Emergency medicine management is directed at relieving pain, assessing kidney function, and determining the likelihood of spontaneous stone passage. This chapter discusses renal and ureteral stones. Bladder stones are discussed in chapter 92, “Acute Urinary Retention.”

The prevalence of kidney stones in the United States has risen from 5.2% in 1994¹ to 8.8% in 2010.² The prevalence is 10.6% in men and 7.1% in women.² Increasing prevalence is documented in Europe and Southeast Asia.³ Obesity and diabetes are strongly associated with kidney stones.² The lifetime risk is approximated at 10% to 15% in the United States and other developed countries. Urinary calculi recur in 37% of patients in the first year, 50% of patients within 10 years, and 75% of patients in 20 years.⁴ Children <16 years old constitute about 7% of all renal stone cases.⁵ Unique to children is a 1:1 sex distribution.⁴ The most common causes in children involve metabolic abnormalities (50%), urologic anomalies (20%), infection (15%), immobilization syndrome (5%), and idiopathic causes (10%).⁵ Ethnically, whites develop stones more frequently than blacks.²

Stone formation requires supersaturation of dissolved salts in the urine, which condense into a solid phase. Increasing the amount of solvent (urine) and decreasing the amount of solute presented to the kidney (i.e., calcium, oxalate, uric acid) can aid in prevention. Inhibitory substances, such as citrate, and magnesium can prevent crystal precipitation and stone formation.

About 80% of calculi are composed of calcium oxalate, calcium phosphate, or a combination of both. Calcium excretion is elevated in conditions that include hyperparathyroidism, absorptive and renal hypercalciuria, and immobilization syndrome. Randall’s plaque, a collection of interstitial suburothelial calcium phosphate particles on the surface of the renal papillae, serves as a nucleation surface for calcium oxalate stones.^6,7 Complex interactions between the gut, kidney, and bones contribute to calcium oxalate stone formation. A diet restricting calcium paradoxically increases calcium stone formation because there is less calcium to bind oxalate in the intestinal lumen, leading to increased absorption of oxalate from the gut, recruitment of calcium from bones, osteoporosis, and symptomatic stone disease in predisposed patients.

About 10% of stones are struvite (magnesium-ammonium-phosphate). These stones are associated with infection by urea-splitting bacteria (Proteus, Klebsiella, Staphylococcus species, Providencia, and Corynebacterium) and are the most common cause of staghorn calculi, which are large stones that form a cast of the renal pelvis. Antibiotic penetration into staghorn calculi is poor, and the potential for urosepsis exists as long as the stones remain.

Uric acid causes about 10% of urolithiasis. Twenty-five percent of patients with gout will develop kidney stones, and they occur at a rate of approximately 1% per year after the first gout attack. Urate stones are radiolucent, and the urine is typically acidic. Cystine stones are rare, account for approximately 1% of all stones, and occur in patients with cystinuria, an autosomal recessive genetic disorder affecting amino acid transport (COLA: cysteine, ornithine, lysine, arginine). Stones can be made of many other miscellaneous substances, including indinavir, triamterene, xanthene, and silicate.

Some medications predispose to stone disease. The protease inhibitor indinavir sulfate, used to treat the human immunodeficiency virus, is associated with a 4% to 10% incidence of symptomatic urolithiasis. Pure indinavir stones are radiolucent on plain abdominal x-ray and CT scan. Carbonic anhydrase inhibitors, triamterene, and laxative abuse also increase the prevalence of renal stones.⁸ With appropriate evaluation, 90% of patients will have a cause identified, and over 50% of calcium oxalate stone recurrences can be prevented.⁹ Table 94-1 lists risk factors associated with kidney stones.^2,3,10

Pain associated with kidney stones is due to obstruction of a hollow viscus organ (ureter) and subsequent hydronephrosis creating pressure against Gerota’s fascia, causing flank pain. Isolated small renal pelvis stones (not staghorn) do not cause pain unless they cause intermittent obstruction of the entrance to the ureter. A migrating but nonobstructive stone also causes pain. During acute obstruction, most patients have no rise in serum creatinine because the unobstructed kidney functions at up to 185% of its baseline capacity. A rise in serum creatinine in acute obstruction suggests a solitary kidney or preexisting renal disease such that the unobstructed kidney is unable to compensate completely. Fortunately, most patients have incomplete ureteral obstruction, and many patients can be safely observed over weeks. Irreversible renal damage from an obstructive kidney stone is rare if obstruction has been present for ≤1 month.¹¹

The probability of spontaneous passage of stones is determined by multiple factors, including size, shape, location, and degree of ureteral obstruction. Bizarre or irregularly shaped stones with spicules or sharp edges have a lower spontaneous passage rate. With complete obstruction, there is a lower rate of spontaneous passage than if the blockage is partial. The most common sites of obstruction include the ureteropelvic junction, where the 1-cm pelvis constricts into the 2- to 3-mm ureter; the pelvic brim, where the ureter courses over both the pelvis and the iliac vessels; and finally, the ureterovesical junction, because this is the most constricted site of the ureter due to the muscular coat of the bladder. Based on stone size alone, 98% of stones <5 mm will pass within 4 weeks without intervention. Sixty percent of stones 5 to 7 mm and 39% of stones >7 mm will pass within 4 weeks. Stone size on plain radiographs is magnified by up to 20%, and a measured stone on CT is 88% of actual stone size.¹²

The classic symptom complex for nephrolithiasis is the acute onset of a crampy intermittent flank pain that radiates toward the groin. As pain originates from a hollow viscus (ureter), the pain is visceral in nature without associated peritoneal irritation. Patients writhe in pain, unable to find a position of comfort. However, patients with renal colic may demonstrate rebound tenderness (29%), guarding (61%), and rigidity (8%).¹³ Pain is commonly accompanied by nausea and vomiting (50%). The adrenergic response to pain can result in tachycardia, hypertension, and diaphoresis. Hematuria is present in only 85% of patients with renal colic, and 30% have gross hematuria.

The location of the pain correlates somewhat with the location of the stone. Stones in the upper ureter refer pain to the flank, whereas those in the mid-ureter radiate to the lower anterior quadrant of the abdomen. A distal ureter stone, which is where 75% of stones are diagnosed, refers pain to the groin. Stones positioned at the ureterovesical junction can mimic a urinary tract infection by causing frequency, urgency, and dysuria in 3% to 24% of patients.¹³ Extracorporeal shock wave lithotripsy fractures stones into small particles with the use of focused sound waves. The resulting “sludge” is passed in the urine. When there are large fragments, an acute episode of renal colic occurs.

In children, symptoms vary with age. Older children are more likely to present with typical adult symptoms. Younger children may complain of nonspecific abdominal or pelvic pain. Although renal colic is rare in infants, symptoms may be mistakenly attributed to intestinal colic. Overall, 20% to 30% of children may have only painless hematuria with urologic stone disease.

During the patient interview, elucidate three important items of history: assess risk factors for stone development (Table 94-1), prior stone-related outcome, and important mimickers. The risk factors for a poor outcome with stones include three categories: renal function at risk, history of difficulty with stones, and infection (Table 94-2). Two mimickers that are very important to exclude are abdominal aortic aneurysm and renal artery infarction. Nephrolithiasis is the most common misdiagnosis given to patients with a rupturing or expanding abdominal aortic aneurysm. Recall that stones do not usually present in men older than age 60 and do not cause hypotension, even transiently. Renal artery thrombosis can mimic stone symptoms due to swelling of the infarcted kidney and can also be associated with hematuria. However, early in the course, noncontrast CT will not necessarily show inflammation around the kidney, and because no contrast is used, the function of the kidney is not assessed.

The diagnosis of urologic stone disease is clinically suspected and supported by the presence of hematuria; imaging confirms the diagnosis with certainty.

Many diagnoses can be confused with renal colic (Table 94-3). History and physical examination can be difficult because the patient’s discomfort may interfere with adequate information collection. The most critical diagnoses to consider are aortic dissection and ruptured abdominal aortic aneurysm. Renal colic and abdominal aortic aneurysm may have similar presentations.

LABORATORY EVALUATION

The laboratory evaluation centers on evaluating for infection, kidney dysfunction, and possibility of pregnancy. Test all females of childbearing potential for pregnancy when considering renal colic. With pregnancy, consider ectopic pregnancy in the differential diagnosis while minimizing radiation exposure to the fetus.