Evaluation of Flank Pain

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etiology. Flank pain that is due to infection, such as acute pyelonephritis, usually is steady and dull, whereas pain that is due to an acutely obstructing calculus can be intense and sharp.

The kidney and its capsule are innervated by sensory fibers traveling to the T10-L1 spinal cord. Pain that originates from the kidney often is felt just lateral to the sacrospinalis muscle beneath the 12th rib posteriorly. The pain often radiates anteriorly, but it also may be referred to the inguinal, labial, penile, or testicular areas. It is not uncommon for a man with a ureteral calculus to complain of pain at the tip of the penis or for a women with the same problem to experience labial pain.

Flank pain that originates from urinary tract pathology may be caused by obstruction, inflammation, or mass. Hydronephrosis occurs when there is obstruction of the urinary tract that results in dilation of the renal collecting system. Dilation of the renal collecting system leads to distention of the renal capsule, and this distention results in flank pain. In the case presented above, flank pain accompanied by crystals in the urine is suggestive of hydronephrosis due to an obstructing renal calculus.

When evaluating a patient with flank pain, the severity of the pain generally correlates inversely with the duration of the problem. That is, chronic, gradual distention of the renal capsule over a long period of time due to a slowly enlarging ureteral tumor often is associated with mild to moderate flank pain. The pain is mild or dull because it results in gradual but possibly severe distention of the renal collecting system and capsule. In contrast, the acute flank pain that is associated with an obstructing renal calculus often is severe, since it results in sudden distention of the renal collecting system and capsule. In the case presented, it is likely that an obstructing calculi is causing the patient’s symptoms. Severe flank pain caused by an acute urinary tract obstruction is termed renal colic.

It is important for the clinician to determine if the pain represents an emergency or if the problem can be managed in the outpatient setting. In this regard, it is important to determine if there is associated fever, dehydration, nausea, or vomiting. Comorbid medical conditions, such as diabetes, immunocompromise, or pregnancy, also need to be considered. When flank pain presents in association with any one of these factors, hospital admission may be necessary to prevent possible complications, such as pyelonephritis or urosepsis, from developing. In the case presented, none of these factors are present, so this patient can be managed in the outpatient setting.

Since a prime objective for the clinician is to determine if the flank pain represents an emergent medical problem, it is helpful to consider the differential diagnosis of flank pain (see Algorithm 38.1).

Differential Diagnosis of Flank Pain

Urinary Calculi

One of the most common causes of acute, severe flank pain is sudden distention of the renal collecting system and capsule secondary to an

Algorithm 38.1. Algorithm for the clinical evaluation of the patient presenting with acute flank pain. CT, computed tomography; H&P, history and physical examination; IVP, intravenous pyelogram; KUB, kidney and urinary bladder; UA, urinalysis; US, ultrasound.

obstructing urinary calculi. Most urinary calculi cause pain only when they obstruct the flow of urine from the kidney into the bladder. A nonobstructing stone usually does not cause significant flank pain. Since the patient in the case presented has pain, it is probable that obstruction is present. Typically, the stone becomes caught in the renal pelvis or ureter and causes obstruction of urine flow. The back pressure results in pain and hydronephrosis.

Types of Urinary Calculi

The most common type of urinary tract calculus is composed of calcium oxalate. Oxalate is found in many green leafy vegetables and teas, and it is considered to be an inducer of stone formation. When urine becomes supersaturated with calcium or oxalate, precipitation of crystals can result in stone formation. Causes for supersaturation with calcium or oxalate include excess bone resorption of calcium from immobility, intestinal hyperabsorbtion of calcium from sarcoidosis, and renal leak of calcium seen with renal tubular acidosis. However, most individuals who form calcium oxalate stones do not drink enough fluids, which results in concentrated urine. This facilitates crystal precipitation and stone formation. Even though the patient in the case presented has a family history of calcium oxalate calculi, dehydration is the most likely cause of her stone formation. For this reason, calcium oxalate stones are more common in the summer months and in the

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southern United States “stone belt,” where it is hot and where dehydration is more likely to occur.

Other common types of stones include magnesium ammonium phosphate and carbonate apatite stones. These stones sometimes are called infection stones, since they form secondary to urinary tract infections with urea splitting bacteria. Urea splitting bacteria raise the pH of the urine, and this facilitates the formation of infection stones by lowering the solubility of magnesium-ammonium and phosphate. Common urea splitting bacteria include Escherichia coli and Proteus mirabilis. Infectious stones can enlarge quickly and sometimes can

fill the entire renal collecting system to form a staghorn calculus.

The term staghorn calculus indicates that the stone is a large stone, but it does not imply stone composition. All urinary calculi have the potential to form staghorn calculi; however, infection stones result in staghorn formation most often.

Some stones, including uric acid and cystine stones, form secondary to metabolic abnormalities. These stones are seen less commonly in clinical practice, but they should be suspected in patients with a history of gout or homozygous cystinuria. It is estimated that 25% of patients with uric acid stones have gout. Uric acid is an end product of purine metabolism. Hyperuricosuria may be seen in gout, myeloproliferative disorders, idiopathic hyperuricosuria, and patients with increased dietary purine. Uric acid stones are clinically unique, since they cannot be seen on a standard abdominal x-ray. They can, however, be visualized on ultrasound or computed tomography (CT) scan. Since the formation of uric acid stones is very dependent on the pH of the urine, they generally form only if the urine pH is consistently below 5.5. Uric acid stones have been dissolved successfully by raising urinary pH to 6.5 or slightly above. Typically, an oral urinary alkalinizing agent, such as potassium citrate, is used to raise urine pH and dissolve uric acid stones. Cystine stones are uncommon and form only in patients who are homozygous for cystinuria. Cystinuria is an inherited defect of the renal tubule causing loss of cystine, ornithine, arginine, and lysine. The loss of cystine is the only clinical problem patients suffer, since they excrete over 250 mg of cystine per liter of urine. This high urinary cystine level is problematic, since stone formation results in urinary cystine levels of 170 mg per liter of urine at pH 5. Patients who are heterozygous for cystinuria excrete less urinary cystine and generally do not suffer from cystine stone formation.

Risk Factors

Some of the common risk factors for developing urinary calculi include inadequate fluid intake, excess sodium intake, metabolic abnormalities, inflammatory bowel disease, dehydration, and family history.

Patients with inflammatory bowel disease form stones composed of calcium oxalate by a unique mechanism. Fat malabsorption caused by the inflammatory bowel disease results in excess fats in the gut, which bind to calcium. This creates a situation in the gut in which oxalate, which normally binds to calcium, enters the bloodstream in its ionic

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form. The oxalate then is excreted by the kidneys, and hyperoxaluria results. Since oxalte is a stone inducer, it binds with urinary calcium and facilitates calcium oxalate stone formation.

Other medical conditions increase the risk for stone formation by causing hypercalciuria, which is excess calcium in the urine. These medical problems include renal tubular acidosis, sarcoidosis, hyperparathyroidism, chronic immobility, and paralysis. In these conditions, hypercalciuria results when excess calcium is absorbed from bone or the gut and ultimately is excreted by the kidneys. In renal tubular acidosis, the renal tubule leaks calcium directly into the urine.

Chronic urinary tract infection also can lead to stone formation due to urea splitting bacteria, which lead to an elevated urine pH. Urease catalyzes the hydrolysis of urea into ammonia and carbon dioxide. These end products cause a rise in urinary pH, which facilitates infectious stone formation. P. mirabilis and E. coli are the most common urea splitting bacteria that are associated with urinary tract infection and urinary calculi formation. These bacteria raise the pH of the urine, and this allows the precipitation of magnesium-ammonium-phosphate or apatite stones. Patients with infected urine and flank pain due to an obstructing calculi may require hospitalization to prevent urosepsis.

Management

As illustrated in the case presented, most patients who present with flank pain secondary to acutely obstructing urinary calculi can be managed on an outpatient basis. Cornerstones of therapy include adequate hydration, pain relief, and control of any associated nausea or vomiting.

If the pain is severe enough to require intravenous morphine sulfate or if there is associated fever or dehydration due to nausea or vomiting, hospital admission may be necessary. Again, one of the most important decisions the clinician has to make is to determine if the patient can be treated as an outpatient or if the patient needs hospital admission. There are several indications for hospital admission, and fever is a common indicator for admission (Table 38.1). As Table 38.1 indicates, appropriate blood and urine cultures need to be performed, and other causes of infection need to be considered. Fever in the presence of obstructing urinary calculi can be an ominous clinical finding that suggests an accumulation of purulent urine proximal to an obstructing stone. This is an especially serious situation if the patient has comorbid medical conditions, such as diabetes. Emergent intravenous antibiotics, aggressive intravenous fluid hydration, and percutaneous or transureteral drainage of the infected urine usually are necessary in these situations. Patients with fever and obstructing urinary calculi should not be discharged from the emergency room, as urosepsis and septic shock can develop quickly.

Following the acute event, it is suggested that all patients who form urinary stones undergo a metabolic evaluation consisting of a complete blood count, urinalysis, serum chemistry profile, and a 24-hour urine collection for calcium, phosphorus, uric acid, creatinine, citrate, and oxalate levels. This evaluation can be done on an outpatient basis.

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Table 38.1. Continued

Suspected urinary tract infection

Level II: Obtain urine for culture and to evaluate for pyuria. If the patient has an indwelling Foley catheter, urine should be collected from the urine port and not the drainage bag.

The specimen should be transported rapidly to the laboratory, or refrigerated if transport will exceed 1 h.

Suspected sinusitis

Level I: Aspirate should be Gram stained and cultured.

Level II: Computed tomography of the facial sinuses is the imaging modality of choice for the diagnosis of sinusitis.

Puncture and aspiration of the sinuses should be performed using sterile technique if mucosal thickening or an air–fluid level is present in the sinus.

Postoperative fever

Level II: Examine the surgical wound for erythema, fluctuance, tenderness, or purulent drainage.

Open the wound for suspicion of infection.

Culture and Gram stain should be obtained from purulent material if from deep within the wound.

Suspected central nervous system infection

Level II: Gram stain and culture of cerebrospinal fluid should be performed in cases of suspected infection. Other tests should be predicated on the clinical situation.

A computed tomographic study is usually required before lumbar puncture, which may need to be deferred if a mass lesion is present.

Consider lumbar puncture for new fever with unexplained alteration of consciousness or focal neurologic signs.

In febrile patients with an intracranial device, cerebrospial fluid should be sent for culture and Gram stain.

Noninfectious causes of fever

Level II: Reevaluate all recent medications and blood products the patient has received. Stop all nonessential medications, or substitute medications for treatments that

cannot be stopped.

a Summary of clinical recommendations, Society of Critical Care Medicine, 1998; level III guidelines excluded. Source: Adapted from O’Grady NP, Barie PS, Bartlett JG, et al. Practice guidelines for evaluating new fever in critically ill adult patients. Task Force of the Society of Critical Care Medicine and the Infectious Diseases Society of America. Clin Infect Dis 1998;26:1042–1059, with permission. Published by the University of Chicago. Reprinted from Norton JA. History of Endocrine Surgery. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.

The most common abnormality detected is a low urine volume, usually less than 1 L/day, due to inadequate fluid intake. In this situation, the patient should be encouraged to increase fluid intake and to maintain a urine volume of 2 to 3 L per day. Water is the best fluid to drink, while teas, cranberry juice, and other drinks that are high in oxalate should be limited. Cranberry juice has been shown to be effective in reducing the risk for recurrent urinary tract infections, but it is high in oxalate and should be limited in patients who form stones. Patients sometimes also are advised to limit the intake of certain foods that are high in calcium and oxalate, such as cheese, spinach, and nuts; however, it is often difficult to maintain these dietary restrictions.

Medications sometimes are necessary to prevent recurrence. Orthophosphates decrease urinary calcium and are used to prevent calcium stone formation. Hydrochlorothiazide prevents reabsorption of sodium and calcium in the loop of Henle; this leads to an increase

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blood cells (WBC), red blood cells (RBC), and bacteria. The finding of WBC casts in the urine sample is strongly suggestive of acute pyelonephritis, and urine Gram stain can establish the diagnosis of bacteriuria.

Risk Factors

Risk factors for acute pyelonephritis include vesicoureteral reflux, obstruction of the urinary tract, and hematogenous infection. Reflux typically occurs in children, and, since their kidneys are still maturing, acute pyelonephritis can interfere with kidney growth and development. Obstructions can be caused by several factors, including stricture, stone, or pregnancy. With pregnancy, the gravid uterus can obstruct the ureters. Obstruction leads to stasis of urine, which facilitates bacterial growth. Normally, bacteria in the urinary tract are washed out by ureteral peristalsis and proper bladder emptying; however, obstruction disables the former defense mechanism.

Other risk factors include diabetes mellitus, since there is increased substrate availability in the kidney. Gas-forming organisms could result in emphysematous pyelonephritis, which may require nephrectomy. Patients with neurogenic bladder and the elderly also are at increased risk, since urinary emptying may not be complete in these patients. Finally, females are more prone to develop acute pyelonephritis due to their shorter urethral length compared to the male urethra.

Management

Treatment of pyelonephritis consists of intravenous fluid hydration and antibiotic therapy. A standard regimen includes an aminoglycoside (gentamicin, 1.5 mg/kg IV q 8 h) plus ampicillin (2 g IV q 6 h). In mild cases, oral antibiotics can be considered; however, if a positive clinical response is not noted within 24 hours, hospitalization with intravenous antibiotics should be implemented. Following intravenous antibiotics, 75% to 80% of patients improve clinically and become afebrile within 72 hours. Once patients have been afebrile for 24 to 48 hours, they may be switched to oral antibiotics. A 14to 21-day total course of antibiotics is recommended to ensure effective sterilization of the kidney and helps reduce the incidence of renal scarring.

Urologic intervention is necessary if pyelonephritis occurs in the presence of an obstruction, such as a ureteral calculus. In this situation, antibiotics are not effective until the purulent urine behind the obstruction is drained via nephrostomy or ureteral stent. In cases of renal abscess formation, percutaneous drainage and intravenous antibiotic therapy usually are effective.

Urinary Tract Tumors

Urinary tract tumors, such as renal cell carcinomas, tumors of the urinary collecting system, and bladder tumors, can cause flank pain when the tumor obstructs the urinary tract. These tumors also cause pain when they are large and stretch the ram capsule or when they invade surrounding structures (Fig. 38.2). Bladder and ureteral tumors

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Figure 38.2. Computed tomography (CT) scan of large renal tumor. In this situation, flank pain could result from stretching of the renal capsule or direct invasion into surrounding tissues.

are seen more commonly in smokers, and gross hematuria usually is associated with the flank pain. There may be prior episodes of gross hematuria, flank pain, or weight loss in patients with urologic malignancies.

Renal cell tumors are relatively uncommon and account for 3% of adult malignancies. Most renal tumors (90%) are adenocarcinomas and originate from the cells of the proximal convoluted tubules. These tumors usually are unilateral and grow inwardly toward the medulla of the kidney. If gross hematuria is present, it indicates that the tumor has invaded the collecting system of the kidney. Only an advanced tumor would produce flank pain, since a stage 1 tumor is confined to the kidney. Tumors that penetrate the renal capsule but remain within Gerota’s fascia are considered grade 2. A grade 3 tumor has spread locally and can cause flank pain, as can a grade 4 tumor, which is metastatic. Treatment for renal tumors stage 1 to 3 is by surgical excision. Grade 4 tumors are treated with chemotherapy, but excision is sometimes necessary for relief of pain or to control bleeding.

Tumors of the urinary collecting system, ureter, and bladder are most commonly transitional cell carcinomas. These tumors can cause flank pain when they obstruct the urinary tract, and they commonly present with gross hematuria. About 30% of patients with a renal pelvic cancer complain of flank pain, whereas only 15% of patients with a ureteral tumor experience flank pain.

Bladder tumors usually present with hematuria; however, when the tumor is located at the ureteral orifice, it can cause flank pain due to ureteral obstruction. Bladder tumors that obstruct the ureter tend to be advanced at the time of discovery, and prognosis is guarded.

Urologic tumors rarely are palpable on physical examination unless they are large; however, most renal tumors are seen during

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upper tract imaging with ultrasound or CT scan (Fig. 38.2). Bladder and ureteral tumors usually require intravenous pyelogram (IVP), contrast-enhanced CT scan, cystoscopy, and sometimes retrograde urography for accurate diagnosis. For this reason, all patients with flank pain who also have gross hematuria require urologic consultation.

Traumatic Flank Pain

Flank pain due to trauma usually is obvious, given the clinical presentation. In the trauma setting, imaging of the urinary system is necessary to exclude serious injury to the urinary tract, such as renal laceration, renal contusion, or ureteral avulsion (Table 38.2). As seen in Table 38.2, CT scan is useful for evaluating the retroperitoneum in cases of blunt abdominal trauma. Renal lacerations and contusions can occur from relatively minor forces and can be diagnosed with CT (Fig. 38.3). In the pediatric population, a hydronephrotic kidney, due to a congenital ureteropelvic junction obstruction, can rupture from a relatively minor traumatic event. Also, the pediatric kidney is more prone to injury since it is not well protected. In the adult, a significant amount of fat, muscle, and bone protect the kidney from injury, but this protective barrier is not well developed in children. Therefore, all children who present with flank pain following a traumatic event require upper tract imaging.

If the magnitude of the injury was severe or involved a sudden deceleration injury, then contrast imaging of the urinary tract with CT scanning is suggested to exclude an injury to the urinary collecting system, such as ureteral injury or avulsion (Table 38.3). However, as seen in Table 38.3, the leading cause of ureteral injury in an adult is a gunshot wound. Injuries to the collecting system of the kidney usually are due to significant trauma, except in the pediatric population for the reasons mentioned above. Administration of intravenous contrast often is necessary to document these injuries, since they usually are not seen on a plain abdominal x-ray or ultrasound examination and urinalysis may be normal (Table 38.4). Thus, a normal urinalysis in the trauma setting does not exclude serious urologic injury.

Renal Artery Emboli

Renal artery emboli can result secondary to mitral valve disease, atrial fibrillation, acute myocardial infarction, endocarditis, and cardiac tumors. In addition, atherosclerotic aortic disease and thrombi originating in renal artery aneurysms have been known to cause renal artery emboli (Table 38.5).

Patients with renal artery emboli present with acute, severe flank pain. There often is a history of cardiac or atherosclerotic disease. Physical examination may demonstrate a cardiac arrhythmia or

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Figure 38.3. CT scan of bilateral areas of renal infarction due to trauma.

Table 38.3. Mechanism and site of ureteral injuries.

j Stutzman RE. Ballistics and the management of ureteral injuries from high velocity missiles. J Urol 1977; 118:947–949.

k Holden S, Hicks CC, O’Brien DP, et al. Gunshot wounds of the ureter: a 15-year review of 63 consecutive cases. J Urol 1976;116:562–564.

l Lankford R, Block NL, Politano VA. Gunshot wounds of the ureter: a review of ten cases. J Trauma 1974;14:848–852. m Carlton CE Jr, Scott R Jr, Guthrie AG. The initial management of ureteral injuries: a report of 78 cases. J Urol 1971;105:335–341.

n Eickenberg H, Amin M. Gunshot wounds to the ureter. J Trauma 1976;16:562–565.

o Presti JC Jr, Carroll PR, McAninch JW. Ureteral and renal pelvic injuries from external trauma: diagnosis and management. J Trauma 1989;29:370–374.

p Steers WD, Corriere JN Jr, Benson GS, et al. The use of indwelling ureteral stents in managing ureteral injuries due to external violence. J Trauma 1985;25:1001–1003.

q Rober PE, Smith JB, Pierce JM. Gunshot injuries of the ureter. J Trauma 1990;30:83–86.

r Campbell EW, Filderman PS, Jacobs SC. Ureteral injury due to blunt and penetrating trauma. Urology 1992;40:216–220.

Source: Reprinted from Presti JC Jr. Urology. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.

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Table 38.4. Urinalysis and intravenous urography in the diagnosis of ureteral injuries.

N/A, not available.

a Number of patients in study.

b Microscopic (>5 red cells/high-power field) or gross hematuria on initial urinalysis. c Intravenous urography demonstrating ureteral injury.

d Peterson NE, Pitts JC. Penetrating injuries of the ureter. J Urol 1981;126:587–590.

e Liroff SA, Pontes JES, Pierce JM Jr. Gunshot wounds of the ureter: 5 years of experience. J Urol 1977;118:551–553.

f Lankford R, Block NL, Politano VA. Gunshot wounds of the ureter: a review of ten cases. J Trauma 1974;14:848–852.

trauma: diagnosis and management. J Trauma 1989;29:370–374.

j Steers WD, Corriere JN Jr, Benson GS, et al. The use of indwelling ureteral stents in managing ureteral injuries due to external violence. J Trauma 1985;25:1001–1003.

k Rober PE, Smith JB, Pierce JM. Gunshot injuries of the ureter. J Trauma 1990;30:83–86. l Campbell EW, Filderman PS, Jacobs SC. Ureteral injury due to blunt and penetrating trauma. Urology 1992;40:216–200.

Source: Reprinted from Presti JC Jr. Urology. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.

murmur, while urologic symptoms, such as urinary frequency, urgency, and dysuria, commonly are absent. Urine analysis may be normal, and a study that evaluates renal function, such as an IVP, intravenous contrast-enhanced CT, or renal angiogram, is necessary to establish the diagnosis (Fig. 38.4).

Patients who present with renal artery emboli usually are medically unstable or recently have suffered a cardiac event. In such

Table 38.5. Arteriosclerotic renovascular hypertension.

Source: Reprinted from Stanley JC. Surgical treatment of renovascular hypertension. Am J Surg 1997;174:102–110. Copyright © 1997 Excerpta Medica. With permission from Excerpta Medica.

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Figure 38.4. Renal artery angiogram demonstrating normal right renal vasculature and abrupt cutoff of left renal artery due to emboli.

patients who usually have unilateral renal infarction, treatment is nonoperative and consists of anticoagulation therapy. For bilateral renal artery emboli or emboli to a solitary kidney, streptokinase catheter embolectomy or surgical treatment may be necessary.

Nonurologic Causes

Other problems that cause flank pain that should be considered by the clinician include intraabdominal pathology that secondarily results in flank pain. Since the kidneys are related anatomically to the colon, pancreas, spleen, ovaries, and psoas muscle, pathology involving these organs can produce flank pain. Usually, the abdominal symptoms are the primary complaint of the patient in these situations.

Musculoskeletal causes of flank pain are not uncommon and also need to be considered. Most patients with a musculoskeletal cause of flank pain present with pain of long-standing duration (12 weeks or more). In contrast to flank pain secondary to a urologic cause, musculoskeletal pain tends to be localized more medially, below the costal margin and above the inferior gluteal folds, with or without leg pain (sciatica).

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Psychological

If the evaluation of a patient with flank pain is normal and the patient continues to complain of pain and seeks narcotic medication for relief of symptoms, consider drug-seeking behavior or Munchausen syndrome. These patients are well aware of the clinical presentation of stone disease and have been known to put a drop of blood from a pricked finger in the urine to simulate microscopic hematuria. Such patients may have an “allergy” to all nonnarcotic analgesics and sometimes indicate the narcotic that works best for them. Such patients also have brought in small stones that they recently have “passed” in the urine. On stone analysis, these stones usually are found to be composed of 100% quartz. Patients with drug-seeking behavior or Munchausen syndrome should not be given narcotics; however, psychiatric evaluation is recommended.

History and Physical Examination

History

The history is the most important component of the evaluation of the patient with flank pain. The onset and severity of the pain provide clues to the etiology of the pain. Long-standing, dull pain is more typical of an infectious, malignant, or congenital problem. Acute, severe pain is characteristic of renal colic and most commonly results from an acute obstruction of the urinary tract due to a calculus, as seen in the case presented. It is not uncommon for patients with renal colic to complain of prior stone episodes, since calculi tend to reoccur in up to 60% of patients.

Nausea and vomiting are common in patients who present with flank pain. These symptoms are due to irritation of the peritoneum and distention of the renal capsule. Nausea and vomiting, therefore, can occur with most causes of flank pain; however, it is most severe when the flank pain is acute and severe, such as from a renal calculi.

Associated urinary frequency and urgency are common with many causes of flank pain and are due to pain that is referred to the bladder area. The presence of gross hematuria is an important sign that can occur during an episode of flank pain and can be due to a renal calculi, infection, or tumor. Gross hematuria mandates a complete urologic evaluation to rule out a malignancy of the urinary tract, such as a renal carcinoma, bladder carcinoma, or ureteral tumor. The evaluation should include imaging of the upper urinary tract with ultrasound or CT scan and evaluation of the bladder with cystoscopy.

A history of fever, in association with flank pain, is an ominous sign that usually indicates infection (Table 38.1). The source of the fever typically is infected urine that remains undrained behind the source of obstruction, such as a calculi, stricture, or tumor. If no obstruction is present, yet the patient complains of flank pain in the presence of fever,

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it is consistent with acute pyelonephritis. In this situation, the renal tissue itself is infected, without obstruction of the urinary tract collecting system.

The presence of comorbid conditions must be considered when evaluating a patient with flank pain. Most healthy individuals with flank pain and no fever can be managed safely as outpatients. Problems that might predispose an individual to developing urosepsis include diabetes, immunosuppression, and pregnancy.

Tobacco use should be determined, since there is an increased risk for developing a transitional cell carcinoma in smokers. Transitional cell epithelium can be found in the bladder, ureter, and renal collecting system. Patients with transitional cell cancer typically present with gross hematuria without significant flank pain. However, if the tumor or a blood clot cause obstruction, flank pain may be identical to that produced by a renal calculi.

Patients with cardiac arrhythmias presenting with acute, severe flank pain should be evaluated for a possible thromboembolic event. In this situation, a cardiac thrombus suddenly is dislodged and obstructs the main renal artery or one of its branches. The resulting pain is identical to that produced by a renal calculi, so a history of cardiac arrhythmia is essential for establishing the diagnosis. A functional imaging study, such as an IVP, contrast-enhanced CT, or renal angiogram, demonstrates absence of renal blood flow, indicating obstruction of the renal artery (Fig. 38.4).

Physical Examination

A complete physical examination is indicated for patients presenting with flank pain to help determine the etiology of the pain and provide insight into the severity of the problem. It is important to perform a complete physical examination and resist the temptation to focus on the urinary tract or flank area exclusively.

Vital signs are important to determine if the flank pain might be associated with dehydration, infection, or urosepsis (Table 38.1). In the patient with flank pain, urosepsis is suggested if the patient is febrile, has a rapid pulse and respiration rate, and has labile blood pressure. If urosepsis is suspected, the patient should be hospitalized to prevent septic shock. In this situation, intravenous antibiotics, aggressive fluid replacement, and urologic relief of any hydronephrosis are indicated.

Fever from a lower urinary tract infection (bladder) may be low grade, while high spiking temperatures suggest upper tract infection (kidney). It is important to note, however, that one always cannot localize the site of the infection by the severity of the temperature. That is, a high temperature necessarily does not indicate upper urinary tract infection and vice versa; this is true especially in children.

The carotid arteries should be auscultated for bruits to evaluate for a possible cardiac etiology of the flank pain, such as a renal artery disease or embolus. Heart auscultation for rate, rhythm, and murmurs should be done for the same reason, since renal artery embolism

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Figure 38.5. Large bladder rhabdomyosarcoma in a 2-year-old causing urinary tract obstruction. Note outline of mass and indwelling catheter.

usually occurs in patients with atrial fibrillation. The abdomen should be examined for bruits, tenderness, and masses. If the pain is more severe during the abdominal examination, consider intraabdominal etiologies for the flank pain. A rectal examination, with stool for guaiac, should be done to exclude a possible intraabdominal cause for the flank pain.

In females, it is essential to determine if the patient is pregnant with a urine or serum b-human chorionic gonadotropin (b-HCG) test. If the patient is pregnant, x-rays should be avoided, and the patient should be evaluated with ultrasound. Both males and females should have a complete genital examination, since referred pain is common. The bladder sometimes is able to be palpated just above the pubic symphysis. If the bladder is distended, it suggests a possible urologic etiology for the pain (Fig. 38.5).

The flank area should be examined for asymmetry, mass, and percussion tenderness. It is uncommon to discover a palpable flank mass, unless there is a large renal tumor present. Patients with acute pyelonephritis or obstructing renal calculi complain of severe pain when the flank is percussed, so it is important to tap lightly in order to maintain patient confidence.

To rule out a musculoskeletal etiology for the flank pain, the lower extremities should be examined for motor and sensory function.

Laboratory and Diagnostic Studies

Laboratory Studies

The history and physical examination help determine the most probable etiology of the flank pain and guide the clinician toward the selection of the most appropriate laboratory and diagnostic tests.

38. Evaluation of Flank Pain 689

In almost all cases, a urinalysis should be performed as the initial diagnostic test. Among the most important parameters to consider on urine analysis are pH, WBCs, RBCs, bacteria, casts, and crystals. Infected urine typically has a high pH secondary to urea splitting bacteria. In contrast, patients with uric acid stones tend to have an acidic urine, since these stones do not form when the urine is alkaline. The presence of WBCs in the urine may signify infection, but it also may be due to inflammation caused by a stone. The presence of WBC casts strongly suggests urinary tract infection or acute pyelonephritis. Tumors of the urinary tract usually result in urinary RBCs, and the urine may appear grossly bloody. A stone similarly can result in RBCs in the urine, so it is important to repeat a urinalysis in patients after they have passed the stone to exclude an underlying urologic cancer. If the patient has RBCs in the urine after the stone has passed, urologic evaluation is necessary. A Gram stain should be done in the emergency room or clinic and can help determine if infection is present. In the case presented, a negative Gram stain suggests sterile urine. Finding bacteria on an unspun specimen suggests infection. Most urinary tract infections are caused by gram-negative bacteria such as E. coli; however, gram-positive organisms can cause urinary tract infections as well. If urinary calculi are present within the urinary tract, it is not uncommon to find crystals in the urine analysis, along with RBCs and WBCs, as seen in the illustrated case. The shape of the crystal can be used by the laboratory technician to help identify its composition. The urinalysis may be normal if the etiology of the flank pain is due to cardiac, intraabdominal, musculoskeletal, or psychological problems.

Limited blood tests are indicated in patients with flank pain. If infection is suspected, a complete blood count is important to determine if the serum WBC count is elevated. Anemia and a low or high platelet count might be seen in the presence of bleeding urologic tumors. An abnormally high hematocrit can be seen if the patient is dehydrated. Evaluation of serum sodium, potassium, chloride, bicarbonate, glucose, blood urea nitrogen (BUN), and creatinine are important. An elevated BUN can be due to renal disease or dehydration. In general, if the BUN is greater than 10 times the serum creatinine level, then the elevation most likely is due to dehydration. If the BUN to serum creatinine ratio is 10 or less, then renal disease is likely. The serum creatinine level directly reflects renal function. An elevated creatinine indicates impaired renal function, regardless of the BUN value. The impaired function could be due to dehydration, obstruction, tumor, infarct, or medical renal disease. Moreover, an elevated serum creatinine indicates bilateral renal disease or disease involving a solitary kidney, since only one healthy kidney is required to maintain a normal serum creatinine. In long-standing renal compromise, it is not uncommon to see a fall in serum bicarbonate along with hyperkalemia. Hyponatremia results from volume overload and can cause nausea, vomiting, and seizures. Hyperkalemia especially is dangerous, since it could result in cardiac arrhythmias. Other useful tests might include a serum uric acid level and serum calcium level, if a urinary calculus is suspected.

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Diagnostic Studies

Following the history, physical exam, and laboratory analysis, a plain film of the abdomen can help identify urinary calculi (Fig. 38.6). This film is called a KUB, since it visualizes the kidney, ureter, and bladder. The entire film should be viewed for intestinal gas pattern, gallstones, bony structure, and free air, which may provide insight into the etiology of the pain. Renal cell carcinomas are osteolytic tumors, and this can be seen radiographically in metastatic disease. An abnormal intestinal gas pattern, gallstones, or free air suggest intraabdominal pathology. Aortic calcifications and aneurysms should be determined, since they might suggest renal artery disease as the etiology of the flank pain. Urinary calculi typically are seen as calcifications overlying the kidney shadow or along the course of the ureter (Fig. 38.6). Small stones, 1 to 2 mm in size, can cause severe flank pain if they obstruct the flow of urine into the bladder. Stones typically become obstructive where the ureter meets the renal pelvis [ureteropelvic junction (UPJ)], where the ureter crosses over the pelvic brim, and where the ureter enters the bladder [ureterovesical junction (UVJ)]. Small stones tend to lodge at the UVJ, whereas bigger stones lodge higher in the urinary tract. It should be noted that uric acid calculi are radiolucent and are not seen on a plain film of the abdomen, but they can be seen on ultrasound or CT scan.

Following the history, physical examination, urinalysis, and abdominal plain film, a preliminary diagnosis is possible in most instances. However, more detailed imaging studies often are performed to confirm the diagnosis and to help plan appropriate therapy. The traditional test of choice for evaluating flank pain in detail has been the IVP (Table 38.4). The IVP is a relatively inexpensive functional study that diagnoses most urologic, infectious, and cardiac causes of flank pain. However, because it requires the administration of iodine-based

Figure 38.6. Plain film of the abdomen demonstrating multiple left renal calculi.

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