Urinary system diseases and chronic kidney disease in a family doctor practice. Differential diagnosis of symptoms and syndromes. The organization of the route the patient. Treatment protocols. Rehabilitation and clinical examination. Employment expertise.

Urinary system diseases and chronic kidney disease in a family doctor practice. Differential diagnosis of symptoms and syndromes. The organization of the route the patient. Treatment protocols. Rehabilitation and clinical examination. Employment expertise.

 

In February 2002, the Kidney Disease Outcome Quality Initiative of the National Kidney Foundation published clinical practice guidelines on chronic kidney disease. The first six of the 15 guidelines are of the greatest relevance to family physicians. Part I of this two-part article reviews guidelines 1, 2, and 3. Chronic kidney disease is defined by the presence of a marker of kidney damage, such as proteinuria (ratio of greater than 30 mg of albumin to 1 g of creatinine on untimed [spot] urine testing), or a decreased glomerular filtration rate for three or more months. Disease staging is based on the glomerular filtration rate. Evaluation should be directed at determining the type and severity of chronic kidney disease. Treatment goals include preventing disease progression and complications. The guidelines place special emphasis on the prevention and treatment of cardiovascular disease in patients with chronic kidney disease. Risk factors for chronic kidney disease include diabetes mellitus, hypertension, family history of chronic kidney disease, age older than 60 years, and U.S. racial or ethnic minority status. The guidelines recommend testing for proteinuria and estimating the glomerular filtration rate in patients at risk for chronic kidney disease. Family physicians should weigh the value of the National Kidney Foundation guidelines for their clinical practice based on the strength of evidence and perceived cost-effectiveness until additional evidence becomes available on the usefulness of the recommended quality indicators.

Chronic kidney disease is a major public health problem throughout the world. In the United States, kidney failure is becoming increasingly common and is associated with poor health outcomes and high medical expenditures. In this country, the number of patients treated with dialysis or transplantation is projected to increase from 340,000 in 1999 to 651,000 in 2010.

Strength of Recommendations

View Table

The major outcomes of chronic kidney disease, regardless of the specific diagnosis (i.e., type of kidney disease), include progression to kidney failure, complications from decreased kidney function, and development of cardiovascular disease. Increasing evidence shows that early detection and treatment often can prevent or delay some of these adverse outcomes. However, opportunities for prevention may be lost because chronic kidney disease is not diagnosed or is treated insufficiently. One reason is lack of agreement about the definition of chronic kidney disease, as well as the classification of its stages. Another reason is lack of uniform application of simple tests for the detection and evaluation of the disease.

In February 2002, the Kidney Disease Outcome Quality Initiative (K/DOQI) of the National Kidney Foundation (NKF) published clinical practice guidelines on chronic kidney disease. The goals of the Work Group that developed the guidelines were as follows: to define chronic kidney disease and classify its stages, regardless of the underlying cause; to evaluate laboratory measurements for clinical assessment of kidney disease; to associate the level of kidney function with the complications of chronic kidney disease; and to stratify risk for the loss of kidney function and the development of cardiovascular disease.

The leaders of the NKF recognized the role of family physicians in providing medical care for patients with chronic kidney disease (particularly during the early stages when interventions might slow disease progression) and therefore wanted the guidelines to be practical and accessible to primary care physicians. To these ends, a family physician was invited to be an active participant in the guidelines Work Group and a member of the K/DOQI Advisory Board, which oversees all guidelines developed under its auspices. At present, there are only about 5,000 nephrologists in the United States. With the projected increase in the number of patients diagnosed with chronic kidney disease (especially as defined by the NKF guidelines), a strong partnership with family physicians and general internists will be necessary.

The first purpose of this article is to disseminate the simple definition and the five-stage classification system of chronic kidney disease that were developed through an evidence-based process and justified with existing literature. The second purpose is to describe the six guidelines with the most immediate relevance to family physicians. Guidelines on evaluation, treatment, and risk factors are reviewed in part I of this two-part article. Part II reviews guidelines on estimation of glomerular filtration rate, assessment of proteinuria, and use of markers of chronic kidney disease other than proteinuria.

 

KIDNEY STONES OVERVIEW

The kidney acts as a filter for blood, removing waste products from the body and making urine. It also helps regulate electrolyte levels that are important for body function. Urine drains from the kidney through a narrow tube called the ureter into the bladder. When the bladder fills and there is an urge to urinate, the bladder empties to the outside through the urethra, a much wider tube than the ureter.

In some people, chemicals crystallize in the urine and form the beginning, or nidus, of a kidney stone. These stones are very tiny when they form, smaller than a grain of sand, but gradually can grow over time to 1/10 of an inch or larger. Urolithiasis is the term that refers to the presence of stones in the urinary tract, while nephrolithiasis refers to kidney stones and ureterolithiasis refers to stones lodged in the ureter. The size of the stone doesn’t matter as much as where it is located and whether it obstructs or prevents urine from draining.

When the stone sits in the kidney, it rarely causes problems, but when it falls into the ureter, it acts like a dam. As the kidney continues to function and make urine, pressure builds up behind the stone and causes the kidney to swell. This pressure is what causes the pain of a kidney stone, but it also helps push the stone along the course of the ureter. When the stone enters the bladder, the obstruction in the ureter is relieved and the symptoms of a kidney stone are resolved.

Kidney Stones Causes

There is no consensus as to why kidney stones form.

·                      Heredity: Some people are more susceptible to forming kidney stones, and heredity may play a role. The majority of kidney stones are made of calcium, andhypercalciuria (high levels of calcium in the urine) is a risk factor. The predisposition to high levels of calcium in the urine may be passed on from generation to generation. Some rare hereditary diseases alsopredispose some people to form kidney stones. Examples include people with renal tubular acidosis and people with problems metabolizing a variety of chemicals including cystine (an amino acid), oxalate, (a type of salt), and uric acid (as in gout).

 

·                      Geographical location: There may be a geographic predisposition, and where a person lives may predispose them to form kidney stones. There are regional “stone belts,” with people living in the southern United States having an increased risk of stone formation. The hot climate in this region combined with poor fluid intake may cause people to be relatively dehydrated, with their urine becoming more concentrated and allowing chemicals to come in closer contact to form the nidus, or beginning, of a stone.

 

·                      Diet: Diet may or may not be an issue. If a person is susceptible to forming stones, then foods high in calcium may increase the risk; however, if a person isn’t susceptible to forming stones, diet probably will not change that risk.

 

·                      Medications: People taking diuretics (or “water pills”) and those who consume excess calcium-containing antacids can increase the amount of calcium in their urine and potentially increase their risk of forming stones. Taking excess amounts of vitamins A and D are also associated with higher levels of calcium in the urine. Patients with HIV who take the medicationindinavir (Crixivan) may form indinavir stones. Other commonly prescribed medications associated with stone formation include dilantin and antibioticslike ceftriaxone (Rocephin) and ciprofloxacin (Cipro).

 

·                      Underlying illnesses: Some chronic illnesses are associated with kidney stone formation, including cystic fibrosis, renal tubular acidosis, andinflammatory bowel disease.

 

Symptoms and Signs

When a tubular structure is blocked in the body, waves of pain occur as the body tries to unblock the obstruction. These waves of pain are called colic. This is opposed to non-colicky type pain, like that associated with appendicitisor pancreatitis, in which movement causes increased pain and the patient tries to hold very still.

·                      Renal colic (renal is the medical term for things related to the kidney) has a classic presentation when a kidney stone is being passed.

o       The pain is intense and comes on suddenly. It may wax and wane, but there is usually a significant underlying ache between the acute spasms of pain.

o       It is usually located in the flank or the side of the mid back and may radiate to the groin. Males may complain of pain in the testicle or scrotum.

o       The patient cannot find a comfortable position and often writhes or paces with pain.

·                      Sweating, nausea, and vomiting are common.

·                      Blood may or may not be visible in the urine because the stone has irritated the kidney or ureter. Blood in the urine (hematuria), however, does not always mean a person has a kidney stone. There may be other reasons for the blood, including kidney and bladder infections, trauma, or tumors. Urinalysis with amicroscope may detect blood even if it is not appreciated by the naked eye. Sometimes, if the stone causes complete obstruction, no blood may be found in the urine because it cannot get past the stone.

 

·                     

Diagnosis

The classic presentation of renal colic associated with blood in the urine suggests the diagnosis of kidney stone. Many other conditions can mimic this disease, and the care provider may need to order tests to confirm the diagnosis. In older patients, it is always important to at least consider the diagnosis of a leaking or ruptured abdominalaortic aneurysm (abnormal widening of the large blood vessel that leads from the heart to supply blood to the body) as a source of this type of pain.

Physical examination is ofteot helpful in patients with kidney stones, aside from the finding of flank (side of the body between the ribs and hips) tenderness. The examination is often done to look for potentially dangerous conditions. The care provider may palpate or feel the abdomen trying to find a pulsatile or throbbing mass that might indicate the presence of an abdominal aortic aneurysm. Listening to the abdomen with a stethoscope may reveal a bruit or rushing noise made by abnormal blood flow through the aneurysm. Tenderness under the right rib cage margin may signal gallbladder disease. Tenderness in the lower quadrants may be associated with appendicitis, diverticulitis, or ovarian disease. Examination of the scrotum may exclude atesticular torsion.

In children, colicky abdominal pain may be associated with intussusception of the intestine.

Symptom control is very important, and medication for pain and nausea may be provided before the confirmation of the diagnosis occurs.

A urinalysis may detect blood in the urine. It is also done to look for evidence of infection, a complication of kidney stone disease.

Blood tests are usually not indicated, unless the health-care provider has concerns about the diagnosis or is worried about kidney stone complications.

 

Computerized tomography (CT) scanning of the abdomen without oral or intravenous contrast dye is the most commonly used diagnostic test. The scan will demonstrate the anatomy of the kidneys, ureter, and bladder and can detect a stone, its location, its size, and whether it is causing dilation of the ureter and inflammation of the kidney. The CT can also evaluate many other organs in the abdomen, including the appendix, gallbladder, liver, pancreas, aorta, and bowel. However, since no contrast material is used, there are some limitations to the detail that can be observed in the images of the scan.

Ultrasound is another way of looking for kidney stones and obstruction and may be useful when the radiation risk of a CT scan is unwanted (for example, if a woman is pregnant). Ultrasound requires a specially trained person to interpret the images and may not always be available.

In those patients who already have the diagnosis of a kidney stone, plain abdominal X-rays may be used to track its movement down the ureter toward the bladder. As well, in patients with known kidney stone disease, no imaging may be necessary if the diagnosis seems certain, so that the amount of X-ray radiation that can accumulate over a lifetime is minimized.

Kidney Stones Treatment

Kidney Stone Home Remedy

·                      Prevention is always the preferable way to treat kidney stones. Remaining well hydrated keeps the urine dilute and helps prevent kidney stones from forming.

 

·                      Those who have never passed a kidney stone may not appreciate the severity of the symptoms. There is little a person can do at home to control the debilitating pain and vomiting that can occur with a kidney stone other than to seek emergency care. If this is the first episode and no previous diagnosis has been established, it is important to be seen by a health-care provider to confirm the diagnosis.

·                      For those who have a history of stones, home therapy may be appropriate. Most kidney stones, given time, will pass on their own, and treatment is directed toward symptom control. The patient should be instructed to drink plenty of oral fluids.Ibuprofen may be used as an anti-inflammatory medication if there is no contraindication to its use. If further pain medication is needed, the primary-care provider may be willing to prescribe stronger narcotic pain medications.

 

·                      Please note, if a fever is associated with the symptoms of a kidney stone, this becomes an emergency, and medical care should be accessed immediately. Urinary tract infections associated with a kidney stone often require urgent assessment and may need intervention by a urologist to remove or bypass the stone.

Medical Treatment

·                      In the emergency department, intravenous fluids may be provided to help with hydration and to allow the administration of medications to control pain and nausea.Ketorolac (Toradol), an injectable anti-inflammatory drug, and narcotics may be used for pain control, with the goal being to relieve suffering and not necessarily to make the patient pain free. Nausea and/or vomiting may be treated with anti-emetic medications like ondansetron (Zofran),promethazine (Phenergan), or droperidol(Inapsine).

Follow-up

·                      For the first-time kidney stone patient, there should be an attempt to catch the stone by straining the urine, so that it can be sent for analysis. The stone may be so tiny that it may not be recognized. While most stones are made of calcium oxalate, stones can also consist of other chemicals. It may be possible to prevent future stone formation by taking medications. For those whose stone disease is recurrent and the kind of stone is known, this instruction is often omitted.

·                      Drinking plenty of water will help push the stone down the ureter to the bladder and hasten its elimination.

·                      A follow-up visit with a urologist may be arranged one to two weeks after the initial visit, allowing the stone to pass on its own.

·                      Patients should call their physician or return to the emergency department if the pain medication is not working to control the pain, if there is persistent vomiting, or if a fever occurs.

 

Kidney Stone Prognosis

Once a patient has passed a stone, there is a great likelihood that another stone will be passed in his or her lifetime. Since kidney stones may also be hereditary, this likelihood is passed on to the next generation. A patient who has experienced a stone is unlikely to forget the experience and often will arrive at the health-care facility already knowing the diagnosis. Those with recurrent stones may be given medication to keep at home should symptoms recur.

 

NEPHROLITHIASIS 

 

Nephrolithiasis specifically refers to calculi in the kidneys, but renal calculi and ureteral calculi (ureterolithiasis) are often discussed in conjunction. The majority of renal calculi contain calcium. The pain generated by renal colic is primarily caused by dilation, stretching, and spasm because of the acute ureteral obstruction.

In one study, investigators found that the routine use of flexible nephroscopy during percutaneous nephrolithotomy (PCNL) provided advantages over standard PCNL in which rigid nephroscopy is used.^{[1, 2]} Flexible nephroscopy resulted not only in a higher stone-free rate relative to rigid nephroscopy but also in fewer interventions and bleeding, particularly in patients who had calculi with low Hounsfield unit density.^{[1, 2]}

The classic presentation for a patient with acute renal colic is the sudden onset of severe pain originating in the flank and radiating inferiorly and anteriorly; at least 50% of patients will also have nausea and vomiting. Patients with urinary calculi may report pain, infection, or hematuria. Patients with small, nonobstructing stones or those with staghorn calculi may be asymptomatic or experience moderate and easily controlled symptoms.

The location and characteristics of pain in nephrolithiasis include the following:

·                       Stones obstructing ureteropelvic junction: Mild to severe deep flank pain without radiation to the groin; irritative voiding symptoms (eg, frequency, dysuria); suprapubic pain, urinary frequency/urgency, dysuria, stranguria, bowel symptoms

·                       Stones within ureter: Abrupt, severe, colicky pain in the flank and ipsilateral lower abdomen; radiation to testicles or vulvar area; intense nausea with or without vomiting

·                       Upper ureteral stones: Radiate to flank or lumbar areas

·                       Midureteral calculi: Radiate anteriorly and caudally

·                       Distal ureteral stones: Radiate into groin or testicle (men) or labia majora (women)

·                       Stones passed into bladder: Mostly asymptomatic; rarely, positional urinary retention

See Clinical Presentation for more detail.

The diagnosis of nephrolithiasis is often made on the basis of clinical symptoms alone, although confirmatory tests are usually performed.

Examination in patients with nephrolithiasis includes the following findings:

·                       Dramatic costovertebral angle tenderness; pain can move to upper/lower abdominal quadrant with migration of ureteral stone

·                       Generally unremarkable abdominal evaluation: Possibly hypoactive bowel sounds; usually absence of peritoneal signs; possibly painful testicles but normal-appearing

·                       Constant body positional movements (eg, writhing, pacing)

·                       Tachycardia

·                       Hypertension

·                       Microscopic hematuria

Testing

The European Association of Urology recommends the following laboratory tests in all patients with an acute stone episode^[3] :

·                       Urinary sediment/dipstick test: To demonstrate blood cells, with a test for bacteriuria (nitrite) and urine culture in case of a positive reaction

·                       Serum creatinine level: To measure renal function

Other laboratory tests that may be helpful include the following:

·                       CBC with differential in febrile patients

·                       Serum electrolyte assessment in vomiting patients (eg, sodium, potassium, calcium, PTH, phosphorus)

·                       Serum and urinary pH level: May provide insight regarding patient’s renal function and type of calculus (eg, calcium oxalate, uric acid, cystine), respectively

·                       Microscopic urinalysis

·                       24-Hour urine profile

Imaging studies

The following imaging studies are used in the evaluation of nephrolithiasis:

·                       Noncontrast abdominopelvic CT scan: The imaging modality of choice for assessment of urinary tract disease, especially acute renal colic

·                       Renal ultrasonography: To determine presence of a renal stone and the presence of hydronephrosis or ureteral dilation; used alone or in combination with plain abdominal radiography

·                       Plain abdominal radiograph (flat plate or KUB): To assess total stone burden, as well as size, shape, composition, location of urinary calculi; often used in conjunction with renal ultrasonography or CT scanning

·                       IVP (urography) (historically, the criterion standard): For clear visualization of entire urinary system, identification of specific problematic stone among many pelvic calcifications, demonstration of affected and contralateral kidney function

·                       Plain renal tomography: For monitoring a difficult-to-observe stone after therapy, clarifying stones not clearly detected or identified with other studies, finding small renal calculi, and determining number of renal calculi present before instituting a stone-prevention program

·                       Retrograde pyelography: Most precise imaging method for determining the anatomy of the ureter and renal pelvis; for making definitive diagnosis of any ureteral calculus

·                       Nuclear renal scanning: To objectively measure differential renal function, especially in a dilated system for which the degree of obstruction is in question; reasonable study in pregnant patients, in whom radiation exposure must be limited

See Workup for more detail.

Management

Supportive care and pharmacotherapy

Medical treatment of nephrolithiasis involves supportive care and administration of agents, such as the following:

·                       IV hydration

·                       Nonnarcotic analgesics (eg, APAP)

·                       PO/IV narcotic analgesics (eg, codeine, butorphanol, morphine sulfate, oxycodone/APAP, hydrocodone/APAP, meperidine, nalbuphine)

·                       NSAIDS (eg, ketorolac, ketorolac intranasal, ibuprofen)

·                       Uricosuric agents (eg, allopurinol)

·                       Antiemetics (eg, metoclopramide)

·                       Antidiuretics (eg, DDAVP)

·                       Antibiotics (eg, ampicillin, gentamicin, ticarcillin/clavulanic acid, ciprofloxacin, levofloxacin, ofloxacin)

·                       Alkalinizing agents (eg, potassium citrate, sodium bicarbonate): For uric acid and cysteine calculi

·                       Corticosteroids (eg, prednisone, prednisolone)

·                       Calcium channel blockers (eg, nifedipine)

·                       Alpha blockers (eg, tamsulosin, terazosin)

Surgical option

Stones that are 7 mm and larger are unlikely to pass spontaneously and require some type of surgical procedure, such as the following:

·                       Stent placement

·                       Percutaneous nephrostomy

·                       Extracorporeal shockwave lithotripsy

·                       Ureteroscopy

·                       Percutaneous nephrostolithotomy

·                       Opeephrostomy

See Treatment and Medication for more detail.

Background

Nephrolithiasis is a common disease that is estimated to produce medical costs of $2.1 billion per year in the United States.^[4] Nephrolithiasis specifically refers to calculi in the kidneys, but this article discusses both renal calculi (see the first image below) and ureteral calculi (ureterolithiasis; see the second image below). Ureteral calculi almost always originate in the kidneys, although they may continue to grow once they lodge in the ureter.

Small renal calculus that would likely respond to extracorporeal shockwave lithotripsy.

Distal ureteral stone observed through a small, rigid ureteroscope prior to ballistic lithotripsy and extraction. The small caliber and excellent optics of today’s endoscopes greatly facilitate minimally invasive treatment of urinary stones.

Urinary tract stone disease has been a part of the human condition for millennia; in fact, bladder and kidney stones have even been found in Egyptian mummies. Some of the earliest recorded medical texts and figures depict the treatment of urinary tract stone disease.

Acute renal colic is probably the most excruciatingly painful event a person can endure. Striking without warning, the pain is often described as being worse than childbirth, broken bones, gunshot wounds, burns, or surgery. Renal colic affects approximately 1.2 million people each year and accounts for approximately 1% of all hospital admissions.

Most active emergency departments (EDs) manage patients with acute renal colic every day, depending on the hospital’s patient population. Initial management consists of proper diagnosis, prompt initial treatment, and appropriate consultations, but concurrently efforts should be directed towards patient education, including initial preventive therapy measures.

Although nephrolithiasis is not a common cause of renal failure, certain problems, such as preexisting azotemia and solitary functional kidneys, clearly present a higher risk of additional renal damage. Other high-risk factors include diabetes, struvite and/or staghorn calculi, and various hereditary diseases such as primary hyperoxaluria, Dent disease, cystinuria, and polycystic kidney disease. Spinal cord injuries and similar functional or anatomical urological anomalies also predispose patients with kidney stones to an increased risk of renal failure.

Recurrent obstruction, especially when associated with infection and tubular epithelial or renal interstitial cell damage from microcrystals, may activate the fibrogenic cascade, which is mainly responsible for the actual loss of functional renal parenchyma.

For other discussions on urolithiasis and nephrolithiasis, see Pediatric Urolithiasis, as well as Imaging Urinary Calculi, Hypercalciuria, Hyperoxaluria, andHypocitraturia.

Anatomy

The basic anatomy of the ureter is as follows (see the image below).

 

Fig. Nephrolithiasis: acute renal colic. Anatomy of the ureter.

 

Most of the pain receptors of the upper urinary tract responsible for the perception of renal colic are located submucosally in the renal pelvis, calices, renal capsule, and upper ureter. Acute distention seems to be more important in the development of the pain of acute renal colic than spasm, local irritation, or ureteral hyperperistalsis.

Stimulation of the peripelvic renal capsule causes flank pain, while stimulation of the renal pelvis and calices causes typical renal colic (see the image below). Mucosal irritation can be sensed in the renal pelvis to some degree by chemoreceptors, but this irritation is thought to play only a minor role in the perception of renal or ureteral colic.

  

Fig. Nephrolithiasis: acute renal colic. Renal colic and flank pain.

 

Renal pain fibers are primarily preganglionic sympathetic nerves that reach spinal cord levels T-11 to L-2 through the dorsal nerve roots (see the images below). Aortorenal, celiac, and inferior mesenteric ganglia are also involved. Spinal transmission of renal pain signals occurs primarily through the ascending spinothalamic tracts.

Fig. Nephrolithiasis: acute renal colic. Nerve supply of the kidney.

Fig.  Nephrolithiasis: acute renal colic. Nerve supply of the kidney.

In the lower ureter, pain signals are also distributed through the genitofemoral and ilioinguinal nerves (see the image below). The nervi erigentes, which innervate the intramural ureter and bladder, are responsible for some of the bladder symptoms that often accompany an intramural ureteral calculus.

Fig. Nephrolithiasis: acute renal colic. Distribution of nerves in the flank.

 

Pathophysiology

Urinary tract stone disease, depicted below, is likely caused by two basic phenomena.

The first phenomenon is supersaturation of the urine by stone-forming constituents, including calcium, oxalate, and uric acid. Crystals or foreign bodies can act as nidi, upon which ions from the supersaturated urine form microscopic crystalline structures. The resulting calculi give rise to symptoms when they become impacted within the ureter as they pass toward the urinary bladder.

The overwhelming majority of renal calculi contain calcium. Uric acid calculi and crystals of uric acid, with or without other contaminating ions, comprise the bulk of the remaining minority. Other, less frequent stone types include cystine, ammonium acid urate, xanthine, dihydroxyadenine, and various rare stones related to precipitation of medications in the urinary tract. Supersaturation of the urine is likely the underlying cause of uric and cystine stones, but calcium-based stones (especially calcium oxalate stones) may have a more complex etiology.

The second phenomenon, which is most likely responsible for calcium oxalate stones, is deposition of stone material on a renal papillary calcium phosphate nidus, typically a Randall plaque (which are always composed of calcium phosphate). Evan et al recently proposed this model based on evidence accumulating from several laboratories.^[5]

Calcium phosphate precipitates in the basement membrane of the thin loops of Henle, erodes into the interstitium, and then accumulates in the subepithelial space of the renal papilla. The subepithelial deposits, which have long been known as Randall plaques, eventually erode through the papillary urothelium. Stone matrix, calcium phosphate, and calcium oxalate gradually deposit on the substrate to create a urinary calculus.

The colicky-type pain known as renal colic usually begins in the upper lateral midback over the costovertebral angle and occasionally subcostally. It radiates inferiorly and anteriorly toward the groin. The pain generated by renal colic is primarily caused by the dilation, stretching, and spasm caused by the acute ureteral obstruction. (When a severe but chronic obstruction develops, as in some types of cancer, it is usually painless.)

In the ureter, an increase in proximal peristalsis through activation of intrinsic ureteral pacemakers may contribute to the perception of pain. Muscle spasm, increased proximal peristalsis, local inflammation, irritation, and edema at the site of obstruction may contribute to the development of pain through chemoreceptor activation and stretching of submucosal free nerve endings.

The term “renal colic” is actually a misnomer, because this pain tends to remain constant, whereas intestinal or biliary colic is usually somewhat intermittent and often comes in waves. The pattern of the pain depends on the individual’s pain threshold and perception and on the speed and degree of the changes in hydrostatic pressure within the proximal ureter and renal pelvis. Ureteral peristalsis, stone migration, and tilting or twisting of the stone with subsequent intermittent obstructions may cause exacerbation or renewal of the renal colic pain.

The severity of the pain depends on the degree and site of the obstruction, not on the size of the stone. A patient can often point to the site of maximum tenderness, which is likely to be the site of the ureteral obstruction (see the image below).

 

Fig.  Nephrolithiasis: acute renal colic. Distribution of renal and ureteral pain.

A stone moving down the ureter and causing only intermittent obstruction actually may be more painful than a stone that is motionless. A constant obstruction, even if high grade, allows for various autoregulatory mechanisms and reflexes, interstitial renal edema, and pyelolymphatic and pyelovenous backflow to help diminish the renal pelvic hydrostatic pressure, which gradually helps reduce the pain.

The interstitial renal edema produced stretches the renal capsule, enlarges the kidney (ie, nephromegaly), and increases renal lymphatic drainage. (Increased capillary permeability facilitates this edema.) It may also reduce the radiographic density of the affected kidney’s parenchyma when viewed on a noncontrast CT scan.

Distention of the renal pelvis initially stimulates ureteral hyperperistalsis, but this diminishes after 24 hours, as does renal blood flow. Peak hydrostatic renal pelvis pressure is attained within 2-5 hours after a complete obstruction.

Within the first 90 minutes of a complete ureteral obstruction, afferent preglomerular arteriolar vasodilation occurs, which temporarily increases renal blood flow. Between 90 minutes and 5 hours after the obstruction, renal blood flow starts to decrease while intraureteral pressure continues to rise. By 5 hours after a complete obstruction, both renal blood flow and intraluminal ureteral pressure decrease on the affected side.

Renal blood flow decreases to approximately 50% of normal baseline levels after 72 hours, to 30% after 1 week, to 20% after 2 weeks, and to 12% after 8 weeks. By this point, intraureteral pressures have returned to normal, but the proximal ureteral dilation remains and ureteral peristalsis is minimal.

Interstitial edema of the affected kidney actually 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 unit.

In summary, by 24 hours after a complete ureteral obstruction, the renal pelvic hydrostatic pressure has dropped because of (1) a reduction in ureteral peristalsis; (2) decreased renal arterial vascular flow, which causes a corresponding drop in urine production on the affected side; and (3) interstitial renal edema, which leads to a marked increase in renal lymphatic drainage.

Additionally, as the ureter proximal to the stone distends, some urine can sometimes flow around the obstruction, relieving the proximal hydrostatic pressure and establishing a stable, relatively painless equilibrium. These factors explain why severe renal colic pain typically lasts less than 24 hours in the absence of any infection or stone movement.

Whether calyceal stones cause pain continues to be controversial. In general, in the absence of infection, how a renal stone causes pain remains unclear, unless the stone also causes obstruction. Arguably, proving that a calyceal stone is causing an obstruction can be difficult. However, a stone trapped in a calyx plausibly could block the outflow tract from that calyx, causing an obstruction and subsequent pain.

Experimental studies in animals have suggested that renal damage may begin within 24 hours of a complete obstruction and that permanent kidney deterioration starts within 5-14 days. Whereas some practitioners wait several months for a stone to pass in an asymptomatic patient, others argue that permanent damage is occurring as long as intervention is delayed.

Based on personal experience and anecdotal cases, the author recommends waiting no longer than 4 weeks for a stone to pass spontaneously before considering intervention. Convincing asymptomatic patients of the need for surgical intervention may be difficult in the absence of a clear consensus in the urological community about the length of time to wait before surgical stone removal, fragmentation, or bypass.

If only a partial obstruction is present, the same changes occur, but to a lesser degree and over a longer period. Proximal ureteric and renal pelvic hydrostatic pressures tend to remain elevated longer, and ureteral peristalsis does not diminish as quickly. If the increased pressure is sufficient to establish a reasonable flow beyond the obstructing stone, glomerular filtration and renal blood flow approximates reference range baseline levels, although pain may be ongoing.

Etiology

A low fluid intake, with a subsequent low volume of urine production, produces high concentrations of stone-forming solutes in the urine. This is an important, if not the most important, environmental factor in kidney stone formation. The exact nature of the tubular damage or dysfunction that leads to stone formation has not been characterized.

Most research on the etiology and prevention of urinary tract stone disease has been directed toward the role of elevated urinary levels of calcium, oxalate, and uric acid in stone formation, as well as reduced urinary citrate levels.

Hypercalciuria is the most common metabolic abnormality. Some cases of hypercalciuria are related to increased intestinal absorption of calcium (associated with excess dietary calcium and/or overactive calcium absorption mechanisms), some are related to excess resorption of calcium from bone (ie, hyperparathyroidism), and some are related to an inability of the renal tubules to properly reclaim calcium in the glomerular filtrate (renal-leak hypercalciuria).

Magnesium and especially citrate are important inhibitors of stone formation in the urinary tract. Decreased levels of these in the urine predispose to stone formation.

The following are the 4 main chemical types of renal calculi, which together are associated with more than 20 underlying etiologies:

·                       Calcium stones

·                       Struvite (magnesium ammonium phosphate) stones

·                       Uric acid stones

·                       Cystine stones

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.^[6]

Calcium stones account for 75% of renal calculi. 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.^[7] 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 account for 15% of renal calculi. They are associated with chronic urinary tract infection (UTI) with gram-negative rods capable of splitting urea into ammonium, which combines with phosphate and magnesium. Usual organisms include Proteus, Pseudomonas, and Klebsiella species. Escherichia coli is not capable of splitting urea and, therefore, is not associated with struvite stones. Urine pH is typically greater than 7.

Underlying anatomical abnormalities that predispose patients to recurrent kidney infections should be sought and corrected. UTI does not resolve until stone is removed entirely.

Uric acid stones account for 6% of renal calculi. 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 account for 2% of renal calculi. They 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.

Cystine stones are treated with a 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.

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.^{[8, 9, 10]}

In developing countries, bladder calculi are more common than upper urinary tract calculi; the opposite is true in developed countries. These differences are believed to be diet-related.

Most urinary calculi develop in persons aged 20-49 years. Peak incidence occurs in people aged 35-45 years, but the disease can affect anyone at any age. Patients in whom multiple recurrent stones form usually develop their first stones while in their second or third decade of life.

An initial stone attack after age 50 years is relatively uncommon. 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.

In general, urolithiasis is more common in males (male-to-female ratio of 3:1). Stones due to discrete metabolic/hormonal defects (eg, cystinuria,hyperparathyroidism) and stone disease in children are equally prevalent between the sexes. Stones due to infection (struvite calculi) are more common in women than in men. Female patients have a higher incidence of infected hydronephrosis.

Urinary tract calculi are far more common in Asians and whites than in Native Americans, Africans, African Americans, and some natives of the Mediterranean region. White males are affected 3-4 times more often than African American males, though African Americans have a higher incidence of infected ureteral calculi than whites.

Although some differences may be attributable to geography (stones are more common in hot and dry areas) and diet, heredity also appears to be a factor. This is suggested by the finding that, in regions with both white and nonwhite populations, stone disease is much more common in whites.

Prognosis

Approximately 80-85% of stones pass spontaneously. Approximately 20% of patients require hospital admission because of unrelenting pain, inability to retain enteral fluids, proximal UTI, or inability to pass the stone.

The most morbid and potentially dangerous aspect of stone disease is the combination of urinary tract obstruction and upper urinary tract infection. Pyelonephritis, pyonephrosis, and urosepsis can ensue. Early recognition and immediate surgical drainage are necessary in these situations.

Because the minimally invasive modalities for stone removal are generally successful in removing calculi, the primary consideration in managing stones is not whether the stone can be removed but whether it can be removed in an uncomplicated manner with minimum morbidity.

The usually quoted recurrence rate for urinary calculi is 50% within 5 years and 70% or higher within 10 years, although a large, prospective study published in 1999 suggested that the recurrence rate may be somewhat lower at 25-30% over a 7.5-year period. Recurrence rates after an initial episode of ureterolithiasis have also been reported to be 14%, 35%, and 52% at 1, 5, and 10 years, respectively.

Metabolic evaluation and treatment are indicated for patients at greater risk for recurrence, including those who present with multiple stones, who have a personal or family history of previous stone formation, who present with stones at a younger age, or who have residual stones after treatment.

Medical therapy is generally effective at delaying (but perhaps not completely stopping) the tendency for stone formation. The most important aspect of medical therapy is maintaining a high fluid intake and subsequent high urinary volume. Without an adequate urinary volume, no amount of medical or dietary therapy is likely to be successful in preventing stone formation.

According to estimates, merely increasing fluid intake and regularly visiting a physician who advises increased fluids and dietary moderation can cut the stone recurrence rate by 60%. This phenomenon is known as the “stone clinic” effect. In contrast, optimal use of metabolic testing with proper evaluation and compliance with therapy can completely eliminate new stones in many patients and significantly reduces new stone formation in most patients.

History

Patients with urinary calculi may report pain, infection, or hematuria. Small nonobstructing stones in the kidneys only occasionally cause symptoms. If present, symptoms are usually moderate and easily controlled. The passage of stones into the ureter with subsequent acute obstruction, proximal urinary tract dilation, and spasm is associated with classic renal colic.

Acute onset of severe flank pain radiating to the groin, gross or microscopic hematuria, nausea, and vomiting not associated with an acute abdomen are symptoms that most likely indicate renal colic caused by an acute ureteral or renal pelvic obstruction from a calculus. Renal colic pain rarely, if ever, occurs without obstruction.

Patients with large renal stones known as staghorn calculi (see the image below) are often relatively asymptomatic. The term “staghorn” refers to the presence of a branched kidney stone occupying the renal pelvis and at least one calyceal system. Such calculi usually manifest as infection and hematuria rather than as acute pain.

Complete staghorn calculus that fills the collecting system of the kidney (no intravenous contrast material in this patient). Although many staghorn calculi are struvite (related to infection with urease-splitting bacteria), the density of this stone suggests that it may be metabolic in origin and is likely composed of calcium oxalate. Percutaneous nephrostolithotomy or perhaps even open surgical nephrolithotomy is required to remove this stone.

 

 

Asymptomatic bilateral obstruction, which is uncommon, manifests as symptoms of renal failure.

Important historical features are as follows:

·                       Duration, characteristics, and location of pain

·                       History of urinary calculi

·                       Prior complications related to stone manipulation

·                       Urinary tract infections

·                       Loss of renal function

·                       Family history of calculi

·                       Solitary or transplanted kidney

·                       Chemical composition of previously passed stones

Location and characteristics of pain

Most calculi originate within the kidney and proceed distally, creating various degrees of urinary obstruction as they become lodged iarrow 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 distention 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.

Pain from upper ureteral stones tends to radiate to the flank and lumbar areas. On the right side, this can be confused with cholecystitis or cholelithiasis; on the left, the differential diagnoses include acute pancreatitis, peptic ulcer disease, and gastritis.

Midureteral calculi cause pain that radiates anteriorly and caudally. This midureteral pain in particular can easily mimic appendicitis on the right or acute diverticulitis on the left.

Distal ureteral stones cause pain that tends to radiate into the groin or testicle in the male or labia majora in the female because the pain is referred from the ilioinguinal or genitofemoral nerves.

Stones lodged at the ureterovesical junction also may cause irritative voiding symptoms, such as urinary frequency and dysuria. If a stone is lodged in the intramural ureter, symptoms may appear similar to cystitis or urethritis. These symptoms include suprapubic pain, urinary frequency, urgency, dysuria, stranguria, pain at the tip of the penis, and sometimes various bowel symptoms, such as diarrhea and tenesmus. These symptoms can be confused with pelvic inflammatory disease, ovarian cyst rupture, or torsion and menstrual pain in women.

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.

Phases of acute renal colic attack

The actual pain attack tends to occur in somewhat predictable phases, with the pain reaching its peak in most patients within 2 hours of onset. The pain roughly follows the dermatomes of T-10 to S-4. The entire process typically lasts 3-18 hours. Renal colic has been described as having 3 clinical phases.

The first phase is the acute or onset phase.The typical attack starts early in the morning or at night, waking the patient from sleep. When it begins during the day, it tends to start slowly and insidiously. The pain is usually steady, increasingly severe, and continuous, sometimes punctuated by intermittent paroxysms of even more excruciating pain. The pain may increase to maximum intensity in as little as 30 minutes after onset or may take up to 6 hours or longer to peak. The typical patient reaches maximum pain 1-2 hours after the start of the renal colic attack.

The second phase is the constant phase. Once the pain reaches maximum intensity, it tends to remain constant until it is either treated or allowed to diminish spontaneously. The period of sustained maximal pain is called the constant phase of the renal colic attack. This phase usually lasts 1-4 hours but can persist longer than 12 hours in some cases. Most patients arrive in the ED during this phase of the attack.

The third phase is the abatement or relief phase.During this final phase, the pain diminishes fairly quickly, and patients finally feel relief. Relief can occur spontaneously at any time after the initial onset of the colic. Patients may fall asleep, especially if they have been administered strong analgesic medication. Upon awakening, the patient notices that the pain has disappeared. This final phase of the attack most commonly lasts 1.5-3 hours.

Other symptoms

Nausea and vomiting occur in at least 50% of patients with acute renal colic. Nausea is caused by the common innervation pathway of the renal pelvis, stomach, and intestines through the celiac axis and vagal nerve afferents. This is often compounded by the effects of narcotic analgesics, which often induce nausea and vomiting through a direct effect on gastrointestinal (GI) motility and an indirect effect on the chemoreceptor trigger zone in the medulla oblongata. Nonsteroidal anti-inflammatory drugs (NSAIDs) can often cause gastric irritation and GI upset.

The presence of a renal or ureteral calculus is not a guarantee that the patient does not have some other, unrelated medical problem causing the GI symptoms.

In some cases, a stone may pass before the definitive imaging procedure has been completed. In these cases, residual inflammation and edema still may cause some transient or diminishing obstruction and pain even without any stone being positively identified.

Physical Examination

The classic presentation for a patient with acute renal colic is the sudden onset of severe pain originating in the flank and radiating inferiorly and anteriorly. The pain is usually, but not always, associated with microscopic hematuria, nausea, and vomiting. Dramatic costovertebral angle tenderness is common; this pain can move to the upper or lower abdominal quadrant as a ureteral stone migrates distally. However, the rest of the examination findings are often unremarkable.

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. Peritoneal signs are usually absent—an important consideration in distinguishing renal colic from other sources of flank or abdominal pain. Testicles may be painful but should not be very tender and should appear normal.

Unlike patients with an acute abdomen, who usually try to lie absolutely still, patients with renal colic tend to move constantly, seeking a more comfortable position. (However, patients with pyonephrosis also tend to remain motionless.) 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.

Findings should correlate with the reports of pain, so that complicating factors (eg, urinary extravasation, abscess formation) can be detected. Beyond this, the specific location of tenderness does not always correlate with the exact location of the stone, although the calculus is often in the general area of maximum discomfort.

Approximately 85% of all patients with renal colic demonstrate at least microscopic hematuria, which means that 15% of all patients with kidney stones do not have hematuria. Lack of hematuria alone does not exclude the diagnosis of acute renal colic. Tachycardia and hypertension are relatively common in these cases, even in patients with no prior personal history of abnormal cardiac or blood pressure problems.

Fever is not part of the presentation of uncomplicated nephrolithiasis. The presence of pyuria, fever, leukocytosis, or bacteriuria suggests the possibility of a urinary infection and the potential for an infected obstructed renal unit or pyonephrosis. Such a condition is potentially life threatening and should be treated as a surgical emergency.

In patients older than 60 years presenting with severe abdominal pain and with no prior history of renal stones, look carefully for physical signs of abdominal aortic aneurysm (AAA) (see Abdominal Aortic Aneurysm).

Complications

The morbidity of urinary tract calculi is primarily due to obstruction with its associated pain, although nonobstructing calculi can still produce considerable discomfort. Conversely, patients with obstructing calculi may be asymptomatic, which is the usual scenario in patients who experience loss of renal function due to chronic untreated obstruction. Stone-induced hematuria is frightening to the patient but is rarely dangerous by itself.

Serious complications of urinary tract stone disease include the following:

·                       Abscess formation

·                       Serious infection of the kidney that diminishes renal function

·                       Urinary fistula formation

·                       Ureteral scarring and stenosis

·                       Ureteral perforation

·                       Extravasation

·                       Urosepsis

·                       Renal loss due to long-standing obstruction

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.

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.

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 ooncontrast 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.

Diagnostic Considerations

The diagnosis is often made on the basis of clinical symptoms alone, although confirmatory tests are usually performed. At this point, the goals and opinions of physicians in different specialties diverge.

From the point of view of the emergency department (ED) physician, making the diagnosis of a renal or ureteral stone and excluding appendicitis or abdominal aortic aneurysm (AAA) is sufficient. A urologist, who must ultimately make the decision about possible surgery, may require additional information. Before such a decision can be made, a urologist must know about the size, orientation, radiolucency, composition, and location of the stone and must know about overall kidney function, the presence of any infection, and other clinical information.

It is important to distinguish nephrolithiasis from the many other conditions (gynecologic and nongynecologic) that can cause flank pain (see Causes of Flank Pain).

Beware of the patient older than 60 years with an apparent first kidney stone. Consider the possibility of symptomatic 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.

Failure to diagnose or delay in diagnosing symptomatic AAA may lead to medicolegal liability. The pain of a leaking AAA often is misdiagnosed initially as renal colic. In one series of 134 patients with symptomatic AAA presenting to the ED, the following statistics were reported^[12] :

·                       Eighteen percent had an initial misdiagnosis of nephrolithiasis.

·                       All were older than 60 years and none had a prior history of renal calculi.

·                       Eighty percent had a pulsatile mass noted by at least one examiner.

·                       Forty-three percent had microhematuria on urinalysis.

·                       Delay of diagnosis of AAA in the ED was associated with higher mortality and morbidity rates than in the group who received the correct diagnosis promptly.

Failure to diagnose and promptly treat a urinary tract infection (UTI) proximal to a ureteral stone is also a potential source of medicolegal liability. Urgent urologic intervention must be sought in these patients.

Other conditions to consider include the following:

·                       Pyonephrosis

·                       Renal artery embolus

Differential Diagnoses

·                       Abdominal Abscess

·                       Acute Glomerulonephritis

·                       Appendicitis

·                       Biliary Colic

·                       Cholecystitis

·                       Cholelithiasis

·                       Diverticulitis

·                       Duodenal Ulcers

·                       Epididymitis

·                       Gastritis and Peptic Ulcer Disease

·                       Gastrointestinal Foreign Bodies

·                       Ileus

·                       Inflammatory Bowel Disease

·                       Large Bowel Obstruction

·                       Liver Abscess

·                       Pancreatitis

·                       Papillary Necrosis

·                       Pelvic Inflammatory Disease

·                       Pyonephrosis

·                       Rectal Foreign Bodies

·                       Renal Arteriovenous Malformation

·                       Renal Cell Carcinoma

·                       Renal Vein Thrombosis Imaging

·                       Small Bowel Obstruction

·                       Splenic Abscess

·                       Testicular Torsion

·                       Urinary Tract Infection in Females

·                       Urinary Tract Infection in Men

·                       Urinary Tract Obstruction

·                       Viral Gastroenteritis

 

Approach Considerations

Acute renal colic with resultant flank pain is a common and sometimes complex clinical problem. Whereas noncontrast abdominopelvic computed tomography (CT) scans have become the imaging modality of choice, in some situations, renal ultrasonography or a contrast study such as intravenous pyelography (IVP) may be preferred.

A kidneys-ureters-bladder (KUB) radiograph, in addition to the renal colic CT scan, facilitates the review and follow-up of stone patients. Alternatively, the “CT scout” (a digital reconstruction from the CT that has an appearance similar to a KUB) is almost as sensitive as a KUB and is a good substitute at the initial assessment if the stone seen on the CT scan is visible on the CT scout. Adding contrast to the CT scan study may sometimes help clarify a difficult or confusing case, but, in general, contrast obscures calcific densities, and, as such, contrast scans are usually indicated only during subsequent evaluation of patients with stones. The noncontrast CT is the cornerstone of initial radiographic assessment.

Most authors recommend diagnostic imaging to confirm the diagnosis in first-time episodes of ureterolithiasis, when the diagnosis is unclear, or if associated proximal urinary tract infection (UTI) is suspected. Lindqvist et al found that patients who are pain-free after receiving analgesics could be discharged from the emergency department (ED) and undergo radiologic imaging after 2-3 weeks without increasing morbidity.^[13]

Initial stones in elderly people and in children are relatively uncommon; however, consider kidney stones whenever acute back or flank pain is encountered, regardless of patient age. When stones occur in persons in these uncommon age groups, a metabolic workup consisting of a 24-hour urine collection and appropriate serum laboratory testing is recommended.

Guidelines from the European Association of Urology recommend the following laboratory tests in all patients with an acute stone episode^[3] :

·                       Urinary sediment/dipstick test for demonstration of blood cells, with a test for bacteriuria (nitrite) and urine culture in case of a positive reaction

·                       Serum creatinine level, as a measure of renal function

In addition, patients with fever warrant a complete blood cell count. Patients with vomiting should have serum or plasma sodium and potassium levels measured. Optional tests that may provide useful information include a pH level (which might provide insight into the type of stone that the patient has formed) and measurement of serum or plasma calcium (which may identify hypercalcemia).^[3]

Urinalysis

Microscopic examination of the urine for evidence of hematuria and infection is a critical part of the evaluation of a patient thought to have renal colic. Gross or microscopic hematuria is only present in approximately 85% of patients with urinary calculi. The lack of microscopic hematuria does not eliminate renal colic as a potential diagnosis. In addition to a dipstick evaluation, always perform a microscopic urinalysis in these patients.

One retrospective study found that 67% of patients with ureterolithiasis had more than 5 red blood cells (RBCs) per high-power field (hpf), and 89% of patients had more than 0 RBCs/hpf on urine microscopic examination.^[14] In addition, 94.5% have hematuria if screened with microscopy plus urine dipstick testing.^[15]

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.

Attention should also be paid to the presence or absence of leukocytes, crystals, and bacteria and to the urinary pH. In general, if the number of white blood cells (WBCs) in the urine is greater than 10 cells per high-power field or greater than the number of RBCs, suspect a UTI. Pyuria (>5 WBCs/hpf on a centrifuged specimen) in a patient with ureterolithiasis should prompt a careful search for signs of infected hydronephrosis.

Urinary crystals of calcium oxalate, uric acid, or cystine may occasionally be found upon urinalysis. When present, these crystals are very good clues to the underlying type and nature of any obstructing calculus.

Determining urinary pH also helps. 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.

Blood Studies

Whereas mild leukocytosis often accompanies a renal colic attack, a high index of suspicion for a possible renal or systemic 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. A depressed RBC count suggests a chronic disease state or severe ongoing hematuria.

Measurements of serum electrolyte, creatinine, calcium, uric acid, parathyroid hormone (PTH), and phosphorus are needed to assess a patient’s current renal function and to begin the assessment of metabolic risk for future stone formation.

A high serum uric acid level may indicate gouty diathesis or hyperuricosuria, while hypercalcemia suggests either renal-leak hypercalciuria (with secondary hyperparathyroidism) or primary hyperparathyroidism. If the serum calcium level is elevated, serum PTH levels should be obtained.

Serum creatinine level is the major predictor of contrast-induced nephrotoxicity. If the creatinine level is higher than 2 mg/dL, use diagnostic techniques that do not require an infusion of contrast, such as ultrasonography or helical CT scanning.

Hypokalemia and decreased serum bicarbonate level suggest underlying distal (type 1) renal tubular acidosis, which is associated with formation of calcium phosphate stones.

24-Hour Urine Profile

To identify urinary risk factors, a 24-hour urine profile, including appropriate serum tests of renal function, uric acid, and calcium, is needed. Such testing is available from various commercial laboratories. This study is designed to provide more information about the exact nature of the chemical problem that caused the stone. This information is useful not only to allow more specific and effective therapy for stone prevention but also to identify patients with renal calculi who might have other significant health problems.

Keep in mind that all of the 24-hour urine chemistry findings may be within the reference range in patients who actively form stones and who are at high risk for stones. In these cases, optimizing the levels is beneficial.

The following are objective indications for a metabolic evaluation with a 24-hour urinalysis:

·                       Residual calculi after surgical treatment

·                       Initial presentation with multiple calculi

·                       Initial presentation before age 30 years

·                       Renal failure

·                       Solitary kidney (including renal transplant)

·                       Family history of calculi

·                       More than 1 stone in the past year

·                       Bilateral calculi

·                       Patient preference: An important consideration in determining whether to perform a 24-hour urine study is the patient’s interest. If a patient is strongly motivated to follow a protracted stone-prevention treatment plan (involving diet, supplements, medications, or a combination), obtain the study. If a patient is unlikely or unwilling to follow a long-term treatment plan, a metabolic evaluation is probably unwarranted. Patients have to understand that stone disease is a chronic disease. If they do not commit to helping themselves in behavior modification, dietary changes, or medical compliance, they are prone to more frequent calculi formation.

The most common findings on 24-hour urine studies include hypercalciuria,hyperoxaluria, hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high urinary sodium and low urinary magnesium concentrations, may also play a role. A finding of hypercalcemia should prompt follow-up with an intact parathyroid hormone study to evaluate for primary and secondary hyperparathyroidism.

Elevation of the 24-hour excretion rate of calcium, oxalate, or uric acid indicates a predisposition to form calculi.

Hypercalciuria can be subdivided into absorptive, resorptive, and renal-leak categories on the basis of the results of blood tests and 24-hour urinalysis on both regular and calcium-restricted diets. Depending on the specific subtype, the treatment of absorptive hypercalciuria may include modest dietary calcium restriction, thiazide diuretics, oral calcium binders, or phosphate supplementation.

Resorptive hypercalciuria is primary hyperparathyroidism and requires parathyroidectomy, when possible. If parathyroid surgery is not possible, phosphate supplementation is usually recommended. Renal-leak hypercalciuria, which is less common than absorptive hypercalciuria, is usually associated with secondary hyperparathyroidism and is best managed with thiazide diuretics.

Another clinical approach to hypercalciuria, when hyperparathyroidism has been excluded with appropriate blood tests, is avoidance of excessive dietary calcium (usual recommendation, 600-800 mg/d), modest limitation of oxalate intake, and thiazide therapy. If thiazide therapy fails, additional workup (eg, calcium-loading test, more thorough evaluation) may be needed.

Indiscriminate dietary calcium restriction is not advantageous and in fact may increase formation of calculi owing to a secondary increase in oxalate absorption. The reduced dietary calcium reduces the oxalate-binding sites in the gastrointestinal (GI) tract, increasing the free dietary oxalate and leading to increased oxalate absorption. The final product of this is a net increase in stone production.

Hyperoxaluria may be primary (a rare genetic disease), enteric (due to malabsorption and associated with chronic diarrhea or short-bowel syndrome), or idiopathic. Oxalate restriction and vitamin B-6 supplementation are somewhat helpful in patients with idiopathic hyperoxaluria. Enteric hyperoxaluria is the type that is most amenable to treatment; dietary calcium supplementation often produces dramatic results.

Calcium citrate is the recommended supplement because it tends to further reduce stone formation. Calcium carbonate supplementation is less expensive but lacks citrate’s added benefit. Calcium works as an oxalate binder, reducing oxalate absorption from the GI tract. It should be administered with meals, especially those that contain high-oxalate foods. The supplement should not contain added vitamin D, because this increases calcium absorption, leaving less calcium in the GI tract to bind to oxalate. The optimal 24-hour urine oxalate level is 20 mg/d or less.

Hyperuricosuria predisposes to the formation of calcium-containing calculi because sodium urate can produce malabsorption of macromolecular inhibitors or can serve as a nidus for the heterogeneous growth of calcium oxalate crystals. Gouty diathesis, a condition of increased stone production associated with high serum uric acid levels, is also possible.

Therapy involves potassium citrate supplementation, allopurinol, or both. In general, patients with pure uric acid stones and hyperuricemia are treated with allopurinol, and those with hyperuricosuric calcium stones are treated with citrate supplementation. The optimal 24-hour urine uric acid level is 600 mg/d or less.

Excess sodium excretion can contribute to hypercalciuria by a phenomenon known as solute drag. Elevated urinary sodium levels are almost always associated with dietary indiscretions. Decreasing the oral sodium intake can decrease calcium excretion, thereby decreasing calcium saturation.

An elevated phosphorus level is useful as a marker for a subtype of absorptive hypercalciuria known as renal phosphate leak (absorptive hypercalciuria type III). Renal phosphate leak is identified by high urinary phosphate levels, low serum phosphate levels, high serum 1,25 vitamin D-3 (calcitriol) levels, and hypercalciuria. This type of hypercalciuria is uncommon and does not respond well to standard therapies.

The above laboratory tests are confirmatory but are performed only if the index of clinical suspicion is high. Any patient with hypercalciuria who has a low serum phosphorus level and a high-normal or high urinary phosphorus level may have this condition. Repeat laboratories along with a 1,25 vitamin D-3 level are confirmatory.

Phosphate supplements are used to correct the low serum phosphate level, which then decreases the inappropriate activation of vitamin D originally caused by the hypophosphatemia. This corrects the hypercalciuria, which is ultimately a vitamin D–dependent function in this condition. This therapy is not well tolerated, however.

Magnesium and, especially, citrate are important chemical inhibitors of stone formation. Hypocitraturia is one of the most common metabolic defects that predispose to stone formation, and some authorities have recommended citrate therapy as primary or adjunctive therapy to almost all patients who have formed recurrent calcium-containing stones.

Many laboratories use 24-hour urine citrate levels of 320 mg/d as the normal threshold, but optimal levels are probably closer to the median level (640 mg/d) in healthy individuals. Periodic monitoring of pH with pH test strips can be very useful to titrate and optimize citrate supplementation. A pH level of 6.5 is usually considered optimal. A pH level over 7.0 should be discouraged, as it prompts calcium phosphate precipitation.

Potassium citrate is the preferred type of pharmacologic citrate supplement, though a potassium/magnesium preparation is under investigation. Liquid or powder pharmacologic citrate preparations are recommended when absorption is a problem or in cases involving chronic diarrhea. Sustained-release tablets are available and may be more convenient for some patients. Lemon juice is an excellent source of citrate; alternatively, large quantities of lemonade can be ingested, and this, of course, has the added benefit of providing increased fluid intake.

Magnesium is a more recently recognized inhibitor of stone formation, and the clinical role of magnesium replacement therapy is less well defined than that of citrate.

Creatinine is the control that allows verification of a true 24-hour sample. Most individuals excrete 1-1.5 g of creatinine daily. Values at either extreme that are not explained by estimates of lean body weight should prompt consideration that the sample is inaccurate.

Patients in whom stones form should strive to achieve a urine output of more than 2 L daily in order to reduce the risk of stone formation. Patients with cystine stones or those with resistant cases may need a daily urinary output of 3 L for adequate prophylaxis.

Some stones, such as those composed of uric acid or cystine, are pH-dependent, meaning that they can form only in acidic conditions. Calcium phosphate and struvite only form when the urine pH is alkaline. Although the other parameters in the 24-hour urine usually identify patients at risk of forming these stones, pH studies can be important in monitoring these patients, in optimizing therapy with citrate supplementation, and in identifying occult stone disease in some patients.

Plain (Flat Plate or KUB) Radiography

Plain abdominal radiography (also referred to as flat plate or KUB radiography) is useful for assessing total stone burden, as well as the size, shape, composition, and location of urinary calculi in some patients. Calcium-containing stones (approximately 85% of all upper urinary tract calculi) are radiopaque, but pure uric acid, indinavir-induced, and cystine calculi are relatively radiolucent on plain radiography.

When used with other imaging studies, such as a renal ultrasonography or, particularly, CT scanning, the plain film helps provide a better understanding of the characteristics of urinary stones revealed with these other imaging studies. This may also be helpful in planning surgical therapy.

The flat plate radiograph uses the same orientation and anatomical presentation that is observed on fluoroscopy images and retrograde pyelograms or during endoscopic ureteral surgery, such as ureteroscopy or intracorporeal lithotripsy. Not all urinary calculi may be visible on the KUB radiograph, whether because of their small size, stone radiolucency, or overlying gas, stool, or bone. The stones that are observed can be correlated with opacities found on other studies for identification and tracking progress.

If a stone is not visible on a flat plate radiograph, it could be a radiolucent uric acid stone that can be dissolved with alkalinizing medication. Such a stone is more likely if the urine pH indicates very acidic urine. In practice, any patient with symptoms of acute renal colic who demonstrates a urine pH lower than 6.0 should be considered at risk for a possible uric acid stone. If a stone of adequate size is visible on a CT scan but not visible on KUB, then uric stones should be considered.

The flat plate radiograph is inexpensive, quick, and usually helpful even if no specific stone is observed. It is extremely useful in following the progress of previously documented radiopaque calculi and checking the position of any indwelling double-J stents. The KUB radiograph can suggest the fluoroscopic appearance of a stone, which determines whether it can be targeted with extracorporeal shockwave lithotripsy (SWL).

The KUB radiograph is also quite accurate for helping determine the exact size and shape of a visible radiopaque stone and sometimes is more accurate than CT in this regard. Note that most stones will appear larger on KUB radiograph than on CT, with CT-based measurement of maximum stone dimension approximately 12% smaller than a corresponding KUB-based measurement.^[16]

Many calcifications observed on the KUB radiograph are phleboliths, vascular calcifications, calcified lymph nodes, appendicoliths, granulomas, various calcified masses, or even bowel contents. All can be confused with urinary tract calculi.

The insoluble radiopaque carrier for osmotically controlled-release oral system (OROS) pharmaceuticals can sometimes be mistaken for urinary calculi on KUB radiographs.

Differentiation between a phlebolith and an obstructing calcific stone becomes easier when the KUB radiograph demonstrates a lucent center, identifying the calcification as a phlebolith. This central lucency may not be observed as often on CT scans. For these reasons, many urologists recommend the flat plate radiograph in addition to CT scan for any renal colic–type scenario.

A number of studies have suggested that the flat plate has a relatively low sensitivity (40-50%) and specificity for renal and ureteral calculi. Many patients have numerous pelvic calcifications that make pinpointing specific stones difficult. Any calcific density observed on a KUB radiograph that happens to overlie the course of the ureter is not guaranteed to be a stone.

A large clinical study from Johns Hopkins University by Jackman et al concluded that “plain abdominal radiograph is more sensitive than scout CT for detecting radiopaque nephrolithiasis.^[17] Of the stones visible on plain abdominal radiograph, 51% were not seen on CT. To facilitate outpatient clinic follow-up of patients with calculi, plain abdominal radiographs should be performed.”

Many urologists, including this author, recommend that in addition to other studies (eg, noncontrast helical or spiral CT scans), a KUB radiograph be obtained in all patients with a clinical presentation of acute flank pain suggestive of renal colic. Knowing the exact size and shape of a stone, its position, fluoroscopic appearance, surgical orientation, and relative radiolucency is an advantage.

In addition, the progress of the stone can be easily monitored with a follow-up KUB radiograph, which may prove 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.

A reasonable practical compromise is to obtain a KUB film only in cases in which the stone is not visible on the digital CT scout radiograph.

Ultrasonography

Renal ultrasonography by itself is frequently adequate to determine the presence of a renal stone. The study is mainly used alone in pregnancy^[18] or in combination with plain abdominal radiography to determine hydronephrosis or ureteral dilation associated with an abnormal radiographic density believed to be a urinary tract calculus. A stone easily identified with renal ultrasonography but not visible on the plain radiograph may be a uric acid or cystine stone, which is potentially dissolvable with urinary alkalinization therapy.

For some stones, ultrasonography works quite well; however, it has been found to be less accurate in diagnosis of ureteral stones (see the image below), especially those in the distal ureter, than IVP or CT. Diagnostic criteria include direct visualization of the stone, hydroureter more than 6 mm in diameter, and perirenal urinoma suggesting calyceal rupture.^[19]

Renal sonogram showing a dilated renal collecting system consistent with ureteral obstruction.

In addition, ultrasonography is not reliable for small stones (ie, those smaller than 5 mm) and does not help in the evaluation of kidney function.

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 definitive on helical CT or IVP (see the image below).

Transabdominal sonogram revealing a ureteral stone at the ureterovesical junction.

Ultrasonography requires no intravenous (IV) contrast and can easily detect any significant hydronephrosis, although this must be differentiated from ureteropelvic junction (UPJ) obstruction or an extrarenal pelvis. A large extrarenal pelvis or UPJ obstruction can easily be misread for hydronephrosis if ultrasonography alone is used.

Middleton et al reported perhaps the most successful use of ultrasonography for renal colic: a 91% stone detection rate. Most authors report rates of approximately 30%. The unusually high success rate achieved by Middleton et al is partly explained by the fact that a radiologist specializing in ultrasonography performed the studies, which typically required at least 15-20 minutes to complete. The success of diagnostic ultrasonography is very dependent on operator skill and experience, which is probably demonstrated by the unique setting of this study.^[20]

Renal ultrasonography works best in the setting of relatively large stones within the renal pelvis or kidney and sometimes at the UPJ. Whether the stones are radiolucent or radio-opaque does not matter because an ultrasound image is based strictly on density, not on calcium content. Ultrasonography is a good way to monitor known stones after medical or surgical therapy if the stones are large enough to be detected by this modality and are in a suitable position.

Ultrasonography can also be used to check the abdomen for a possible abdominal aortic aneurysm (AAA) or cholelithiasis, which can sometimes be mistaken for acute renal colic. It is also useful in differentiating filling defects observed on contrast studies because stones are much more echogenic than tumors, clots, or tissue. It is the initial imaging modality of choice for pregnant patients with acute renal colic because it avoids all potentially hazardous ionizing radiation.

Ultrasonography relies on indirect visualization clues to identify stones. Differentiating an extrarenal pelvis from an obstructed one is sometimes difficult when using ultrasonography alone. Intermittent obstruction or mild hydronephrosis can be easily missed with ultrasonography, and, with the few exceptions mentioned above, it generally does not provide much information about most other disease processes capable of causing acute flank pain.

Sometimes, a KUB abdominal flat plate radiograph is used in addition to ultrasonography to help identify and monitor suspected stones, especially if renal dilation is detected. As with the KUB radiograph alone, any density detected along the expected course of the ureter is not guaranteed to be an actual stone within the collecting system.

The combination of renal ultrasonography with KUB radiography has been proposed as a reasonable initial evaluation protocol when a CT scan cannot be performed or is unavailable. When combined with KUB radiography, ultrasonography can quickly and inexpensively provide substantial information about the urinary tract without the risk of contrast nephrotoxicity or hypersensitivity. IVP can then be limited to those patients for whom additional information is required for a diagnosis or for whom the etiology of the pain remains unclear.

The intrarenal resistive index, as measured on Doppler studies, has been proposed as one way to diagnose acute renal obstruction using ultrasound. Under normal conditions, renal vascular resistance is relatively low and renal blood flow is excellent throughout the cardiac cycle, with a reasonable flow continuing even during diastole. During conditions associated with increased vascular resistance (eg acute ureteric obstruction), the decrease in renal blood flow during diastole is proportionately of greater magnitude than that during systole.

The resistive index is calculated as peak systolic velocity minus end-diastolic velocity divided by peak systolic velocity. An elevated resistive index of 0.7 or more is considered indicative of an acute ureteral obstruction. A change in the resistive index between the affected and contralateral (healthy) kidney of 0.04 or more also suggests a ureteral obstruction. (The affected kidney has the higher resistive index value.)

This study may be particularly useful in pregnancy (when exposure to ionizing radiation must be minimized), severe contrast media allergy, and azotemia. For best results, measure the intrarenal resistive index during a pain attack but before any nonsteroidal anti-inflammatory drugs (NSAIDs) or other anti-inflammatory medications are administered.

However, the intrarenal resistive index does not identify partial or intermittent obstructions and is less helpful in the early phase of even complete ureteral blockage. It also does not provide any information about the radiolucency, size, shape, or position of any stone and cannot be used to differentiate between intrinsic and extrinsic urinary obstructions.

Pyelosinus extravasation or fornix rupture, which occurs in up to 20% of patients with acute ureteral obstructions, leads to a loss of dilation and may be responsible for false-negative findings from studies. Other nonobstructive renal problems, such as renal failure, diabetic nephropathy, and renal compression, can affect the readings.

Considering that up to perhaps 35% of patients with documented acute ureteral obstruction do not demonstrate any significant hydroureteronephrosis, the use of a noninvasive study such as Doppler ultrasonography and intrarenal resistive index, which does not depend on visual ureteral or renal pelvic dilation, may eventually prove very useful. For now, additional studies on this technique are needed before the intrarenal resistive index can be reliably used for diagnosing acute renal colic and ureteric obstruction.

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.^[21]

Intravenous Pyelography (Urography)

Before the advent of helical CT, IVP, also known as intravenous urography (IVU), was the test of choice in diagnosing ureterolithiasis. IVP is widely available and fairly inexpensive but less sensitive thaoncontrast helical CT. CT scanning with delayed contrast series and thin slices has reduced the need for IVP in the evaluation of problematic ureteral stones.

The main advantage of IVP is the clear outline of the entire urinary system that it provides, making visualization of even mild hydronephrosis relatively easy. IVP is helpful in identifying the specific problematic stone among numerous pelvic calcifications, as well as in demonstrating renal function and establishing that the other kidney is functional. These determinations are particularly helpful if the degree of hydronephrosis is mild and the noncontrast CT scan findings are not definitive. IVP can also show nonopaque stones as filling defects.

Disadvantages include the need for IV contrast material, which may provoke an allergic response or renal failure, and the need for multiple delayed films, which can take up to 6 hours. Obtaining the IVP is also a relative labor-intensive process. In addition, IVP may fail to reveal alternative pathology if a stone is not discovered, delaying the final diagnosis. False-negative results usually occur with stones located at the ureterovesical junction.

The dose of IV contrast is usually about 1 mL/kg. Bolus administration is usually recommended for renal colic evaluations because it allows for a nephrogram-effect phase film. This normally occurs within the first minute after bolus contrast injection and cannot be obtained with slow-drip infusion.

Acute ureteral obstruction causes an intense persistent finding on nephrograms. This may take several hours or more to fully visualize, which necessarily delays completion of the study. The so-called delayed nephrogram on IVP is one of the hallmark signs of acute urinary tract obstruction. The relative delay in penetration of IV contrast passing through an obstructed kidney elicits this sign. The kidney appears to develop a whitish color, and contrast appearance within the collecting system of the affected renal unit is significantly delayed.

KUB radiographs are obtained immediately before contrast administration and at 1, 5, 10, and 15 minutes afterwards or until visible contrast material fills both ureters (see the image below). Prone films are sometimes obtained to enhance visualization of the ureters. When the bladder is full of contrast and the distal ureters contain sufficient contrast for visualization, the patient is asked to void; then a postvoid film is taken. Sometimes, oblique views are needed when bone or bowel contents overlie the area of interest.

 

I

Fig. Intravenous pyelogram (IVP) demonstrating dilation of the right renal collecting system and right ureter consistent with right ureterovesical stone.

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.

Typically, an IVP positive for a ureteral stone is one that shows a delayed nephrogram effect and columnization. The ureter is peristaltic, so the entire ureter is not usually visualized on a single film except when an obstruction is present, such as from a stone. Even without observing any specific stone, the presence of a nephrogram effect in one kidney with normal function of the opposite kidney is highly suggestive, but not diagnostic, of ureteral obstruction.

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.

However, no published study has indicated that the clinical course, treatment outcome, or residual renal damage is altered in any way in these patients. In fact, this information about the radiological assessment of the relative severity of the obstruction rarely affects clinical treatment decisions, except perhaps in persons with solitary kidneys.

Contrast-induced nephropathy (CIN) is the third leading cause of hospital-acquired acute renal failure. A serum creatinine level of more than 2 mg/dL is a relative contraindication to the use of IV contrast agents. Patients with azotemia, multiple myeloma, pregnancy, or diabetes, especially if dehydrated, are particularly susceptible to acute CIN (25% or greater increase in serum creatinine within 2-3 days of IV contrast exposure). Ischemia, direct intracellular high–contrast-concentration toxicity, and free-radical injury are thought to be the causative mechanisms of CIN.

Low osmolarity or iso-osmolar contrast may help to reduce the risk of CIN. The renal vasodilator fenoldopam mesylate has been used to minimize renal complications in higher-risk patients requiring IV contrast studies who would otherwise be at high risk for azotemia. Fenoldopam is a dopamine type 1A agonist that has been shown to increase renal plasma flow and to help prevent contrast nephropathy.

Theophylline and N-acetylcysteine have also been used with some success, but the standard prophylactic therapy is IV saline at a rate of 1-3 mL/kg/h. Hemodialysis before and after IV contrast can also be used to minimize renal toxicity, but such a regimen is costly and too cumbersome for general use except in special high-risk situations.

A randomized study by Merten et al comparing standard IV saline hydration prophylaxis with a 154-mEq/L sodium bicarbonate solution found a substantial benefit with the latter.^[22] Patients treated with saline were 8 times more likely to develop nephropathy after contrast exposure than those treated with sodium bicarbonate. Such a treatment plan is practical, inexpensive, simple, safe, and effective, and the author now recommend IV sodium bicarbonate hydration as the method of choice for prevention of CIN.^[22]

Anaphylaxis to ionic contrast agents occurs in 1-2 patients per 1000 IVP studies. Risk of recurrence is approximately 15% if reexposed to ionic agents but falls to 5% wheonionic 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.

Nonionic contrast media is more expensive but less likely to provoke an allergic response than the older ionic media, especially if the patient has a history of mild or moderate allergic reactions to contrast or injected dye. 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.

Many institutions currently use only nonionic agents for all IV contrast studies, despite the added cost, because of the increased safety. Glucophage should be discontinued at least 1 day before any IV contrast study, particularly in patients with proven or borderline azotemia, because of the risk of worsening renal function and the rare development of potentially life-threatening lactic acidosis. It can be resumed 48 hours after the contrast study if renal function has normalized.

Medullary sponge kidney (MSK), also called tubular or ductal ectasia or cystic dilation of the collecting ducts, is a generally benign congenital condition that demonstrates dilation of the distal renal collecting tubules on IVP as the tubules fill with contrast. These normally invisible microscopic tubules show a whitish blush in the papilla in persons with MSK. In severe cases, stones, cysts, and diverticula can be present. The condition can be unilateral, or even limited to one calyceal system, but it is bilateral in 70% of patients. It is not usually discovered until the second or third decade of life, even though MSK is congenital.

MSK is the most common anatomical problem found in calcium nephrolithiasis patients, affecting approximately 2% overall. Most stones in patients who have MSK are composed of calcium oxalate with or without calcium phosphate. Stones tend to be small and are usually passed spontaneously.

In most cases, MSK is not hereditary, although rare autosomal inherited forms have been described. The exact cause is unknown, but it could be caused by tubular obstruction due to calcium oxalate calculi from infantile hypercalciuria or collecting duct dilation from blockage by fetal uric acid stones, embryonal remnants, or other material.

The most accurate way to demonstrate MSK is to employ high-quality excretory urography (ie, IVP) with serial renal tomography starting just before the injection of the contrast media and continuing every 4 minutes for the next 20 minutes.

Most patients with MSK are asymptomatic; unless they have an IVP for an unrelated reason, the condition may never be diagnosed. Of patients who are symptomatic, renal colic and calcium urinary stones are the most common problems. (UTIs and hematuria are the others.) Women are more likely to have MSK than men.

Some patients with MSK may report severe chronic renal pain without any evidence of infection, stones, or obstruction. The etiology of this pain is unclear. These patients may be treated best by physicians comfortable with the management of chronic pain disorders, although recent reports suggest that ureteroscopic laser papillotomy may provide temporary relief.^[23]

Long-term management of MSK, as in any frequent stone former, is aimed toward identifying metabolic risk factors for continuing stone formation, with serum and 24-hour urine testing. The most common metabolic problems in MSK are hypercalciuria and hypocitraturia.

Computed Tomography Scanning

At most institutions that offer this examination, CT scanning has replaced IVP, the historic criterion standard, for the assessment of urinary tract stone disease, especially for acute renal colic. CT scans are readily available in most hospitals and can be performed and read in just a few minutes. Numerous studies have demonstrated that CT has a sensitivity of 95-100% and superior specificity and accuracy when compared with IVP.^[19]

A renal colic study consists of a noncontrast or unenhanced CT scan of the abdomen and pelvis, including very narrow cuts taken through the kidneys and bladder areas, where symptomatic stones are most likely to be encountered.

Technically, a relatively high pitch of more than 1.5 with thin collimation of 2-3 mm is generally considered a good compromise between imaging quality and radiation dosage. No rectal, oral, or IV contrast is used, because contrast material obscures any calcium-containing stones; both the stone and the contrast material would appear bright on the scans. Optimally, the patient’s bladder is filled, which facilitates viewing the ureterovesical junction (see the image below).

Fig. Noncontrast helical CT scan of the abdomen demonstrating a stone at the right ureterovesical junction.

In equivocal cases in which an indeterminate calcification is found along the course of the ureter or an abrupt change in ureteral caliber is found without a conclusively identified stone, an overlapping retrospective series can be performed to better evaluate this specific area and eliminate any sampling error.

An abdominal flat plate or KUB radiograph is sometimes automatically included in a renal colic study, depending on the institution and the preferences of the medical staff.

Advantages of CT scanning include the following:

·                       It can reveal other pathology (eg, AAAs, appendicitis, pancreatitis, cholecystis, ovarian disorders, diverticular disease, renal carcinoma).^[24] If the patient’s true underlying pathology is something other than a kidney stone, the CT scan is more clinically useful than an IVP for examining the possibilities.

·                       It can be performed quickly (< 5 min acquisition time)

·                       It avoids the use of IV contrast materials.

·                       The density of the stone can assist in predicting stone composition and response to shockwave lithotripsy.

Disadvantages of CT scanning include the following:

·                       It cannot be used to assess individual renal function or degree of obstruction.

·                       It can fail to reveal some unusual radiolucent stones, such as those caused by indinavir and atazanavir, which are typically invisible on the CT scan (though some serve as a nidus for deposition of calcium oxalate or calcium phosphate deposition and thus become radiopaque). Because of this possibility, IVP with contrast should be used for patients taking indinavir or atazanavir. Sulfadiazine stones are also difficult to visualize on CT because of relatively low attenuation.^[25]

·                       It is relatively expensive.

·                       It exposes the patient to a relatively high radiation dose (and thus should not be performed on pregnant women).

·                       Precise identification of small distal stones is occasionally difficult.

·                       Stone size as measured on CT KUB correlates poorly with actual size of the stone measured after spontaneous passage.^[26] 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.

·                       Although CT scans can be used to estimate the overall size, width, and location of a stone, they can only approximate its shape.^[27] Stone location can be described in anatomical terms, but the CT scan lacks the surgical orientation that most urologists prefer.

·                       It is not suitable for tracking the progress of the stone over time, supporting the recommendation for KUB radiography along with the CT scan.

If a KUB or flat plate radiograph is performed at the same time as the CT scan, some of these objections and problems disappear. However, obtaining the extra films involves some additional delay, the patient is exposed to more ionizing radiation, and the total cost for the workup increases.

The “scout” reconstruction of the CT scan, formatted to look like a plain radiograph, is a reasonable substitute for a formal KUB radiograph in some cases. Stones 3 mm and larger can be observed routinely on these studies. If the findings from a noncontrast CT scan are positive for a stone and the findings from the scout CT radiograph are negative, a separate KUB radiograph should be performed.

A digital scout CT radiograph is not nearly as sensitive as a good plain radiograph in detecting calculi; however, if the stone is visible on the “scout” reconstruction, only plain radiography may be needed later to determine if the stone has moved or passed.

Differentiation of phleboliths from urinary tract stones

Phleboliths are often confused with calcific ureteral stones. On a KUB radiograph, the characteristic lucent center of a phlebolith is often visible; thiis not present in a true calculus. Unfortunately, CT scans usually fail to reveal this central lucency or a bifid peak if a central lucency cannot be identified. Why this finding of a central transparency is so uncommon with CT scanning is unclear, but it may involve the orientation of the veins that form the phleboliths.

The “rim sign,” originally reported by Smith in 1995, is described as a rim, ring, or halo of soft tissue visible on CT scans that completely surrounds ureteral stones.^[22] The effect is enhanced by the local inflammation a stone produces in the ureteral wall, with subsequent edema at the site of the calculus. The rim sign is generally missing or incomplete with phleboliths.

While not absolutely definitive, the rim sign is strong evidence that the calcific density it surrounds is a stone and not a phlebolith. In several studies, more than 75% of all ureteral stones demonstrated a rim sign, while only 2-8% of phleboliths demonstrated it. The rim sign is more likely to be present in small or medium stones up to 5 mm in diameter. Larger stones (>6 mm) tend to lose the rim sign, presumably from stretching and thinning of the ureteral wall around a relatively large calculus.

Another way to differentiate a phlebolith from a calculus is to find a comet’s tail or comet sign, which is the noncalcified portion of a pelvic vein that is contiguous with the phlebolith. It appears as a small linear area of soft tissue that seems to pass obliquely through the CT scan section and attaches to the calcific density at one end. This is not observed in ureteral stones, although a ureter can mimic this sign to some degree. The comet sign is found in less than 20% of phleboliths, so its absence helps little, and its reliability is still unproved.

Currently, CT scans can be used to estimate the relative stone density and composition to some extent, although the results have not replaced the formal stone chemical composition analysis. However, this information can still help to plan therapy. Low-density stones are more amenable to shockwave lithotripsy, whereas higher-density stones may require ureteroscopy.

For example, a lucent stone that is not visible on the KUB radiograph that is clearly visible on the CT scan may indicate a uric acid calculus. This suggests a different diagnosis and therapy (urinary alkalinization) than for a calcium stone. For these reasons, many institutions routinely perform KUB radiography whenever renal colic noncontrast CT scanning is performed.

The Hounsfield unit density of the calculus on CT scanning can also be useful in predicting whether the stone is composed of uric acid. In a study of the unenhanced CT scans of 129 patients with renal stones, researchers from the University of Wisconsin concluded that the peak Hounsfield attenuation level of a kidney stone, used either by itself or divided by the size of the calculus in millimeters, may be a useful indicator of the stone’s chemical composition.

An attenuation-to-size ratio of 80 or greater was found to be highly suggestive of calcium oxalate stone material, especially in larger calculi. Uric acid stones have relatively low peak attenuation levels, and their attenuation-to-size ratios were generally below 80. In this Wisconsin study, uric acid stones averaged a mean peak Hounsfield reading of 344 HU, while the mean for calcium oxalate calculi was 652 HU.

Calculating the peak attenuation level and attenuation-to-size ratio adds no financial cost, patient morbidity, or time delay. While this study and similar reports are interesting and suggestive, the precise clinical role of CT scans in predicting stone fragility and chemical composition remains unclear.

Secondary signs of obstruction may be visible only on CT scans. In some cases, if a stone was passed shortly before the study, these signs may be the only evidence that the patient has or ever had a stone. These secondary signs include ureteral dilation with hydronephrosis, renal enlargement from interstitial edema (nephromegaly), and inflammatory changes, such as stranding or streaking in the perinephric fatty tissue.

In a 1996 study of 54 ureteral stone patients reported by Katz et al, hydronephrosis was present in 69%, proximal ureteral dilation was found in 67%, and perinephric stranding was detected in 65%. The other secondary signs had a similar frequency in adults and children. In the study, only 2 of the patients with ureteral calculi did not demonstrate any of the secondary signs of obstruction. The other secondary signs had a similar frequency in adults and children.^[28]

A similar 1996 study by Smith et al involving 220 patients found an even higher correlation between these 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%.^[29]

However, perinephric stranding was found less often in children with ureteral calculi than in adults in a 2001 study by Smergel and associates; therefore, this secondary sign, at least in the pediatric population, may be less reliable.^[30]

An additional secondary sign of acute renal obstruction ooncontrast CT scans has been reported by investigators from Johns Hopkins University. This sign is defined as a reduction in renal parenchymal attenuation (radiologic density) on the nonenhanced CT scan of the acutely obstructed renal unit compared with the normal unobstructed contralateral kidney. The difference in density is at least 2 standard deviations. This sign was identified in 95% of patients with acute ureteral obstruction, which suggests it is a reliable indicator.

Rarely, in indeterminate cases in which the secondary signs are negative and a stone is strongly suspected clinically but not clearly visible on the unenhanced CT scan, IV contrast can be used to help visualize the ureter. Repeat scanning after contrast infusion allows for improved visualization of the ureters. This allows physicians to make direct comparisons with the earlier studies to help make the correct diagnosis. Flat abdominal radiograph films taken after the contrast provide information similar to IVP, but delayed films or scans are likely to be needed.

In current clinical practice, the renal colic noncontrast CT scan is the standard of care in most EDs when a patient is thought to have renal colic or presents with acute flank pain. Guidelines from the American College of Radiology (ACR) recommend noncontrast CT as the most appropriate radiologic procedure for both suspected stone disease and recurrent symptoms of stone disease. Reduced-dose techniques are preferred.^[31]

Because of the limitations of CT scans, some urologists request additional studies, such as KUB radiography or IVP, to help them make critical decisions about management, follow-up, and possible surgical interventions. In cases of suspected stone disease in pregnant patients and in patients allergic to iodinated contrast or wheoncontrast CT is unavailable, the ACR considers ultrasonography of the kidney and bladder retroperitoneal with Doppler and KUB the preferred examination.^[31]

As noted earlier, obtaining a KUB radiograph when a renal colic CT scan study is performed for acute flank pain provides more precise information about the size and shape of any stone and quickly reveals whether stones are nonopaque and radiolucent. Follow-up evaluations are easier because only a repeat KUB radiograph is needed for comparison. A KUB radiograph also helps the urologist determine if a stone will be visible on fluoroscopic images, which is useful for possible shockwave lithotripsy since for most lithotripters used in the United States, fluoroscopic visualization is needed for stone targeting and positioning.

While the addition of an abdominal flat plate study (KUB radiograph) adds to the overall financial cost and requires additional time, the extra information the study provides is often quite valuable and ultimately beneficial to the patient. If the stone is visible on the CT scout image, however, then this provides the same information as a KUB and thus the latter is not needed.

CT has largely supplanted IVP in a number of settings. However, a comparison of the pros and cons of the two modalities suggests IVP retains some advantages (see Table, below).

Table. Intravenous Pyelography Versus CT Scanning: Which Is Better? (Open Table in a new window)

The noncontrast or renal colic-type CT scan is good for the initial diagnosis of a stone, especially in unusual or atypical cases or when patients are unable to tolerate intravenous contrast because of allergy or azotemia. Without definite hydronephrosis, a CT scan may not be able to isolate a specific stone, although secondary signs, such as perinephric streaking and nephromegaly, may be present.

The CT scan can be performed quickly in most institutions, even with an additional KUB radiograph, but it usually costs more than the IVP. In one series of 397 consecutive emergency urolithiasis patients from several university centers, the average fee for a CT scan was $1407, compared with $445 for an IVP.

CT scans are generally preferred by most ED physicians for the initial evaluation of patients with acute flank pain, except for HIV-positive patients who may be on protease inhibitors, who require an IVP, and pregnant women, who require ultrasonography for their initial imaging modality.

The IVP is better for clearly outlining the entire urinary tract and determining relative renal function. This test clearly shows stones causing blockage, whether the stones are radiolucent or opaque. While an IVP can reliably help in the diagnosis of an MSK, the clinical importance of this diagnosis is limited. The IVP is sometimes preferred by urologists in certain situations because of its better orientation and superior value in predicting possible stone passage, although these advantages are mostly negated if a KUB radiograph routinely accompanies the CT scan.

Plain Renal Tomography

Plain renal tomography requires moving the radiograph projector and film in such a way that a zone of photographic clarity is positioned at the stationary focus point of the radiograph beam. All other overlying material is eliminated. The focal point is adjusted along the anteroposterior axis a distance of 1 cm, and the radiograph procedure is repeated. Usually, a series of 4-6 films is needed to completely image both kidneys. If such a series of films is needed, it should be obtained before any IV contrast is administered; contrast obscures any stones present.

Although largely replaced by CT scanning without contrast, plain renal tomography has some uses and advantages. It does not require extensive preparation and can be performed quickly. In addition, the cost and radiation dosage to the patient are less than with CT scanning.

Plain renal tomography can be useful for monitoring a difficult-to-observe stone after therapy. Observing even a relatively large radiopaque stone located in the kidney or renal pelvis on a standard abdominal flat plate radiograph can be difficult or impossible if the patient has abundant gas or stool overlying the area, and plain renal tomography can often overcome this difficulty.

Plain renal tomography may be helpful for clarification of stones not clearly detected or identified with other studies (eg, differentiating intrarenal calcifications that are likely to be stones from extrarenal opacities that are clearly not renal calculi). It is often helpful in finding small stones in the kidneys, especially in patients who are large or obese whose bowel contents complicate observation of any renal calcifications.

Plain renal tomography is also useful for determining the number of stones present in the kidneys before a stone-prevention program is instituted. This information is used to better differentiate stones formed before therapy began from those formed later.

Retrograde Pyelography

The most precise imaging method for determining the anatomy of the ureter and renal pelvis and for making a definitive diagnosis of any ureteral calculus is not IVP or renal colic CT scanning but retrograde pyelography.

In this study, the patient is taken to the operating room (OR) cystoscopy suite, and an endoscopic examination is performed with the patient under anesthesia. After a cystoscope is placed in the bladder, a thin ureteral catheter is inserted into the ureteral orifice on the affected side. A radiographic picture is taken while contrast material is injected through the ureteral catheter directly into the ureter. Any stone, even if radiolucent, and any ureteral kinks, strictures, or tortuousities that may not be visualized easily on other studies become clearly visible.

Urologists perform retrograde pyelograms when a precise diagnosis cannot be made by other means or when a need clearly exists for an endoscopic surgical procedure and the exact anatomical characteristics of the ureter must be clarified.

Retrograde pyelograms are rarely performed merely for diagnostic purposes, because other less invasive studies are usually sufficient. They are considered essential when surgery is deemed necessary because of uncontrollable pain, severe urinary infection or urosepsis with a blocked kidney, a solitary obstructed kidney, a stone that is considered unlikely to pass spontaneously because of its large size (generally ≥8 mm), or the presence of possible anatomical abnormalities (eg, ureteral strictures).

Retrograde pyelograms can be performed safely both in patients highly allergic to IV contrast media and in patients with renal failure because the contrast medium never enters the bloodstream and therefore requires no renal filtration or excretion and causes no anaphylaxis.

Nuclear Renal Scanning

A nuclear renal scan can be used to objectively measure differential renal function, especially in a dilated system for which the degree of obstruction is in question. This is also a reasonable study in pregnant patients, in whom radiation exposure must be limited.

The intravenously injected radioisotope is eliminated via the nephron, with the rate of clearance from the renal unit providing an excellent estimate of the glomerular filtration rate and the relative rate of drainage or clearing from each kidney. A drainage half-time that is 20 minutes or longer indicates obstruction, while a drainage half-time of 10 minutes or less is considered unobstructed. If the drainage half-time is 10-20 minutes, the result is indeterminate.

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) has virtually no role in the current evaluation of acute renal colic in the typical patient. Direct detection of most stones is not possible with MRI, and MRI should not be used for that purpose in most instances. MRIs are generally more expensive than other studies, such as CT scans, which reveal stones much better.

On the other hand, MRI produces no dangerous radiation, the gadolinium contrast it uses has minimal nephrotoxicity, and it can readily reveal urinary obstruction even if the stones themselves are not easily visualized. These attributes make using MRI reasonable in selected cases in which other technologies are too toxic or potentially dangerous, such as in some children and in pregnant women (see below). Gadolinium contrast, however, is contraindicated if the estimated glomerular filtration rate is less than 30, owing to the risk of nephrogenic systemic fibrosis.

Use of MRI in pregnant patients is somewhat controversial. Long-term effects on the fetus are unknown, and MRI is not specifically indicated in pregnancy, although it is not specifically contraindicated either. Anecdotal reports suggest that MRI has no immediately detectable deleterious effects. When other imaging modalities cannot be used or are insufficient, magnetic resonance urographic imaging can be considered on a case-by-case basis when the benefits to the mother and fetus outweigh the potential risks.

Although MRI does not play a major role in the diagnosis of ureteral stones, it can be used for this purpose. 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.^[32] Sensitivity and specificity increased to 96.2-100% and 100%, respectively, using gadolinium-enhanced 3-D FLASH MR urography. Its lack of radiation makes MRI a good choice in this setting for pregnant women who have nondiagnostic findings from a sonogram.

Approach Considerations

Treatment of nephrolithiasis involves emergency management of renal (ureteral) colic, including surgical interventions where indicated, and medical therapy for stone disease.

In emergency settings where concern exists about possible renal failure, the focus of treatment should be on correcting dehydration, treating urinary infections, preventing scarring, identifying patients with a solitary functional kidney, and reducing risks of acute renal failure from contrast nephrotoxicity, particularly in patients with preexisting azotemia (creatinine >2 mg/dL), diabetes, dehydration, or multiple myeloma. Adequate intravenous (IV) hydration is essential to minimize the nephrotoxic effects of IV contrast agents. Choosing imaging studies that do not require IV contrast (eg, ultrasonography, plain abdominal flat plate radiographs, noncontrast computed tomography [CT] scans) is wise, especially in patients at increased risk for developing renal failure.

Most small stones with relatively mild hydronephrosis can be treated with observation and acetaminophen. More serious cases with intractable pain may require drainage with a stent or percutaneous nephrostomy. The internal ureteral stent is usually preferred in these situations because of decreased morbidity.

Acetaminophen can be used in pregnancy for mild-to-moderate pain. Opioid drugs, such as morphine and meperidine, are pregnancy category C medications, which means they can be used but they cross the placental barrier. Opioids can cause respiratory depression in the fetus; therefore, they should not be used near delivery or when other medications are adequate.

A stone chemical composition analysis should be performed whenever possible, and information should be provided to motivated patients about possible 24-hour urine testing for long-term nephrolithiasis prophylaxis. This is particularly important in patients with only 1 functioning kidney, those with medical risk factors, and children. However, any strongly motivated patient can benefit from a prevention analysis and prophylactic treatment if they are willing to pursue long-term therapy.

The size of the stone is an important predictor of spontaneous passage. 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. However, stone passage also depends on the exact shape and location of the stone and the specific anatomy of the upper urinary tract in the particular individual. For example, the presence of a ureteropelvic junction (UPJ) obstruction or a ureteral stricture could make passing even very small stones difficult or impossible. Most experienced emergency department (ED) physicians and urologists have observed very large stones passing and some very small stones that do not move.

Aggressive medical therapy has shown promise in increasing the spontaneous stone passage rate and relieving discomfort while minimizing narcotic usage. Aggressive treatment of any proximal urinary infection is important to avoid potentially dangerous pyonephrosis and urosepsis. In these cases, consider percutaneous nephrostomy drainage rather than retrograde endoscopy, especially in very ill patients.

Medical therapy for stone disease takes both short- and long-term forms. The former includes measures to dissolve the stone (possible only with noncalcium stones) or to facilitate stone passage, and the latter includes treatment to prevent further stone formation. Stone prevention should be considered most strongly in patients who have risk factors for increased stone activity, including stone formation before age 30 years, family history of stones, multiple stones at presentation, and residual stones after surgical treatment.

The decision to hospitalize a patient with a stone is usually made based on clinical grounds rather than on any specific finding on a radiograph. Generally, hospitalization for an acute renal colic attack is now officially termed an observation because most patients recover sufficiently to go home within 24 hours. Admission rate for patients with acute renal colic is approximately 20%.

Hospital admission is clearly necessary when any of the following is present:

·                       Oral analgesics are insufficient to manage the pain.

·                       Ureteral obstruction from a stone occurs in a solitary or transplanted kidney.

·                       Ureteral obstruction from a stone occurs in the presence of a urinary tract infection (UTI), fever, sepsis, or pyonephrosis.

Infected hydronephrosis, defined as UTI proximal to an obstructing stone, mandates hospital 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.^[33]

The clinical presentation of infected hydronephrosis is variable. Pyuria (>5 white blood cells [WBCs] per high-power field [hpf]) is almost always present but is 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.^[34]

Renal ultrasonography or computed tomography (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, ultrasonographic sensitivity for pyonephrosis was found to be 62-67%. CT sensitivity for pyonephrosis has not been reliably determined.^{[35, 36]} The emergency physician must maintain a high index of suspicion.^[37]

Antibiotics should cover Escherichia 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%.^[38]

Relative indications to consider for a possible admission include comorbid conditions (eg, diabetes), dehydration requiring prolonged intravenous (IV) fluid therapy, renal failure, or any immunocompromised state. Patients with complete obstruction, perinephric urine extravasation, a solitary kidney, 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.

Larger stones (ie, ≥ 7 mm) that are unlikely to pass spontaneously require some type of surgical procedure. In some cases, hospitalizing a patient with a large stone to facilitate surgical stone intervention is reasonable. However, most patients with acute renal colic can be treated on an ambulatory basis.

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, including extracorporeal shock wave lithotripsy (SWL), ureteroscopy, and percutaneous nephrolithotomy.^[39]

Emergency Management of Renal Colic

Initial treatment of a renal colic patient in the ED starts with obtaining IV access to allow fluid, analgesic, and antiemetic medications to be administered. Many of these patients are dehydrated from poor oral intake and vomiting. Although the role of supranormal hydration in the management of renal (ureteral) colic is controversial (see below), patients who are dehydrated or ill need adequate restoration of circulating volume.

After diagnosing renal (ureteral) colic, determine the presence or absence of obstruction or infection. Obstruction in the absence of infection can be initially managed with analgesics and with other medical measures to facilitate passage of the stone. Infection in the absence of obstruction can be initially managed with antimicrobial therapy. In either case, promptly refer the patient to a urologist.

If neither obstructioor infection is present, analgesics and other medical measures to facilitate passage of the stone (see below) can be initiated with the expectation that the stone will likely pass from the upper urinary tract if its diameter is smaller than 5-6 mm (larger stones are more likely to require surgical measures).

If both obstruction and infection are present, emergency decompression of the upper urinary collecting system is required (see Surgical Care). In addition, immediately consult with a urologist for patients whose pain fails to respond to ED management.

Pain relief

The cornerstone of ureteral colic management is analgesia, which can be achieved most expediently with parenteral narcotics or nonsteroidal anti-inflammatory drugs (NSAIDs). If oral intake is tolerated, the combination of oral narcotics (eg, codeine, oxycodone, hydrocodone, usually in a combination form with acetaminophen), NSAIDs, and antiemetics, as needed, is a potent outpatient management approach for renal (ureteral) colic.

Parenteral narcotics are the mainstay of analgesia for patients with acute renal colic. They work primarily on the central nervous system (CNS) to reduce the perception of pain. They are inexpensive and quite effective. When considering a medication and dosage range, remember that acute renal colic is probably the most painful malady to affect humans. Adverse effects of narcotic analgesics include respiratory depression, sedation, constipation, a potential for addiction, nausea, and vomiting.

Choosing any particular agent tends to be somewhat arbitrary. Morphine, meperidine, and butorphanol are the most commonly used.

Morphine is a potent narcotic analgesic that controls severe pain primarily through a CNS mechanism via specific receptor site interactions. The usual dosage is 10 mg/70 kg body weight intramuscularly (IM) or subcutaneously (SC) every 4 hours. The actual dosage required varies according to each individual patient’s tolerance and severity of discomfort. For more rapid results, morphine sulfate can be administered IV in doses of 4-10 mg, but this must be done slowly or in small increments to avoid excessive adverse effects.

Adverse effects of morphine include respiratory depression, drowsiness, mood changes, nausea, vomiting, increases in the cerebrospinal fluid pressure, and cough reflex depression. The most bothersome is respiratory depression caused by a direct effect on the brain stem respiratory center. This effect is most severe in patients who are elderly, debilitated, or both.

Meperidine is a potent parenteral narcotic analgesic that is very similar in overall effect to morphine sulfate. A 60-80 mg dose of meperidine is roughly equivalent to 10 mg of morphine. Meperidine offers a slightly more rapid onset of action and slightly shorter duration of analgesic activity than morphine sulfate. Some evidence suggests that meperidine may have slightly fewer adverse effects than morphine.

The dosage range is usually 50-150 mg IM or SC every 3-4 hours; it is reduced by at least 50% with IV administration. The actual effective dosage varies according to the source of the pain and the individual’s tolerance. As with morphine sulfate, IV administration should be performed slowly. Meperidine is contraindicated in patients taking monoamine oxidase inhibitors.

Butorphanol has some theoretical advantages based on studies that suggest it causes less smooth muscle spasm and respiratory depression than either morphine or meperidine. Butorphanol costs approximately $10/mg, compared with approximately $0.05/mg for meperidine. Because 1 mg of butorphanol is roughly equivalent in pain relieving efficacy to 20 mg of meperidine, butorphanol effectively is about 10 times as costly.

Naloxone (0.4 mg or 1 mL) is a specific narcotic antagonist for both meperidine and morphine sulfate that can be administered to counteract inadvertent narcotic overdosage or unusual opioid sensitivity. Naloxone has no analgesic properties.

Nalbuphine is a potent parenteral analgesic that is partly antagonistic to narcotics. Its overall effectiveness in relieving pain is equivalent to the opioids. The usual starting dose is 0.5 mg IV or 1-1.5 mg IM every 4-6 hours as needed.

Of the NSAIDs, the only one approved by the US Food and Drug Administration (FDA) for parenteral use is ketorolac. Ketorolac works at the peripheral site of pain production rather than on the CNS. It has been proven in multiple studies to be as effective as opioid analgesics, with fewer adverse effects.^{[40, 41]} The dosage is 30-60 mg IM or 30 mg IV initially followed by 30 mg IV or IM every 6-8 hours. A dose of 15 mg is recommended in patients older than 65 years.

In more severe cases, ketorolac is particularly effective when used together with narcotic analgesics. Oral ketorolac is available in 10-mg pills, but the efficacy of this form in persons with acute renal colic is less clear. Some practitioners use parenteral ketorolac in the hospital but recommend either ibuprofen or oral cyclooxygenase-2 inhibitors (eg, celecoxib or meloxicam) for pain management in outpatients.

An intranasal ketorolac preparation is now available for moderate-to-severe pain and may be particularly useful for outpatient use in patients unable to take oral medication. A maximum of 5 days of ketorolac therapy is recommended.

Chemically, ketorolac is similar to aspirin and may increase the prothrombin time when administered with anticoagulants. Ketorolac can increase methotrexate toxicity and phenytoin levels. It is potentiated by probenecid and should be avoided in patients with peptic ulcer disease, renal failure, or recent gastrointestinal (GI) bleeding.

Because nausea and vomiting frequently accompany acute renal colic, antiemetics often play a role in renal colic therapy. Several antiemetics have a sedating effect that is often helpful.

Metoclopramide is the only antiemetic that has been specifically studied in the treatment of renal colic. In 2 double-blinded studies, it apparently provided pain relief equivalent to narcotic analgesics in addition to relieving nausea. Its antiemetic effect stems from its dopaminergic receptor blockage in the CNS. It has no anxiolytic activity and is less sedating than other centrally acting dopamine antagonists. The effect of metoclopramide begins within 3 minutes of an IV injection, but it may not take effect for as long as 15 minutes if administered IM.

The usual dose in adults is 10 mg IV or IM every 4-6 hours as needed. Metoclopramide is not available as a suppository.

Other medications commonly used as antiemetics include promethazine, prochlorperazine, and hydroxyzine. The author usually recommends antiemetics when patients with renal colic have been vomiting actively or report nausea sufficient to interfere with oral therapy. They also may be useful as anxiolytics in some cases. Whereas metoclopramide is the antiemetic of choice in the hospital or ED setting, a suppository formulation such as promethazine or prochlorperazine is recommended for outpatient use.

Several studies have now demonstrated that desmopressin (DDAVP), a potent antidiuretic that is essentially an antidiuretic hormone, can dramatically reduce the pain of acute renal colic in many patients. It acts quickly, has no apparent adverse effects, reduces the need for supplemental analgesic medications, and may be the only immediate therapy necessary for some patients. It is available as a nasal spray (usual dose of 40 mcg, with 10 mcg per spray) and as an IV injection (4 mcg/mL, with 1 mL the usual dose). Generally, only 1 dose is administered.

Animal studies have demonstrated a significant reduction in mean intraureteral pressure after an acute obstruction in subjects administered desmopressin compared with controls. In human studies, approximately 50% of 126 patients tested had complete relief of their acute renal colic pain within 30 minutes after the administration of intranasal desmopressin without any analgesic medication. For patients in whom desmopressin therapy failed, suitable analgesics were administered. No adverse effects from the antidiuretic medication occurred.

Although desmopressin is thought to work by reducing the intraureteral pressure, it may also have some direct relaxing effect on the renal pelvic and ureteral musculature. A central analgesic effect through the release of hypothalamic beta-endorphins has been proposed but remains unproved. Whether this therapy significantly affects eventual stone passage is unknown.

While some of the human studies lack adequate controls and further studies must be conducted, desmopressin therapy currently appears to be a promising alternative or adjunct to analgesic medications in patients with acute renal colic, especially in patients in whom narcotics cannot be used or in whom the pain is unusually resistant to standard medical treatment.

Antibiotic use in patients with kidney stones remains controversial. Overuse of the more effective agents leaves only highly resistant bacteria, but failure to adequately treat a UTI complicated by an obstructing calculus can result in potentially life-threatening urosepsis and pyonephrosis.

Use antibiotics if a kidney stone or ureteral obstruction has been diagnosed and the patient has clinical evidence of a UTI. Evidence of a possible UTI includes an abnormal finding upon microscopic urinalysis, showing pyuria of 10 WBCs/hpf (or more WBCs than RBCs), bacteriuria, fever, or unexplained leukocytosis. Perform a urine culture in these cases because a culture cannot be performed reliably later should the infection prove resistant to the prescribed antibiotic.

Approximately 3% of patients being treated for renal colic are reported to develop a newly acquired UTI. While case numbers are not high, such an infection can dramatically complicate the clinical outcome for that patient. Base selection of the antibiotic on the patient’s presentation, reserving the most effective parenteral antibiotics for patients with frank sepsis or other high-risk characteristics.

The author’s preference for initial medical therapy for pain in patients with acute renal colic is to use IV or IM ketorolac for pain with metoclopramide for nausea. If this therapy is unsuccessful or if the case is deemed more severe, a narcotic such as morphine sulfate or meperidine is added as needed to control pain. An antibiotic is administered if any question of potential infection exists. An oral antibiotic is always used if the patient is able to return home.

The traditional outpatient treatment approach detailed above has recently been improved with the application of a more aggressive treatment approach known as active medical expulsive therapy (MET). Many randomized trials have confirmed the efficacy of MET in reducing the pain of stone passage, increasing the frequency of stone passage, and reducing the need for surgery.^{[42, 43, 44, 45, 46, 47, 48, 49]}

MET should be considered in any patient with a reasonable probability of stone passage. Given that stones smaller than 3 mm are already associated with an 85% chance of spontaneous passage, MET is probably most useful for stones 3-10 mm in size. Overall, MET is associated with a 65% greater likelihood of stone passage.^[50]

The original rationale for MET was based on the possible causes of failure to spontaneously pass a stone, including ureteral stricture, muscle spasm, local edema, inflammation, and infection. Various common drugs were considered that would potentially benefit these problems, improve spontaneous stone passage, and alleviate renal colic discomfort.

Although NSAIDs have ureteral-relaxing effects and, as such, can be considered a form of MET, patient outcomes have been significantly improved only with the use of more potent (off-label) medications. The initially popularized regimens for MET included corticosteroids such as prednisone, as in the following example:

·                       Ketorolac at 10 mg orally every 6 hours for 5 days

·                       Nifedipine XL at 30 mg/d PO for 7 days

·                       Prednisone 20 mg PO twice a day for 5 days

·                       Trimethoprim/sulfamethoxazole DS once a day for 7 days

·                       Acetaminophen 2 tablets 4 times a day for 7 days

·                       An oral opioid pain medication (oxycodone-acetaminophen) as needed for breakthrough pain

·                       Prochlorperazine suppository as needed for control of nausea

Although corticosteroids are effective, concerns about their side effects (admittedly not supported by randomized data) limited the acceptance of MET. More recently, randomized studies have demonstrated great efficacy of the following individual agents, sparing the corticosteroid component.

The calcium channel blocker nifedipine is indicated for angina, migraine headaches, Raynaud disease, and hypertension, but it can also reduce muscle spasms in the ureter, which helps reduce pain and facilitate stone passage. Ureteral smooth muscle uses an active calcium pump to produce contractions, so a calcium channel blocker such as nifedipine would be expected to relax ureteral muscle spasms.

The alpha-blockers, such as terazosin, and the alpha-1 selective blockers, such as tamsulosin, also relax the musculature of the ureter and lower urinary tract, markedly facilitating passage of ureteral stones. Some literature suggests that the alpha-blockers are more effective in this setting than the calcium channel blockers, and most practitioners currently use alpha-blockers preferentially over calcium channel blockers.

Multiple prospective randomized controlled studies 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.^{[43, 44, 45]}The best studied of these is tamsulosin, 0.4 mg administered daily.

A systematic review by Singh et al found that MET 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.^[51]

A systematic review by Beach et al found that MET 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.^[52]

Not all data support MET. A randomized study of 77 ED 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 MET highly likely.^[53]

MET with calcium channel blockers and alpha-blockers also appears to improve the results of ESWL (see Surgical Care) inasmuch as the stone fragments resulting from treatment appear to clear the system more effectively.

Analgesic therapy combined with MET dramatically improves the passage of stones, addresses pain, and reduces the need for surgical treatment. Ibuprofen can be substituted for the ketorolac tablets recommended in the original studies. Fewer complications with ibuprofen occur while maintaining efficacy for pain relief. An oral narcotic (eg, oxycodone/acetaminophen) is used as needed to control breakthrough pain.

·                       A typical regimen for this aggressive therapy is as follows:

·                       1-2 oral narcotic/acetaminophen tablets every 4 hours as needed for pain

·                       600-800 mg ibuprofen every 8 hours

MET with 30 mg nifedipine extended-release tablet once daily, 0.4 mg tamsulosin once daily, or 4 mg of terazosin once daily

Limit MET to a 10- to 14-day course, as most stones that pass during this regimen do so in that time frame. If outpatient treatment fails, promptly consult a urologist.

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 MET.

Intravenous hydration

IV hydration in the setting of acute renal colic is controversial. Whereas some authorities believe that IV 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 L of saline over 2 hours versus those who received 20 mL of saline per hour.^[54]

IV hydration should be given to patients with clinical signs of dehydration or to those with a borderline serum creatinine level who must undergo intravenous pyelography (IVP).

Straining urine for stones

Collecting any passed kidney stones is extremely important in the evaluation of a patient with nephrolithiasis for stone-preventive therapy. Yet, in a busy ED, the simple instruction to strain all the urine for stones can be easily overlooked.

Knowing when a stone is going to pass is impossible regardless of its size or location. Even after a stone has passed, residual swelling and spasms can cause continuing discomfort for some time. Be certain that all urine is actually strained for any possible stones. An aquarium net makes an excellent urinary stone strainer for home use because of its tight nylon weave, convenient handle, and collapsible nature, making it very portable; it easily fits into a pocket or purse.

Surgical Care

In general, stones that are 4 mm in diameter or smaller will probably pass spontaneously, and stones that are larger than 8 mm are unlikely to pass without surgical intervention. With MET, stones 5-8 mm in size often pass, especially if located in the distal ureter. The larger the stone, the lower the possibility of spontaneous passage (and thus the greater the possibility that surgery will be required), although many other factors determine what happens with a particular stone.

Indications and contraindications

The primary indications for surgical treatment include pain, infection, and obstruction. Infection combined with urinary tract obstruction is an extremely dangerous situation, with significant risk of urosepsis and death, and must be treated emergently in virtually all cases. Additionally, certain occupational and health-related reasons exist.

General contraindications to definitive stone manipulation include the following:

·                       Active, untreated UTI

·                       Uncorrected bleeding diathesis

·                       Pregnancy (a relative, but not absolute, contraindication)

Specific contraindications may apply to a given treatment modality. For example, do not perform SWL if a ureteral obstruction is distal to the calculus or in pregnancy.

Surgical options

For an obstructed and infected collecting system secondary to stone disease, virtually no contraindications exist for emergency surgical relief either by ureteral stent placement (a small tube placed endoscopically into the entire length of the ureter from the kidney to the bladder) or by percutaneous nephrostomy (a small tube placed through the skin of the flank directly into the kidney).

Many urologists have a preference for one technique or the other, but, in general, patients who are acutely ill, who have significant medical comorbidities, or who harbor stones that probably cannot be bypassed with ureteral stents undergo percutaneous nephrostomy, while others receive ureteral stent placement.

In patients who are floridly septic or hemodynamically unstable, a percutaneous nephrostomy is a faster and safer way to establish drainage of an infected and obstructed kidney. In these situations, retrograde approaches to drainage, if used at all, should be reserved for relatively mild cases in which patients are medically stable. Use appropriate urine cultures and antibiotics whenever a UTI is suspected in conjunction with hydronephrosis or renal colic.

The vast majority of symptomatic urinary tract calculi are now treated with noninvasive or minimally invasive techniques, while open surgical excision of a stone from the urinary tract is now limited to isolated atypical cases.

Guidelines are now available to assist the urologist in selecting surgical treatments. The 2005 American Urological Association (AUA) staghorn calculus guidelines recommend percutaneous nephrostolithotomy as the cornerstone of management.^[55] In the ureteral stone guidelines produced by a joint effort of the AUA and the European Association of Urology, SWL and ureteroscopy are both recognized as first-line treatments for ureteral stones.^[56]

Stent placement

Internal ureteral stents form a coil at either end when the stiffening insertion guide wire is removed. One coil forms in the renal pelvis and the other in the bladder. Stents are available in lengths from 20-30 cm and in 3 widths from 4.6F to 8.5F. Some are designed to soften after placement in the body; others are rather stiff to resist crushing and obstruction by large stones or external compression with occlusion from an extrinsic tumor or scar tissue.

To select the correct-size stent, estimates can be made based on the height of the patient, or the ureteral length can be measured. This is best performed by means of a retrograde pyelogram. The distance from the tip of the retrograde catheter to the UPJ is measured in centimeters with a tape measure. To account for the average magnification effect of the film, 10% of this reading is subtracted. If the result is an odd number, a double-J stent one size longer is used. The most common lengths used are 26 cm in men and 24 cm in women.

The optimal stent width depends on both the relative diameter and course of the ureter and the purpose of the stent. If the patient has a stricture or a tortuous ureter, a stiffer or larger-diameter stent is placed if possible.

When used for stone disease, stents perform several important functions. They virtually guarantee drainage of urine from the kidney into the bladder and bypass any obstruction. This relieves patients of their renal colic pain even if the actual stone remains. Over time, stents gently dilate the ureter, making ureteroscopy and other endoscopic surgical procedures easier to perform later.

Because they are also quite radiopaque, stents provide a stable landmark when performing SWL. A landmark is particularly important with small or barely visible stones, especially in the ureter, because the SWL machine uses radiographic visualization to target the stone.

Once large stones are broken up, stents tend to prevent the rapid dumping of large amounts of stone fragments and debris into the ureter (called steinstrasse). The stent forces the fragments to pass slowly, which is more efficient and prevents clogging.

Stents do have drawbacks. They can become blocked, kinked, dislodged, or infected. A KUB radiograph can be used to determine stent position, while infection is easily diagnosed by urinalysis. A renal sonogram can sometimes be helpful if there is concern for obstruction.

Questionable cases can be evaluated further using a radiographic cystogram or an IVP. The cystogram is performed by filling the urinary bladder with diluted contrast media through a Foley catheter under gravity pressure. A stent that is unclogged and functioning normally should show free reflux of contrast from the bladder into the stented renal pelvis.

The major drawback of stents, however, is that they are often quite uncomfortable for patients due to direct bladder irritation, spasm, and reflux. This discomfort can be alleviated to some extent by pain medications, anticholinergics (eg, oxybutynin, tolterodine), alpha-blockers, and topical analgesics (eg, phenazopyridine).

Percutaneous nephrostomy

In some cases, drainage of an obstructed kidney is necessary and stent placement is inadvisable or impossible. In particular, such cases include patients with pyonephrosis who have a UTI or urosepsis exacerbated by an obstructing calculus. In these patients, retrograde endourological procedures like retrograde pyelography and stent placement may exacerbate infection by pushing infected urinary material into the obstructed renal unit. Percutaneous nephrostomy is useful in such situations.^[57]

Extracorporeal shockwave lithotripsy

SWL, the least invasive of the surgical methods of stone removal, utilizes an underwater energy wave focused on the stone to shatter it into passable fragments.

It is especially suitable for stones that are smaller than 2 cm and lodged in the upper or middle calyx. It is contraindicated in pregnancy, untreatable bleeding disorders, tightly impacted stones, or in cases of ureteral obstruction distal to the stone. In addition, the effectiveness is limited for very hard stones (which tend to be dense on CT scan), cystine stones, and in very large patients.

The patient, under varying degrees of anesthesia (depending on the type of lithotriptor used), is placed on a table or in a gantry that is then brought into contact with the shock head. The deeper the anesthesia (general endotracheal), the better the results. In addition, evidence is mounting that slower shockwave delivery (60-80 per min) improves the results. New lithotriptors that have 2 shock heads, which deliver a synchronous or asynchronous pair of shocks (possibly increasing efficacy), have attracted great interest.

The shock head delivers shockwaves developed from an electrohydraulic, electromagnetic, or piezoelectric source. The shockwaves are focused on the calculus, and the energy released as the shockwave impacts the stone produces fragmentation. The resulting small fragments pass in the urine.

SWL is limited somewhat by the size and location of the calculus. A stone larger than 1.5 cm in diameter or one located in the lower section of the kidney is treated less successfully. Fragmentation still occurs, but the large volume of fragments or their location in a dependent section of the kidney precludes complete passage. In addition, results may not be optimal in large patients, especially if the skin-to-stone distance exceeds 10 cm.^[58]

Ureteroscopy

Along with SWL, ureteroscopic manipulation of a stone (see the image below) is a commonly applied method of stone removal. A small endoscope, which may be rigid, semirigid, or flexible, is passed into the bladder and up the ureter to directly visualize the stone.

 

 

Two calculi in a dependent calyx of the kidney (lower pole) visualized through a flexible fiberoptic ureteroscope. In another location, these calculi might have been treated with extracorporeal shockwave lithotripsy (ESWL), but, after being counseled regarding the lower success rate of ESWL for stones in a dependent location, the patient elected ureteroscopy. Note that the image provided by fiberoptics, although still acceptable, is inferior to that provided by the rod-lens optics of the rigid ureteroscope in the previous picture.

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. The typical patient has acute symptoms caused by a distal ureteral stone, usually measuring 5-8 mm. 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 SWL or are fragmented using an endoscopic direct-contact fragmentation device.

Often, a ureteral stent must be placed after ureteroscopy in order to prevent obstruction from ureteral spasm and edema. Since a ureteral stent is often uncomfortable, many urologists eschew stent placement following ureteroscopy in selected patients.^[59]

Percutaneous nephrostolithotomy allows fragmentation and removal of large calculi from the kidney and ureter. Because of their increased morbidity compared with SWL and ureteroscopy, percutaneous procedures are generally reserved for large and/or complex renal stones and failures from the other 2 modalities. Percutaneous nephrostolithotomy is especially useful for stones larger than 2 cm in diameter.

A needle and then a wire, over which is passed a hollow sheath, are inserted directly into the kidney through the skin of the flank. Percutaneous access to the kidney typically involves a sheath with a 1-cm lumen, which will admit relatively large endoscopes with powerful and effective lithotrites that can rapidly fragment and remove large stone volumes. Renal calyces, pelvis, and proximal ureter can be examined and stones extracted with or without prior fragmentation.

In some cases, a combination of SWL and a percutaneous technique is necessary to completely remove all stone material from a kidney. This technique, called sandwich therapy, is reserved for staghorn or other complicated stone cases. In such cases, experience has shown that the final procedure should be percutaneous nephrostolithotomy.

Opeephrostomy has been used less and less often since the development of SWL and endoscopic and percutaneous techniques; it now constitutes less than 1% of all interventions. Disadvantages include longer hospitalization, longer convalescence, and increased requirements for blood transfusion.

Medical Therapy for Stone Disease

Urinary calculi composed predominantly of calcium cannot be dissolved with current medical therapy; however, medical therapy is important in the long-term chemoprophylaxis of further calculus growth or formation.

Uric acid and cystine calculi can be dissolved with medical therapy. Patients with uric acid stones who do not require urgent surgical intervention for reasons of pain, obstruction, or infection can often have their stones dissolved with alkalization of the urine. Sodium bicarbonate can be used as the alkalizing agent, but potassium citrate is usually preferred because of the availability of slow-release tablets and the avoidance of a high sodium load.

The dosage of the alkalizing agent should be adjusted to maintain the urinary pH between 6.5 and 7.0. Urinary pH of more than 7.5 should be avoided because of the potential deposition of calcium phosphate around the uric acid calculus, which would make it undissolvable. Both uric acid and cystine calculi form in acidic environments.

Even very large uric acid calculi can be dissolved in patients who comply with therapy. Roughly 1 cm per month dissolution can be achieved. Practical ability to alkalinize the urine significantly limits the ability to dissolve cystine calculi.

Prophylactic therapy might include limitation of dietary components, addition of stone-formation inhibitors or intestinal calcium binders, and, most importantly, augmentation of fluid intake. (See Dietary Measures and Prevention of Nephrolithiasis.) Besides advising patients to avoid excessive salt and protein intake and to increase fluid intake, base medical therapy for long-term chemoprophylaxis of urinary calculi on the results of a 24-hour urinalysis for chemical constituents.

Chemoprophylaxis of uric acid and cystine calculi consists primarily of long-term alkalinization of urine. If hyperuricosuria or hyperuricemia is documented in patients with pure uric acid stones (present in only a relative minority), allopurinol (300 mg qd) is recommended because it reduces uric acid excretion.

Pharmaceuticals that can bind free cystine in the urine (eg, D-penicillamine, 2-alpha-mercaptopropionyl-glycine) help reduce stone formation in cystinuria. Therapy should also include long-term urinary alkalinization and aggressive fluid intake. Captopril has been shown to be effective in some trials, although, again, strong data are lacking. Routine use should be avoided but can be added in patients who have difficulty in dissolving and preventing cystine stones.

Dietary Measures

In almost all patients in whom stones form, an increase in fluid intake and, therefore, an increase in urine output is recommended. This is likely the single most important aspect of stone prophylaxis. 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. The goal is a total urine volume in 24 hours in excess of 2 liters.

The only other general dietary guidelines are to avoid excessive salt and protein intake. Moderation of calcium and oxalate intake is also reasonable, but great care must be takeot to indiscriminately instruct the patient to reduce calcium intake.

Dietary calcium should not be restricted beyond normal unless specifically indicated based on 24-hour urinalysis findings. Urinary calcium levels are normal in many patients with calcium stones. Reducing dietary calcium in these patients may actually worsen their stone disease, because more oxalate is absorbed from the GI tract in the absence of sufficient intestinal calcium to bind with it. This results in a net increase in oxalate absorption and hyperoxaluria, which tends to increase new kidney stone formation in patients with calcium oxalate calculi.

An empiric restriction of dietary calcium may also adversely affect bone mineralization and may have osteoporosis implications, especially in women. This practice should be condemned unless indicated based on a metabolic evaluation.

As a rule, dietary calcium should be restricted to 600-800 mg/d in patients with diet-responsive hypercalciuria who form calcium stones. This is roughly equivalent to a single high-calcium or dairy meal per day.

Prevention of Nephrolithiasis

The most common causes of kidney stones are hypercalciuria, hyperuricosuria, hyperoxaluria, hypocitraturia, and low urinary volume. Each of these major factors can be measured easily with a 24-hour urine sample using one of several commercial laboratory packages now available. Kidney stone preventive therapy consists of dietary adjustments, nutritional supplements, medications, or combinations of these.

Strongly encourage patients who have a stone at a young age (ie, < 25 y), multiple recurrences, a solitary functioning kidney, or a history of prior kidney stone surgery to obtain a 24-hour urine collection for stone prevention analysis, especially if they are motivated to comply with a long-term stone prevention program. These 24-hour urine collection kits can be obtained from a number of commercial medical laboratories.

Consultations

Consultation with a urologist is required when immediate ED management of renal (ureteral) colic fails. Referral to a urologist is necessary for all stones that prove refractory to outpatient management or that fail to pass spontaneously.

Consult a urologist immediately in cases of ureterolithiasis with proximal UTI. Infected hydronephrosis is a true urologic emergency and requires hospital admission, IV fluids, IV antibiotics, and immediate drainage of the infected hydronephrosis via percutaneous nephrostomy or ureteral stent placement.

Urologic consultation is also appropriate in patients with unusually large stones, high-risk medical conditions, inability to tolerate oral fluids and medications, unrelenting pain, renal failure, renal transplant, a solitary functioning kidney, or a history of prior stones that required invasive intervention.

Patients who are pregnant require a consultation with an obstetrician-gynecologist, and those with a history of severe cardiac disease or congestive heart failure may benefit from involvement of an internal medicine specialist or cardiologist.

Patients with strong motivation to prevent all future stones, those with multiple recurrences or single functioning kidneys, and all children younger than 16 years with nephrolithiasis should be referred to a specialist iephrolithiasis prevention. A medical expert in metabolic stone prevention testing, interpretation, and prophylactic therapy is available in most communities.

Long-Term Monitoring

Patients who do not meet admission criteria may be discharged from the ED in anticipation that the stone will pass spontaneously at home. Arrangements should be made 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.

Postsurgical follow-up

After surgical treatment of urinary tract calculi, the major issues include infection, ureteral obstruction, and hemorrhage. The postoperative course of minimally invasive stone-removal modalities is generally characterized by short-lived discomfort easily managed with oral medications. Continued or severe pain should prompt evaluation for complications. Repeat urine cultures and imaging studies should be performed to assess for ureteral obstruction and perforation, and the degree of circulating blood volume should be evaluated for ongoing hemorrhage.

A follow-up examination that includes abdominal radiography is often adequate after an uncomplicated stone-removal procedure. Further imaging is often unnecessary in a patient with a previous radiopaque stone who has no further symptoms. Imaging that includes assessment of renal drainage (eg, IVP, ultrasonography, CT scanning) is usually indicated in the following cases:

·                       Stones with unusual characteristics

·                       Difficult or complicated procedures

·                       Patients with unusual symptoms

Once postoperative complications have been excluded and the patient is clinically healthy, standard radiographic follow-up care includes abdominal radiography every 6-12 months. Radiography is often performed in conjunction with metabolic chemoprophylaxis.

Ongoing medical therapy

If a patient older than 40 years has formed a single stone that passed spontaneously or was easily treated, follow-up care for recurrent stones may be unnecessary. This patient is at a reasonably low risk for recurrence if adequate fluid intake is maintained. In other patients, whether or not they have elected directed metabolic therapy, routine follow-up care consists of plain abdominal radiography (or renal ultrasonography in the case of radiolucent stones) every 6-12 months.

If medical therapy is instituted, a 24-hour urinalysis 3 months after starting any new therapy should be performed to assess the degree of patient compliance and the adequacy of the metabolic response. Checking all possible metabolic parameters—not just the previously abnormal ones—is necessary because of the possibility of new problems arising as a result of the new therapy. Once a stable regimen has been established, annual 24-hour urinalyses are adequate.

Medication Summary

Please see Cystinuria, Hypercalciuria, Hyperoxaluria, Hyperuricosuria and Gouty Diathesis, Hypocitraturia, and struvite topics for specific information regarding medical therapy for stone disease. The medications listed below include those used in the emergency department (ED) and in outpatient management of renal (ureteral) colic, as well as selected antibiotics

Analgesics, Narcotic

Class Summary

Narcotic analgesics act at the central nervous system (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.

View full drug information

Butorphanol (Stadol)

 

Butorphanol is a mixed agonist-antagonist narcotic with central analgesic effects for moderately severe to severe pain. It causes less smooth muscle spasm and respiratory depression than morphine or meperidine. Weigh these advantages against the increased cost of butorphanol.

View full drug information

Morphine sulfate (Astramorph, Infumorph 200, Infumorph 500)

 

Morphine is the principal opium alkaloid product. It is the drug of choice for parenteral use in the immediate management of pain due to renal (ureteral) colic.

View full drug information

Oxycodone and acetaminophen (Percocet, Endocet, Roxicet, Tylox)

 

Oxycodone-acetaminophen is a drug combination indicated for oral relief of moderate to severe pain. It is employed in medical expulsive therapy (MET).

View full drug information

Hydrocodone and acetaminophen (Vicodin, Vicodin ES, Lortab, Norco)

 

Hydrocodone is also combined with acetaminophen. This drug combination is indicated for oral relief of moderate to severe pain.

View full drug information

Meperidine (Demerol)

 

Meperidine is a narcotic analgesic with multiple actions similar to those of morphine. It may produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine.

View full drug information

Nalbuphine

 

Nalbuphine is a synthetic opioid agonist-antagonist potent analgesic. It stimulates kappa opioid receptor in the CNS, which causes inhibition of ascending pain pathways. It is indicated for the relief of moderate to severe pain.

Analgesics, Miscellaneous

Class Summary

Analgesics such as acetaminophen can be used to provide relief of mild to moderate pain.

View full drug information

Acetaminophen

 

Acetaminophen is a nonopioid analgesic that is effective in relieving mild to moderate pain; however, it has no peripheral anti-inflammatory effects but can be used in pregnancy.

Nonsteroidal anti-inflammatory drugs

Class Summary

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit pain and inflammatory reactions by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. Both properties are beneficial in the management of renal (ureteral) colic.

These agents are at least as effective as narcotic analgesics iumerous randomized controlled trials. NSAIDs cause less nausea and less sedation thaarcotic analgesics, do not cause respiratory depression, and have no abuse potential. Their principal disadvantage is cost. Potential adverse effects on renal function, gastrointestinal (GI) mucosa, and platelet aggregation do not appear clinically important when they are used for short-term pain relief.

View full drug information

Ketorolac

 

Ketorolac is the only NSAID approved for parenteral use in adults in the United States. Its onset of action is evident within 10 min.

View full drug information

Ketorolac intranasal (Sprix)

 

Intranasal ketorolac inhibits cyclooxygenase, an early component of the arachidonic acid cascade, resulting in reduced synthesis of prostaglandins, thromboxanes, and prostacyclin. It elicits anti-inflammatory, analgesic, and antipyretic effects. It is indicated for short-term (up to 5 d) management of moderate to moderately severe pain. Bioavailability of a 31.5-mg intranasal dose (2 sprays) is approximately 60% of a 30-mg intramuscular (IM) dose. The intranasal spray delivers 15.75 mg per 100-µL spray; each 1.7-g bottle contains 8 sprays.

View full drug information

Ibuprofen (Motrin, Advil)

 

Ibuprofen is an oral NSAID. It has antipyretic, analgesic, and anti-inflammatory properties and is used for outpatient management.

Corticosteroids

Class Summary

These are strong anti-inflammatory agents that reduce ureteral inflammation. They also have profound metabolic and immunosuppressive effects.

View full drug information

Prednisone

 

Prednisone has been used in MET. Only a short course of prednisone therapy (5-10 d) should be administered.

View full drug information

Prednisolone (Prelone, Pediapred, Millipred, Orapred, Orapred ODT)

 

In combination with nifedipine or tamsulosin, prednisolone is 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.

Calcium channel blockers

Class Summary

Calcium channel blockers are smooth-muscle relaxants. In combination with prednisolone, they have facilitated ureteral stone passage in several small prospective studies.

View full drug information

Nifedipine (Nifedical XL, Procardia, Procardia XL, Adalat CC)

 

Nifedipine facilitates the passage of ureteral stones. The extended-release formulation simplifies treatment and encourages compliance. Only short-term therapy (10 d) should be considered for this indication.

Alpha blockers

Class Summary

Alpha-blockers are smooth-muscle relaxants. They have been shown to facilitate ureteral stone passage.

View full drug information

Tamsulosin (Flomax)

 

Tamsulosin, an alpha-1 selective blocker, is indicated for the treatment of lower urinary tract symptoms due to prostatic enlargement. An off-label use, as discussed above, is to facilitate passage of ureteral stones. Only short-term therapy (10 d) should be considered for this indication.

View full drug information

Terazosin (Hytrin)

 

Terazosin is indicated for the treatment of hypertension, as well as lower urinary tract symptoms due to prostatic enlargement. An off-label use is to facilitate passage of ureteral stones. Only short-term therapy (10 d) should be considered for this indication.

Uricosuric agents

Class Summary

Uricosuric agents help prevent nephropathy. They also help prevent recurrent calcium oxalate calculi.

View full drug information

Allopurinol (Zyloprim)

 

Allopurinol inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. It reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines.

Alkalinizing agents, oral

Class Summary

Oral alkalinizing agents are used for the treatment of metabolic acidosis. They are also employed when long-term maintenance of alkaline urine is desirable.

View full drug information

Potassium citrate (Polycitra-K, Urocit K)

 

Potassium citrate is absorbed and metabolized to potassium bicarbonate, thus acting as a systemic alkalizer. Its effects are essentially those of chlorides before absorption and those of bicarbonates subsequently. Oxidation is virtually complete so that < 5% of the potassium citrate is excreted in the urine unchanged. It is highly concentrated and, when administered after meals and before bedtime, allows maintenance of an alkaline urinary pH at all times, usually without necessity of 2 AM dose. In the recommended dosage, it alkalinizes urine without producing systemic alkalosis.

Antiemetics

Class Summary

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.

View full drug information

Metoclopramide (Reglan)

 

Metoclopramide is the only antiemetic that has been studied specifically in treatment of renal colic. In 2 small double-blinded studies, it provided relief of nausea and pain relief equal to that of narcotic analgesics. Metoclopramide’s antiemetic effect is due to blockade of dopaminergic receptors in chemoreceptor trigger zone in CNS. Metoclopramide does not possess antipsychotic or tranquilizing activity and is less sedating than other central dopamine antagonists. Onset of action is 1-3 min after intravenous (IV) injection and 10-15 min after IM injection.

Antibiotics

Class Summary

Infected hydronephrosis mandates IV antibiotic therapy in addition to urgent drainage via percutaneous nephrostomy or urethral stent placement. Aerobic gram-negative enteric organisms, including Escherichia coli and Klebsiella, Proteus, Enterobacter, and Citrobacter species, are typical pathogens. Enterococcal infection occasionally is seen in patients recently on antibiotics. Candida albicanssometimes is responsible in diabetic or immunosuppressed patients. Initial empiric antibiotic therapy should cover common bacterial pathogens.

View full drug information

Ampicillin

 

Ampicillin is a 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. Ampicillin is usually combined with gentamicin.

View full drug information

Gentamicin

 

Gentamicin is an 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.

View full drug information

Ticarcillin and clavulanic acid (Timentin)

 

Ticarcillin is an extended-spectrum penicillin, beta-lactam antibiotic. Clavulanic acid is a beta-lactamase inhibitor that, in combination with ticarcillin, extends the spectrum of ticarcillin to include many beta-lactamase–producing bacteria. Ticarcillin-clavulanate is excreted via the urinary tract.

This combination is 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; the anaerobic spectrum includes Peptococcus and Peptostreptococcus species, Clostridium perfringens, Clostridium tetani, and Bacteroides species, including many strains of B fragilis. It is not effective against Enterococcus species or methicillin-resistant staphylococci.

View full drug information

Ciprofloxacin (Cipro, Proquin XR)

 

Ciprofloxacin is a reasonable alternative for treating infected hydronephrosis in penicillin-allergic patients. Fluoroquinolones are active against aerobic gram-negative organisms and generally effective against aerobic gram-positive organisms, though some resistance has beeoted in S aureus and Streptococcus pneumoniae. Ciprofloxacin is not effective against anaerobes. It is variably effective against E faecalis, though ampicillin and gentamicin are likely to be more effective.

View full drug information

Levofloxacin (Levaquin)

 

Levofloxacin is a reasonable alternative for treating infected hydronephrosis in penicillin-allergic patients. Fluoroquinolones are active against aerobic gram-negative organisms and generally effective against aerobic gram-positive organisms, though some resistance has beeoted in S aureus and S pneumoniae. Levofloxacin is not effective against anaerobes. It is variably effective against E faecalis, though ampicillin and gentamicin are likely to be more effective.

View full drug information

Ofloxacin

 

Ofloxacin is a reasonable alternative for treating infected hydronephrosis in penicillin-allergic patients. It is active against aerobic gram-negative organisms and generally effective against aerobic gram-positive organisms, though some resistance has beeoted in S aureus and S pneumoniae. It is not effective against anaerobes. It is variably effective against E faecalis, though ampicillin and gentamicin are likely to be more effective.