66 Marius C. Conradie Netcare Waterfall City Hospital, Johannesburg, South Africa Acute renal colic is probably the most painful event a person can endure. Renal colic affects approximately 1.2 million people each year and accounts for approximately 1% of all hospital admissions. Most active emergency rooms treat an average of at least one patient with acute renal colic every day, depending on the size of the hospital [1]. Renal colic is often the supposed diagnosis made in the emergency room in patients presenting with an acute onset of flank or loin pain. Often, multiple investigations are done before the diagnosis is confirmed. Frequently this causes a delay in appropriate management. It is up to the attending physician or urologist not only to make a prompt diagnosis but also to initiate effective pain control and identify potentially complicated renal colic. Patients with acute renal colic classically present with a sudden onset of severe pain originating in the flank. The initial presentation typically lasts 3–18 hours. The progression of pain has been described as having three clinical phases. The typical attack starts slowly and insidiously. The pain typically waxes and wanes in severity, and develops in waves or paroxysms that are related to movement of the stone in the ureter and associated ureteral spasm. Paroxysms of severe pain usually last 20–60 minutes. Pain is thought to occur primarily from urinary obstruction with distension of the renal capsule. The pain reaches its maximum 1–2 hours after the start. In the constant phase, the period of sustained maximal pain, the pain tends to remain constant until it is either treated or allowed to improve spontaneously. Most patients arrive in the emergency room during this phase of the attack. In the final phase of renal colic, relief can occur spontaneously at any time after the initial onset and most commonly lasts 1.5–3 hours. The pain may localize at different sites of the abdomen depending on the exact position of the calculus in the urinary tract. Stones commonly become impacted in the urinary tract in a calyx, at the ureteropelvic junction, at the pelvic brim where the ureter begins to arch over the iliac vessels, at the broad ligament in females, and at the ureterovesical junction, which is the most common site of impaction. Pain from upper ureteral calculi tends to radiate to the flank and lumbar areas. Mid‐ureteral calculi cause pain that radiates anteriorly and caudally. Distal ureteral calculi cause pain that tends to radiate into the groin or testicle in the male or labia majora in the female. If a calculus is lodged in the distal intramural part of the ureter, symptoms may mimic detrusor overactivity or cystitis. These symptoms include suprapubic pain, urinary frequency, urgency, dysuria, or pain at the tip of the penis in men. On examination of the abdomen, the pain localizes to the costovertebral angle. The remaining examination findings are often unremarkable. The characteristic difference between patients with renal colic and those with an acute abdomen lies in the restlessness of patients with renal colic. Patients with an acute abdomen of surgical origin usually lie as still as possible. Rebound tenderness will be present in an abdomen with peritonitis. The pain is generally diffuse in an acute abdomen as opposed to renal colic where the patient can often point to the site of maximum tenderness, which is likely to be the site of the ureteral obstruction. Hematuria is often associated with renal colic. However, 15% of all patients with urinary calculi do not have hematuria [2]. Therefore, the lack of hematuria does not exclude the possibility of acute renal colic. Other clinical signs that may be encountered are fever, chills, nausea, vomiting, and tachycardia. The presence of pyuria, fever, leukocytosis, or bacteriuria suggests the possibility of a urinary infection and the potential for an infected obstructed kidney. This is a potentially life‐threatening situation and should be treated as a surgical emergency. Renal colic is the consequence of the acute dilation of the urinary tract proximal to an obstruction along with smooth muscle spasm at the site of the obstruction. High intrarenal pressure promotes local synthesis and release of prostaglandin E2 with subsequent vasodilation of the afferent arterioles, which promotes diuresis and a further rise in renal–pelvic pressure, potentially exacerbating the patient’s pain. In addition, ureteral smooth muscle spasm is directly stimulated by prostaglandin E2 [3]. Most of the pain receptors of the upper urinary tract responsible for the perception of renal colic are located submucosally in the renal pelvis, calyces, renal capsule, and upper ureter. Acute distension seems to be most important in the development of the pain of acute renal colic. Muscle spasm, increased proximal peristalsis, and local inflammation at the site of obstruction may contribute to the development of pain through chemoreceptor activation and stretching of submucosal free nerve endings. Renal colic pain rarely, if ever, occurs without obstruction. The initial renal response to acute unilateral ureteral obstruction is the release of prostaglandins, especially E2, resulting in vasodilatation of the afferent arterioles and worsening of ureteral smooth muscle spasm. Subsequently, the dilation of the afferent arterioles results in an increase in renal blood flow and glomerular filtration rate [4]. As a consequence, more urine is produced, and the renal pelvis and ureter dilate further. Distension of the renal pelvis initially stimulates ureteral hyperperistalsis. Peak hydrostatic renal pelvis pressure is attained within 2–5 hours after a complete obstruction. The initial phase of obstruction lasts approximately 1.5 hours and is followed by vasoconstriction of the efferent arterioles with a resultant decrease in renal blood flow. Eventually, the afferent arterioles constrict and ureteral pressures fall [4]. By this time, intraureteral pressures have returned to normal, but the proximal ureteral dilation remains and ureteral peristalsis is minimal. The interstitial edema of the ipsilateral kidney enhances fluid reabsorption, which helps to increase the renal lymphatic drainage to establish a new, relatively stable, equilibrium. At the same time, renal blood flow increases in the contralateral kidney as renal function decreases in the obstructed kidney. The return of renal function after a period of complete unilateral ureteral obstruction is an important clinical concern for the urologist. The renal function recovery rate after 1 week of ureteral obstruction is 100%, but after 4 weeks only a 30% recovery can be expected [5]. If only a partial obstruction is present, the same changes occur, but to a lesser degree. The diagnosis of renal colic is often made based on clinical symptoms alone, although confirmatory tests are usually performed. Additional tests are useful not only to confirm the diagnosis but also to facilitate in the decision‐making process on further treatment. Before a decision on treatment can be made, a urologist must know the size, shape, orientation, radiolucency, and location of the stone. Other factors that may influence further treatment are kidney function and the presence of infection, as well as all other clinical information and comorbid conditions the patient may have. Patient history, physical examination, and urinalysis alone cannot help confirm or exclude urolithiasis with sufficient accuracy. In particular, hematuria testing has a sensitivity of 81–84% and a specificity and negative predictive value of 48 and 65%, respectively [6, 7]. In addition to the presence of blood in the urine, the presence or absence of leukocytes, crystals, and bacteria, and the urinary pH should be documented. A urinary tract infection should be suspected if the number of white blood cells (WBCs) in the urine is greater than 10 per high‐power field. Determining urinary pH may be helpful in planning treatment. With a pH lower than 6.0, a uric acid stone should be considered. The observation of cystine, uric acid, struvite, or calcium oxalate crystals in the urine may be an indication of the type of calculus ultimately found. While mild leukocytosis often accompanies a renal colic attack, a high index of suspicion for a possible infection should accompany any serum WBC count of 15 000/µl or higher in a patient presenting with an apparent acute kidney stone attack, even if afebrile. Urea, creatinine, and electrolyte testing may be helpful in identifying patients with renal function impairment as well as in giving some information on the hydration status of the patient, which may determine their further management. The historical cornerstone of the evaluation of renal colic was a radiograph of the kidneys–ureters–bladder (KUB). Not all urinary calculi will be visible on the KUB radiograph because of their small size, calculus radiolucency, or overlying bowel gas. Typically, 90% of calculi are radiopaque. However, many calcifications that can be observed on the KUB radiograph are not calculi, but phleboliths, vascular calcifications, calcified lymph nodes, or bowel contents. Typically the differentiation between a phlebolith and a urinary calculus becomes easier when the KUB radiograph demonstrates a lucent center, identifying the calcification as a phlebolith. However, this central lucency is not observed as often on computed tomography (CT) scans. The KUB radiograph is also quite accurate for helping determine the size and shape of a visible radiopaque calculus. It uses the same orientation and anatomic presentation that is observed on fluoroscopy images during endoscopic ureteral surgery. Also, the progress of the stone can be easily monitored with a follow‐up radiograph. For these reasons, many urologists recommend a KUB in addition to a CT scan in the workup of renal colic (Figure 66.1). Figure 66.1 (a) Distinguishing renal calculi from phleboliths in the pelvis can be intricate. This axial noncontrast CT demonstrates two phleboliths in the pelvis. One demonstrates the comet‐tail sign, which is a soft‐tissue attenuation leading to the phlebolith and represents a vein in which it is located. (b) On a KUB radiograph, a phlebolith classically demonstrates a central lucency whereas ureteral calculi do not. Renal ultrasound is most useful in diagnosing relatively large calculi within the renal pelvis or kidney. However, it is less useful than other modalities for detecting ureteral calculi. One benefit is that it can easily diagnose any significant hydronephrosis. Ultrasound can also be used to diagnose other pathologic conditions such as abdominal aortic aneurysm or cholelithiasis, which can sometimes be mistaken for acute renal colic. Combining a renal ultrasound with a KUB radiograph can be adopted as a reasonable alternative when a CT scan cannot be performed. Intravenous urography (IVU) has been the imaging modality of choice for investigating acute renal colic since Osborne et al. first described it in 1923 [8]. It provides detailed information about the anatomy of the renal collecting system and ureters, offers some information about renal function and the degree of obstruction, and is good for the planning of calculus surgery (Figure 66.2). When a patient has multiple pelvic calcifications, identifying the actual stone is simple with an IVU and it can also show nonopaque calculi as filling defects. Figure 66.2 (a) An IVU obtained in a patient with renal colic demonstrates a calculus <6 mm, normal anatomy, and no signs of obstruction, which makes for the ideal candidate for conservative management or medical expulsive therapy. (b) IVU image demonstrates a calculus >6 mm at the ureteropelvic junction in the lower moiety of a kidney with complete ureteral duplication. This represents a clear indication for a surgical intervention. There are, however, limitations: adequate bowel preparation is necessary for good‐quality studies, and there is a risk of contrast‐related allergic and anaphylactic reactions (10 and 1% of patients, respectively) [9]. Also, in patients with renal failure and diabetes mellitus, the risk of contrast‐induced nephrotoxicity is 25% [10]. A serum creatinine level of more than 2 mg/ml is a relative contraindication to the use of intravenous contrast. Furthermore, there may be a need for delayed films if there is high‐grade obstruction, which can lead to delays in diagnosis and treatment. The classic finding of acute ureteral obstruction is a persistent nephrogram, caused by an increase in the intrarenal concentration of the contrast. Even without observing any specific calculus, the presence of a persistent nephrogram in one kidney with prompt contrast excretion by the contralateral kidney is highly suggestive of ureteral obstruction secondary to a calculus. There may also be columnization on the delayed films. Extravasation of contrast around the collecting system may be a sign of a ruptured fornix, while pyelolymphatic backflow indicates that contrast has entered into the renal lymphatic drainage system. Both are considered signs of a more severe ureteric obstruction. The use of a noncontrast helical CT (NCCT) scan to assess patients with acute flank pain was first reported in 1995 by Smith et al. [11]. Recent studies have shown that NCCT is more accurate and reliable than IVU in making a diagnosis in patients presenting with acute flank pain. NCCT has both sensitivity and specificity of 94–100% compared with 60–94% for IVU, partly because NCCT clearly demonstrates both radiopaque and radiolucent stones, as well as detecting alternative causes for a patient’s symptoms [12, 13]. Unrelated pathology may be detected by NCCT in 28% of patients [14]. Moreover, NCCT does not require special preparation or intravenous contrast, thus avoiding the risk of contrast‐associated reactions and allowing imaging studies to be completed in a few seconds, which improves image quality by reducing respiratory motion and artifact [15, 16]. For these reasons, NCCT has displaced IVU to become the investigation of choice for acute flank pain in many institutions across North America, Europe, and Australasia [13, 17, 18]. Very finely spaced scans are taken through the kidneys and bladder areas, where symptomatic calculi are most likely to be encountered (Figure 66.3). A KUB radiograph is sometimes automatically included in a renal colic study, as mentioned. Figure 66.3 Classic example of a calculus <6 mm in the intramural part of the ureter. Conservative management or medical expulsive therapy would be an appropriate course of action. Katz et al. found that CT scan estimates of stone size to be similar to those determined by plain film radiography [19]. Both the estimated mean stone diameter and the length were similar on CT and KUB. The limitation of this method is that if CT collimation is too large relative to the stone, the entire stone may not be scanned, leading to underestimation of stone length. This inaccuracy can be best compensated for by making sure that slices are small in relation to stone size. Therefore, 5 mm collimation is preferred to 10 mm collimation. In addition to verifying similarity of stone size estimates by CT and KUB, Katz et al. also found that the prediction of spontaneous stone passage was similar using the two imaging modalities. It is widely believed that transverse stone dimension is more important than length in predicting the likelihood of spontaneous passage. Interestingly, the study demonstrated the measured anteroposterior stone diameter on CT to be wider in many cases than the measured transverse diameter on CT and plain film. This result could be explained by orthogonal imaging in curved portions of the ureter, where larger anteroposterior diameters were found irrespective of stone location. At any given point along the CT scan, the ureter is either ascending or descending; therefore, an anteroposterior cut would slice tangentially, and cause a wider anteroposterior than transverse diameter. Phleboliths are often confused with ureteral calculi. On a KUB radiograph, the characteristic lucent center of a phlebolith is often visible, but is not present in a true calculus. Unfortunately, as mentioned above, CT scans usually fail to reveal this central lucency. The “rim sign,” originally reported by Smith et al. in 1995, is described as a rim or halo of soft tissue, visible on CT scans, that completely surrounds ureteral calculi [11]. This effect is enhanced by the local inflammation in the ureteral wall with subsequent edema at the site of the calculus. The rim sign is generally incomplete with phleboliths. The rim sign is more likely to be present in small stones up to 5 mm in diameter. Calculi, including relatively radiolucent uric acid calculi, and cystine and matrix stones, are easily identifiable on CT scan. While they do not contain calcium, they are still much denser than the surrounding soft tissue. The only exception is indinavir calculi, which are not visible on CT scans. These patients require an IVU that will demonstrate a filling defect. Currently, CT scans can be used to estimate the relative density of the calculus and composition to some extent. The mean peak Hounsfield reading of uric acid calculi and calcium oxalate calculi are around 344 ± 152 and 652 ± 490 HU, respectively [20]. Secondary signs of obstruction may be visible on CT scans. In some cases, if the stone passed shortly before the study, these signs may be the only evidence that the patient had a stone. These secondary signs include ureteral dilation with hydronephrosis and renal enlargement with streaking of the perinephric fatty tissue [2]. Although NCCT is unable to provide direct information on function and drainage, the degree of obstruction can be assessed by secondary signs, such as the severity of hydronephrosis and ureteral dilation and the presence of perinephric fluid, indicating forniceal rupture. Smith et al. found a high correlation between secondary signs of obstruction and the presence of a ureteral calculus. In particular, the combination of collecting system dilation and perinephric stranding had a positive predictive value of 98%, while the absence of both of these secondary signs had a negative predictive value of 91% [21]. The biggest advantage of a CT scan over an IVU lies in its ability to diagnose other underlying pathology mistaken for renal colic, such as aortic aneurysms, pancreatitis, appendicitis, ovarian problems, and bowel disorders. Disadvantages of a CT scan include difficulties in identifying a stone if the patient exhibits limited hydronephrosis with additional pelvic calcifications and the little information it gives on the renal function. Stone location can be described in anatomic terms, but the scan lacks the surgical orientation that most urologists prefer. Spiral CT scans can, however, allow for anatomic three‐dimensional image reconstruction, which may be useful in the evaluation and pretreatment planning (Figure 66.4).
Management of Renal Colic and Triage in the Emergency Department
Introduction
Classic presentation of renal colic: symptoms and signs
Mechanism of renal colic
Autoregulatory process associated with obstruction
Diagnosis
Laboratory investigations
Urinalysis
Hematologic tests
Imaging studies
Plain abdominal radiograph
Renal ultrasound
Intravenous urogram
Computed tomography scan
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