Sandy Craig, MD,
Adjunct Associate Professor, Department of
Emergency Medicine, University of North Carolina at Chapel
Hill, Carolinas Medical Center
Nothing to disclose.
Specialty Editor(s)
David S Howes, MD,
Professor of Medicine and Pediatrics, Section
Chief and Residency Program Director, Emergency Medicine,
University of Chicago/Pritzker School of
Medicine
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Francisco Talavera, PharmD, PhD,
Senior Pharmacy Editor,
eMedicine
eMedicine Salary Employment
John D Halamka, MD, MS,
Associate Professor of Medicine, Harvard
Medical School, Beth Israel Deaconess Medical Center; Chief
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Medical School; Attending Physician, Division of Emergency
Medicine, Beth Israel Deaconess Medical
Center
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Richard H Sinert, DO,
Associate Professor of Emergency Medicine,
Clinical Assistant Professor of Medicine, Research Director,
State University of New York College of Medicine; Consulting
Staff, Department of Emergency Medicine, Kings County
Hospital Center
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Chief Editor
Robert E O'Connor, MD, MPH,
Professor and Chair, Department of Emergency
Medicine, University of Virginia Health
System
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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.
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.
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.
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.
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.
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 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]
One retrospective study found that 67% of patients with ureterolithiasis had more than 5 RBC per high power field (hpf) and 89% of patients had more than 0 RBC/hpf on urine microscopic examination.[7] In addition, 94.5% have hematuria if screened with microscopy plus urine dipstick testing.[8]
Degree of hematuria is not predictive of stone size or likelihood of passage.
No literature exists to support the theory that ureterolithiasis without hematuria is indicative of complete ureteral obstruction.
Pyuria (>5 WBC/hpf on a centrifuged specimen) in a patient with ureterolithiasis should prompt a careful search for signs of infected hydronephrosis. Obtain a complete blood count (CBC), creatinine, and urine culture. Treatment with antibiotics is indicated in patients with ureterolithiasis and pyuria. Admission to the hospital is mandatory if the patient has any signs of infected hydronephrosis (fever, elevated WBC count, elevated creatinine), or if follow-up within 24 hours is not reliably available.
A urine pH greater than 7 suggests presence of urea-splitting organisms, such as Proteus, Pseudomonas, or Klebsiella species, and struvite stones.
A urine pH less than 5 suggests uric acid stones.
Electrolytes
Serum creatinine level is the major predictor of contrast-induced nephrotoxicity.
If creatinine level is greater than 2 mg/dL, use diagnostic techniques that do not require an infusion of contrast, such as ultrasonography or helical CT scan.
Hypokalemia and decreased serum bicarbonate level suggest underlying distal (type 1) renal tubular acidosis, which is associated with formation of calcium phosphate stones.
Most authors recommend diagnostic imaging to confirm the diagnosis in first-time episodes of ureterolithiasis, when the diagnosis is unclear, or if associated proximal UTI is suspected. Lindqvist et al found that patients who are pain-free after receiving analgesics could be discharged from the ED and undergo radiologic imaging after 2-3 weeks without increasing morbidity.[9]
Kidney, ureter, and bladder (KUB) radiography
Multiple studies show that the KUB radiography has low (40-50%) sensitivity and specificity for the presence of ureterolithiasis and adds nothing to the emergent clinical impression. At follow-up, the urologist may find the KUB radiograph to be helpful in determining the exact size and shape of the stone, in establishing a baseline for follow-up studies, and for visualization of the surgical orientation.
KUB radiographs can be used to monitor passage of a previously documented opaque stone. Note that most stones will appear larger on KUB radiograph than on CT, with CT-based measurement of maximum stone dimension approximately 12% smaller compared with a KUB-based measurement.[10]
Computed tomography (CT): Noncontrast helical CT has become the criterion standard imaging study in the ED diagnosis of ureterolithiasis (see Media file 1).
View Image
Noncontrast helical CT scan of the abdomen demonstrating a stone at the right ureterovesical junction.
Numerous studies have demonstrated that CT has a sensitivity of 95-100% and superior specificity and accuracy compared with the historic criterion standard, intravenous pyelogram (IVP).[11]
Other advantages of helical CT include rapid (< 5 min) acquisition time, avoidance of intravenous (IV) contrast, and potential for diagnosis of other pathology including AAA, pancreatitis, appendicitis, ovarian disorders, diverticular disease, renal carcinoma, and biliary tract disorders.[12]
Principal disadvantages are that helical CT gives no information on renal function or degree of urinary obstruction. A recent study also demonstrated that stone size as measured on CT KUB correlates poorly with actual size of the stone measured after spontaneous passage.[13] For this reason, caution should be used in counseling patients on the likelihood of spontaneous stone passage when stone size is determined using CT-based measurement.
Pure indinavir stones are radiolucent and may not be visualized well by helical CT scan. However, indinavir stones often serve as a nidus for deposition of calcium oxalate or calcium phosphate deposition and thus become radioopaque. CT KUB remains the test of choice for patients on indinavir who present with apparent renal colic.
Sulfadiazine stones, most often seen in AIDS patients taking sulfadiazine for treatment of toxoplasmosis, are also difficult to visualize on CT because of relatively low attenuation.[14]
Intravenous pyelogram: Prior to the advent of helical CT, IVP was the test of choice in diagnosing ureterolithiasis. IVP is widely available and fairly inexpensive but less sensitive than noncontrast helical CT.
Contrast is administered intravenously at a dose of 1 mL/kg, and KUB films are taken immediately and at 1, 5, 10, and 15 minutes until contrast fills both distal ureters (see Media file 2). Look for direct visualization of stone within the ureter, unilateral ureteral dilation, delayed appearance of the nephrogram phase, lack of normal peristalsis pattern of the ureter, or perirenal contrast extravasation. Degree of obstruction is graded based on delay in appearance of the nephrogram.
View Image
Intravenous pyelogram (IVP) demonstrating dilation of the right renal collecting system and right ureter consistent with right ureterovesical stone.
Anaphylaxis to ionic contrast agents (eg, Renografin, Conray) occurs in 1-2 patients per 1000 IVP studies. Risk of recurrence is approximately 15% if reexposed to ionic agents but falls to 5% when nonionic agents are used. Risk of anaphylaxis can be reduced further by pretreatment with a combination of H1- and H2-blockers and steroids, but studies showing the benefit of pretreatment began pretreatment more than 12 hours prior to study. Risk of nephrotoxicity is not clearly reduced with use of nonionic agents. Indications for use of nonionic contrast agents vary among institutions but consistently include history of prior mild to moderately severe reaction to ionic contrast, asthma, multiple allergies, or severe cardiac disease.
Disadvantages of IVP include radiation exposure and risk of nephrotoxicity or anaphylactoid reaction to contrast agent. IVP is relatively contraindicated in pregnant or dehydrated patients or if serum creatinine level exceeds 2 mg/dL. IVP is absolutely contraindicated in patients with a history of severe contrast-induced anaphylaxis. False-negative results usually occur with stones located at the ureterovesical junction.
Ultrasonography: This is a good imaging modality in patients who are pregnant or to rule out the presence of an AAA in patients older than 60 years with a first or atypical presentation of nephrolithiasis.[15]
A handful of small studies have found sensitivities of 65-100% (see Media files 3-4). Ultrasonography has been found to be less accurate in diagnosis of ureteral stones when compared with IVP or helical CT. Diagnostic criteria include direct visualization of the stone, hydroureter more than 6 mm in diameter, and perirenal urinoma suggesting calyceal rupture.[11]
View Image
Renal sonogram showing a dilated renal collecting system consistent with ureteral obstruction.
View Image
Transabdominal sonogram revealing a ureteral stone at the ureterovesical junction.
Advantages include lack of radiation exposure and ability to complete the study at the bedside in patients who are potentially in unstable condition.
Disadvantages include inferior sensitivity, lack of universal availability, dependence on operator expertise, and inability to accurately estimate the degree of urinary obstruction.
A urine-filled bladder provides an excellent acoustic window for ultrasound imaging; sonograms occasionally may demonstrate a stone at the ureterovesical junction that is not seen on helical CT or IVP.
Future studies may utilize 2-dimensional ultrasonography in combination with color Doppler analysis of the ureteral jets to enhance sensitivity of ultrasonography in patients with ureteral colic.[16]
Magnetic resonance imaging: MRI can be used to detect ureteral stones. One study of 40 consecutive patients with acute flank pain found sensitivity of 54-58% and specificity of 100% using breath-hold heavily T2-weighted sequences.[17] Sensitivity and specificity increased to 96.2-100% and 100%, respectively, using gadolinium-enhanced 3-D FLASH MR urography. Although MRI does not play a major role in the diagnosis of ureteral stones, lack of radiation makes MRI a good choice in pregnant women who have nondiagnostic findings from a sonogram.
Intravenous access should be obtained to facilitate delivery of analgesic and antiemetic medications.
Intravenous hydration is controversial.
Some authorities believe that intravenous fluids hasten passage of the stone through the urogenital system. Others express concern that additional hydrostatic pressure exacerbates the pain of renal colic. One small study of 43 ED patients found no difference in pain score or rate of stone passage in patients who received 2 liters of saline over 2 hours versus those who received 20 mL of saline per hour.[18]
Intravenous hydration should be given to patients with clinical signs of dehydration or to those with a borderline serum creatinine level who must undergo IVP.
Analgesia should be provided promptly.
The pain of renal colic is mediated by prostaglandin E2. Nonsteroidal anti-inflammatory drugs inhibit formation of this mediator, and ketorolac (the only parenteral NSAID approved by the US FDA) has been proven in multiple studies to be as effective as opioid analgesics, with fewer adverse effects.[19, 20]
Opioid analgesics can be added in cases of incomplete pain control.
Antiemetics should be administered as needed.
Medical expulsive therapy
Multiple prospective randomized controlled studies[21, 22, 23] in the urology literature have demonstrated that patients treated with oral alpha-blockers have an increased rate of spontaneous stone passage and a decreased time to stone passage. The best studied of these is tamsulosin, 0.4 mg administered daily.
Calcium channel blockers in combination with oral steroids have also proven efficacious in multiple studies. The most common regimen is 30-mg slow-release nifedipine daily plus oral corticosteroid such as prednisolone.
A systematic review by Singh et al in November 2007 found that medical expulsive therapy using either alpha antagonists or calcium channel blockers augmented the stone expulsion rate for moderately sized distal ureteral stones. Adverse effects were noted in 4% of those taking alpha antagonists and in 15.2% of those taking calcium channel blockers.[24]
A systematic review by Beach et al in August 2006 found that medical expulsive therapy with alpha antagonists for 28 days increased the rate of stone passage, decreased the time to stone passage, and decreased the rates of hospitalization and ureteroscopy, with minimal adverse effects.[25]
A 2009 randomized study of 77 emergency department patients with ureterolithiasis found no benefit to a 14-day course of tamsulosin, though the study group was small and the average stone size was 3.6 mm, making spontaneous passage without expulsive therapy highly likely.[26]
Future studies may identify a subgroup of patients such as those with larger stones or history of inability to pass stones that would benefit from medical expulsive therapy.
Consult a urologist immediately in cases of ureterolithiasis with proximal UTI. Infected hydronephrosis is a true urologic emergency and requires hospital admission, intravenous antibiotics, and immediate drainage of the infected hydronephrosis via percutaneous nephrostomy or ureteral stent placement.
Urologic consultation is also appropriate in patients who are unable to tolerate oral fluids and medications and in those with unrelenting pain, renal failure, renal transplant, a solitary functioning kidney, and history of prior stones that required invasive intervention.
Pain of renal colic is mediated locally primarily by prostaglandin E2. Ureteral obstruction stimulates synthesis of prostaglandin E2 in the renal medulla, which increases ureteral contractility and renal blood flow, leading to increased ureteral pressures and painful renal colic.
These agents act at the CNS mu receptors and are the standard of care for treatment of renal colic. They are inexpensive and proven effective. Disadvantages include sedation, respiratory depression, smooth muscle spasm, and potential for abuse and addiction.
Clinical Context:
Mixed agonist-antagonist narcotic with central analgesic effects for moderately severe to severe pain. Causes less smooth muscle spasm and respiratory depression than morphine or meperidine. Weigh these advantages against increased cost of butorphanol.
These agents inhibit synthesis of prostaglandin E2 and are at least as effective as narcotic analgesics in numerous randomized controlled trials. NSAIDs cause less nausea and less sedation than narcotic analgesics, do not cause respiratory depression, and have no abuse potential. Principal disadvantage is cost. Potential adverse effects on renal function, GI mucosa, and platelet aggregation do not appear clinically important when used for short-term pain relief.
Clinical Context:
Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which, in turn, decreases formation of prostaglandin precursors. Only NSAID approved for IV or IM use in adults in United States. Single IM dose of 30 mg provides pain relief comparable to meperidine 100 mg IM with fewer adverse effects. Also can be administered IV. Onset of analgesic action is evident within 10 min of IM administration. Efficacy of PO formulation for outpatient treatment of renal colic has not yet been studied.
Clinical Context:
NSAID; inhibits cyclooxygenase (COX), an early component of the arachidonic acid cascade, resulting in reduced synthesis of prostaglandins, thromboxanes, and prostacyclin. Elicits anti-inflammatory, analgesic, and antipyretic effects. Indicated for short-term (up to 5 d) management of moderate to moderately severe pain. Bioavailability of 31.5-mg intranasal dose (2 sprays) is approximately 60% of 30-mg IM dose. Intranasal spray delivers 15.75 mg per 100-μ L spray; each 1.7-g bottle contains 8 sprays.
Patients with acute renal colic frequently experience intense nausea and/or vomiting. Effective pain control often is accompanied by resolution of nausea and vomiting, but some patients may require antiemetics in addition to analgesics. Various antiemetic medications are used, including phenothiazines and butyrophenones.
Clinical Context:
Only antiemetic that has been studied specifically in treatment of renal colic. In 2 small double-blinded studies, provided relief of nausea and pain relief equal to that of narcotic analgesics.
Antiemetic effect due to blockade of dopaminergic receptors in chemoreceptor trigger zone in CNS. Does not possess antipsychotic or tranquilizing activity and is less sedating than other central dopamine antagonists. Onset of action is 1-3 min after IV injection and 10-15 min after IM injection.
Infected hydronephrosis mandates IV antibiotic therapy in addition to urgent drainage via percutaneous nephrostomy or urethral stent placement. Aerobic gram-negative enteric organisms, including E coli and Klebsiella, Proteus, Enterobacter, and Citrobacter species, are typical pathogens. Enterococcal infection occasionally is seen in patients recently on antibiotics. Candida albicans sometimes is responsible in diabetic or immunosuppressed patients. Initial empiric antibiotic therapy should cover common bacterial pathogens.
Clinical Context:
Ampicillin is beta-lactam aminopenicillin antibiotic. Non–penicillinase-producing staphylococci and most streptococci are susceptible. Ampicillin is effective against E coli and Proteus and Enterococcus species, but most Klebsiella, Serratia, Acinetobacter, indole-positive Proteus, and Pseudomonas species and Bacteroides fragilis are resistant.
Gentamicin is aminoglycoside antibiotic, which is active against Staphylococcus aureus and Enterobacteriaceae organisms including E coli and Proteus, Klebsiella, Serratia, Enterobacter, and Citrobacter species. Pseudomonas aeruginosa is usually sensitive, although its sensitivity varies somewhat. When used in combination with ampicillin, gentamicin also effective against Enterococcus faecalis.
Clinical Context:
Ticarcillin is extended-spectrum penicillin, beta-lactam antibiotic. Clavulanic acid is beta-lactamase inhibitor that, in combination with ticarcillin, extends spectrum of ticarcillin to include many beta-lactamase–producing bacteria.
Timentin active against most staphylococci and streptococci and gram-negative organisms including E coli, Morganella morganii, Proteus mirabilis, Proteus vulgaris, Neisseria gonorrhoeae, and Pseudomonas and Providencia species. Anaerobic spectrum includes Peptococcus and Peptostreptococcus species, Clostridium perfringens, Clostridium tetani, and Bacteroides species, including many strains of B fragilis. Timentin not effective against Enterococcus species or methicillin-resistant staphylococci.
Clinical Context:
Reasonable alternative for treating infected hydronephrosis in penicillin-allergic patients. Fluoroquinolones active against aerobic gram-negative organisms and generally effective against aerobic gram-positive organisms, though some resistance has been noted in S aureus and Streptococcus pneumoniae. Not effective against anaerobes. Variably effective against E faecalis, though ampicillin and gentamicin likely to be more effective.
Clinical Context:
Reasonable alternative for treating infected hydronephrosis in penicillin-allergic patients. Fluoroquinolones active against aerobic gram-negative organisms and generally effective against aerobic gram-positive organisms, though some resistance has been noted in S aureus and S pneumoniae. Not effective against anaerobes. Variably effective against E faecalis, though ampicillin and gentamicin likely to be more effective.
Clinical Context:
Reasonable alternative for treating infected hydronephrosis in penicillin-allergic patients. Active against aerobic gram-negative organisms and generally effective against aerobic gram-positive organisms, though some resistance has been noted in S aureus and S pneumoniae.
Not effective against anaerobes. Variably effective against E faecalis, though ampicillin and gentamicin likely to be more effective.
Clinical Context:
In combination with nifedipine or tamsulosin, proven to facilitate spontaneous passage of a ureteral stone in several small prospective studies. Only a short course of therapy (5-10 d) should be administered.
These agents are smooth muscle relaxants that, in combination with prednisolone, facilitate ureteral stone passage in several small prospective studies.
Clinical Context:
Sustained-release (SR) formulation simplifies treatment and encourages compliance. Only short-term therapy (5-10 d) should be considered for this indication.
Clinical Context:
Alpha-adrenergic blocker specifically targeted to alpha1-receptors. Has advantage of relatively less orthostatic hypotension and requires no gradual up-titration from initial introductory dosage. Inhibits postsynaptic alpha-adrenergic receptors, resulting in vasodilation of veins and arterioles and decrease in total peripheral resistance and blood pressure. Improves irritative and obstructive voiding symptoms. Only short-term therapy (5-10 d) should be considered for this indication.
Admission rate for patients with acute renal colic is approximately 20%. Three absolute indications for admission are (1) infected hydronephrosis, (2) unrelenting pain or vomiting despite analgesics and antiemetics, and (3) dehydration.
Infected hydronephrosis is defined as UTI proximal to an obstructing stone. Infected hydronephrosis mandates admission for antibiotics and prompt drainage.
Midstream urine culture and sensitivity was a poor predictor of infected hydronephrosis in one series, being positive in only 30% of cases.[27]
The clinical presentation of infected hydronephrosis is variable. Pyuria (>5 WBC/hpf) is almost always present but not diagnostic of proximal infection. In one small series of 23 patients with infected hydronephrosis, the temperature was higher than 38°C in 15 patients, the peripheral WBC count was more than 10 X 109/L in 13 patients, and the creatinine level was greater than 1.3 mg/dL in 12 patients.[28]
Renal ultrasonography or helical CT may distinguish pyonephrosis from simple hydronephrosis by demonstrating a fluid-fluid level in the renal pelvis (urine on top of purulent debris). In 2 small studies, the ultrasonographic sensitivity for pyonephrosis was found to be 62-67%. CT sensitivity for pyonephrosis has not been reliably determined.[29, 30] The emergency physician must maintain a high index of suspicion.[31] Antibiotics should cover E coli and Staphylococcus, Enterobacter, Proteus, and Klebsiella species.
In another small study of 38 patients with hydronephrosis, 16 had infected hydronephrosis and 22 had sterile hydronephrosis. Ultrasonography alone detected 6 of 16 cases of pyonephrosis, a sensitivity of 38%. Using a cutoff value of 3 mg/dL for C-reactive protein and 100 mm/h for erythrocyte sedimentation rate, the diagnostic accuracy of detecting infected hydronephrosis and pyonephrosis increased to 97%.[32]
Patients with complete obstruction, perinephric urine extravasation, a solitary kidney, renal transplant, renal failure, or pregnancy, and those with a poor social support system, also should be considered for admission, especially if rapid urologic follow-up is not reliably available.
A stone less than 4 mm in diameter has an 80% chance of spontaneous passage; this falls to 20% for stones larger than 8 mm in diameter. The urologist may choose to admit a patient with a ureteral stone larger than 6 mm because of low likelihood of spontaneous passage.
About 15-20% of patients require invasive intervention due to stone size, continued obstruction, infection, or intractable pain. Several techniques are available to the urologist when the stone fails to pass spontaneously.[33]
Extracorporeal shock wave lithotripsy (ESWL) utilizes an underwater energy wave focused on the stone to shatter it into passable fragments. Approximately 70% of stones can be treated with ESWL alone. This technique is especially suitable for stones that are smaller than 2 cm and lodged in the upper or middle calyx. Anesthesia or sedation is required. ESWL is contraindicated in pregnancy, untreatable bleeding disorders, patients weighing more than 300 lb, tightly impacted or cystine stones, or in cases of ureteral obstruction distal to the stone.
Ureteroscopy is especially suitable for removal of stones that are 1-2 cm, lodged in the lower calyx or below, cystine stones, and high attenuation ("hard") stones. Stones smaller than 5 mm in diameter generally are retrieved using a stone basket, whereas tightly impacted stones or those larger than 5 mm are manipulated proximally for ESWL or are fragmented using an endoscopic direct-contact fragmentation device.
Percutaneous nephrolithotomy involves entering the renal pelvis percutaneously using the Seldinger technique after ultrasonography or fluoroscopic localization. Renal calyces, pelvis, and proximal ureter can be examined and stones extracted with or without prior fragmentation. This technique is especially useful for stones larger than 2 cm in diameter. A percutaneous nephrostomy can be used as an emergency procedure to relieve obstruction in a high-risk patient in whom other treatments are not feasible.[34]
Open nephrostomy rarely is used since the development of ESWL and endoscopic and percutaneous techniques. Open nephrostomy now constitutes only 1-2% of all interventions. Disadvantages include longer hospitalization, longer convalescence, and increased requirements for blood transfusion.
Patients who do not meet admission criteria may be discharged from the ED in anticipation that the stone will pass spontaneously at home.
Arrange for follow-up with a urologist in 2-3 days. Patients should be told to return immediately for fever, uncontrolled pain, or vomiting.
Patients should be discharged with a urine strainer and encouraged to submit any recovered calculi to a urologist for chemical analysis.
Follow-up for patients with first-time incidence of stones should consist of stone analysis and abbreviated metabolic evaluation to rule out hyperparathyroidism, renal tubular acidosis, and chronic infection with urea-splitting bacteria.
Patients with recurrent ureterolithiasis should undergo a more thorough metabolic evaluation. Patients with recurrent stones who undergo thorough metabolic evaluation and specific therapy enjoy a remission rate in excess of 80% and can decrease the rate of stone formation by 90%. A stone chemical analysis together with serum and appropriate 24-hour urine metabolic tests can identify the etiology in more than 95% of patients. A typical 24-hour urine determination should include urinary volume, pH, specific gravity, calcium, citrate, magnesium, oxalate, phosphate, and uric acid. Most common findings are hypercalciuria, hyperuricosuria, hyperoxaluria, hypocitraturia, and low urinary volume. Therefore, the emergency physician should encourage urologic follow-up.
Discharge on an oral analgesic and an antiemetic if needed. No studies exist that demonstrate superiority of one oral analgesic over another. Typical choices include agents such as hydrocodone, oxycodone, meperidine, or oral anti-inflammatory agents.
Medical therapies to aid in passage of a stone have been studied. Multiple randomized controlled prospective studies show that outpatient treatment with sustained-release nifedipine 30 mg/d plus prednisolone 25 mg/d or tamsulosin 0.4 mg/d decreases the time to spontaneous passage of the stone; increases the overall spontaneous expulsion rate; and decreases the need for analgesics, hospitalization, and endoscopic intervention.[21, 22, 23]
Patients with recurrent nephrolithiasis traditionally have been instructed to drink 8 glasses of fluid daily to maintain adequate hydration and decrease chance of urinary supersaturation with stone-forming salts.
Prospective studies suggest that daily consumption of coffee, tea, beer, or wine decreases risk of stone formation, while daily consumption of apple or grapefruit juice increases risk of stone formation.[35]
Infected hydronephrosis is the most deadly complication because the presence of infection adjacent to the highly vascular renal parenchyma places the patient at risk for rapidly progressive sepsis and death.
Calyceal rupture with perinephric urine extravasation due to high intracaliceal pressures occasionally is seen and usually is treated conservatively.
Complete ureteral obstruction may occur in patients with tightly impacted stones. This is best diagnosed via IVP and is not discernible on noncontrast CT scan. Patients with 2 healthy kidneys can tolerate several days of complete unilateral ureteral obstruction without long-term effects on the obstructed kidney. If a patient with complete obstruction is well hydrated and pain and vomiting are well controlled, the patient can be discharged from the ED with urologic follow-up within 1-2 days.
Approximately 80% of ureteral stones pass spontaneously without hospitalization or invasive intervention.
Approximately 20% of patients require hospitalization due to dehydration, continued pain or vomiting, or inability to pass the stone spontaneously.
Recurrence rates after an initial episode of ureterolithiasis are 14%, 35%, and 52% at 1, 5, and 10 years, respectively. Risk of recurrence can be reduced drastically by specific medical therapy based on analysis of the stone and serum and urine metabolic profiles.
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