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RENAL AND PERIRENAL ABSCESSES
URINARY TRACT INFECTIONS
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RENAL AND PERIRENAL ABSCESSES Louise-Marie Dembry, MD, and Vincent T. Andriole, MD
Infections in the kidney and perinephric space occur as a variety of clinical entities that can be divided into intrarenal and perirenal pathology. Newer and more sensitive renal imaging techniques have enhanced our knowledge of the spectrum of intrarenal pathology. The classification of intrarenal abscess currently includes acute focal bacterial nephritis, acute multifocal bacterial nephritis, renal cortical abscess, renal corticomedullary abscess, and xanthogranulomatous p yelonephritis. Perirenal abscesses occur in the perinephric fascia external to the capsule of the kidney, usually as a result of extension of an intrarenal abscess into this area. The incidence of these suppurative intrarenal and perirenal infections ranges from 1 to 10 cases per 10,000 hospital admissions. Most cases are complications of a lower urinary tract infection and affect men and women with equal frequency. INTRARENAL ABSCESSES Renal Cortical Abscess (Renal Carbuncle)
Etiology Renal carbuncle was first described by Israel in 1905 before the Free Society of Berlin Surgeons.40The case was that of a previously healthy 37-year-old army officer who was kicked in the left flank several weeks after he had had a carbuncle on his neck. He immediately experienced a brief episode of pain in the left lumbar region. The next day, the pain recurred and his temperature was 102°F. The fever and flank pain persisted for 3 weeks. He was then found to have a left lumbar fluctuant mass, pyuria, proteinuria, and hematuria. At the
From the Department of Internal Medicine, Infectious Disease Section, Yale University School of Medicine, New Haven, Connecticut
INFECTIOUS DISEASE CLINICS OF NORTH AMERICA VOLUME 11 * NUMBER 3 SEPTEMBER 1997
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time of nephrectomy, an intrarenal abscess extending from the cortex to the medulla was found and the cultures grew Staphylococcus uuycus. The patient 41) Renal carbuncles are uncommon, although many reeventually re~overed.3~. ports and reviews have followed Israel’s first description.* The recognition of this entity is important because of the difference in pathogenesis and bacteriology from other intrarenal abscesses. Pathogenesis
A renal carbuncle results from hematogenous spread of bacteria from a primary focus of infection elsewhere in the body. Primary foci of infection include skin lesions, especially cutaneous carbuncles, furuncles, paronychia, cellulitis, osteomyelitis, and endovascular infections. Conditions associated with an increased risk for staphylococcal bacteremia such as hemodialysis, diabetes mellitus, and injection drug use are also predisposing conditions for renal carbuncle. The primary focus of infection is not apparent in up to one third of the patients=, 73 because the interval between the original staphylococcal infection and presentation of renal carbuncle ranges from a few days to months, with an average interval of 7 weeks.3 The most common causative agent is S. aweus (90%). In contrast to other intrarenal abscesses, ascending infection is an infrequent cause of renal cortical abscesses.I*,75 Once the cortical parenchyma is seeded hematogenously with the infecting organism, the development of cortical microabscesses follows. Several interconnecting microabscesses then enlarge and coalesce, forming a fluid-filled mass with a thick wall (Fig. 1). Ten percent of cortical abscesses rupture through the renal capsule and form a perinephric *References 3, 14, 15, 19, 21, 33, 39, 48, 54, 58, 73, and 77.
Route of Infection Hematogenous
Chief Findings Fever (high or low grade)
C.V.A.pain
Tenderness or no localizing sign5 or bladder symptoms
Normal urine
Figure 1. Pathogenesis of a staphylococcal renal carbuncle. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983.New York, Plenum Publishing Co, 1983; with permission.)
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abscess. Most carbuncles are unilateral (97%), single lesions (77%) occurring in the right kidney (63%). Clinical Features
In contrast to other intrarenal abscesses, the renal carbuncle is approximately three times more common in men than in women. Although it can occur at any age, it is more common between the second and fourth decades.b 33, 3y Patients usually present with chills, fever, and back or abdominal pain,” 4H, 78 with few or no localizing signs.“’* Most patients do not have urinary symptoms because this is a circumscribed process in the cortex, and as such does not generally communicate with the excretory passages.33,39, 48. 54* 73, 7x Costovertebral angle tenderness and involuntary guarding in the upper lumbar and abdominal musculature are often present on physical examination. A flank mass or a bulge in the lumbar region with loss of lumbar lordosis may also be noted. Chest examination on the affected side may be abnormal, with decreased inspiratory effort, dullness, diminished breath sounds, or rales. Basic laboratory data are nonspecific and variable; however, 95’x of patients 33 The urinalysis usually does not reveal have elevated white blood cell any abnormalities unless the abscess communicates with the collecting system.’, 4x, 73 Blood cultures, when obtained, are generally negative.3 Diagnosis
Other intrarenal pathology such as renal tumors, cysts, intrarenal abscesses caused by aerobic gram-negative rods, and perinephric abscesses can mimic renal cortical abscesses. In the past, surgical exploration was generally done to differentiate the mass from a renal carcinoma.21An anterior renal carbuncle may also resemble an intra-abdominal process. In addition, renal cortical abscesses are difficult to distinguish from renal medullary abscesses, especially in children.%18, 24, ha, 73. 75, no Radiologic techniques are useful in characterizing the renal mass and making the diagnosis.* Excretory urograms are generally nonspecific with the carbuncle appearing as an intrinsic mass, frequently with caliceal distortion. The kidney is not displaced, however, as it frequently is with a perinephric abscess. An intrinsic mass with caliceal distortion but without kidney displacement in a patient with sterile urine suggests a renal carbuncle or tumor. Ultrasonography is useful in the diagnosis of this entity because it provides information about renal morphology and locates and characterizes an intrarenal lesion as cystic, 31, 4R, 56, 73 The abscess appears as a fluid-filled tumor-like, or mass with a thick wall after coalescence (Figs. 2 A , B ) . Ultrasonography may also be used to drain the abscess percutaneously and follow its response to antimicrobial therapy.62.73 Some internal echoes may be seen early in a renal carbuncle, giving the appearance of a solid or semisolid mass. This early appearance may be confused with a tumor, and renal angiography may be needed to differentiate the two lesions (Figs. 3A,B).3,12, 19, 28, 44, 48, 55, h4, 73 Angiographically, the renal carbuncle shows increased vascularization in the periphery of the mass as the abscess wall is usually hypervascular and the major portion of the abscess is avascular (Fig. 4). In addition, the vasculature in an abscess may be displaced or compressed by the mass but retains a normal branching pattern and organiza*References 12, 26, 28, 29, 31, 43, 44, 55, 62, and 64.
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Figure 2. Ultrasonogram of the right kidney on admission to the hospital. A, Longitudinal view demonstrating two echolucent fluid-filled lesions. 9, Transverse view demonstrating fluid filled masses with thickened margins. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
tion. In contrast, renal carcinomas are usually hypervascular but can be hypovascular; they are rarely both. Tumor neovascularity has an irregular branching pattern and abnormal organization. Chronic inflammatory lesions may look like a tumor angiographically if the mass is solid and appears to have central vascularity; however, normal peripheral vasculature will establish the diagnosis. Occasionally, oblique views may be required to rule out central 71 Gallium (h7Gacitrate) scans have also facilitated the diagnosis of renal abscessJ6,35 h7Ga normally concentrates in the kidneys, liver, spleen, and gastrointestinal tract, which can make interpretation d i f f i ~ u l tNonspecific .~~ concentration of h7Gain the kidney (Fig. 5) occurs with renal carcinoma, ureteral obstruction, and severe pyelonephritis without abscess formation. A subtraction technique using "Ga citrate and 9qTcglucoheptonate can differentiate these false positives from a true intrarenal absce~s.7~
Figure 3. Ultrasonogram of right kidney after 4 weeks of antibiotic therapy. Longitudinal view (A) and transverse view (9)showing a decrease in the size of the fluid-filled echolucent lesions. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
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Figure 4. Arterial phase of the left renal arteriogram. Peripheral vessels of the lower pole are attenuated and separated in comparison to the normal vessels in the upper pole. No tumor vessels are present. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
Figure 5. Radionuclide scan with gallium itr rate-^' Ga at 48 hr, showing abnormal uptake in the right upper quadrant, inferior to the liver and right in the area of the kidney. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
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Computed tomography (CT) yields the most accurate anatomic information, detects abscesses less than 2 cm in size, and is the most precise noninvasive technique currently in widespread The CT may be particularly useful if ultrasonography is equivocal or negative, and it can also be used as a guide to percutaneous aspiration. Most abscesses appear as low density masses with enhancement of the wall caused by dilated and inflamed vessels.5hGas within a low density mass is pathognomonic for an abscess. With the advent of CT scanning, angiography is rarely required to define an intrarenal mass. These radiologic techniques are extremely useful once the diagnosis of renal cortical abscess is considered, but because the clinical presentation of renal cortical abscess is often vague, the diagnosis is frequently delayed from days to weeks.3 Treatment
In the past, the treatment of renal carbuncle was surgical drainage.?"3y, 54, 77 Surgical strategies varied with the patient's condition, but in general three techniques were used: primary nephrectomy, enucleation of the carbuncle, and incision and drainage followed by nephrectomy if necessary.33Because S. uureus is usually the cause of renal carbuncle, however, it often responds to antistaphylococcal antibiotics alone and surgical intervention is not required.?,4R, 73 If the diagnosis of renal cortical abscess is suspected from the history, physical examination, radiographic evaluation, and if bacteriologic evaluation of the urine reveals large, gram-positive cocci or no bacteria, antistaphylococcal therapy should be started. A semisynthetic penicillin (oxacillin or nafcillin), 1 to 2 g every 4 to 6 hours, is appropriate therapy. For patients with a penicillin allergy, a first generation cephalosporin (cephalothin or cephapirin 2 g every 4 hours or cefazolin 2 g every 8 hours) or vancomycin for patients with severe immediate beta-lactam allergy (1 g or 15 mg/kg every 12 hours) intravenously are the recommended alternatives. Parenteral antibiotics should be continued for 10 days to 2 weeks, followed by oral antistaphylococcal therapy for at least 2 to 4 weeks. Typically, fever resolves 5 to 6 days after institution of therapy, and flank pain improves within 24 hours of instituting therapy. A clinical course other than this suggests an incorrect diagnosis or uncontrolled infection, such as a perinephric abscess, or bacteria resistant to administered therapy. If there is no response to therapy in 48 hours, percutaneous aspiration should be attempted,'" and if unsuccessful, open drainage should be undertaken. Renal Corticomedullary Abscess Etiology
The development of a corticomedullary abscess is usually associated with an underlying urinary tract abnormality, such as vesicoureteral reflux or urinary tract obstruction. Enteric aerobic gram-negative bacilli, including Esckerickiu coli, Klebsiella species, and Proteus species are commonly responsible for this infection. Pathogenesis
Several acute and chronic inflammatory processes are designated as renal corticomedullary infections. Acute focal bacteriul nephritis (acute lobar nephronia or focal pyelonephritis) is a focal inflammation of the kidney without frank abscess formation. This entity represents a severe form of acute bacterial intersti-
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tial nephritis affecting a single renal lobe.41,52, 67 The tissue shows interstitial inflammation and marked infiltration with polymorphonuclear leukocytes. Acute focal bacterial nephritis may represent an early phase of another acute severe inflammatory entity, acute multifocal bacterial nephritis. The pathology of acute multifocal bacterial nephritis reveals a heavy polymorphonuclear infiltrate present throughout the kidney with frank liquefaction and abscess formation.’h Emphysematous pyelonephritis is an uncommon but distinctive entity representing a severe, necrotizing form of acute multifocal bacterial nephritis in which retroperitoneal, extraluminal gas is seen in the renal parenchyma and perirenal space on an abdominal radiograph. The presence of this gas suggests a perinephric abscess caused by gas-forming, gram-negative facultative anaerobic uropathogens. E. coli is the most common organism associated with this disease, but other gram-negative uropathogens have been reported, including Klebsiella species, Proteus mirabilis, and Citrobacter specie^.'^, 53, 6u This condition occurs most commonly in diabetes with or without urinary obstructions. Rarely, it may occur in nondiabetics with urinary ob~truction’~, 53 and immunocompromised patients. Xanthogranulomatous pyelonephritis is an uncommon but severe chronic infection of the renal parenchyma. It was first described by Schlagenhaufer in 191674 and is largely a pathologic entity and diagnosis. Gross pathologic examination of the involved kidney shows it to be enlarged and fixed to the retroperitoneum by perirenal fibrosis or extension of the granulomatous process. Maleksodevised a pathologic classification of this disease into three stages based on the amount of renal and perirenal involvement. The characteristic xanthogranulomatous process is confined to the kidney in Stage I (nephric). Stage I1 (perinephric) involvement includes Gerota’s fat and the renal parenchyma, and Stage I11 (paranephric) involves widespread extension of the process to the retroperitoneum. Each stage is further subdivided into focal or diffuse depending on the amount of parenchymal involvement. Microscopic pathology characteristically shows destruction of the renal parenchyma, which is replaced by granulomatous tissue containing lipid-laden macrophages (foam cells). Although its cause is still not entirely clear, it seems to be related to a combination of renal obstruction and chronic urinary tract infection. Predisposing factors include renal calculi (75% of cases, 50% of which are staghorn calculi), urinary obstruction, lymphatic obstruction, partially treated chronic urosepsis, renal ischemia and secondary metabolic alterations in lipid metabolism, abnormal host immune response, diabetes mellitus, and primary hyperparathyroidism.”.45, 4y Acute focal bacterial nephritis, acute multifocal bacterial nephritis, and xanthogranulomatous pyelonephritis occur most commonly as a complication of bacteriuria and ascending infection caused by an accompanying renal tract abnormality. The most common abnormalities include obstructive problems such as tubular scarring from previous infections and renal calculi, genitourinary abnormalities associated with diabetes mellitus or primary hyperparathyroidism, and vesicoureteral reflux, particularly in children.*.3, 16, 37, 4y, 67, 70. 75, Two thirds of the intrarenal abscesses caused by aerobic gram-negative bacilli in adults are associated with damaged kidneys or renal calculi; in children these infections are often associated only with vesicoureteral reflux. These factors allow bacteria access to the renal parenchyma by reflux followed by intrarenal reflux into the renal papillae and bacterial inoculation of the renal medulla. Parenchymal infection develops if the urinary tract abnormality, such as reflux or obstruction, persists after bacterial inoculation of the renal medulla. The infection may extend into the renal pelvis and drain into the lower urinary tract, remain undrained, or develop into a chronic The pathogenesis of renal corticomedullary abscesses accounts for the difference in the bacterial cause and
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anatomic location compared with staphylococcal renal cortical abscesses. Another contrast between the two entities is that the gram-negative bacillary corticomedullary infection frequently causes a severe parenchymal infection that may extend to and perforate the renal capsule, thus forming a perinephric abscess. Clinical Features
Corticomedullary abscesses affect men and women with approximately equal frequency except for xanthogranulomatous pyelonephritis in adults, which is more common in women than in men!, 45 There is a higher incidence in older age groups, but it can occur at any age. The typical presentation of the three described intrarenal entities (acute focal bacterial nephritis, acute multifocal bacterial nephritis, xanthogranulomatous pyelonephritis) includes fever, chills, and flank or abdominal pain. Dysuria may not necessarily be present; however, up to two thirds of patients have nausea and vomiting, thus mimicking an abdominal process. Nonspecific constitutional complaints of malaise, fatigue, and weight loss may be present in persons with a chronic process; they are especially common in patients with xanthogranulomatous pyelonephritis.22Patients may have a previous history of recurrent urinary tract infections (65‘%), renal calculi (30%),or a history of prior genitourinary instrumentation (26%).h1 Significant physical findings include a flank mass (60%)),hepatomegaly (30%), and rarely a draining flank sinus. Leukocytosis is generally present and the urinalysis is often abnormal with bacteriuria, pyuria, proteinuria, or hematuria because the intrarenal abscess drains into the urinary collecting system. The urinalysis may be normal up to 30% of the time, however. The most common pathogens recovered from urine cultures are E. coli, Klebsiella species, and Proteus mirabilis. Bacteremia is frequently present with acute focal bacterial nephritis and acute multifocal bacterial nephritis. Other laboratory abnormalities include anemia (75%), abnormal liver function tests (38% to 63%), hypoalbuminemia (6O%), and hypergammaglobulinemia (alpha-1 and alpha-2 globulin) (79%)? Up to 50% of patients with xanthogranulomatous pyelonephritis have hyperuricemia.”, 49 Diagnosis
The nonspecific clinical presentation of fever, chills, and back pain may be seen with a variety of intrarenal processes including corticomedullary abscesses, renal carbuncle, perinephric abscess, renal cyst, and renal tumor. One clinical feature that may assist in differentiating these entities is the presence of bacteremia, which is associated with corticomedullary abscesses and to a lesser degree, perinephric abscesses. In contrast, urosepsis does not usually occur in patients with cysts and tumors.4In addition, the urinalysis is abnormal in 70% of patients with a corticomedullary abscess, whereas it is usually normal in the patient with a renal cortical abscess. The diagnosis is difficult to establish from clinical and laboratory data alone. Radiographic techniques are necessary to differentiate these various intrarenal processes. Acute Focal Bacterial Nephritis (Acute Lobar Nephronia)
Ultrasonography reveals a poorly defined mass with low amplitude echoes compared with the renal cortex and disruption of the corticomedullary junction.‘“,42, 52, 5h, h7 This entity has three characteristics on CT: lobar distribution of inflammatory areas, wedge-shaped hypodense lesions on postcontrast CT,
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and mass-like hypodense lesions in more severe cases.'" The major factor that differentiates acute focal bacterial nephritis from abscess is the lack of a definable wall on visualization with either ultrasound or CT.s6 Liquefaction is generally not seen in this entity.Ih,41, hb Needle aspiration or open biopsy is usually not necessary to make the diagnosis.52, " Acute Multifocal Bacterial Nephritis
Radiographic lesions are similar to those of acute focal bacterial nephritis except that multiple renal lobes are involved.'', 20, 34, 46 Xanthogranulomatous Pyelonephritis
The radiographic presentation is varied because of the heterogeneous underlying causes of this chronic disease. The process may be diffuse or localized, and the most common urographic finding is a stone-bearing (70%), nonfunctioning (80%) kidney.27,On, 32, 4y, li2 This entity should be considered in the presence of a focal mass and staghorn calculi. CT findings include large renal calculi, nonfunctioning kidney, spherical areas of low attenuation, rim enhancement of the low attenuation areas with contrast, and thickening of Gerota's fascia.O'l,5h, 6s The diagnosis is suggested by CT in 44% of cases3"and is useful in planning the operative procedure for treatment of this entity. Ultrasound findings are less specific than the CT findings and MR imaging offers no additional information over CT scan. Treatment
In the past, surgical drainage, debridement, and sometimes nephrectomy were used for treatment of renal corticomedullary abscesses. More recent experience has indicated that, just as with renal carbuncles, treatment of acute, focal and multifocal bacterial nephritis with antimicrobial agents alone produces clinical response within 1 week in most cases with no sequelae.Ih,ls, 37, hy After clinical resolution, radiologic techniques should be used to ensure resolution of the parenchymal abnormalities. Medical therapy is successful in most cases; however, a well-established, large abscess may be more difficult to treat with antimicrobial agents alone than an abscess identified early. In most cases, an intensive trial of appropriate antibiotic therapy should be attempted before considering surgical drainage for lesions localized to the renal parenchyma. Parenteral antimicrobial agents and intravenous hydration should be administered promptly when the diagnosis is considered. Empiric antimicrobial therapy should be directed against the common bacterial organisms in this setting, including E. coli, Klebsiella, and Pvoteus specie^.^ Monotherapy can be given with an extended spectrum penicillin (mezlocillin, piperacillin), an extended spectrum cephalosporin (ceftriaxone, cefotaxime, or ceftazidime) or ciprofloxacin. If combination therapy is to be used, a beta-lactam antibiotic, such as ampicillin (1 g every 4 to 6 hours) or cefazolin (1 g every 8 hours) intravenously should be used with an aminoglycoside until culture and sensitivity results are known. There is no evidence that combination therapy is more effective than a single agent in treating acute focal or multifocal bacterial nephritis." When urine or blood culture and sensitivity results are available, antimicrobial therapy should be modified to the most appropriate agent. Duration of therapy is not specifically defined and must be determined on a case-by-case basis. Current recommendations are to continue parenteral antimicrobial therapy for at least 24 to 48 hours
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after clinical improvement of symptoms and resolution of fever. Depending on antimicrobial susceptibility results, oral antibiotic therapy can be continued for an additional 2 weeks. Acute focal bacterial nephritis typically responds to antimicrobial therapy alone, with follow-up radiographic studies showing complete resolution of the intrarenal 1esi0n.~52 Most patients with acute multifocal bacterial nephritis improve with antibiotics alone, albeit slowly, and only occasionally is a drainage procedure necessary. Factors associated with failure to respond to antimicrobial therapy alone include large abscesses, obstructive uropathy, advanced age, and urosepsis.2,Ih, 37, 6q Pediatric patients with gramnegative bacillary multifocal bacterial nephritis who have severe vesicoureteral reflux and accompanying extensive parenchymal involvement often do not respond to antimicrobial therapy alone. Percutaneous aspiration of the abscess combined with parenteral antimicrobials has been successful in those requiring drainage.'",69, 76 If obstructive uropathy is present, prompt drainage by percutaneous nephrostomy until the patient is stable and afebrile is appropriate; then the lesion can be corrected.I6If open drainage is required, incision and drainage are done when possible. Nephrectomy is reserved for patients with diffusely damaged renal parenchyma or elderly, septic patients requiring urgent intervention for survival.*Patients in the pediatric age group who present with corticomedullary abscess caused by gram-negative bacilli should be evaluated by voiding cystourethrography to rule out correctable lower urinary tract abnormalities. Patients with xanthogranulomatous pyelonephritis are generally not cured by antimicrobials alone. Surgical excision of the xanthogranulomatous process is usually necessary to cure this disease, although there have been several case reports of successful treatment with antibiotics without surgical intervention.x The diagnosis is often not made preoperatively because the entity resembles other diseases, but once the tissue is removed, the xanthogranulomatous process ceases and does not seem to recur. After excision, the prognosis in those without other urinary pathologic conditions is excellent. Although total nephrectomy is the usual procedure, Malek and Elder49have recommended partial nephrectomy for focal disease confined to the kidney (Stage I) or perinephric fat (Stage 11). A partial nephrectomy is particularly appropriate in children because this disease is usually localized in ~hildren.4~ The more common presentation in adults, however, is diffuse disease involving most of the kidney and extending to the perinephric fat (Stage 11) or beyond (Stage 111). Removal of the involved kidney and perirenal fat is preferred in these cases but may be very difficult and complicated by adjacent bowel fistulas. Although the xanthogranulomatous process does not recur after excision, bacteriuria may recur and require treatment.32,49 Infected Renal Cyst
Spontaneous infection of preexisting solitary renal cysts has been documented in several reports.13,16, 47 Patients with polycystic kidney disease may have a single or multiple cysts become infected. The most common etiologic agents are gram-negative uropathogens, which are thought to infect the cyst by way of an ascending route following bacteriuria.h Iatrogenic infection has also been reported after cyst instrumentation.lh The clinical presentation is similar to patients with other renal abscesses-hills, fever, back or flank pain, nausea or vomiting, and dysuria. Radiographic techniques can differentiate the infected cyst from other intrarenal infections. CT or ultrasonography typically show a solitary lesion characteristic of an uncomplicated simple renal cyst. Gallium scanning can identify the cyst or cysts as the source of infection. The definitive
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diagnosis is made by percutaneous cyst aspiration and culture performed under ultrasound or CT guidance. Percutaneous drainage combined with a 2-week course of antibiotics results in resolution of infection.61If urine or blood cultures reveal the bacteriologic cause, percutaneous drainage may not be necessary to make an etiologic diagnosis. Open drainage is rarely required in the therapy of a solitary infected cyst. In polycystic renal disease patients, however, treatment is more difficult and not well defined. A conservative approach has been to use a long (6 to 8 week) course of oral antibiotics directed against the most likely pathogens or those isolated from urine or blood cultures? Surgical intervention is generally avoided because of the difficulty in identifying the infected cyst and is usually a measure of last resort. PERINEPHRIC ABSCESS
Etiology
A perinephric abscess may be caused by a variety of bacterial organisms. The common causes of intrarenal abscess, E . coli, Proteus species, and S. aureus, are also the most common etiologic agents of perinephric abscesses. Other gramnegative bacilli associated with this entity are Klebsiella species, Enterobacter species, Pseudomonas species, Serratia species, and Citrobacter species. Occasionally, enterococci are implicated, and at least one case caused by Streptococcus pneumoniae has been reported.57Anaerobic bacteria, such as Clostridium species, Bacteroides species, and Actinomyces species, may cause perinephric abscesses 23, hy Fungi, particularly Candida and may account for culture-negative absce~ses.~, species, are important causes of perinephric abscesses, as is Mycobacterium tuberculosis. Perinephric abscesses are polymicrobial in cause in 25% of cases." 21,69, 7y,81 Results of urine cultures often correlate with cultures from the abscess, but in some patients, the urine culture is positive for bacteria different from those 23, 5', 6y, 79 From 20% to 40% of patients have positive isolated from the blood culture^.^, 7y
Pathogenesis A perinephric abscess is a collection of suppurative material in the perinephric space between the renal capsule and Gerota's fascia (Fig. 6). Most of perirenal abscesses result from either the rupture of an intrarenal abscess into the perinephric space, renal cortical abscess, chronic or recurrent pyelonephritis, particularly in the presence of obstruction, xanthogranulomatous pyelonephritis, or renal carbuncle.z4,5 1 , 69, 70, 79,Ro The most common mechanism for development of a gram-negative aerobic bacillary perinephric abscess is rupture of a renal corticomedullary abscess, whereas the most common mechanism for development of a staphylococcal perinephric abscess is rupture of a renal cortical abscess into the perinephric space.'*,2', 24 Other initiating events include hematogenous or regional lymphatic seeding from skin sites.", 69, Dissemination from other sites of infection include the liver, gallbladder, pancreas, pleura, prostate, or the female reproductive tract. Other inflammatory processes that may be the primary focus for spread of infection include appendicitis, diverticulitis, perforated colon, carcinoma, and osteomyelitis of adjacent ribs or vertebrae.', 25, 59,6y A subphrenic abscess, empyema, or nephrobronchial fistula may result 14, 5y, h9, Perforation into the from cephalad extension of a perinephric absces~.~,
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soul-ce of Infection ; or
Dir*ectExtension
Low Fever
V.A. pain Tenderness Pwas \ P a m
Figure 6. Pathogenesis of a perinephric abscess. (From Patterson J E , Andriole VT: Renal and perirenal abscesses. Infect Dis Clin North Am 1:918, 1987.)
peritoneal cavity or rupture into the colon is rare. The abscess is usually confined to the perinephric space, but it may extend to pararenal areas as determined by The abscess may extend into the flank or psoas the anatomy of Gerota‘s muscles and may even extend through Petit’s triangle and present as a draining flank abscess. Extension can occur caudally between diverging layers of Gerota’s fascia, and the abscess presents in the groin or paravesical area.7n Predisposing conditions for perinephric abscess are similar to those for intrarenal abscess. Most patients have underlying urinary tract abnormalities, usually obstruction. Predisposing factors include renal or ureteral calculi, neurogenic bladder, ureteral stricture, vesicoureteral reflux, bladder outlet obstruction, neoplasm, polycystic kidney disease, renal papillary necrosis, genitourinary tuberculosis, renal transplantation, trauma (renal biopsy, urinary tract instrumentation, or urologic surgery), steroid administration, and injection drug use. Patients with chronic or recurrent urinary tract infections, with or without calculi, may also be at increased risk.Z3Up to 25% of patients with perinephric abscesses are diabetic.” Clinical Features
The symptoms of a perinephric abscess develop insidiously making early recognition difficult. Patients are usually symptomatic for 2 or more weeks before presentation. Fever is the most common presenting symptom and occurs
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in virtually all patients. Unilateral flank pain is present in 70% to 80%; chills and dysuria are present in 40% of patients.z3,6y, 72,79 Other symptoms include nausea, vomiting and weight loss in 25% of the patients. The most common findings on physical examination are flank and costovertebral angle tenderness. Abdominal tenderness is present in about 60% of patients and may confuse the clinical picture. A flank or abdominal mass is present in less than 50% of patients.'" 6y, 7y Referred pain is common, and patients may complain of hip, thigh, or knee pain. Splinting, with secondary scoliosis, may be noted. The musculoskeletal examination may reveal pain on bending toward the contralatera1 side, active flexion of the ipsilateral thigh against resistance, or extension of the thigh while walking. Routine laboratory tests are nonspecific. The peripheral white blood cell count is usually elevated with a left shift. Anemia is present in 40% and azotemia in 25% of 7y Pyuria and proteinuria are common; however, the urinalysis may be normal up to one third of the time, and 40% of patients have sterile urine. Bacteremia is documented in approximately 40% of patients." 6y, 7y Diagnosis The diagnosis of perinephric abscesses can be difficult because of its insidious onset and nonspecific symptoms, physical examination, and laboratory tests. The diagnosis is made on admission in only one third of patient^.^, h9. 70, 7x Another one third of patients are diagnosed only at autopsy.69,7y A perinephric abscess should be considered in patients who have fever of unknown origin and in patients with unexplained peritonitis, pelvic abscess, or empyema that may have resulted from extension of the abscess. The key to making the diagnosis is in considering this entity in the differential and performing the appropriate radiologic examinations. The chest radiograph may show an ipsilateral pleural effusion, elevated diaphragm, or lower lobe infiltrate, or it may be completely normal.6y,7y Abnormalities on a supine abdominal radiograph may be subtle and include vertebral scoliosis, obliteration of the renal outline, an upper quadrant mass, or obliteration of the psoas shadow. An absent psoas margin must be interpreted with caution and is not necessarily diagnostic of a perinephric abscess.?,24 Ultrasonography, CT, MR imaging, and gallium67 imaging have greatly improved the ability to diagnose this disease. The ultrasound will show a sonolucent mass, often with irregular walls, and may be multiloculated with internal echoes. In one study, however, the ultrasound was falsely negative in 36% of cases when compared to CT e v a l ~ a t i o n CT . ~ ~ scan is considered the diagnostic technique of choice as it identifies the abscess and defines its extent beyond the renal capsule and the surrounding anatomy, including extension into the psoas muscle (Fig. 7A,B).72MR imaging and CT are equally efficacious in the evaluation of abdominal fluid collections, although MR imaging may be better able to define the extension of infection into adjacent organs and is advantageous for those patients who should not receive contrast agents caused by allergies or renal insuffi~iency.~~ Gallium 67 radionuclide imaging may confirm the evidence of renal or perirenal inflammation; however, it does not provide anatomical detail nor differentiate a perinephric abscess from intrarenal abscess, pyelonephritis, renal carcinoma, or ureteral obstr~ction.~, 35 Findings on excretory urography include decreased renal mobility with respiration or position, diminished to absent renal function, caliectasis or other caliceal abnormalities, and displacement of the kidney or ureter (usually medially and upward). Although extrarenal extravasation of contrast material is rare,
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Figure 7. A, CT scan through midabdomen demonstrating marked enlargement of the right psoas major muscle with a bilobed fluid-filled cavity, labeled A. B, Transverse CT scan through the level of the femoral head showing the inferior extent of the abscess (arrow) pointing below the inguinal ligament. (From Andriole VT: The clinician’sviewpoint. Clinics in Diagnostic Ultrasound 11:1, 1982. New York, Churchill Livingstone, 1982; with permission.)
it is of diagnostic importance when it occurs because this is virtually diagnostic of perirenal abscess.”, 6y Fistulas may form with pararenal structures. Although retrograde pyelography is not usually necessary, it is sometimes helpful in characterizing obstruction that occurs distal to the renal pelvis. Angiography typically shows an increase in the number and size of perforating arteries from the kidney into the abscess. Renal capsular arteries are prominent, stretched, and tortuous around the abscess, and a contrast blush is seem3,43, ?’ This appearance is distinct from the angiographic appearance of a tumor. Angiography is rarely necessary with the widespread use of CT and MR imaging. Treatment
Perinephric abscesses have been associated with high mortality rates (20% to 50%), although with early recognition, prompt drainage, and antimicrobial
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therapy, mortality has decreased.16,23, hq, 72, 7q Antimicrobial therapy alone is not adequate in contrast to most types of intrarenal abscesses, and antibiotics should be used as an adjunct to percutaneous drainage performed under CT or ultrasound guidance. Surgical drainage is undertaken when percutaneous drainage fails or is contraindicated. Acute nephrectomy is still sometimes necessary.'" hq, 72 Empiric antimicrobial therapy should be directed against the common gramnegative uropathogens and s. aureus. An aminoglycoside (gentamicin or tobramycin) and an anti-staphylococcal beta-lactam (oxacillin, nafcillin, cephalothin, cephapirin, or cefazolin) are appropriate initial antibiotics. An extended spectrum beta-lactam may be used in place of an aminoglycoside for gram-negative coverage in patients with abnormal renal function. Once culture results are obtained, therapy should be modified accordingly. If Pseudomonas aeruginosa is present, an anti-pseudomonal beta-lactam (mezlocillin, piperacillin, cefoperazone, or ceftazidime) should be added to the aminoglycoside. If enterococcus is isolated, ampicillin plus gentamicin is the treatment of choice. Isoniazid plus rifampin are indicated for M . tuberculosis infections; ethambutol or streptomycin may also be used in combination with these. Amphotericin B is necessary for abscesses caused by fungi.
SUMMARY
Our knowledge of the spectrum of renal abscesses has evolved as a result
of more sensitive radiologic techniques. The classification of intrarenal abscesses currently includes acute focal bacterial nephritis, acute multifocal bacterial nephritis, renal cortical abscess, renal corticomedullary abscess, and xanthogranulomatous pyelonephritis. The clinical presentation of these entities does not differentiate them, however, and various radiographic studies are helpful in making the diagnosis. The intrarenal abscess is usually treated successfully with antibiotic therapy alone. Antistaphylococcal therapy is indicated for the renal cortical abscess, whereas therapy directed against the common gram-negative uropathogens is indicated for most of the other entities. The perinephric abscess is often an elusive diagnosis, has a more serious prognosis, and is more difficult to treat. Drainage of the abscess and sometimes partial or complete nephrectomy, in addition to antibiotic therapy, are required for resolution. ACKNOWLEDGMENT The authors thank Brenda Smith and Susan Marino for their help in preparing the manuscript.
References 1. Altemeier WA, Alexander J S Retroperitoneal abscess. Arch Surg 85:512, 1961 2. Anderson KA, McAninch JW: Renal abscesses: Classification and review of 40 cases. Urology 16333, 1980 3. Andriole VT: Renal carbuncle. Medical Grand Rounds 2:250, 1983 4. Andriole VT: Renal and perirenal abscess. In Schrier, Gottschalk (eds): Diseases of the Kidney, ed 4. Boston, Little Brown, 1987, pp 1049-1063 5. Atcheson DW: Perinephric abscess with a review of 117 cases. J Urol46:201, 1941
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6. Baker DA, Andriole V T The treatment of difficult urinary-tract infections with carbenicillin indanyl sodium. J Infect Dis 127(suppl):136,1973 7. Brook I: The role of anaerobic bacteria in perinephric and renal abscesses in children. Pediatrics 93261, 1994 8. Brown BS, Dodson M, Weintraub P S Xanthogranulomatous pyelonephritis: Report of nonsurgical management of a case and review of the literature. Clin Infect Dis 22:308, 1996 9. Caberwal D, Katz J, Reid R, et al: A case of nephrobronchial and colobronchial fistula presenting as lung abscess. J Urol 117:371, 1977 10. Caldamone AA, Frank I N Percutaneous aspiration in the treatment of renal abscess. J Urol 123:92, 1980 11. Campbell M F Perinephritic abscess. Surg Obstet Gynecol 51:674, 1930 12. Caplan LH, Siegelman SS, Bosniak MA: Angiography in inflammatory space-occupying lesions of the kidney. Radiology 88:14, 1967 13. Cho KJ, Maklad N, Curran J, et al: Angiographic and ultrasonic findings in infected simple cysts of the kidney. Am J Roentgenol 127:1015, 1976 14. Cobb OE: Carbuncle of the kidney. Br J Urol 38262, 1966 15. Colby FH, Baker MP, St Goar W T Renal carbuncle: Report of a response to modern treatment. N Engl J Med 256:1147, 1957 16. Corriere JN Jr, Sandler CM: The diagnosis and immediate therapy of acute renal and perirenal infections. Urol Clin North Am 9219, 1982 17. Costas S: Renal and perirenal emphysema. Br J Urol 44:311, 1972 18. Costas S, Ripopey JJ, van Blerk PJP: Segmental acute pyelonephritis: A precursor to renal carbuncle or abscess? Br J Urol44399,1972 19. Craven JD, Hardy 8, Stanley P, et al: Acute renal carbuncle: The importance of preoperative angiography. J Urol 111:727, 1974 20. Davidson AJ, Talner LB: Urographic and angiographic abnormalities in adult-onset acute bacterial nephritis. Radiology 106949, 1973 21. Doolittle KH, Taylor JN: Renal abscess in the differential diagnosis of mass in kidney. J Urol 80:649, 1963 22. Eastham J, Ahlering T, Skinner E Xanthogranulomatous pyelonephritis: Clinical findings and surgical considerations. Urology 43:295, 1994 23. Edelstein H, McCabe RE: Perinephric abscess: Modern diagnosis and treatment in 47 cases. Medicine 67118, 1988 24. Evans JA, Meyers MA, Bosniak MA: Acute renal and perirenal infections. Semin Roentgenol 6:274, 1971 25. Falk VS: Obstructive jaundice and perinephric abscess. Arch Surg 113:778, 1978 26. Frankel RS, Richman SD, Levenson SM, et al: Renal localization of gallium-67 citrate. Radiology 114:393, 1975 27. Gammill S, Rabinowitz JG, Peace R, et al: New thoughts concerning xanthogranulomatous pyelonephritis (X-P). AJR 125:154, 1975 28. Gardrinab NM, Lome LG, Presman D Renal abscess: Role of renal arteriography. Urology 239, 1973 29. Gelman ML, Stone LB: Renal carbuncle: Early diagnosis by retroperitoneal ultrasound. Urology 7:103, 1976 30. Goldman SM, Hartman DS, Fishman EK, et al: CT of xanthogranulomatous pyelonephritis: Radiologic-pathologic correlation. AJR 142963, 1984 31. Goldman SM, Minkin SD, Naraval DC, et al: Renal carbuncle: The use of ultrasound in its diagnosis and treatment. J Urol 118:525, 1977 32. Goodman M, Curry T, Russell T: Xanthogranulomatous pyelonephritis (XGP): A local disease with systemic manifestations. Report of 23 patients and review of the literature. Medicine 58:171, 1979 33. Graves RC, Parkins LE: Carbuncle of the kidney. J Urol 35:1, 1936 34. Hoffman EP, Mindelzun RE, Anderson RU: Computed tomography in acute pyelonephritis associated with diabetes. Radiology 135:691, 1980 35. Hopkins GB, Hall RL, Mende C W Gallium-67 scintigraphy for the diagnosis and localization of perinephric abscesses. J Urol 115:126, 1976 36. Hotchkiss RS Perinephric abscess. Am J Surg 85:471, 1953
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37. Hoverman IV, Gentry LO, Jones DW, et a 1 Intrarenal abscess: Report of 14 cases. Arch Intern Med 140:914, 1980 38. Huang JJ, Sung JM, Chen KW, et al: Acute bacterial nephritis: A Clinicoradiologic correlation based on computed tomography. Am J Med 93:289, 1992 39. Ingrish GA: Carbuncle of the kidney: Report of ten cases. J Urol 42:326, 1939 40. Israel J: Metastatischer karbunkel der niere. Deutsche Med Wochnschr 1660, 1905 41. June CH, Browning MD, Smith LP, et al: Ultrasonography and computed tomography in severe urinary tract infection. Arch Intern Med 1452341, 1985 42. Klar A, Hurvitz H, Berkun Y, et al: Focal bacterial nephritis (lobar nephronia) in children. J Pediatr 128:850,1996 43. Koehler PR Roentgen diagnosis of inflammatory renal masses: Emphasis on radiographic clues. Radiology 112:257, 1974 44. Levin DC, Gordon D, Kinkhabwala MN, et al: Reticular neovascularity in malignant and inflammatory renal masses. Radiology 120:61, 1976 45. Levy M, Baumal R, Eddy AA: Xanthogranulomatous pyelonephritis in children. Clin Pediatr 33:360, 1994 46. Lilienfeld RM, Lande A: Acute adult onset bacterial nephritis: Long-term urographic and angiographic follow-up. J Urol 11414, 1975 47. Limjoco UR, Strauch AE: Infected solitary cysts of the kidney: Report of a case and review of the literature. J Urol96625, 1966 48. Lyons RW, Long JM, Lytton B, et al: Arteriography and antibiotic therapy of renal carbuncle. J Urol 107524, 1972 49. Malek RS, Elder JS: Xanthogranulomatous pyelonephritis: A critical analysis of 26 cases and of the literature. J Urol 119:589, 1978 50. Malek RS, Greene LF, DeWeerd JH, et al: Xanthogranulomatous pyelonephritis. Br J Urol 44:296, 1972 51. Malgieri JJ, Kursh ED, Persky L The changing clinicopathological pattern of abscesses in or adjacent to the kidney. J Urol 118:230, 1977 52. McDonough WD, Sandler CM, Benson GS: Acute focal bacterial nephritis: Focal pyelonephritis that may simulate renal abscess. J Urol 126:670, 1981 53. McMurray SD, Luft FC, Maxwell DR, et al: Emphysematous pyelonephritis. J Urol 115:604, 1976 54. McNulty PH: Carbuncle of the kidney: Review of the literature, discussion of unilateral localized lesions of the kidney and report of a case. J Urol 35:15, 1936 55. Meany TF: Errors in angiographic diagnosis of renal masses. Radiology 93:361, 1969 56. Merenich WM, Popky G L Radiology of renal infection. Med Clin North Am 75425, 1991 57. Merimsky E, Feldman C: Perinephric abscess: Report of 19 cases. Int Surg 6679, 1981 58. Moore CA, Gangai MP: Renal cortical abscess. J Urol 98:303, 1967 59. Murray HW, Molavi A: Perinephric abscess: An unusual presentation of perforation of the colon. Johns Hopkins Med J 140:15, 1977 60. Patel NP, Lavengood RW, Fernandes M, et al: Gas-Forming Infections in Genitourinary Tract. Urology 39:341, 1992 61. Patterson JE, Andriole VT: Renal and Perirenal Abscesses. Infect Dis Clin North Am 1:907, 1987 62. Pedersen JF, Hancke S, Kristensen JK: Renal carbuncle: Antibiotic therapy governed by ultrasonically guided aspiration. J Urol 109:777, 1973 63. Pfister RC, Stanley RJ, Geisse G, et al: Percutaneous aspiration of inflammatory renal masses: Separation of medical from surgical disease [abstract]. AJR 128:522, 1977 64. Rabinowitz JG, Kinkhabwala MN, Robinson T: Acute renal carbuncle: The roentgenographic clarification of a medical enigma. AJR 116:740, 1972 65. Rabushka LS, Fishman EK, Goldman SM: Pictorial review: Computed tomography of renal inflammatory disease. Urology 44:473, 1994 66. Rauschkolb EN, Sandler CM, Patel S, et al: Computed tomography of renal inflammatory disease. J Comp Assist Tomog 6502, 1982 67. Rosenfield AT, Glickman MG, Taylor KJW, et al: Acute focal bacterial nephritis (acute lobar nephronia). Radiology 132:553, 1979 68. Rote AR, Bauer SB, Retik AB: Renal abscess in children. J Urol 119:254, 1978
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69. Saiki J, Vaziri ND, Barton C: Perinephric and intranephric abscesses: A review of the literature. West J Med 136:95, 1982 70. Salvatierra 0 Jr, Bucklew WB, Morrow JW: Perinephric abscess: A report of 71 cases. J Urol 98:296, 1967 71. Schajnuck LI, Fouty R, Cutler RE: Emphysematous pyelonephritis: A new case and review of previous observations. Am J Med 44:134-139, 1968 72. Scheinfeld J, Erturk E, Spataro RF, et al: Perinephric abscess: Current concepts. J Urol 137191, 1987 73. Schiff M, Glickman M, Weiss RM, et al: Antibiotic treatment of renal carbuncle. Ann Intern Med 87305, 1977 74. Schlagenhaufer F: Uber eigentumliche Staphylomykosen der Nieren und des pararenalen Bindegewebes. Frankfurt Z Path 19:139, 1916 75. Segura JW, Kelalis PP: Localized renal parenchymal infections in children. J Urol 109:1029, 1973 76. Siege1 JF, Smith A, Moldwin R: Minimally Invasive Treatment of Renal Abscess. J Urol 155:52, 1996 77. Spence HM, Johnston LW: Renal carbuncle. Ann Surg 109:99, 1939 78. Taylor KJW, Wasson JFMcI, deGraaff C, et al: Accuracy of grey scale ultrasound diagnosis of abdominal and pelvic abscesses in 220 patients. Lancet 1233, 1978 79. Thorley JD, Jones SR, Sanford JP: Perinephric abscess. Medicine 53:41, 1974 80. Timmons JW, Perlmutter A D Renal abscess: A changing concept. J Urol 115:229, 1976 81. Truesdale BH, Rous SN, Nelson RP: Perinephric abscess: A review of 26 cases. J Urol 118910, 1977 82. Van Kirk OC, Go RT, Wedel VJ: Sonographic features of xanthogranulomatous pyelonephritis. AJR 1341035, 1980
Address reprint requests to Vincent T. Andriole, MD Infectious Disease Section Department of Internal Medicine 201-202 Laboratory of Clinical Investigation 333 Cedar Street New Haven, CT 0652M022
0891-5520/97 $0.00
+ .20
RENAL AND PERIRENAL ABSCESSES Louise-Marie Dembry, MD, and Vincent T. Andriole, MD
Infections in the kidney and perinephric space occur as a variety of clinical entities that can be divided into intrarenal and perirenal pathology. Newer and more sensitive renal imaging techniques have enhanced our knowledge of the spectrum of intrarenal pathology. The classification of intrarenal abscess currently includes acute focal bacterial nephritis, acute multifocal bacterial nephritis, renal cortical abscess, renal corticomedullary abscess, and xanthogranulomatous p yelonephritis. Perirenal abscesses occur in the perinephric fascia external to the capsule of the kidney, usually as a result of extension of an intrarenal abscess into this area. The incidence of these suppurative intrarenal and perirenal infections ranges from 1 to 10 cases per 10,000 hospital admissions. Most cases are complications of a lower urinary tract infection and affect men and women with equal frequency. INTRARENAL ABSCESSES Renal Cortical Abscess (Renal Carbuncle)
Etiology Renal carbuncle was first described by Israel in 1905 before the Free Society of Berlin Surgeons.40The case was that of a previously healthy 37-year-old army officer who was kicked in the left flank several weeks after he had had a carbuncle on his neck. He immediately experienced a brief episode of pain in the left lumbar region. The next day, the pain recurred and his temperature was 102°F. The fever and flank pain persisted for 3 weeks. He was then found to have a left lumbar fluctuant mass, pyuria, proteinuria, and hematuria. At the
From the Department of Internal Medicine, Infectious Disease Section, Yale University School of Medicine, New Haven, Connecticut
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time of nephrectomy, an intrarenal abscess extending from the cortex to the medulla was found and the cultures grew Staphylococcus uuycus. The patient 41) Renal carbuncles are uncommon, although many reeventually re~overed.3~. ports and reviews have followed Israel’s first description.* The recognition of this entity is important because of the difference in pathogenesis and bacteriology from other intrarenal abscesses. Pathogenesis
A renal carbuncle results from hematogenous spread of bacteria from a primary focus of infection elsewhere in the body. Primary foci of infection include skin lesions, especially cutaneous carbuncles, furuncles, paronychia, cellulitis, osteomyelitis, and endovascular infections. Conditions associated with an increased risk for staphylococcal bacteremia such as hemodialysis, diabetes mellitus, and injection drug use are also predisposing conditions for renal carbuncle. The primary focus of infection is not apparent in up to one third of the patients=, 73 because the interval between the original staphylococcal infection and presentation of renal carbuncle ranges from a few days to months, with an average interval of 7 weeks.3 The most common causative agent is S. aweus (90%). In contrast to other intrarenal abscesses, ascending infection is an infrequent cause of renal cortical abscesses.I*,75 Once the cortical parenchyma is seeded hematogenously with the infecting organism, the development of cortical microabscesses follows. Several interconnecting microabscesses then enlarge and coalesce, forming a fluid-filled mass with a thick wall (Fig. 1). Ten percent of cortical abscesses rupture through the renal capsule and form a perinephric *References 3, 14, 15, 19, 21, 33, 39, 48, 54, 58, 73, and 77.
Route of Infection Hematogenous
Chief Findings Fever (high or low grade)
C.V.A.pain
Tenderness or no localizing sign5 or bladder symptoms
Normal urine
Figure 1. Pathogenesis of a staphylococcal renal carbuncle. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983.New York, Plenum Publishing Co, 1983; with permission.)
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abscess. Most carbuncles are unilateral (97%), single lesions (77%) occurring in the right kidney (63%). Clinical Features
In contrast to other intrarenal abscesses, the renal carbuncle is approximately three times more common in men than in women. Although it can occur at any age, it is more common between the second and fourth decades.b 33, 3y Patients usually present with chills, fever, and back or abdominal pain,” 4H, 78 with few or no localizing signs.“’* Most patients do not have urinary symptoms because this is a circumscribed process in the cortex, and as such does not generally communicate with the excretory passages.33,39, 48. 54* 73, 7x Costovertebral angle tenderness and involuntary guarding in the upper lumbar and abdominal musculature are often present on physical examination. A flank mass or a bulge in the lumbar region with loss of lumbar lordosis may also be noted. Chest examination on the affected side may be abnormal, with decreased inspiratory effort, dullness, diminished breath sounds, or rales. Basic laboratory data are nonspecific and variable; however, 95’x of patients 33 The urinalysis usually does not reveal have elevated white blood cell any abnormalities unless the abscess communicates with the collecting system.’, 4x, 73 Blood cultures, when obtained, are generally negative.3 Diagnosis
Other intrarenal pathology such as renal tumors, cysts, intrarenal abscesses caused by aerobic gram-negative rods, and perinephric abscesses can mimic renal cortical abscesses. In the past, surgical exploration was generally done to differentiate the mass from a renal carcinoma.21An anterior renal carbuncle may also resemble an intra-abdominal process. In addition, renal cortical abscesses are difficult to distinguish from renal medullary abscesses, especially in children.%18, 24, ha, 73. 75, no Radiologic techniques are useful in characterizing the renal mass and making the diagnosis.* Excretory urograms are generally nonspecific with the carbuncle appearing as an intrinsic mass, frequently with caliceal distortion. The kidney is not displaced, however, as it frequently is with a perinephric abscess. An intrinsic mass with caliceal distortion but without kidney displacement in a patient with sterile urine suggests a renal carbuncle or tumor. Ultrasonography is useful in the diagnosis of this entity because it provides information about renal morphology and locates and characterizes an intrarenal lesion as cystic, 31, 4R, 56, 73 The abscess appears as a fluid-filled tumor-like, or mass with a thick wall after coalescence (Figs. 2 A , B ) . Ultrasonography may also be used to drain the abscess percutaneously and follow its response to antimicrobial therapy.62.73 Some internal echoes may be seen early in a renal carbuncle, giving the appearance of a solid or semisolid mass. This early appearance may be confused with a tumor, and renal angiography may be needed to differentiate the two lesions (Figs. 3A,B).3,12, 19, 28, 44, 48, 55, h4, 73 Angiographically, the renal carbuncle shows increased vascularization in the periphery of the mass as the abscess wall is usually hypervascular and the major portion of the abscess is avascular (Fig. 4). In addition, the vasculature in an abscess may be displaced or compressed by the mass but retains a normal branching pattern and organiza*References 12, 26, 28, 29, 31, 43, 44, 55, 62, and 64.
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Figure 2. Ultrasonogram of the right kidney on admission to the hospital. A, Longitudinal view demonstrating two echolucent fluid-filled lesions. 9, Transverse view demonstrating fluid filled masses with thickened margins. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
tion. In contrast, renal carcinomas are usually hypervascular but can be hypovascular; they are rarely both. Tumor neovascularity has an irregular branching pattern and abnormal organization. Chronic inflammatory lesions may look like a tumor angiographically if the mass is solid and appears to have central vascularity; however, normal peripheral vasculature will establish the diagnosis. Occasionally, oblique views may be required to rule out central 71 Gallium (h7Gacitrate) scans have also facilitated the diagnosis of renal abscessJ6,35 h7Ga normally concentrates in the kidneys, liver, spleen, and gastrointestinal tract, which can make interpretation d i f f i ~ u l tNonspecific .~~ concentration of h7Gain the kidney (Fig. 5) occurs with renal carcinoma, ureteral obstruction, and severe pyelonephritis without abscess formation. A subtraction technique using "Ga citrate and 9qTcglucoheptonate can differentiate these false positives from a true intrarenal absce~s.7~
Figure 3. Ultrasonogram of right kidney after 4 weeks of antibiotic therapy. Longitudinal view (A) and transverse view (9)showing a decrease in the size of the fluid-filled echolucent lesions. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
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Figure 4. Arterial phase of the left renal arteriogram. Peripheral vessels of the lower pole are attenuated and separated in comparison to the normal vessels in the upper pole. No tumor vessels are present. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
Figure 5. Radionuclide scan with gallium itr rate-^' Ga at 48 hr, showing abnormal uptake in the right upper quadrant, inferior to the liver and right in the area of the kidney. (From Andriole VT: Renal carbuncle. Medical Grand Rounds 2:259, 1983. New York, Plenum Publishing Co, 1983; with permission.)
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Computed tomography (CT) yields the most accurate anatomic information, detects abscesses less than 2 cm in size, and is the most precise noninvasive technique currently in widespread The CT may be particularly useful if ultrasonography is equivocal or negative, and it can also be used as a guide to percutaneous aspiration. Most abscesses appear as low density masses with enhancement of the wall caused by dilated and inflamed vessels.5hGas within a low density mass is pathognomonic for an abscess. With the advent of CT scanning, angiography is rarely required to define an intrarenal mass. These radiologic techniques are extremely useful once the diagnosis of renal cortical abscess is considered, but because the clinical presentation of renal cortical abscess is often vague, the diagnosis is frequently delayed from days to weeks.3 Treatment
In the past, the treatment of renal carbuncle was surgical drainage.?"3y, 54, 77 Surgical strategies varied with the patient's condition, but in general three techniques were used: primary nephrectomy, enucleation of the carbuncle, and incision and drainage followed by nephrectomy if necessary.33Because S. uureus is usually the cause of renal carbuncle, however, it often responds to antistaphylococcal antibiotics alone and surgical intervention is not required.?,4R, 73 If the diagnosis of renal cortical abscess is suspected from the history, physical examination, radiographic evaluation, and if bacteriologic evaluation of the urine reveals large, gram-positive cocci or no bacteria, antistaphylococcal therapy should be started. A semisynthetic penicillin (oxacillin or nafcillin), 1 to 2 g every 4 to 6 hours, is appropriate therapy. For patients with a penicillin allergy, a first generation cephalosporin (cephalothin or cephapirin 2 g every 4 hours or cefazolin 2 g every 8 hours) or vancomycin for patients with severe immediate beta-lactam allergy (1 g or 15 mg/kg every 12 hours) intravenously are the recommended alternatives. Parenteral antibiotics should be continued for 10 days to 2 weeks, followed by oral antistaphylococcal therapy for at least 2 to 4 weeks. Typically, fever resolves 5 to 6 days after institution of therapy, and flank pain improves within 24 hours of instituting therapy. A clinical course other than this suggests an incorrect diagnosis or uncontrolled infection, such as a perinephric abscess, or bacteria resistant to administered therapy. If there is no response to therapy in 48 hours, percutaneous aspiration should be attempted,'" and if unsuccessful, open drainage should be undertaken. Renal Corticomedullary Abscess Etiology
The development of a corticomedullary abscess is usually associated with an underlying urinary tract abnormality, such as vesicoureteral reflux or urinary tract obstruction. Enteric aerobic gram-negative bacilli, including Esckerickiu coli, Klebsiella species, and Proteus species are commonly responsible for this infection. Pathogenesis
Several acute and chronic inflammatory processes are designated as renal corticomedullary infections. Acute focal bacteriul nephritis (acute lobar nephronia or focal pyelonephritis) is a focal inflammation of the kidney without frank abscess formation. This entity represents a severe form of acute bacterial intersti-
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tial nephritis affecting a single renal lobe.41,52, 67 The tissue shows interstitial inflammation and marked infiltration with polymorphonuclear leukocytes. Acute focal bacterial nephritis may represent an early phase of another acute severe inflammatory entity, acute multifocal bacterial nephritis. The pathology of acute multifocal bacterial nephritis reveals a heavy polymorphonuclear infiltrate present throughout the kidney with frank liquefaction and abscess formation.’h Emphysematous pyelonephritis is an uncommon but distinctive entity representing a severe, necrotizing form of acute multifocal bacterial nephritis in which retroperitoneal, extraluminal gas is seen in the renal parenchyma and perirenal space on an abdominal radiograph. The presence of this gas suggests a perinephric abscess caused by gas-forming, gram-negative facultative anaerobic uropathogens. E. coli is the most common organism associated with this disease, but other gram-negative uropathogens have been reported, including Klebsiella species, Proteus mirabilis, and Citrobacter specie^.'^, 53, 6u This condition occurs most commonly in diabetes with or without urinary obstructions. Rarely, it may occur in nondiabetics with urinary ob~truction’~, 53 and immunocompromised patients. Xanthogranulomatous pyelonephritis is an uncommon but severe chronic infection of the renal parenchyma. It was first described by Schlagenhaufer in 191674 and is largely a pathologic entity and diagnosis. Gross pathologic examination of the involved kidney shows it to be enlarged and fixed to the retroperitoneum by perirenal fibrosis or extension of the granulomatous process. Maleksodevised a pathologic classification of this disease into three stages based on the amount of renal and perirenal involvement. The characteristic xanthogranulomatous process is confined to the kidney in Stage I (nephric). Stage I1 (perinephric) involvement includes Gerota’s fat and the renal parenchyma, and Stage I11 (paranephric) involves widespread extension of the process to the retroperitoneum. Each stage is further subdivided into focal or diffuse depending on the amount of parenchymal involvement. Microscopic pathology characteristically shows destruction of the renal parenchyma, which is replaced by granulomatous tissue containing lipid-laden macrophages (foam cells). Although its cause is still not entirely clear, it seems to be related to a combination of renal obstruction and chronic urinary tract infection. Predisposing factors include renal calculi (75% of cases, 50% of which are staghorn calculi), urinary obstruction, lymphatic obstruction, partially treated chronic urosepsis, renal ischemia and secondary metabolic alterations in lipid metabolism, abnormal host immune response, diabetes mellitus, and primary hyperparathyroidism.”.45, 4y Acute focal bacterial nephritis, acute multifocal bacterial nephritis, and xanthogranulomatous pyelonephritis occur most commonly as a complication of bacteriuria and ascending infection caused by an accompanying renal tract abnormality. The most common abnormalities include obstructive problems such as tubular scarring from previous infections and renal calculi, genitourinary abnormalities associated with diabetes mellitus or primary hyperparathyroidism, and vesicoureteral reflux, particularly in children.*.3, 16, 37, 4y, 67, 70. 75, Two thirds of the intrarenal abscesses caused by aerobic gram-negative bacilli in adults are associated with damaged kidneys or renal calculi; in children these infections are often associated only with vesicoureteral reflux. These factors allow bacteria access to the renal parenchyma by reflux followed by intrarenal reflux into the renal papillae and bacterial inoculation of the renal medulla. Parenchymal infection develops if the urinary tract abnormality, such as reflux or obstruction, persists after bacterial inoculation of the renal medulla. The infection may extend into the renal pelvis and drain into the lower urinary tract, remain undrained, or develop into a chronic The pathogenesis of renal corticomedullary abscesses accounts for the difference in the bacterial cause and
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anatomic location compared with staphylococcal renal cortical abscesses. Another contrast between the two entities is that the gram-negative bacillary corticomedullary infection frequently causes a severe parenchymal infection that may extend to and perforate the renal capsule, thus forming a perinephric abscess. Clinical Features
Corticomedullary abscesses affect men and women with approximately equal frequency except for xanthogranulomatous pyelonephritis in adults, which is more common in women than in men!, 45 There is a higher incidence in older age groups, but it can occur at any age. The typical presentation of the three described intrarenal entities (acute focal bacterial nephritis, acute multifocal bacterial nephritis, xanthogranulomatous pyelonephritis) includes fever, chills, and flank or abdominal pain. Dysuria may not necessarily be present; however, up to two thirds of patients have nausea and vomiting, thus mimicking an abdominal process. Nonspecific constitutional complaints of malaise, fatigue, and weight loss may be present in persons with a chronic process; they are especially common in patients with xanthogranulomatous pyelonephritis.22Patients may have a previous history of recurrent urinary tract infections (65‘%), renal calculi (30%),or a history of prior genitourinary instrumentation (26%).h1 Significant physical findings include a flank mass (60%)),hepatomegaly (30%), and rarely a draining flank sinus. Leukocytosis is generally present and the urinalysis is often abnormal with bacteriuria, pyuria, proteinuria, or hematuria because the intrarenal abscess drains into the urinary collecting system. The urinalysis may be normal up to 30% of the time, however. The most common pathogens recovered from urine cultures are E. coli, Klebsiella species, and Proteus mirabilis. Bacteremia is frequently present with acute focal bacterial nephritis and acute multifocal bacterial nephritis. Other laboratory abnormalities include anemia (75%), abnormal liver function tests (38% to 63%), hypoalbuminemia (6O%), and hypergammaglobulinemia (alpha-1 and alpha-2 globulin) (79%)? Up to 50% of patients with xanthogranulomatous pyelonephritis have hyperuricemia.”, 49 Diagnosis
The nonspecific clinical presentation of fever, chills, and back pain may be seen with a variety of intrarenal processes including corticomedullary abscesses, renal carbuncle, perinephric abscess, renal cyst, and renal tumor. One clinical feature that may assist in differentiating these entities is the presence of bacteremia, which is associated with corticomedullary abscesses and to a lesser degree, perinephric abscesses. In contrast, urosepsis does not usually occur in patients with cysts and tumors.4In addition, the urinalysis is abnormal in 70% of patients with a corticomedullary abscess, whereas it is usually normal in the patient with a renal cortical abscess. The diagnosis is difficult to establish from clinical and laboratory data alone. Radiographic techniques are necessary to differentiate these various intrarenal processes. Acute Focal Bacterial Nephritis (Acute Lobar Nephronia)
Ultrasonography reveals a poorly defined mass with low amplitude echoes compared with the renal cortex and disruption of the corticomedullary junction.‘“,42, 52, 5h, h7 This entity has three characteristics on CT: lobar distribution of inflammatory areas, wedge-shaped hypodense lesions on postcontrast CT,
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and mass-like hypodense lesions in more severe cases.'" The major factor that differentiates acute focal bacterial nephritis from abscess is the lack of a definable wall on visualization with either ultrasound or CT.s6 Liquefaction is generally not seen in this entity.Ih,41, hb Needle aspiration or open biopsy is usually not necessary to make the diagnosis.52, " Acute Multifocal Bacterial Nephritis
Radiographic lesions are similar to those of acute focal bacterial nephritis except that multiple renal lobes are involved.'', 20, 34, 46 Xanthogranulomatous Pyelonephritis
The radiographic presentation is varied because of the heterogeneous underlying causes of this chronic disease. The process may be diffuse or localized, and the most common urographic finding is a stone-bearing (70%), nonfunctioning (80%) kidney.27,On, 32, 4y, li2 This entity should be considered in the presence of a focal mass and staghorn calculi. CT findings include large renal calculi, nonfunctioning kidney, spherical areas of low attenuation, rim enhancement of the low attenuation areas with contrast, and thickening of Gerota's fascia.O'l,5h, 6s The diagnosis is suggested by CT in 44% of cases3"and is useful in planning the operative procedure for treatment of this entity. Ultrasound findings are less specific than the CT findings and MR imaging offers no additional information over CT scan. Treatment
In the past, surgical drainage, debridement, and sometimes nephrectomy were used for treatment of renal corticomedullary abscesses. More recent experience has indicated that, just as with renal carbuncles, treatment of acute, focal and multifocal bacterial nephritis with antimicrobial agents alone produces clinical response within 1 week in most cases with no sequelae.Ih,ls, 37, hy After clinical resolution, radiologic techniques should be used to ensure resolution of the parenchymal abnormalities. Medical therapy is successful in most cases; however, a well-established, large abscess may be more difficult to treat with antimicrobial agents alone than an abscess identified early. In most cases, an intensive trial of appropriate antibiotic therapy should be attempted before considering surgical drainage for lesions localized to the renal parenchyma. Parenteral antimicrobial agents and intravenous hydration should be administered promptly when the diagnosis is considered. Empiric antimicrobial therapy should be directed against the common bacterial organisms in this setting, including E. coli, Klebsiella, and Pvoteus specie^.^ Monotherapy can be given with an extended spectrum penicillin (mezlocillin, piperacillin), an extended spectrum cephalosporin (ceftriaxone, cefotaxime, or ceftazidime) or ciprofloxacin. If combination therapy is to be used, a beta-lactam antibiotic, such as ampicillin (1 g every 4 to 6 hours) or cefazolin (1 g every 8 hours) intravenously should be used with an aminoglycoside until culture and sensitivity results are known. There is no evidence that combination therapy is more effective than a single agent in treating acute focal or multifocal bacterial nephritis." When urine or blood culture and sensitivity results are available, antimicrobial therapy should be modified to the most appropriate agent. Duration of therapy is not specifically defined and must be determined on a case-by-case basis. Current recommendations are to continue parenteral antimicrobial therapy for at least 24 to 48 hours
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after clinical improvement of symptoms and resolution of fever. Depending on antimicrobial susceptibility results, oral antibiotic therapy can be continued for an additional 2 weeks. Acute focal bacterial nephritis typically responds to antimicrobial therapy alone, with follow-up radiographic studies showing complete resolution of the intrarenal 1esi0n.~52 Most patients with acute multifocal bacterial nephritis improve with antibiotics alone, albeit slowly, and only occasionally is a drainage procedure necessary. Factors associated with failure to respond to antimicrobial therapy alone include large abscesses, obstructive uropathy, advanced age, and urosepsis.2,Ih, 37, 6q Pediatric patients with gramnegative bacillary multifocal bacterial nephritis who have severe vesicoureteral reflux and accompanying extensive parenchymal involvement often do not respond to antimicrobial therapy alone. Percutaneous aspiration of the abscess combined with parenteral antimicrobials has been successful in those requiring drainage.'",69, 76 If obstructive uropathy is present, prompt drainage by percutaneous nephrostomy until the patient is stable and afebrile is appropriate; then the lesion can be corrected.I6If open drainage is required, incision and drainage are done when possible. Nephrectomy is reserved for patients with diffusely damaged renal parenchyma or elderly, septic patients requiring urgent intervention for survival.*Patients in the pediatric age group who present with corticomedullary abscess caused by gram-negative bacilli should be evaluated by voiding cystourethrography to rule out correctable lower urinary tract abnormalities. Patients with xanthogranulomatous pyelonephritis are generally not cured by antimicrobials alone. Surgical excision of the xanthogranulomatous process is usually necessary to cure this disease, although there have been several case reports of successful treatment with antibiotics without surgical intervention.x The diagnosis is often not made preoperatively because the entity resembles other diseases, but once the tissue is removed, the xanthogranulomatous process ceases and does not seem to recur. After excision, the prognosis in those without other urinary pathologic conditions is excellent. Although total nephrectomy is the usual procedure, Malek and Elder49have recommended partial nephrectomy for focal disease confined to the kidney (Stage I) or perinephric fat (Stage 11). A partial nephrectomy is particularly appropriate in children because this disease is usually localized in ~hildren.4~ The more common presentation in adults, however, is diffuse disease involving most of the kidney and extending to the perinephric fat (Stage 11) or beyond (Stage 111). Removal of the involved kidney and perirenal fat is preferred in these cases but may be very difficult and complicated by adjacent bowel fistulas. Although the xanthogranulomatous process does not recur after excision, bacteriuria may recur and require treatment.32,49 Infected Renal Cyst
Spontaneous infection of preexisting solitary renal cysts has been documented in several reports.13,16, 47 Patients with polycystic kidney disease may have a single or multiple cysts become infected. The most common etiologic agents are gram-negative uropathogens, which are thought to infect the cyst by way of an ascending route following bacteriuria.h Iatrogenic infection has also been reported after cyst instrumentation.lh The clinical presentation is similar to patients with other renal abscesses-hills, fever, back or flank pain, nausea or vomiting, and dysuria. Radiographic techniques can differentiate the infected cyst from other intrarenal infections. CT or ultrasonography typically show a solitary lesion characteristic of an uncomplicated simple renal cyst. Gallium scanning can identify the cyst or cysts as the source of infection. The definitive
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diagnosis is made by percutaneous cyst aspiration and culture performed under ultrasound or CT guidance. Percutaneous drainage combined with a 2-week course of antibiotics results in resolution of infection.61If urine or blood cultures reveal the bacteriologic cause, percutaneous drainage may not be necessary to make an etiologic diagnosis. Open drainage is rarely required in the therapy of a solitary infected cyst. In polycystic renal disease patients, however, treatment is more difficult and not well defined. A conservative approach has been to use a long (6 to 8 week) course of oral antibiotics directed against the most likely pathogens or those isolated from urine or blood cultures? Surgical intervention is generally avoided because of the difficulty in identifying the infected cyst and is usually a measure of last resort. PERINEPHRIC ABSCESS
Etiology
A perinephric abscess may be caused by a variety of bacterial organisms. The common causes of intrarenal abscess, E . coli, Proteus species, and S. aureus, are also the most common etiologic agents of perinephric abscesses. Other gramnegative bacilli associated with this entity are Klebsiella species, Enterobacter species, Pseudomonas species, Serratia species, and Citrobacter species. Occasionally, enterococci are implicated, and at least one case caused by Streptococcus pneumoniae has been reported.57Anaerobic bacteria, such as Clostridium species, Bacteroides species, and Actinomyces species, may cause perinephric abscesses 23, hy Fungi, particularly Candida and may account for culture-negative absce~ses.~, species, are important causes of perinephric abscesses, as is Mycobacterium tuberculosis. Perinephric abscesses are polymicrobial in cause in 25% of cases." 21,69, 7y,81 Results of urine cultures often correlate with cultures from the abscess, but in some patients, the urine culture is positive for bacteria different from those 23, 5', 6y, 79 From 20% to 40% of patients have positive isolated from the blood culture^.^, 7y
Pathogenesis A perinephric abscess is a collection of suppurative material in the perinephric space between the renal capsule and Gerota's fascia (Fig. 6). Most of perirenal abscesses result from either the rupture of an intrarenal abscess into the perinephric space, renal cortical abscess, chronic or recurrent pyelonephritis, particularly in the presence of obstruction, xanthogranulomatous pyelonephritis, or renal carbuncle.z4,5 1 , 69, 70, 79,Ro The most common mechanism for development of a gram-negative aerobic bacillary perinephric abscess is rupture of a renal corticomedullary abscess, whereas the most common mechanism for development of a staphylococcal perinephric abscess is rupture of a renal cortical abscess into the perinephric space.'*,2', 24 Other initiating events include hematogenous or regional lymphatic seeding from skin sites.", 69, Dissemination from other sites of infection include the liver, gallbladder, pancreas, pleura, prostate, or the female reproductive tract. Other inflammatory processes that may be the primary focus for spread of infection include appendicitis, diverticulitis, perforated colon, carcinoma, and osteomyelitis of adjacent ribs or vertebrae.', 25, 59,6y A subphrenic abscess, empyema, or nephrobronchial fistula may result 14, 5y, h9, Perforation into the from cephalad extension of a perinephric absces~.~,
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soul-ce of Infection ; or
Dir*ectExtension
Low Fever
V.A. pain Tenderness Pwas \ P a m
Figure 6. Pathogenesis of a perinephric abscess. (From Patterson J E , Andriole VT: Renal and perirenal abscesses. Infect Dis Clin North Am 1:918, 1987.)
peritoneal cavity or rupture into the colon is rare. The abscess is usually confined to the perinephric space, but it may extend to pararenal areas as determined by The abscess may extend into the flank or psoas the anatomy of Gerota‘s muscles and may even extend through Petit’s triangle and present as a draining flank abscess. Extension can occur caudally between diverging layers of Gerota’s fascia, and the abscess presents in the groin or paravesical area.7n Predisposing conditions for perinephric abscess are similar to those for intrarenal abscess. Most patients have underlying urinary tract abnormalities, usually obstruction. Predisposing factors include renal or ureteral calculi, neurogenic bladder, ureteral stricture, vesicoureteral reflux, bladder outlet obstruction, neoplasm, polycystic kidney disease, renal papillary necrosis, genitourinary tuberculosis, renal transplantation, trauma (renal biopsy, urinary tract instrumentation, or urologic surgery), steroid administration, and injection drug use. Patients with chronic or recurrent urinary tract infections, with or without calculi, may also be at increased risk.Z3Up to 25% of patients with perinephric abscesses are diabetic.” Clinical Features
The symptoms of a perinephric abscess develop insidiously making early recognition difficult. Patients are usually symptomatic for 2 or more weeks before presentation. Fever is the most common presenting symptom and occurs
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in virtually all patients. Unilateral flank pain is present in 70% to 80%; chills and dysuria are present in 40% of patients.z3,6y, 72,79 Other symptoms include nausea, vomiting and weight loss in 25% of the patients. The most common findings on physical examination are flank and costovertebral angle tenderness. Abdominal tenderness is present in about 60% of patients and may confuse the clinical picture. A flank or abdominal mass is present in less than 50% of patients.'" 6y, 7y Referred pain is common, and patients may complain of hip, thigh, or knee pain. Splinting, with secondary scoliosis, may be noted. The musculoskeletal examination may reveal pain on bending toward the contralatera1 side, active flexion of the ipsilateral thigh against resistance, or extension of the thigh while walking. Routine laboratory tests are nonspecific. The peripheral white blood cell count is usually elevated with a left shift. Anemia is present in 40% and azotemia in 25% of 7y Pyuria and proteinuria are common; however, the urinalysis may be normal up to one third of the time, and 40% of patients have sterile urine. Bacteremia is documented in approximately 40% of patients." 6y, 7y Diagnosis The diagnosis of perinephric abscesses can be difficult because of its insidious onset and nonspecific symptoms, physical examination, and laboratory tests. The diagnosis is made on admission in only one third of patient^.^, h9. 70, 7x Another one third of patients are diagnosed only at autopsy.69,7y A perinephric abscess should be considered in patients who have fever of unknown origin and in patients with unexplained peritonitis, pelvic abscess, or empyema that may have resulted from extension of the abscess. The key to making the diagnosis is in considering this entity in the differential and performing the appropriate radiologic examinations. The chest radiograph may show an ipsilateral pleural effusion, elevated diaphragm, or lower lobe infiltrate, or it may be completely normal.6y,7y Abnormalities on a supine abdominal radiograph may be subtle and include vertebral scoliosis, obliteration of the renal outline, an upper quadrant mass, or obliteration of the psoas shadow. An absent psoas margin must be interpreted with caution and is not necessarily diagnostic of a perinephric abscess.?,24 Ultrasonography, CT, MR imaging, and gallium67 imaging have greatly improved the ability to diagnose this disease. The ultrasound will show a sonolucent mass, often with irregular walls, and may be multiloculated with internal echoes. In one study, however, the ultrasound was falsely negative in 36% of cases when compared to CT e v a l ~ a t i o n CT . ~ ~ scan is considered the diagnostic technique of choice as it identifies the abscess and defines its extent beyond the renal capsule and the surrounding anatomy, including extension into the psoas muscle (Fig. 7A,B).72MR imaging and CT are equally efficacious in the evaluation of abdominal fluid collections, although MR imaging may be better able to define the extension of infection into adjacent organs and is advantageous for those patients who should not receive contrast agents caused by allergies or renal insuffi~iency.~~ Gallium 67 radionuclide imaging may confirm the evidence of renal or perirenal inflammation; however, it does not provide anatomical detail nor differentiate a perinephric abscess from intrarenal abscess, pyelonephritis, renal carcinoma, or ureteral obstr~ction.~, 35 Findings on excretory urography include decreased renal mobility with respiration or position, diminished to absent renal function, caliectasis or other caliceal abnormalities, and displacement of the kidney or ureter (usually medially and upward). Although extrarenal extravasation of contrast material is rare,
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Figure 7. A, CT scan through midabdomen demonstrating marked enlargement of the right psoas major muscle with a bilobed fluid-filled cavity, labeled A. B, Transverse CT scan through the level of the femoral head showing the inferior extent of the abscess (arrow) pointing below the inguinal ligament. (From Andriole VT: The clinician’sviewpoint. Clinics in Diagnostic Ultrasound 11:1, 1982. New York, Churchill Livingstone, 1982; with permission.)
it is of diagnostic importance when it occurs because this is virtually diagnostic of perirenal abscess.”, 6y Fistulas may form with pararenal structures. Although retrograde pyelography is not usually necessary, it is sometimes helpful in characterizing obstruction that occurs distal to the renal pelvis. Angiography typically shows an increase in the number and size of perforating arteries from the kidney into the abscess. Renal capsular arteries are prominent, stretched, and tortuous around the abscess, and a contrast blush is seem3,43, ?’ This appearance is distinct from the angiographic appearance of a tumor. Angiography is rarely necessary with the widespread use of CT and MR imaging. Treatment
Perinephric abscesses have been associated with high mortality rates (20% to 50%), although with early recognition, prompt drainage, and antimicrobial
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therapy, mortality has decreased.16,23, hq, 72, 7q Antimicrobial therapy alone is not adequate in contrast to most types of intrarenal abscesses, and antibiotics should be used as an adjunct to percutaneous drainage performed under CT or ultrasound guidance. Surgical drainage is undertaken when percutaneous drainage fails or is contraindicated. Acute nephrectomy is still sometimes necessary.'" hq, 72 Empiric antimicrobial therapy should be directed against the common gramnegative uropathogens and s. aureus. An aminoglycoside (gentamicin or tobramycin) and an anti-staphylococcal beta-lactam (oxacillin, nafcillin, cephalothin, cephapirin, or cefazolin) are appropriate initial antibiotics. An extended spectrum beta-lactam may be used in place of an aminoglycoside for gram-negative coverage in patients with abnormal renal function. Once culture results are obtained, therapy should be modified accordingly. If Pseudomonas aeruginosa is present, an anti-pseudomonal beta-lactam (mezlocillin, piperacillin, cefoperazone, or ceftazidime) should be added to the aminoglycoside. If enterococcus is isolated, ampicillin plus gentamicin is the treatment of choice. Isoniazid plus rifampin are indicated for M . tuberculosis infections; ethambutol or streptomycin may also be used in combination with these. Amphotericin B is necessary for abscesses caused by fungi.
SUMMARY
Our knowledge of the spectrum of renal abscesses has evolved as a result
of more sensitive radiologic techniques. The classification of intrarenal abscesses currently includes acute focal bacterial nephritis, acute multifocal bacterial nephritis, renal cortical abscess, renal corticomedullary abscess, and xanthogranulomatous pyelonephritis. The clinical presentation of these entities does not differentiate them, however, and various radiographic studies are helpful in making the diagnosis. The intrarenal abscess is usually treated successfully with antibiotic therapy alone. Antistaphylococcal therapy is indicated for the renal cortical abscess, whereas therapy directed against the common gram-negative uropathogens is indicated for most of the other entities. The perinephric abscess is often an elusive diagnosis, has a more serious prognosis, and is more difficult to treat. Drainage of the abscess and sometimes partial or complete nephrectomy, in addition to antibiotic therapy, are required for resolution. ACKNOWLEDGMENT The authors thank Brenda Smith and Susan Marino for their help in preparing the manuscript.
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6. Baker DA, Andriole V T The treatment of difficult urinary-tract infections with carbenicillin indanyl sodium. J Infect Dis 127(suppl):136,1973 7. Brook I: The role of anaerobic bacteria in perinephric and renal abscesses in children. Pediatrics 93261, 1994 8. Brown BS, Dodson M, Weintraub P S Xanthogranulomatous pyelonephritis: Report of nonsurgical management of a case and review of the literature. Clin Infect Dis 22:308, 1996 9. Caberwal D, Katz J, Reid R, et al: A case of nephrobronchial and colobronchial fistula presenting as lung abscess. J Urol 117:371, 1977 10. Caldamone AA, Frank I N Percutaneous aspiration in the treatment of renal abscess. J Urol 123:92, 1980 11. Campbell M F Perinephritic abscess. Surg Obstet Gynecol 51:674, 1930 12. Caplan LH, Siegelman SS, Bosniak MA: Angiography in inflammatory space-occupying lesions of the kidney. Radiology 88:14, 1967 13. Cho KJ, Maklad N, Curran J, et al: Angiographic and ultrasonic findings in infected simple cysts of the kidney. Am J Roentgenol 127:1015, 1976 14. Cobb OE: Carbuncle of the kidney. Br J Urol 38262, 1966 15. Colby FH, Baker MP, St Goar W T Renal carbuncle: Report of a response to modern treatment. N Engl J Med 256:1147, 1957 16. Corriere JN Jr, Sandler CM: The diagnosis and immediate therapy of acute renal and perirenal infections. Urol Clin North Am 9219, 1982 17. Costas S: Renal and perirenal emphysema. Br J Urol 44:311, 1972 18. Costas S, Ripopey JJ, van Blerk PJP: Segmental acute pyelonephritis: A precursor to renal carbuncle or abscess? Br J Urol44399,1972 19. Craven JD, Hardy 8, Stanley P, et al: Acute renal carbuncle: The importance of preoperative angiography. J Urol 111:727, 1974 20. Davidson AJ, Talner LB: Urographic and angiographic abnormalities in adult-onset acute bacterial nephritis. Radiology 106949, 1973 21. Doolittle KH, Taylor JN: Renal abscess in the differential diagnosis of mass in kidney. J Urol 80:649, 1963 22. Eastham J, Ahlering T, Skinner E Xanthogranulomatous pyelonephritis: Clinical findings and surgical considerations. Urology 43:295, 1994 23. Edelstein H, McCabe RE: Perinephric abscess: Modern diagnosis and treatment in 47 cases. Medicine 67118, 1988 24. Evans JA, Meyers MA, Bosniak MA: Acute renal and perirenal infections. Semin Roentgenol 6:274, 1971 25. Falk VS: Obstructive jaundice and perinephric abscess. Arch Surg 113:778, 1978 26. Frankel RS, Richman SD, Levenson SM, et al: Renal localization of gallium-67 citrate. Radiology 114:393, 1975 27. Gammill S, Rabinowitz JG, Peace R, et al: New thoughts concerning xanthogranulomatous pyelonephritis (X-P). AJR 125:154, 1975 28. Gardrinab NM, Lome LG, Presman D Renal abscess: Role of renal arteriography. Urology 239, 1973 29. Gelman ML, Stone LB: Renal carbuncle: Early diagnosis by retroperitoneal ultrasound. Urology 7:103, 1976 30. Goldman SM, Hartman DS, Fishman EK, et al: CT of xanthogranulomatous pyelonephritis: Radiologic-pathologic correlation. AJR 142963, 1984 31. Goldman SM, Minkin SD, Naraval DC, et al: Renal carbuncle: The use of ultrasound in its diagnosis and treatment. J Urol 118:525, 1977 32. Goodman M, Curry T, Russell T: Xanthogranulomatous pyelonephritis (XGP): A local disease with systemic manifestations. Report of 23 patients and review of the literature. Medicine 58:171, 1979 33. Graves RC, Parkins LE: Carbuncle of the kidney. J Urol 35:1, 1936 34. Hoffman EP, Mindelzun RE, Anderson RU: Computed tomography in acute pyelonephritis associated with diabetes. Radiology 135:691, 1980 35. Hopkins GB, Hall RL, Mende C W Gallium-67 scintigraphy for the diagnosis and localization of perinephric abscesses. J Urol 115:126, 1976 36. Hotchkiss RS Perinephric abscess. Am J Surg 85:471, 1953
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Address reprint requests to Vincent T. Andriole, MD Infectious Disease Section Department of Internal Medicine 201-202 Laboratory of Clinical Investigation 333 Cedar Street New Haven, CT 0652M022