Introduction

Background
Acute passage of a kidney stone from the renal pelvis through the ureter gives rise to pain at times so
excruciating that it has been likened to the discomfort of childbirth. The often sudden, extremely painful
episode of renal colic prompts more than 450,000 visits to EDs annually and places emergency
physicians on the front line of management of acute nephrolithiasis. ED management is focused on
excluding other serious diagnoses and providing adequate pain relief.

Pathophysiology
Most calculi arise in the kidney when urine becomes supersaturated with a salt that is capable of forming
solid crystals. Symptoms arise as these calculi become impacted within the ureter as they pass toward
the urinary bladder.

Frequency
United States

The lifetime prevalence of nephrolithiasis is approximately 12% for men and 7% for women in the United
States, and it is rising. Recurrence rates after the first stone episode are 14%, 35%, and 52% at 1, 5, and
10 years, respectively. An increased incidence has been noted in the southeastern United States,
prompting the term "stone belt" for this region of the country.1

International

Nephrolithiasis occurs in all parts of the world, with a lower lifetime risk of 2-5% in Asia, 8-15% in the
West, and 20% in Saudi Arabia.

Mortality/Morbidity
• Approximately 80-85% of stones pass spontaneously.
• Approximately 20% of patients require hospital admission because of unrelenting pain, inability to
retain enteral fluids, proximal urinary tract infection (UTI), or inability to pass the stone.
• A ureteral stone associated with obstruction and upper UTI is a true urologic emergency.
Complications include perinephric abscess, urosepsis, and death. Immediate involvement of the
urologist is essential.
Race
• White males are affected 3-4 times more often than African American males.
• African Americans have a higher incidence of infected ureteral calculi than whites.
Sex
• The male-to-female ratio is approximately 3:1.
• Female patients have a higher incidence of infected hydronephrosis.
Age
Peak onset of symptomatic nephrolithiasis is in the third and fourth decades of life.
 • Beware of the patient older than 60 years with an apparent first kidney stone. Consider the
possibility of symptomatic abdominal aortic aneurysm (AAA) in the older patient, and rule out this
possibility before pursuing the diagnosis of nephrolithiasis. Use bedside ultrasonography if the
patient's condition is potentially unstable. CT scan is a reasonable alternative in the stable
patient.
• Nephrolithiasis in children is rare; approximately 5-10 children aged 10 months to 16 years are
seen annually for the condition at a typical US pediatric referral center.
Clinical

History
Most calculi originate within the kidney and proceed distally, creating various degrees of urinary
obstruction as they become lodged in narrow areas, including the ureteropelvic junction, pelvic brim, and
ureterovesical junction. Location and quality of pain are related to position of the stone within the urinary
tract. Severity of pain is related to the degree of obstruction, presence of ureteral spasm, and presence of
any associated infection.

• Stones obstructing the ureteropelvic junction may present with mild-to-severe deep flank pain
without radiation to the groin, due to distension of the renal capsule.
• Stones impacted within the ureter cause abrupt, severe, colicky pain in the flank and ipsilateral
lower abdomen with radiation to the testicles or the vulvar area. Intense nausea, with or without
vomiting, usually is present.
• Stones lodged at the ureterovesical junction also may cause irritative voiding symptoms, such as
urinary frequency and dysuria.
• Calculi that have entered the bladder are usually asymptomatic and are passed relatively easily
during urination.
• Rarely, a patient reports positional urinary retention (obstruction precipitated by standing, relieved
by recumbency), which is due to the ball-valve effect of a large stone located at the bladder
outlet.
Physical
The classic patient with renal colic is writhing in pain, pacing about, and unable to lie still, in contrast to a
patient with peritoneal irritation, who remains motionless to minimize discomfort.

• Fever is not part of the presentation of uncomplicated nephrolithiasis. If present, suspect infected
hydronephrosis, pyonephrosis, or perinephric abscess.
• The most common finding in ureterolithiasis is flank tenderness due to the dilation and spasm of
the ureter from transient obstruction as the stone passes from the kidney to the bladder.
• Abdominal examination usually is unremarkable. Bowel sounds may be hypoactive, a reflection of
mild ileus, which is not uncommon in patients with severe, acute pain.
• In patients older than 60 years with no prior history of renal stones, the emergency physician
should look carefully for physical signs of AAA (see Aneurysm, Abdominal).
• Testicles may be painful but should not be very tender and should appear normal.
Causes
The formation of the 4 basic chemical types of renal calculi is associated with more than 20 underlying
etiologies. Stone analysis, together with serum and 24-hour urine metabolic evaluation, can identify an
etiology in more than 95% of patients. Specific therapy can result in a remission rate of more than 80%
and can decrease the individual recurrence rate by 90%. Therefore, emergency physicians should stress
the importance of urologic follow-up, especially in patients with recurrent stones, solitary kidneys, or
previous kidney or stone surgery and in all children.2

• Calcium stones (75%): Recent data suggest that a low-protein, low-salt diet may be preferable to
a low-calcium diet in hypercalciuric stone formers for preventing stone
recurrences.3 Epidemiological studies have shown that the incidence of stone disease is inversely
related to the magnitude of dietary calcium intake in first-time stone formers. There is a trend in
the urology community not to restrict dietary intake of calcium in recurrent stone formers. This is
especially important for postmenopausal women in whom there is an increased concern for the
development of osteoporosis. Calcium oxalate, calcium phosphate, and calcium urate are
associated with the following disorders:
○ Hyperparathyroidism - Treated surgically or with orthophosphates if the patient is not a
surgical candidate
○ Increased gut absorption of calcium - The most common identifiable cause of
hypercalciuria, treated with calcium binders or thiazides plus potassium citrate
○ Renal calcium leak - Treated with thiazide diuretics
○ Renal phosphate leak - Treated with oral phosphate supplements
○ Hyperuricosuria - Treated with allopurinol, low purine diet, or alkalinizing agents such as
potassium citrate
○ Hyperoxaluria - Treated with dietary oxalate restriction, oxalate binders, vitamin B-6, or
orthophosphates
○ Hypocitraturia - Treated with potassium citrate
○ Hypomagnesuria - Treated with magnesium supplements
• Struvite (magnesium ammonium phosphate) stones (15%)
○ Struvite stones are associated with chronic UTI with gram-negative rods capable of
splitting urea into ammonium, which combines with phosphate and magnesium.
Underlying anatomical abnormalities that predispose patients to recurrent kidney
infections should be sought and corrected.
○ Usual organisms include Proteus, Pseudomonas, and Klebsiella species. Escherichia
coli is not capable of splitting urea and, therefore, is not associated with struvite stones.
○ UTI does not resolve until stone is removed entirely.
○ Urine pH is typically greater than 7.
• Uric acid stones (6%): These are associated with urine pH less than 5.5, high purine intake (eg,
organ meats, legumes, fish, meat extracts, gravies), or malignancy (ie, rapid cell turnover).
Approximately 25% of patients with uric acid stone have gout. Serum and 24-hour urine sample
should be sent for creatinine and uric acid determination. If serum or urinary uric acid is elevated,
the patient may be treated with allopurinol 300 mg daily. Patients with normal serum or urinary
uric acid are best managed by alkali therapy alone.
• Cystine stones (2%)
○ Cystine stones arise because of an intrinsic metabolic defect resulting in failure of renal
tubular reabsorption of cystine, ornithine, lysine, and arginine.
○ Urine becomes supersaturated with cystine with resultant crystal deposition.
○ These are treated with low-methionine diet (unpleasant), binders such as penicillamine or
a-mercaptopropionylglycine, large urinary volumes, or alkalinizing agents. A 24-hour
quantitative urinary cystine determination helps to titrate the dose of drug therapy to
achieve a urinary cystine concentration of less than 300 mg/L.
• Drug-induced stone disease: A number of medications or their metabolites can precipitate in urine
causing stone formation. These include indinavir; atazanavir; guaifenesin; triamterene; silicate
(overuse of antacids containing magnesium silicate); and sulfa drugs including sulfasalazine,
sulfadiazine, acetylsulfamethoxazole, acetylsulfasoxazole, and acetylsulfaguanidine.4,5,6