Download 38 Evaluation of Flank Pain

38
Evaluation of Flank Pain
Joseph G. Barone
Objectives
1. To discuss the potential etiologies of flank pain.
2. To discuss the imaging modalities available for
the evaluation of flank pain.
3. To discuss the evaluation of a patient with flank
pain.
4. To discuss the clinical presentation of a patient
with urinary calculi.
Case
You are asked to examine a 65-year-old woman with left flank pain.
The pain is acute, severe, and radiates to the left lower quadrant. The
patient complains of nausea, but there is no vomiting or diarrhea. Past
medical history is significant only for hypertension. The patient does
not smoke and denies alcohol and drug use.
On physical examination, the patient is afebrile, and the remaining
vital signs also are normal. The only abnormality detected on physical
examination is severe left costovertebral angle tenderness on percussion. Laboratory evaluations, including a complete blood count and
serum chemistries, are normal. Urine Gram stain demonstrates no bacteria on an unspun specimen. Urinalysis demonstrates the presence of
red blood cells and irregular crystals. An abdominal plain film demonstrates a 2-mm calcification at the level of the left pelvic brim.
Introduction
Flank pain often is due to a urologic etiology, such as renal calculus
disease or acute pyelonephritis; however, cardiac, intraabdominal,
musculoskeletal, and psychological causes also need to be considered. The quality and severity of the pain may provide a clue to its
670
38. Evaluation of Flank Pain
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
671
672
J.G. Barone
Flank pain
(H&P, UA, KUB)
IVP/CT/US
Normal
Muscular
Intraabdominal
Psychological
Mass
Therapy
Nonvisualization
Delayed visualization
Fever/pyuria
Hospitalization
Hydration
Relieve obstruction
Drain abscesses
Antibiotics
Cardiac
Arrhythmia
Calculi
Uncomplicated
Complicated
Fever
Comorbid conditions
Cardiology consult
Control arrhythmia
Oral analgesics
Oral hydration
Strain urine
Hospitalization
Hydration
Relieve obstruct
Antibiotics
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
38. Evaluation of Flank Pain
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
673
674
J.G. Barone
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.
38. Evaluation of Flank Pain
675
Table 38.1. Evidence-based practice management guideline for the evaluation of fever in
critically ill adult patients.a
Temperature measurement
Level I:
Record the temperature and the site of measurement in the patient’s medical record.
The nosocomial spread of pathogens must be avoided when using temperature
measurement devices.
Level II: Temperature is measured most accurately by indwelling vascular or bladder
thermistors, but most other sites are acceptable. Axillary measurements should not
be used.
Laboratory testing for the evaluation of fever should be individualized for each
patient.
Blood cultures
Level I:
For skin preparation, povidone-iodine should be allowed to dry for 2 min, or tincture
of iodine for 30 s. Alcohol skin preparation, an acceptable alternative for iodineallergic patients, need not be allowed to dry.
Level II: Obtain a single pair of blood cultures after appropriate skin disinfection after the
initial temperature elevation, and another pair within 24 h thereafter from a
second peripheral site. Additional cultures should be based on high clinical
suspicion of bacteremia or fungemia, and not instituted automatically for each
temperature elevation.
If two peripheral sites are not available, one pair of cultures may be drawn through
the most recently inserted catheter, but the diagnostic accuracy is reduced.
Draw at least 10–15 mL blood/culture.
Suspected intravascular catheter infection
Level II: Examine the catheter insertion site for purulence, and distally on the extremity for
signs of vascular compromise or embolization.
Any expressed purulence from an insertion site should be collected for culture and
Gram stain.
The catheter should be removed and cultured for evidence of a tunnel infection,
embolic phenomena, vascular compromise, or sepsis.
Two blood cultures should be drawn peripherally, or one may be drawn from the
most proximal port (if a multilumen catheter).
Both the introducer and the catheter itself should be cultured for suspected
pulmonary artery catheter infection.
It is not routinely necessary to culture the intravenous fluid infusate.
Suspected ICU-acquired pneumonia
Level I:
A chest x-ray should be obtained to evaluate for suspected pneumonia.
Posteroanterior and lateral films or computed tomography of the chest can offer
more information.
Level II: Lower respiratory tract secretions should be sampled for direct examination and
culture. Bronchoscopy may be considered.
Respiratory secretions should be transported to the laboratory within 2 h of
collection.
Pleural fluid should be obtained for culture and Gram stain if there is an adjacent
infiltrate or another reason to suspect infection.
Evaluation of the febrile patient with diarrhea
Level II: If more than two diarrheal stools occur, a single stool sample should be sent for
Clostridium difficile evaluation. A second sample should be sent if the first is
negative and suspicion remains high.
If illness is severe and rapid testing is unavailable or nondiagnostic, consider
flexible sigmoidoscopy.
If illness is severe, consider empiric therapy with metronidazole until the results of
studies are available. Empiric therapy (especially with vancomycin) is not
recommended if two stool evaluations have been negative for C. difficile, and is
discouraged because of the risk of producing resistant pathogens.
Stool cultures are rarely indicated for other enteric pathogens if the patient is HIVnegative or did not present to the hospital with diarrhea.
Continued
676
J.G. Barone
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
38. Evaluation of Flank Pain
in proximal tubular reabsorption of sodium and calcium, which
decreases total urinary calcium excretion.
Acute Pyelonephritis
Acute pyelonephritis indicates infection of the kidney and renal
pelvis accompanied by fever, flank pain, and infected urine. In the
case presented, there is no clinical evidence for pyelonephritis. The
diagnosis is made clinically. Bacterial pyelonephritis typically involves
an infection of the renal interstitium and collecting system. Bacterial
invasion of the kidney results in a humoral response that activates the
complement cascade. The polymorphonuclear leukocytes release
superoxide radicals that damage not only bacteria but also the surrounding renal tissue. If the damage is severe, renal scar or loss can
occur.
In the United States, the majority of cases of pyelonephritis are
due to the Enterobacteriaceae group of bacteria, mainly E. coli.
Proteus, Pseudomonas, Enterobacter, Klebsiella, and Staphylococcus also can
cause pyelonephritis. The urea splitting bacteria include E. coli, Proteus,
and Klebsiella and are important, since they may facilitate the development of infection stones.
Patients can present with mild gram-negative bacteremia to septic
shock. Renal abscess can form if treatment is delayed, with resultant
renal parenchyma loss. In the pediatric population, children with vesicoureteral reflux are at risk for pylonephritis and renal scarring, since
the kidney matures until approximately age 7 (Fig. 38.1). The clinical
onset of acute pyelonephritis can be sudden and dramatic; shaking
chills with fevers of 38° to 40°C are not uncommon. Symptoms of
lower urinary tract infection, such as frequency, urgency, and dysuria,
may have preceded the acute event by several days. Costovertebral
angle tenderness usually is severe due to inflammation of the kidney
and surrounding anatomy. Urine analysis typically demonstrates white
Figure 38.1. Voiding cystourethrogram demonstrating reflux. Note dilation at
renal collecting system due to reflux.
677
678
J.G. Barone
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 14- to 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
38. Evaluation of Flank Pain
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
679
680
J.G. Barone
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
30–50
5–10
Abdominal CT
Abdominal
ultrasonography
(FAST)
Test
Diagnostic
peritoneal
lavage (DPL)
Time
required
(min)
5–15
Fast. Sensitive for
hemoperitoneum in
experienced hands.
Noninvasive and no
contrast required. May
be performed in a
variety of locations if
equipment is available.
Pros
Fast. Very sensitive.
Minimal equipment
required. Specialized
training not required.
May be performed in
a variety of locations.
Results are quantitative,
objective, and
operator independent.
Very specific with good
sensitivity. Good for
evaluating posterior
(back and flank,
retroperitoneal) injuries.
Allows staging of blunt
organ injuries for
nonoperative
management. Most
major injuries operator
(reader) independent.
Not useful for most
anterior penetrating
injuries. Requires
time and patient
transport. Some
operator (reader)
dependence. May
miss blunt
intestinal injuries
and, initially, some
pancreatic injuries.
Limited findingspecific or
quantitative
criteria mandating
operation exist.
Not useful for
penetrating
injuries. Requires
immediately
accessible
equipment and
specialized training
and experience.
Nonquantitative
and substantially
operator dependent.
Cons
Invasive. Not
recommended if
prior laparotomy.
Not injury specific.
May miss
retroperitoneal and
diaphragm injuries.
92% {95}
83% {100}
95% {95}
97% {97}
82% {99}
Sensitivity
{specificity}
and injury type
97% {99%} blunt
85–93% {67–99}
penetr
99% {43%}
penetr
99% {86%}
penetr
100% {84%}
blunt
85% {100} blunt
99% {100} blunt
97% {95} blunt
Liud
McKenneyg
Yoshiih
Singhi
Rozyckij
Fabiane
Peitzmanf
Liud
Reference
Alyonoa
Alyonoa
Oreskovichb
Merlottic
Liud
Table 38.2. Comparison of diagnostic methods for evaluating blunt and penetrating abdominal trauma.
Continued
Good sensitivity for
clinically significant
blunt injuries. Poor
sensitivity for
penetrating injuries.
Utility: blunt vs.
penetrating
Good sensitivity for
both blunt and
penetrating trauma.
Nonspecific for
both. Sensitivity
and specificity
highly dependent
on cell count
criteria used.
Good sensitivity and
specificity for blunt
injuries and most
posterior penetrating
injuries. Insensitive
for anterior
penetrating injuries.
38. Evaluation of Flank Pain
681
Pros
Excellent for diagnosis of
diaphragmatic injuries.
Good for nonquantitative
dx. of hemoperitoneum.
Good for determining
peritoneal penetration
for SW/GSW. High
degree of injury
specificity when
visualized.
Cons
Invasive. Poor
sensitivity for some
injuries. Requires
specialized training,
experience, and
equipment.
Nonquantitative
and substantially
operator dependent.
Typically requires
more conscious
sedation than other
methods. General
anesthesia may be
needed in some
circumstances.
Sensitivity
{specificity}
and injury type
88% liver/spleen
83% diaphragm
50% panc/
kidney
25% hollow
viscous
100% periton
penetr
18% GI injuries
Reference
Ortegak
Ortegak
Ortegak
Ortegak
Sosal
Ivaturym
Utility: blunt vs.
penetrating
Good sensitivity for
peritoneal
penetration,
hemoperitoneum,
and diaphragmatic
injuries. Poor
sensitivity for GI
and retroperitoneal
injuries.
GSW, gunshot wound; SW, stab wound.
a
Alyono D, Morrow CE, Perry JF. Reappraisal of diagnostic peritoneal lavage criteria for operation in penetrating and blunt trauma. Surgery (St. Louis) 1982;92:751–757.
b
Oreskovich MR, Carrico CJ. Stab wounds of the anterior abdomen: analysis of a management plan using local wound exploration and quantitative peritoneal lavage.
Ann Surg 1983;198:411–418.
c
Merlotti GJ, Marcet E, Sheaff CM, et al. Use of peritoneal lavage to evaluate abdominal penetration. J Trauma 1985;25:228–231.
d
Liu M, Lee CH, P’eng FK. Prospective comparison of diagnostic peritoneal lavage, computed tomographic scanning, and ultrasonography for the diagnosis of blunt
abdominal trauma. J Trauma 1993;35(2):267–270.
e
Fabian TC, Mangiante EC, White TJ, et al. A prospective study of 91 patients undergoing both computed tomography and peritoneal lavage following blunt abdominal trauma. J Trauma 1986;26:602.
f
Peitzman AB, Makaroun MS, Slasky BS, Ritter P. Prospective study of computed tomography in initial management of blunt abdominal trauma. J Trauma
1986;26:585–592.
g
McKenney M, Lentz K, Nunez D, et al. Can ultrasound replace diagnostic peritoneal lavage in the assessment of blunt trauma? [see comments]. J Trauma
1994;37(3):439–441.
h
Yoshii H, Sato M, Yamamoto S, et al. Usefulness and limitations of ultrasonography in the initial evaluation of blunt abdominal trauma. J Trauma 1998;45(1):45–50.
i
Singh G, Arya N, Safaya R, et al. Role of ultrasonography in blunt abdominal trauma. Injury 1997;28(9–10):667–670.
j
Rozycki GS, Ochsner MG, Schmidt JA, et al. A prospective study of surgeon-performed ultrasound as the primary adjuvant modality for injured patient assessment.
J Trauma 1995;39(3):492–498.
k
Ortega AE, Tang E, Froes ET, Asensio JA, Katkhouda N, Demetriades D. Laparoscopic evaluation of penetrating thoracoabdominal traumatic injuries. Surg Endosc
1996;10(1):19–22.
l
Sosa JL, Arrillaga A, Puente I, Sleeman D, Ginzburg E, Martin L. Laparoscopy in 121 consecutive patients with abdominal gunshot wounds. J Trauma 1995;39(3):501–504,
discussion 504–506.
m
Ivatury RR, Simon RJ, Stahl WM. A critical evaluation of laparoscopy in penetrating abdominal trauma. J Trauma 1993;34(6):822–827, discussion 827–828.
Source: Reprinted from Mackersie RC. Abdominal trauma. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York:
Springer-Verlag, 2001, with permission.
Test
Diagnostic
laparoscopy
Time
required
(min)
20–60+ +
Table 38.2. Continued
682
J.G. Barone
38. Evaluation of Flank Pain
683
Figure 38.3. CT scan of bilateral areas of renal infarction due to trauma.
Table 38.3. Mechanism and site of ureteral injuries.
Reference
Petersonh
Liroffi
Stutzmanj
Holdenk
Lankfordl
Carltonm
Eickenbergn
Prestio
Steersp
Roberq
Campbellr
Totals
na
18
20
22
63
10
39
17
18
18
16
15
256
GSWb
17
N/A
22
63
10
36
17
10
17
16
12
219
SWc
1
N/A
0
0
0
1
0
6
0
0
0
8
Bluntd
0
N/A
0
0
0
2
0
2
1
0
3
8
Uppere
5
5
6
20
6
N/A
6
15
12
8
7
90 (41%)
Midf
7
11
3
27
3
N/A
2
1
4
4
4
66 (30%)
Lowerg
6
4
13
16
1
N/A
9
2
2
4
4
61 (28%)
Data class
III
III
III
III
III
III
III
III
III
III
III
N/A, not available.
a
Number of patients in study.
b
Gunshot wound.
c
Stab wound.
d
Blunt trauma.
e
Upper one third of ureter or renal pelvis.
f
Middle one third of ureter.
g
Lower one third of ureter.
h
Peterson NE, Pitts JC. Penetrating injuries of the ureter. J Urol 1981;126:587–590.
i
Liroff SA, Pontes JES, Pierce JM Jr. Gunshot wounds of the ureter: 5 years of experience. J Urol 1977;118:551–553.
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.
684
J.G. Barone
Table 38.4. Urinalysis and intravenous urography in the diagnosis of
ureteral injuries.
Reference
Petersond
Liroffe
Lankfordf
Carltong
Eickenbergh
Prestii
Steersj
Roberk
Campbelll
Totals
na
18
20
10
39
17
18
18
16
15
171
Urinalysisb
10/13
9/13
9/9
N/A
N/A
11/16
14/16
8/11
10/13
71/91 (78%)
IVUc
7/11
N/A
8/8
17/21
7/9
3/11
7/8
8/8
4/12
61/88 (69%)
Data class
III
III
III
III
III
III
III
III
III
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.
g
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.
h
Eickenberg H, Amin M. Gunshot wounds to the ureter. J Trauma 1976;16:562–565.
i
Presti JC Jr, Carroll PR, McAninch JW. Ureteral and renal pelvic injuries from external
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.
Institution
Bowman Gray
University of Michigan
University of California, San Francisco
Cleveland Clinic
Number of
patients
152
135
84
78
Operative outcome (%)
Cured
15
29
39
40
Improved
75
52
23
51
Failed
10
19
38
9
Surgical
mortality
(%)
1.3
4.4
2.4
2
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.
38. Evaluation of Flank Pain
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).
685
686
J.G. Barone
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,
38. Evaluation of Flank Pain
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
687
688
J.G. Barone
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
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.
689
690
J.G. Barone
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.
38. Evaluation of Flank Pain
Figure 38.7. Renal ultrasound demonstrating hydronephrosis.
intravenous contrast medium, an allergic reaction to the contrast is possible. These reactions can be severe and have resulted in hemodynamic
and respiratory collapse. To avoid contrast reactions, an ultrasound or
noncontrast CT can be used instead of an IVP (Fig. 38.7). Ultrasound
and noncontrast CT are noninvasive and do not require intravenous
contrast administration. The disadvantage, compared to IVP, is that
these studies do not provide any functional information about the
kidney. These tests demonstrate anatomy, not function, and this consideration may be important in a patient’s evaluation. For example, if
the clinician is concerned about a possible renal infarct secondary to an
arterial embolus, a renal ultrasound and noncontrast CT scan might be
normal, since they do not assess renal function. In this instance, the
kidney looks normal; however, it is no longer functioning due to the
recent infarct. To assess function, either an IVP or intravenous contrastenhanced CT scan could be done.
Summary
The urologist frequently evaluates patients with flank pain and diagnoses and treats conditions that may have local or systemic ramifications. Nonurologic causes for the pain always are considered during
the initial evaluation. Although the history and physical examination
are the most important aspect of the evaluation, laboratory and diagnostic tests help confirm the diagnosis. Since this is a commonly
encountered clinical problem, all practitioners should have some familiarity with the diagnosis and management of flank pain.
Selected Readings
Ahya SN, Coyne DW. Renal disease. In: Ahya SN, Flood K, Paranjothi S, eds.
The Washington Manual of Medical Therapeutics, 30th ed. Philadelphia: Lippincott Williams & Wilkins, 2001.
691
692
J.G. Barone
Dunn DL. Diagnosis and treatment of infection. In: Norton JA, Bollinger RR,
Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York:
Springer-Verlag, 2001.
McLeod RS. Evidence-based surgery. In: Norton JA, Bollinger RR, Chang AE,
et al, eds. Surgery: Basic Science and Clinical Evidence. New York: SpringerVerlag, 2001.
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.
Presti JC Jr, Stoller ML, Carroll PR. Urology. In: Tierny LM Jr, McPhee SJ,
Papadikis M, eds. Current Medical Diagnosis and Treatment, 39th ed. New
York: Lange Medical Books/McGraw-Hill, 2000.
Stack RS. Acute pyelonephritis. In Rakel R, ed. Conn’s Current Therapy, 9th
ed. Philadelphia: WB Saunders, 2000.