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 percus- sion. Laboratory evaluations, including a complete blood count and serum chemistries, are normal. Urine Gram stain demonstrates no bac- teria on an unspun specimen. Urinalysis demonstrates the presence of red blood cells and irregular crystals. An abdominal plain film demon- strates 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 consid- ered. The quality and severity of the pain may provide a clue to its
670
etiology. Flank pain that is due to infection, such as acute pyelone- phritis, 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 travel- ing 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 pos- teriorly. 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
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 prob- able 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 pre- cipitation and stone formation. Even though the patient in the case pre- sented 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
Flank pain
(H&P, UA, KUB) IVP/CT/US
Normal Mass Nonvisualization
Delayed visualization
Calculi
Muscular Intraabdominal Psychological
Therapy Fever/pyuria Cardiac Uncomplicated Arrhythmia
Complicated Fever
Comorbid conditions
Hospitalization Hydration Relieve obstruct Antibiotics Hospitalization
Hydration
Relieve obstruction Drain abscesses Antibiotics
Cardiology consult Control arrhythmia
Oral analgesics Oral hydration Strain urine
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.
southern United States “stone belt,” where it is hot and where dehy- dration 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 sec- ondary to metabolic abnormalities. These stones are seen less com- monly 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, myelo- proliferative 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 alkalin- izing 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 inher- ited 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 for- mation 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
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, hyper- parathyroidism, chronic immobility, and paralysis. In these condi- tions, 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 infec- tious 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 vomit- ing, 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 pres- ence of obstructing urinary calculi can be an ominous clinical find- ing 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 intra- venous antibiotics, aggressive intravenous fluid hydration, and per- cutaneous 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 com-
plete 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.
Table 38.1. Evidence-based practice management guideline for the evaluation of fever in critically ill adult patients.
aTemperature 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 iodine- allergic 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 HIV- negative or did not present to the hospital with diarrhea.
Continued
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 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 criti-
cally 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.
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 sur- rounding 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 develop- ment 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 vesi- coureteral 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.
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 matur- ing, acute pyelonephritis can interfere with kidney growth and devel- opment. 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 facili- tates 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 nephrec- tomy. 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 pyelonephri- tis 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 aminoglyco- side (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 situa- tion, 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 anti- biotic 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
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
Figure 38.2. Computed tomography (CT) scan of large renal tumor. In this sit-
uation, flank pain could result from stretching of the renal capsule or direct
invasion into surrounding tissues.
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 retro- grade 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 pre- sentation. In the trauma setting, imaging of the urinary system is nec- essary 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 rel- atively minor traumatic event. Also, the pediatric kidney is more prone to injury since it is not well protected. In the adult, a signifi- cant 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 decel- eration injury, then contrast imaging of the urinary tract with CT scan- ning 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 nec- essary 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
T able 38.2. Comparison of diagnostic methods for evaluating blunt and penetrating abdominal trauma. T ime Sensitivity required {specificity} Utility: blunt vs. T est (min) Pros Cons and injury type Reference penetrating Diagnostic 5–15 Fast. V ery sensitive. Invasive. Not 97% {99%} blunt Alyono
aGood sensitivity for peritoneal Minimal equipment recommended if 85–93% {67–99} Alyono
aboth blunt and lavage (DPL) required. Specialized prior laparotomy . penetr Oreskovich
bpenetrating trauma. training not required. Not injury specific. 99% {43%} Merlotti
cNonspecific for May be performed in May miss penetr Liu
dboth. Sensitivity a variety of locations. retroperitoneal and 99% {86%} and specificity Results are quantitative, diaphragm injuries. penetr highly dependent objective, and 100% {84%} on cell count operator independent. blunt criteria used. Abdominal CT 30–50 V ery specific with good Not useful for most 85% {100} blunt Fabian
eGood sensitivity and sensitivity . Good for anterior penetrating 99% {100} blunt Peitzman
fspecificity for blunt evaluating posterior injuries. Requires 97% {95} blunt Liu
dinjuries and most (back and flank, time and patient posterior penetrating retroperitoneal) injuries. transport. Some injuries. Insensitive Allows staging of blunt operator (reader) for anterior organ injuries for dependence. May penetrating injuries. nonoperative miss blunt management. Most intestinal injuries major injuries operator and, initially , some (reader) independent. pancreatic injuries. Limited finding- specific or quantitative criteria mandating operation exist. Abdominal 5–10 Fast. Sensitive for Not useful for 92% {95} Liu
dGood sensitivity for ultrasonography hemoperitoneum in penetrating 83% {100} McKenney
gclinically significant (F AST) experienced hands. injuries. Requires 95% {95} Y oshii
hblunt injuries. Poor Noninvasive and no immediately 97% {97} Singh
isensitivity for contrast required. May accessible 82% {99} Rozycki
jpenetrating injuries. be performed in a equipment and variety of locations if specialized training equipment is available. and experience. Nonquantitative and substantially operator dependent. Continued
T able 38.2. Continued T ime Sensitivity required {specificity} Utility: blunt vs. T est (min) Pros Cons and injury type Reference penetrating Diagnostic 20–60 ++ Excellent for diagnosis of Invasive. Poor 88% liver/spleen Ortega
kGood sensitivity for laparoscopy diaphragmatic injuries. sensitivity for some 83% diaphragm Ortega
kperitoneal Good for nonquantitative injuries. Requires 50% panc/ Ortega
kpenetration, dx. of hemoperitoneum. specialized training, kidney Ortega
khemoperitoneum, Good for determining experience, and 25% hollow Sosa
land diaphragmatic peritoneal penetration equipment. viscous Ivatury
minjuries. Poor for SW/GSW . High Nonquantitative 100% periton sensitivity for GI degree of injury and substantially penetr and retroperitoneal specificity when operator dependent. 18% GI injuries injuries. visualized. T ypically requires more conscious sedation than other methods. General anesthesia may be needed in some circumstances. GSW , gunshot wound; SW , stab wound.
aAlyono D, Morr ow CE, Perry JF . Reappraisal of diagnostic peritoneal lavage criteria for operation in penetrating and blunt trau ma. Sur gery (St. Louis) 1982;92:751–757.
bOr eskovich MR, Carrico CJ. Stab wounds of the anterior abdomen: analysis of a management plan using local wound exploration and quantitative peritoneal lavage. Ann Sur g 1983;198:41 1–418.
cMerlotti GJ, Mar cet E, Sheaf f CM, et al. Use of peritoneal lavage to evaluate abdominal penetration. J T rauma 1985;25:228–231.
dLiu M, Lee CH, P’eng FK. Pr ospective comparison of diagnostic peritoneal lavage, computed tomographic scanning, and ultrasonogr aphy for the diagnosis of blunt abdominal trauma. J T rauma 1993;35(2):267–270.
eFabian TC, Mangiante EC, White TJ, et al. A p rospective study of 91 patients under going both computed tomography and peritoneal lavage following blunt abdomi- nal trauma. J T rauma 1986;26:602.
fPeitzman AB, Makar oun MS, Slasky BS, Ritter P . Pr ospective study of computed tomography in initial management of blunt abdomina l trauma. J T rauma 1986;26:585–592.
gMcKenney M, Lentz K, Nunez D, et al. Can ultrasound r eplace diagnostic peritoneal lavage in the assessment of blunt trauma? [se e comments]. J T rauma 1994;37(3):439–441.
hY oshii H, Sato M, Y amamoto S, et al. Usefulness and limitations of ultrasonography in the initial evaluation of blunt abdominal trauma. J T rauma 1998;45(1):45–50.
iSingh G, Arya N, Safaya R, et al. Role of ultrasonography in blunt abdominal trauma. Injury 1997;28(9–10):667–670.
jRozycki GS, Ochsner MG, Schmidt JA, et al. A p rospective study of sur geon-performed ultrasound as the primary adjuvant modality for injur ed patient assessment. J T rauma 1995;39(3):492–498.
kOrtega AE, T ang E, Fr oes ET , Asensio JA, Katkhouda N, Demetriades D. Lapar oscopic evaluation of penetrating thoracoabdominal tr aumatic injuries. Sur g Endosc 1996;10(1):19–22.
lSosa JL, Arrillaga A, Puente I, Sleeman D, Ginzbur g E, Martin L. Lapar oscopy in 121 consecutive patients with abdominal gunshot wounds. J T rauma 1995;39(3):501–504, discussion 504–506.
mIvatury RR, Simon RJ, Stahl WM. A critical evaluation of lapar oscopy in penetrating abdominal trauma. J T rauma 1993;34(6):822–82 7, discussion 827–828. Sour ce: Reprinted fr om Mackersie RC. Abdominal trauma. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Sur gery: Basic Science and Cl inical Evidence. New Y ork: Springer -V erlag, 2001, with permission.
Table 38.3. Mechanism and site of ureteral injuries.
Reference n
aGSW
bSW
cBlunt
dUpper
eMid
fLower
gData class
Peterson
h18 17 1 0 5 7 6 III
Liroff
i20 N/A N/A N/A 5 11 4 III
Stutzman
j22 22 0 0 6 3 13 III
Holden
k63 63 0 0 20 27 16 III
Lankford
l10 10 0 0 6 3 1 III
Carlton
m39 36 1 2 N/A N/A N/A III
Eickenberg
n17 17 0 0 6 2 9 III
Presti
o18 10 6 2 15 1 2 III
Steers
p18 17 0 1 12 4 2 III
Rober
q16 16 0 0 8 4 4 III
Campbell
r15 12 0 3 7 4 4 III
Totals 256 219 8 8 90 (41%) 66 (30%) 61 (28%)
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 man- agement. 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.
Figure 38.3. CT scan of bilateral areas of renal infarction due to trauma.
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 med- ically unstable or recently have suffered a cardiac event. In such Table 38.4. Urinalysis and intravenous urography in the diagnosis of ureteral injuries.
Reference n
aUrinalysis
bIVU
cData class
Peterson
d18 10/13 7/11 III
Liroff
e20 9/13 N/A III
Lankford
f10 9/9 8/8 III
Carlton
g39 N/A 17/21 III
Eickenberg
h17 N/A 7/9 III
Presti
i18 11/16 3/11 III
Steers
j18 14/16 7/8 III
Rober
k16 8/11 8/8 III
Campbell
l15 10/13 4/12 III
Totals 171 71/91 (78%) 61/88 (69%)
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 experi- ence. 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
