggestive of acute obstruction, but it is not reliable.31Ureteral jets are compared for symmetry but are only useful if the patient has sufficient urinary output.
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Despite these limitations, ultrasound remains the study for pregnant women and perhaps children (see Fig. 1A and B). IVP
In the discussion of ultrasound versus the gold standard of IVP, the clinician must remember three pearls. Stones are irregularly shaped, often causing incomplete obstruction without hydronephrosis. Administration of contrast causes a brisk diuresis, which may accentuate the degree of dilation. Most importantly, the IVP evaluates renal function. The IVP has long been considered the gold standard in evaluating
Figure 1. Ultrasounds. A, Dilation of the ureter associated with obstruction. B, identifying a stone with shadowing.
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for urolithiasis. However, the helical CT in many institutions has recently supplanted it for the evaluation of acute renal colic in the ED. IVP remains an effective method for detecting urolithiasis and its complications. It can identify the stone or the obstruction related to it with a sensitivity approaching go%.* The IVP visualizes the entire urinary tract and assesses the functional status of the kidney. Relative contraindications to IVP include allergy to contrast agents, renal insufficiency with creatinine > 1.8 mg/dL, diabetes, multiple myeloma, and dehydration. The incidence of allergic reactions resulting from the IVP contrast is approximately 0.1% and may be highest in patients with iodine and shellfish allergies. Those with a questionable history of contrast allergy can receive intravenous steroids and antihistamines or undergo a helical CT. Patients with a known history of contrast allergy should avoid the use of contrast media. Patients with an iodine allergy may receive nonionic contrast. The IVP may show the position of the stone. A delayed nephrogram or hydronephrosis is associated with obstruction. Columnization may occur at the point of obstruction. It is important to obtain delayed films until the diagnosis is made. Because obstruction and delay are common, it is typical ED practice to take successive films at increasing time intervals until two successive films document columnization at the site of the stone. All of these patients should receive urologic follow-up. Extravasation may be due to rupture of a renal calyx or less commonly, the ureter (Fig. 2A). In the absence of infection, rupture typically does
Figure 2. IVPs. A, Extravasation of contrast within Gerota’s fascia. B, Complete obstruction. Note the lack of uptake in the left.
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not require any specific therapy. If the kidney shows no uptake at all, concern for complete obstruction or a renal infarction must be raised (Fig. 2B). An ultrasound or arteriogram can evaluate the latter. MRI
The new modality of MRI urography was evaluated for the assessment of ureteric obstruction in a recent study (Fig. 3). With the HASTE MRI urography, all 41 cases of acute and chronic obstruction were noted. The MRI was able to determine chronic versus acute obstruction by signals read as perirenal fluid surrounding 20 of the 23 acutely obstructed kidneysz5MRI is difficult to use in the ED setting for all the usual reasons (cost, access, presence of magnetically active implants, and patient monitoring), but it may be beneficial in the patient with renal failure or contrast dye allergies. It needs to be compared against the less expensive helical CT scan. One benefit is that the functional status of the kidneys can probably be assessed using gadolinium contrast while the patient is in the MRI.3 HELICAL CT SCANS
The advent of noncontrast helical CT scanning has added a new diagnostic modality to the evaluation of renal stones. A small 1995 study (20 patients) compared noncontrast helical CT to IVP in the evaluation
Figure 3. MRI image of kidneys, ureter, and bladder. This is a normal study.
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of acute flank pain. Of the 20 patients, 12 were shown to have obstruction. All 12 were identified by both IVP and noncontrast helical CT. The CT showed a stone as the presumptive cause of obstruction in 11, whereas the IVP identified the stone in only five patients. Also, CTdiagnosed torsion of a paratubal cyst as the cause of pain in one patient who did not subsequently undergo an IVP. This small study suggests that noncontrast CT scans are as effective as IVP in diagnosing obstruction and better delineated the position of the It also suggests that the helical CT can identify other sources of pain when a stone is not the cause. A 1997 study prospectively evaluated 100 patients who presented to the ED with acute flank pain using helical CT scanning. The results were compared with the gold standard of spontaneous passage, retrieval, or identification of the stone on retrograde pyelography. CT demonstrated a stone in 55 patients and no ureteral obstruction in the other 45. CT was able to determine an apparent cause of the flank pain in 14 of the patients without a stone. Incidental extra-renal disease was identified in 11 additional patients (11Y0).The results showed that 50 of the documented 51 stones were identified, and that 38 of the 38 patients without stones were appropriately identified: a sensitivity of 98%, specificity of loo%, positive predictive value of loo%, and negative predictive value of 97%. The authors mention that the spiral CT would not be expected to evaluate renal function or the urothelium without the additional step of giving c o n t r a ~ t . ~ In many institutions, the non-contrast helical CT has become the study of choice for suspected renal colic (Fig. 4). It is able to identify radiolucent and radiopaque stones and/or hydronephrosis. It can help diagnose other causes of flank pain such as AAA, ovarian cysts, and
Figure 4. CT scan showing left hydronephrosis with perinephric stranding.
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appendicitis. The helical CT does not, however, evaluate the functional status of the kidney. Another advantage of the helical CT scan is that the test is completed quickly, whereas an IVP may require hours of follow-up film. In the ED, this time advantage may be significant. In this author’s opinion (JT), the helical CT scan is the imaging modality of choice for renal colic in the ED. ED TREATMENT Hydration
Patients who have clinical dehydration secondary to vomiting and decreased oral intake should receive intravenous fluid hydration. The idea that aggressively hydrating the patient will cause a ”pressure head” that would help the stone migrate down the ureter is debatable. Previously mentioned studies show that glomerular filtration rate for the obstructed kidney decreases. As well, overly aggressive hydration may dilute the IVP contrast and produce a less than optimal study. Conversely, giving IVP contrast to a dehydrated obstructed kidney is not advisable. The prudent approach is gentle rehydration. Analgesia
Rapid and adequate pain control should be a top priority in the initial management of a patient with renal colic. Opiate analgesics with antiemetics have long been the standard. However, it has recently been shown that nonsteroidal anti-inflammatory drugs (NSAIDs) will not only decrease the pain, but also have anti-prostaglandin effects that decrease the subsequent inflammatory response, and may even promote relaxation of the ureteral smooth m ~ s c l e . ~ The only available parenteral NSAID is ketorolac. If the patient is not vomiting, the NSAID can be given orally. Ketorolac is safe in the majority of patients with renal colic, despite case reports to the contrary. However, NSAIDS should be avoided in patients with know peptic ulcer disease, renal insufficiency, and pregnancy. They should be used judiciously in elderly patients and patients with diabetes, hypertension, and dehydration. Ketorolac should be avoided in those patients with greater than 1 week of o b s t r ~ c t i o n . ~ ~ ADMISSION
Admission criteria vary from institution to institution (List 2). Regional variations should be learned. However, there are some frequently quoted absolute and relative indications for admission.
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List 2. Admission Criteria Absolute Indications Intractable vomiting Intractable pain Single kidney or transplanted kidney with obstruction Concomitant urinary tract infection with obstruction Hypercalcemic crisis Relative Indications Fever Stone larger than 6 mm Solitary kidney Kidney transplantation High grade obstruction Intrinsic renal disease Urinary extravasation Social issues
Patients with an obstructing stone and evidence of infection should be admitted for decompression and intravenous antibiotics. Patients with intractable vomiting and/or pain should be admitted for intravenous hydration and symptom control. A single functional kidney or history of transplantation with obstruction should be admitted. Febrile patients due to UTI with a stone should be admitted because this probably represents a subclinical pyelonephritis. Hypercalcemic crisis in a patient with stones should also be admitted. Relative indications for admission include a solitary kidney or transplantation without obstruction, an unobstructed stone with a concomitant UTI, patients with intrinsic renal disease, and social issues preventing proper outpatient management. Complete obstruction and/or extravasations were previously considered to be absolute indications for admission. However, most urologists feel that these patients require only close follow-up, because they are not going to intervene emergently. CONSULTATION
The urologic consultant is available to the emergency medicine physician for three issues: admission, request for consultation on patients with relative indications for admission, and clarification of care on a complicated case. The goal of this monograph is to clarify the care of a majority of patients with renal colic. OUTPATIENT CARE
Patients should be discharged with a combination of an NSAID and a narcotic analgesic. They should be encouraged to maintain adequate
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hydration to maintain clear urine. Patients should strain their urine until the stone passes. They should return for medical evaluation for a fever of greater than 100.4 F, uncontrollable pain or vomiting, or if they develop abdominal pain and tenderness. If they pass the stone, they should bring it in for analysis if the etiology of their stones has not been previously established. COMPLICATIONS Obstruction
Does the presence of obstruction cause any change in the treatment or disposition of a patient with renal colic? If obstruction occurs in the presence of an infection, the obstruction must be relieved emergentlypossible. However, if obstruction occurs in the absence of infection, how long does it take for irreversible damage to occur? Decreases in renal blood flow as well as in ureteral pressures in the obstructed kidney begin 5-18 hours after obstruction. The degree of the reversibility of this process is not clear.20A decrease in both the glomerular filtration rate and renal plasma flow has been noted in both partially and completely obstructed kidneys.", l5 Hypertrophy of the ureteral musculature occurs after as little as three days of obstru~tion.~ Scar formation was noted if the obstruction continued for 2 weeks. One 1954 study evaluated the effect of 1 week of complete ureteral obstruction on kidney function. Within 1 hour of release, the obstructed kidney functioned at only 25% of its preobstructed glomerular filtration rate. However, the contralateral kidney was functioning at 165% its baseline glomerular filtration rate. The function of the obstructed kidney continued to improve for up to 2 months but stabilized at a level below its pre-morbid ~0ndition.l~ In contrast, a more recent 1997 study reviewed the role of renal resistive indexes in stages of obstruction and release. After relief of obstruction, the previous decrease in effective renal plasma flow and increase in the renal resistive index returned to near baseline levels.31 Despite the conflicting studies, a prominent urologic textbook states that "detectable renal damage does not occur in previously normal kidneys until complete obstruction has been present for 4 weeks."19 Although the studies reviewed would suggest that some damage may occur, urologists concur that obstruction in the absence of infection does not need to be acutely treated as long as there is a functioning contralateral kidney. Infection
A UTI in the presence of an obstructed stone is a urologic emergency. Obstruction causes increased renal pelvic pressure. Hydrostatic
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pressure represents the net difference between the renal capillary and Bowman’s space. Thus, obstruction reduces hydrostatic pressure and reduces glomerular filtration. Antibiotics cannot be excreted unless obstruction is decompressed. Intravenous antibiotics (Floroquinones, Gentamycin) to cover for the usual organisms should be administered. A urologist should be consulted for decompression of the obstruction as it effectively causes an abscess. UTIs in the patient with ureteral stones without obstruction can often be treated with oral antibiotics and close follow-up (24 hours). Renal Stents The care of patients with renal stents in patients with renal stones is covered elsewhere in this text under the chapter ”Infections in Patients with Indwelling Devices.” Patients with stents that complain of increasing pain or bleeding should be evaluated for migration of the stints as well as for obstruction. This can be done with a KUB and ultrasound or a helical CT. The urologist should be consulted as to the disposition and continued care of this patient. SPECIAL CONCERNS Pregnancy Issues The evaluation for a possible kidney stone in a pregnant patient arises in two unique problems: the dose of radiation to the fetus and the normal physiologic dilation of the ureters.35Ionizing irradiation of the fetus may increase the risk of teratogenicity, childhood cancer, or mental retardation. For these reasons, the dose of ionizing radiation should be minimized in pregnant women, especially those at less than 16 weeks gestation. The upper urinary tract begins to dilate in the first trimester and progresses until delivery. Involvement is greatest on the right. Ultrasound may be able to distinguish between physiologic dilation and calculus and does not carry the risk of radiation. With improvements in ultrasound diagnosis as well as the use of transvaginal ultrasound, the ability to detect a stone is increasing.lO, Ultrasound should therefore be the modality of choice in the evaluation of a possible renal stone in pregnant patients. If it is negative, the IVP may be performed if the benefit outweighs the risk to the fetus. A limited IVP ( 3 4 films) is relatively contraindicated after the first 16 weeks of pregnancy (Fig. 5) because this yields a radiation dose of less than 2 rads. A dose of approximately 20 rads in the first trimester is considered teratogenic. Consultation with an obstetrician/gynecologist and the urologist should be made to determine the best approach for women less than 16 weeks pregnant, or if more extensive testing is needed.
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Figure 5. IVP during pregnancy showing hydronephrosis.
Pediatric
Stone disease is uncommon in children. Therefore, one must maintain a high level of suspicion to be able to diagnose these patients. Of note, unusual dietary patterns, such as the ketogenic diet for intractable seizures, have been associated with stone formation. As well, these patients should be referred for a metabolic work-up for the etiology of their stone formation. Some authors suggest that ultrasound is the study of choice for children because of the radiation exposure and/or use of contrast.34The indications for admission remain the same. All children with urinary calculi need to be followed by a urologist, as there is a likelihood that they have metabolic stone disease. Thus, all pediatric stone formers eventually should be worked up for metabolic stone disease as outpatients. Geriatric
Remember that first-time stones do not usually first occur beyond the age of 50. Therefore, the differential diagnosis of diseases that mimic renal colic is very important in these patients. Acute abdominal aortic aneurysms and acute myocardial infarctions top this list. It is imperative to establish a diagnosis in these patients. This will invariably include imaging the patient with a helical CT to evaluate both the aorta and the renal system. Remember that without dye, the helical CT cannot diagnose an infarcted kidney. Finally, these patients do not tolerate narcotics or NSAIDS as well as the younger population. Concurrent medications and/or diseases may preclude their use.
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Pitfalls
1. Failure to image the elderly or first-time stone-patient to establish a definitive diagnosis. 2. Failure to consider stone disease in a patient with absence of hematuria. 3. Failure to diagnose infection with an obstructed stone. References 1. Begun FP, Foley WD, Peterson A, White B: Patient evaluation: Laboratory and imaging studies. Urologic Clin North Am 24:l-11, 1997 2. Balaji KC, Menon M Mechanism of stone formation. Urologic Clin North Am 24:l11, 1997 3. Choo SW, Kim SH, Jeong YG, et al: MR Imaging of segmental renal infarction: An experimental study. Clin Rad 52:6568,1997 4. Coe FL, Parks JH, Asplin Jr: The pathogensis and treatment of kidney stones. N Engl J Med 3271141-1152, 1992 5. Cordell WH, Wright SW, Wolfson AB: Comparison of intravenous ketorolac, meperidine, and both (balanced analgesia) for renal colic. Ann Emerg Med 28:151-158, 1996 6. Elliot JS, Eusebio E: Calcium oxalate solubility: The effects of trace metals. Invest Urol 4:428430, 1967 7. Fielding JR, Steele G, Fox LA, et al: Spiral computerized tomography in the evaluation of acute flank pain: A replacement for excretory urography. J Urol 1572071-2073, 1997 8. Finlayson B, Smith A: Stability of first dissociable proton of uric acid. J Chem Eng Data 19394-97, 1974 9. Gee WF, Kiviat M D Ureteral response to partial obstruction. Smooth muscle hyperplasia and connective tissue proliferation. Invest Urol 12:309-316, 1975 10. Gorton E, Whitfield H N Renal calculi in pregnancy. Br J Urol 8O(supp 1):4-9, 1997 11. Jones DA, Atherton JC, OReilly Ph, et al: Assessment of the nephron segments involved in post-obstructive diuresis in man, using lithium clearance. Br J Urol64:559563, 1989 12. Juul N, Brons J, Torp-Pedersen S, et a1 Ultrasound versus intravenous urography in the initial evaluation of patients with suspected obstructing urinary calculi. Scand J Urol Nephrol Supp113745-47,1991 13. Kerr WS Jr: Effect of complete ureteral obstruction for one week on kidney function. J Applied Physiol 6762-772, 1954 14. Labrecque M, Dostaler LP, Rousselle R. Efficacy of nonsteroidal anti-inflammatory drugs in the treatment of acute renal colic. Arch Int Med 1541381-1387, 1994 15. Lackner H, Barton LJ: Cortical blood flow in ureteral obstruction. Invest Urol 8:319323, 1970 et a1 Renal Artery embolism: Clinical features 16. Lessman RK, Johnson SF, Coburn JW, and long term follow-up of 17 cases. Ann Intern Med 89:477-482, 1978 17. Mandel NS, Mandel GS: Urinary tract stone disease in the United States veteran population: I. Geographical frequency of occurrence. J Urol 142:1513-1515,1989 18. Marston WA, Ahlquist R, Johnson G Jr, Meyer AA. Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg 16:17-22, 1992 19. Menon M, Parulkar BG, Drach G W Urinary lithiasis: Etiology, diagnosis, and medical management. In Walsh PC, Retik AB, Vaughan ED, Wein AJ (eds): Campbell’s Urology, ed 7. Philadelphia, WB Saunders, 1998, pp 2661-2705 20. Moody TE, Vaughan ED Jr, Gillenwater JY Relationship between renal blood flow and ureteral pressure during 18 hours of total unilateral ureteral occlusion. Invest Urol 13:246-251, 1975 21. Murthy LNS: Urinary tract obstruction during pregnancy: Recent developments in imaging. Br J Urol; 8O(suppl 1):l-3, 1997
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22. Mutgi A, Williams JW, Nettleman M Renal colic: Utility of the plain abdominal radiograph. Arch Intern Med 151:1589-1592, 1991 23. Perlmutter A, Miller L, Trimble LA, et al: Toradol, an NSAID used for renal colic, decreases renal perfusion and ureteral pressure in a canine model of unilateral ureteral obstruction. J Urol 149:92&930, 1993 24. Prince CL, Scardino PL, Wolan TC: The effect of temperature, humidity, and dehydration on the formation of renal calculi. J Urol 75:209, 1956 25. Regan F, Bohlman ME, Khazan R, et al: MR Urography Using HASTE Imaging in the Assessment of Ureteric Obstruction. AJR 167 1115-1120, 1996 26. Rizolli R, Bonjour JP: Management of disorders of calcium homeostasis. Baillieres Clin Endocrinol Metab 6129-142, 1992 27. Robertson WG, Peacock M The pattern of urinary stone disease in the United Kingdom in relation to animal protein intake during the period 1960-1980. Urol Int 373394-399, 1982 28. Roth CS, Bowyer BA, Berquist TH: Utility of the plain abdominal radiograph for diagnosing ureteral calculi. Ann Emerg Med 14311-315, 1985 29. Sharma RN, Shah I, Gupta S, et al: Thermogravimetric analysis of urinary tones. Br J Urol64:564566, 1989 30. Shokeir AA, Nijman RJ, El-Azab M, et al: Partial ureteral obstruction: Role of renal resistive index in stages of obstruction and release. Urology 49:52%535, 1997 31. Sinclair D, Wilson S, Toi A, et al: The evaluation of suspected renal colic: Ultrasound scan versus excretory urography. Ann Emerg Med 18:55&559, 1989 32. Smith RC, Rosenfield AT, Choe KA, et a1 Acute flank pain: Comparison of noncontrast-enhanced CT and intravenous urography. Radiology 194:789-794, 1995 33. Stapleton FB: Clinical approach to children with urolithiasis. Semin Nephrol 16:387397, 1996 34. Strothers L, Lee LM. Renal colic in pregnancy. J Urol 1483383-1387, 1992 35. Tasso SR, Shields CP, Rosenberg CR, et al: Effectiveness of selective use of intravenous pyelography in patients presenting to the emergency department with ureteral colic. Acad Emerg Med 4:780-785, 1997 36. Twinem FP: Some radiographic aspects of urinary calculi. Am J Surg 17389-394, 1932 37. Wrenn K. Emergency intravenous pyelography in the setting of possible renal colic: Is it indicated? Ann Emerg Med 26, 1995
Address reprint requests to David E. Manthey, MD, FACEP, FAAEM Department of Emergency Medicine Wake Forest University School of Medicine Medical Center Boulevard Winston-Salem, NC 27157