Renal Colic:

Renal colic, the most common presentation of nephrolithiasis, is encountered by primary care and emergency physicians alike. Although a number of other potentially serious disorders can cause renal colic, the diagnosis of stone disease is usually clinically evident and can be confirmed by laboratory investigations.

In this article, we describe a cost-effective diagnostic approach to the patient with renal colic. We also discuss appropriate management strategies, including newer therapies currently under investigation.

PATHOPHYSIOLOGY

Renal colic occurs in the setting of a fixed or dynamic urinary tract obstruction. Pain associated with urinary tract obstruction results from stretching of the mucosal or submucosal nerve endings of the collecting system or ureteral mucosa by stones and from interstitial edema and distention of the renal capsule.

The location of the obstruction largely determines the nature of the symptoms experienced by the patient. Table 1 lists symptoms associated with each anatomic area.

MAKING THE DIAGNOSIS

The term "renal colic" is a misnomer. Renal colic does not wax and wane like intestinal or biliary colic, but is relatively constant. The pain is of sudden onset and radiates across the abdomen along the course of the ureter; it may be referred to the groin or genital area. Changing position does not relieve the pain. In contrast, patients with acute peritonitis lie still and resist moving.

In patients with renal colic attributable to stone disease, the severity and location of the pain can vary depending on stone size, location and severity of the obstruction, and variations in anatomy and pain threshold. Occasionally, pain may be intermittent as a result of ureteral spasms caused by changes in intraluminal pressure. The character of the pain may vary as the stone passes down the ureter, or it may diminish with the transition from a hyperperistaltic to an aperistaltic ureter.¹

In addition to pain, patients with acute urinary tract obstruction often present with constitutional symptoms such as anorexia, nausea, vomiting, and abdominal distention. Fever, chills, tachycardia, and hypotension suggest infection.

History. In addition to a detailed history of pain and other constitutional symptoms, risk factors for stone formation should be identified as part of the initial screening and evaluation process.

Although an in-depth discussion of the risk factors for stone disease is beyond the scope of this article, careful consideration must be given to such factors as diet, physical activity, fluid intake, medications (such as indinavir, antacids, or acetazolamide), and a history of urinary tract infections (UTIs) or bowel surgery. If a patient has risk factors for or a family history of stone disease, a personal history of bilateral stone disease, or chronic recurrent UTIs, or if nephrocalcinosis is found on radiographic studies, a full metabolic evaluation is warranted.²

Small renal calculi-3 to 4 mm in diameter-are most commonly responsible for acute obstruction of the mid or distal ureter, which causes the most severe episodes of colic. Patients with large "staghorn" calculi are usually asymptomatic.

Physical examination. Examine the patient for signs of trauma, bruises, and skin changes over the area of pain. Chest examination may reveal diminished breath sounds resulting from atelectasis secondary to splinting of the chest wall. An abdominal examination is necessary to rule out appendicitis. In women, a pelvic examination is required to exclude ectopic pregnancy. An inguinal evaluation will help rule out hernias or scrotal lesions. Perform a digital rectal examination to evaluate the prostate gland for enlargement or masses. Hypoactive bowel sounds suggest peritoneal irritation. Palpate the neck to determine if a parathyroid adenoma is present. Although these tumors occur only rarely, they are associated with hypercalcemia and stone formation.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of renal colic is broad. Flank pain may originate from either renal or nonrenal causes (Table 2). Causes of blood clots that result in obstruction include glomerulonephritis, hemophilia, sickle cell disease, and tumors. Fungal bezoars (usually Candida or Aspergillus) are common in neonates and immunocompromised hosts. Commonly seen conditions that must be distinguished from renal colic include ectopic pregnancy, aortic aneurysm, and acute intestinal obstruction. One must also be alert for malingerers seeking pain medication or secondary gain.

DIAGNOSTIC STUDIES

Urinalysis. Hematuria (gross or microscopic) is the single most discriminate indicator of a kidney stone (other than the actual passing of gravel or a stone).³ An estimated 60% to 80% of patients with stones have hematuria.⁴ In one emergency department (ED) study, acute unilateral flank pain, hematuria, and positive results of abdominal radiography were present in about 90% of patients with a suspected stone.⁵ Hematuria may be absent in patients with complete obstruction and in some patients with ureterolithiasis.⁶ The presence of bacteria and white blood cells in the urine may suggest pyelonephritis (with or without renal stones). Crystals (oxalate, urate, cystine, or struvite) may be seen in the urine as well.

Serum chemistries. In the ED, a complete blood cell count and a renal function panel (electrolytes, blood urea nitrogen, and creatinine) give valuable clues to systemic involvement and to the presence of renal failure. Leukocytosis is usually associated with infection. Assessment of serum calcium, magnesium, phosphorus, and uric acid levels can help identify the pathophysiologic basis of stone formation. However, stone analysis remains the gold standard for determining the type of stone involved.

A patient with renal colic who presents with recurrent stone disease and/or risk factors for stone disease requires a comprehensive workup; this can be done on an outpatient basis or at a follow-up evaluation. Tests may include a 24-hour urine collection for pH, sodium, potassium, magnesium, phosphorus, oxalate, calcium, uric acid, and citrate. Urine volume and creatinine are measured to confirm the adequacy of the collection. Urine cultures are helpful in selecting appropriate antibiotics for UTIs and pyelonephritis.

Imaging options. Imaging is the cornerstone of an accurate diagnosis in a patient with renal colic.Kidney, ureter, and bladder (KUB) radiography is simple, inexpensive, and readily available. Sensitivity and specificity are limited by radiolucent uric acid stones, interference from bony structures, relatively inferior contrast resolution, and operator skills.More than 60% of calculi (calcium, struvite, and cystine) are radiopaque and demonstrable on KUB radiography. Stone mimics include calcified structures that may overlie the urinary tract. Examples of such structures are phleboliths, calcified lymph nodes, lateral margin of vertebral body transverse process, gallstones, and costochondral calcifications.

Ultrasonography is useful for evaluating pregnant women and patients with contrast allergy. It can detect urinary tract obstruction and radiolucent stones, as well as assess renal architecture, size, and echogenicity. Ultrasound scanning is highly sensitive for hydronephrosis, but it cannot detect small stones or ureteral stones. (In 1 study, sensitivity was only 19%.⁷) Moreover, it is expensive, and results are highly dependent on operator skills. Although massive hydronephrosis is easy to detect, subtle degrees may easily be missed.

Some experts have suggested that combining ultrasound with pulsed and color Doppler allows interrogation of the physiology of the urinary system to assess resistive indices and ureteral jets. However, because this technique is operator dependent and very tedious, it has not been employed routinely. A combination of imaging modalities may increase sensitivity and specificity.

Intravenous pyelography (IVP)(also called excretory urography)was long considered the preferred investigative procedure for the diagnosis of urolithiasis (Figure 1). IVP can identify the location, size, shape, and number of stones and provide information about the functional status of the kidney. It is highly sensitive and specific for obstructive uropathy. Limitations to its use include contrast allergy, cost, inadequate bowel preparation, renal failure, and the presence of ureteric stones. IVP is not usually ordered in the ED when the diagnosis is clinically evident. Caution is advised when intravenous contrast dye is administered to patients with diabetes who are taking metformin. Contrast dye is best avoided in diabetic patients with preexisting kidney disease; however, it is considered safe for those with normal renal function. Metformin should be withheld for 48 hours after the administration of contrast dye.^8,9

Noncontrast CT. This has now replaced IVP in the workup of renal colic and the diagnosis of nephrolithiasis and, where available, is considered the modality of choice (Figure 2). Noncontrast CT has a sensitivity of 95% and a specificity of 98%; it is 97% accurate for diagnosing stone disease. It is superior to IVP in identifying ureteral stones and as good as IVP in determining the presence or absence of ureteric obstruction.^10-12 CT is extremely valuable in patients in whom the clinical diagnosis is not certain, because it also picks up extra-urinary abnormalities, such as masses. One report found that, compared with IVP, helical CT was faster (26 vs 69 minutes) and only slightly more expensive.¹³

MANAGEMENT OPTIONS

Analgesia and volume expansion are cornerstones of the management of renal colic.

Analgesia. A summary of options is given in Table 3.

In addition to their analgesic and antipyretic properties,NSAIDs work at the site of injury to decrease inflammation and hyperperistalsis. They also seem to work centrally in synergy with narcotic agents.

Use NSAIDs with caution in patients with chronic kidney disease or acute renal failure; they may be contraindicated in patients with allergies, a history of peptic ulcer disease, gastritis, or bleeding diathesis. Because of the increased risk of perinephric-nephric bleeding, do not use NSAIDs in patients who are scheduled to undergo extracorporeal shock wave lithotripsy in the next 5 to 7 days.

Ketorolac is more effective and faster than meperidine.¹⁴

Narcotics.Opioids are first-line therapy for the relief of severe renal colic.Many of these agents have a spasmogenic effect on smooth muscle, although whether this is clinically significant is unclear. The most common side effects include nausea, sedation, mood alteration, hypotension, constipation, and rash. Combinations of narcotics, such as codeines with aspirin or acetaminophen, are also effective.

Selective cyclooxygenase (COX)-2 inhibitors.These agents have analgesic and anti-inflammatory properties with less severe GI and antiplatelet side effects than nonselective NSAIDs. Intravenous formulations of COX-2 inhibitors are not yet available, a factor that limits their use in patients who experience the nausea and vomiting that often accompany severe pain. In vitro work has shown selective COX-2 inhibitors to have the same inhibitory effect as indomethacin on human ureteral contractility.¹⁵ Studies are under way to establish the role of these agents in renal colic analgesia.

Desmopressin.This vasopressin analogue is being studied for pain relief in acute renal colic. Two trials have demonstrated its use in clinical practice, either alone or with diclofenac.^16,17

A recent case report described the successful use of subcutaneous paravertebral block in patients with persistent renal colic pain who were candidates for stone extraction.¹⁸

In a recent study, the addition of sustained-release nifedipine, corticosteroids, trimethoprim/sulfamethoxazole, and acetaminophen to a standard pain-relief regimen resulted in a higher stone passage rate and fewer lost work days, ED visits, and surgical interventions.¹⁹ However, the study was inadequately powered to assess the effect of any one intervention.

Volume expansion. This is an integral component of management because an increase in urine output helps patients pass stones. Patients should drink 2 to 3 liters of fluid or have a similar volume administered intravenously if they are experiencing nausea or vomiting. However, an increase in urine output can worsen pain because of the increase in hydronephrosis and ureteral function.²⁰

When to consider hospitalization. Table 4 lists several indications for hospitalization. However, most patients who present with acute renal colic and flank pain resulting from calculi are young and healthy and can be treated for their acute symptoms in the ED.

The results of imaging studies help determine whether hospitalization and urgent urologic referral are required. A patient with established stone disease can be discharged if the stone is smaller than 5 mm; most patients pass such stones spontaneously. Stones between 5 and 10 mm pass spontaneously in about 50% of cases; stones larger than 10 mm usually require surgical removal. A urologic consultation is warranted if the patient appears to have infection or renal insufficiency. If IVP reveals a nonfunctioning kidney or partially obstructed ureter, urgent urologic referral is necessary. You may wish to consult a urologist if you have chosen to hospitalize the patient. n

References:

REFERENCES:

1.

Gupta M, Stoller ML. Acute and chronic renal pain.In: Coe F, Favus MJ, Pak CYC, et al, eds. Kidney Stones:Medical and Surgical Management. Philadelphia: Lippincott-Raven; 1996:463-497.

2.

Nseyo UO, Weinman E, Lamm DL. Urology forPrimary Care Physicians. Philadelphia: WB SaundersCompany; 1999:93-107.

3.

Aronson MD, Rose BO. Approach to the patientwith possible urolithiasis. UpToDate. Available at:

http://www.uptodate.com

. Accessed July 16, 2002.

4.

Bretland PM. Acute ureteric obstruction-clinicaland radiological aspects. Proc R Soc Med. 1974;67:1215-1217.

5.

Elton TJ, Roth CS, Berquist TH, Silverstein MD.A clinical prediction rule for the diagnosis of ureteralcalculi in emergency departments. J Gen InternMed. 1993;8:57-62.

6.

Bove P, Kaplan D, Dalrymple N, et al. Reexaminingthe value of hematuria testing in patients withacute flank pain. J Urol. 1999;162:685-687.

7.

Yilmaz S, Sindel T, Arslan G, et al. Renal colic:comparison of spiral CT, US, and IVU in the detectionof ureteral calculi. Eur Radiol. 1998;8:212-217.

8.

Rasuli P, Hammond DI. Metformin and contrastmedia: where is the conflict? Can Assoc Radiol J. 1998;49:161-166.

9.

McCartney MM, Gilbert FJ, Murchison LE, et al.Metformin and contrast media-a dangerous combination?Clin Radiol. 1999;54:29-33.

10.

Smith RC, Verga M, McCarthy S, Rosenfield AT.Diagnosis of acute flank pain: value of unenhancedhelical CT. Am J Roentgenol. 1996;166:97-101.

11.

Vieweg J, Teh C, Freed K, et al. Unenhanced helicalcomputerized tomography for the evaluation ofpatients with acute flank pain. J Urol. 1998;160:679-684.

12.

Dalrymple NC, Verga M, Anderson KR, et al.The value of unenhanced helical computerized tomographyin the management of acute flank pain.J Urol. 1998;159:735-740.

13.

Chen MY, Zagoria RJ. Can noncontrast helicalcomputed tomography replace intravenous urographyfor evaluation of patients with acute urinary tract colic?J Emerg Med. 1999;17:299-303.

14.

Larkin GL, Peacock WF 4th, Pearl SM, et al. Efficacyof ketorolac tromethamine versus meperidinein the ED treatment of acute renal colic. Am J EmergMed. 1999;17:6-10.

15.

Nakada SY, Jerde TJ, Bjorling DE, Saban R. Selectivecyclooxygenase-2 inhibitors reduce ureteralcontraction in vitro: a better alternative for renal colic?J Urol. 2000;163:607-612.

16.

el-Sherif AE, Salem M, Yahia H, et al. Treatmentof renal colic by desmopressin intranasal spray anddiclofenac sodium. J Urol. 1995;153:1395-1398.

17.

Lopes T, Dias JS, Marcelino J, et al. An assessmentof the clinical efficacy of intranasal desmopressin sprayin the treatment of renal colic. BJU Int. 2001;87:322-325.

18.

Nikiforov S, Cronin AJ, Murray WB, Hall VE.Subcutaneous paravertebral block for renal colic.Anesthesiology. 2001;94:531-532.

19.

Cooper JT, Stack GM, Cooper TP. Intensivemedical management of ureteral calculi. Urology.2000;56:575-578.

20.

Bihl G, Meyers A. Recurrent renal stone disease-advances in pathogenesis and clinical management.Lancet. 2001;358:651-656.