You are in: eMedicine Specialties > Urology > Infections and Related Inflammatory Conditions Renal Corticomedullary AbscessArticle Last Updated: Nov 19, 2005AUTHOR AND EDITOR INFORMATIONSection 1 of 12
  Author: T Brian Willard, MD, Consulting Staff, Department of Surgery, Division of Urology, Lexington Urological Associates T Brian Willard is a member of the following medical societies: American Urological Association Coauthor(s): J Lynn Teague, MD, FACS, FAAP, Clinical Assistant Professor, Department of Surgery, Division of Urology, University of Missouri at Columbia; Keith Steinbecker, MD, Consulting Staff, Department of Urology, St John's Mercy Medical Center Editors: Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Shlomo Raz, MD, Professor, Department of Surgery, Division of Urology, University of California at Los Angeles School of Medicine; J Stuart Wolf, Jr, MD, FACS, David A Bloom Professor of Urology, Director, Division of Minimally Invasive Urology, Department of Urology, University of Michigan Medical Center; Stephen W Leslie, MD, FACS, Founder and Medical Director of the Lorain Kidney Stone Research Center, Clinical Assistant Professor, Department of Urology, Medical College of Ohio Author and Editor Disclosure Synonyms and related keywords: renal corticomedullary abscess, intrarenal abscess, acute focal bacterial nephritis, lobar nephronia, focal pyelonephritis, acute multifocal bacterial nephritis, emphysematous pyelonephritis, xanthogranulomatous pyelonephritis, XGP, kidney infections, perirenal space infections, intrarenal inflammatory processes, intra-renal inflammatory processes, diabetes mellitus, enteric gram-negative bacteria, enteric gram-negative bacilli, renal corticomedullary infections, renal inflammatory disease, recurrent urinary tract infections, renal calculi, diabetic cystopathy, vesicoureteral reflux, Proteus species, Pseudomonas species, Klebsiella species, Enterobacter species, Streptococcus faecalis, S faecalis, Staphylococcus aureus, S aureus, Proteus mirabilis, P mirabilis, Escherichia coli, E coli INTRODUCTIONSection 2 of 12
  Kidney and perirenal space infections are uncommon. However, when present, they can exact a significant degree of morbidity and mortality. Renal corticomedullary abscess is a spectrum of disease encompassing various intrarenal inflammatory processes. These processes include acute focal bacterial nephritis (eg, lobar nephronia, focal pyelonephritis), acute multifocal bacterial nephritis, emphysematous pyelonephritis, and xanthogranulomatous pyelonephritis (XGP). Renal corticomedullary abscess differs from renal cortical abscess (ie, renal carbuncle) because it develops from ascending rather than hematogenous spread of bacteria. History of the ProcedureDevelopment of a corticomedullary abscess is usually associated with an underlying urinary tract abnormality (eg, vesicoureteral reflux [VUR], urinary tract obstruction). It most commonly occurs in patients with diabetes mellitus with or without urinary tract obstruction. The following history is suggestive of the diagnosis:
ProblemRecurrent urinary tract infections Enteric gram-negative bacteria are the usual infecting organisms among all age groups. Approximately 66% of patients have a history of recurrent urinary tract infections. Bacterial pathogens causing cystitis ascend to the upper tract to infect the renal medulla. Subsequent liquefaction of the renal parenchyma and eventual involvement of the renal cortex is the postulated pathogenesis for the development of corticomedullary abscess. Scarring of the ureters and the ureteral pelvic junction also may occur, causing obstructive symptoms. Renal calculi Nephrolithiasis is present in approximately 30% of patients with corticomedullary abscess. These patients often have associated bladder infections that may result in bacterial seeding of the renal calculi. Furthermore, the presence of renal calculi may result in tubular scarring. Struvite stones (magnesium-ammonium-phosphate) are produced by urea-splitting bacteria such as Proteus, Pseudomonas, and Klebsiella species. Genitourinary instrumentation Urologic procedures such as ureteroscopy or endopyelotomy may cause ureteral trauma resulting in ureteral stricture and obstruction. Approximately two thirds of patients with corticomedullary abscess have a history of prior urinary instrumentation. Vesicoureteral reflux Normal human anatomy dictates that the ureterovesical junction (UVJ) should allow urine to enter the bladder but prevent urine from refluxing back into the kidney. Thus, the kidney is protected from contamination by infected urine. When the UVJ is incompetent, the risk of ascending urinary tract infections increases. The major cause of VUR is weak detrusor backing in combination with a short intramural tunnel. Primary causes of VUR include congenital trigonal weakness or complete ureteral duplication with refluxing lower pole moiety. Secondary causes of reflux include poorly compliant neurogenic bladder or infravesical obstruction resulting in a high-pressure bladder. Refluxing infected urine increases the risk of reflux nephropathy, hypertension, pyelonephritis, and corticomedullary abscess. Diabetes mellitus More than 50% of patients with corticomedullary abscess have diabetes mellitus. Factors that predispose patients with diabetes mellitus to intrarenal abscess include diabetic neuropathy, diabetic cystopathy, and impaired leukocyte function. Diabetes mellitus causes sensory paralytic bladder followed by motor paralytic bladder. This occurs as a result of ischemic damage to the sensory and motor fibers innervating the detrusor muscle. Initially, an areflexic bladder has a normal compliance with low intravesical pressure. However, over time, the detrusor undergoes fibrosis and becomes poorly compliant with high intravesical pressure. This high intravesical pressure is transmitted to the renal parenchyma, and reflux nephropathy results. In the setting of bacterial cystitis, reflux of infected urine may result in parenchymal infection and renal scarring. An impaired immune system may increase the incidence of recurrent urinary tract infections and abscess formation. FrequencyPyelonephritis that subsequently leads to corticomedullary abscess is rare. Incidence of these suppurative intrarenal infections ranges from 1-10 cases per 10,000 hospital admissions. Both males and females are affected, with approximately equal frequency. However, renal cortical abscesses are 3 times more common in males. XGP, by contrast, is more common in females. Prevalence of XGP is exceedingly rare and accounts for less than 1% of renal inflammatory cases. Although it can occur at any age, XGP is more common in patients who are older, typically in the fifth to seventh decades of life. EtiologyRenal corticomedullary abscess is caused by enteric gram-negative bacilli often coupled with urinary tract abnormalities. Escherichia coli is responsible for 75% of infections. Approximately 15-20% of cases are caused by Klebsiella, Proteus, Enterobacter, and Serratia species. The remaining small percentage of infections is divided among gram-positive bacteria, including Streptococcus faecalis and, less commonly, Staphylococcus aureus. PathophysiologyRenal cortical abscess results from hematogenous spread of bacteria from a primary focus of infection outside the kidney. The source is no longer apparent in up to one third of cases at the time of diagnosis. S aureus is the etiologic agent in 90% of cortical abscess cases. In contrast, renal corticomedullary abscess develops as an ascending infection by organisms already isolated within the urinary tract. Severe renal parenchymal involvement observed with corticomedullary abscess is more likely to extend to the renal capsule and perforate, thus forming a perinephric abscess. Several acute and chronic inflammatory processes are designated as renal corticomedullary infections. Acute focal bacterial nephritis Acute focal bacterial nephritis (eg, lobar nephronia, focal pyelonephritis) is a well-localized inflammation of the kidney without frank abscess formation. It is a form of bacterial interstitial nephritis that usually causes interstitial inflammation within a focal area of the kidney. Histologic characteristics include marked infiltration with polymorphonuclear leukocytes at the apex of the medulla with distortion of the glomeruli and renal tubules. In many patients, infection may represent an early phase that progresses to the more severe acute multifocal bacterial nephritis. With this entity, a heavy polymorphonuclear infiltrate is present throughout the kidney with areas of liquefaction and abscess formation. Emphysematous pyelonephritis Emphysematous pyelonephritis is an uncommon but severe necrotizing form of acute multifocal bacterial nephritis. Abdominal radiography (ie, kidneys, ureter, bladder [KUB]) exhibits characteristic intraparenchymal gas. The gas is within the renal parenchyma, not within the collecting system. The presence of gas suggests the presence of gas-forming anaerobic or facultative anaerobic pathogens. The gas is produced by bacterial fermentation of glucose in the necrotic infected tissue. Although E coli is the most common organism associated with this disease, any lactose-fermenting organism may be involved. Diabetes mellitus is the most common risk factor associated with emphysematous pyelonephritis, carrying an overall mortality rate of approximately 45%. Xanthogranulomatous pyelonephritis XGP is a chronic long-term infection of a renal unit often associated with a renal calculus. As a result of long-standing infection, the kidney enlarges and fixes itself to the retroperitoneum by perirenal fibrosis and extension of the granulomatous inflammation. Native tissue planes, such as the plane between Gerota fascia, adjacent retroperitoneal structures, and the peritoneum, are disrupted. Histologically, granulomatous tissue that contains lipid-laden macrophages (ie, foam cells) destroys and replaces the renal parenchyma. Renal calculi are usually present with XGP (75% of patients), and approximately 50% of those are staghorn calculi. Proteus mirabilis is the most common bacteria associated with XGP, but E coli is also common. A pathologic classification system stratifies the disease into the following 3 stages according to the amount of renal and perirenal involvement:
XGP is known as the great imitator because of its clinical, radiologic, and pathologic similarities to renal tumors. Association of XGP with renal cell carcinoma, transitional cell carcinoma, and squamous cell carcinoma has been described. ClinicalClinical features that are typically present in patients with corticomedullary abscess include fever, chills, and flank or abdominal pain. Dysuria and other urinary tract symptoms are variably present. Nonspecific constitutional symptoms (eg, malaise, fatigue, weight loss) may manifest in patients with a chronic process, especially those with XGP. Medical history Medical history is extremely important when evaluating patients suspected of having a renal process consistent with corticomedullary abscess. Several host factors influence the development and severity of renal infection. Most patients have a history of recurrent urinary tract infections, renal calculi, and/or prior genitourinary tract instrumentation. A history of urinary tract obstruction is an important predisposing factor. Most patients report flank or abdominal pain. Associated gastrointestinal symptoms, such as nausea and vomiting, are also common. Physical examination Signs of renal abscess vary greatly and have no specific characteristics to aid in making the diagnosis. However, begin with evaluation of vital signs and general appearance. Most patients with renal infection appear ill and in distress. They often are febrile and may demonstrate signs of hemodynamic instability. Some may be tachycardic and hypotensive, manifesting the clinical picture of sepsis. Although palpable masses are not consistent findings, they are often encountered. A flank mass is present in 70% of patients with XGP. Costovertebral angle tenderness is almost uniformly present with each type of corticomedullary infection. Basic laboratory data are variable. However, most patients demonstrate a leukocytosis with a left shift on CBC and differential. Urine and blood culture results are often positive. Urinalysis also shows signs of infection; however, bacteruria and pyuria may be absent if the ureter is completely obstructed. INDICATIONSSection 3 of 12
Indications to intervene aggressively include persistent infection unresponsive to appropriate antibiotics, impending sepsis, and ongoing hemodynamic instability. RELEVANT ANATOMYSection 4 of 12
The kidneys lie along the borders of the psoas muscle and are placed obliquely. The right kidney is lower than the left kidney because of the overlying liver. The kidneys demonstrate mobility with inspiration and expiration. Lack of mobility suggests abnormal fixation, which often occurs with either acute inflammatory processes (eg, acute pyelonephritis) or chronic fibrosing processes such as xanthogranulomatous pyelonephritis (XGP). The kidney is composed of an outer cortex, central medulla, internal calices, and pelvis. The cortex is homogenous in appearance. The medulla consists of numerous pyramids formed by converging collecting renal tubules, which drain into minor calices. The minor calices unite to form 2 or 3 major calices, which join to form the renal pelvis. Renal calices (most often at the upper and lower poles) affected by the intrarenal reflux of infected urine may result in corticomedullary abscess formation. The ureter courses from the renal pelvis to the posterolateral aspect of the bladder. Areas of relative narrowing occur at the ureteropelvic junction (UPJ), where the ureter crosses over the iliac vessels, and at the UVJ. These are sites where a ureteral calculus is likely to become obstructed. The relative incidence of ureteral obstruction is as follows: UVJ is greater than UPJ, which is greater than crossing of the iliacs. The nephron is the functioning unit of the kidney. It is composed of the glomerulus, proximal convoluted tubule, descending and ascending limbs of the loop of Henle, distal convoluted tubule, and collecting duct. The renal arteries carry approximately 20% of the entire cardiac output, and of this, approximately 90% is filtered by the glomeruli in the renal cortex. The blood supply to the kidney arises from a single renal artery and leads to multiple branching end arteries. These are without collateral circulation. Therefore, occlusion of any of these vessels produces infarction of the affected renal segment. Infarction of the entire kidney occurs if the main renal artery is occluded. Usually, one renal artery arising from the aorta enters the renal hilum. At the renal hilum, the renal artery divides into anterior and posterior segmental branches. The posterior branch supplies a large portion of the posterior segment of the kidney. The anterior branch further divides to supply the upper and lower poles and the entire anterior surface of the kidney. Segmental arteries divide into interlobar arteries that ascend between the renal pyramids. At the corticomedullary junction, interlobar arteries branch into arcuate arteries that course along the base of the pyramids, parallel to the surface of the kidney. Arcuate arteries give rise to the interlobular arteries that run into the renal cortex and divide into the afferent glomerular arterioles of the glomerulus. Filtration occurs within the glomerulus. Efferent glomerular arterioles leave the glomerulus to descend as vasa recta to supply the renal medulla. An intrarenal abscess occurs within the renal capsule. Untreated and fulminant infections can rupture through the capsule and involve the perinephric space as well as the retroperitoneum. Because the kidneys are positioned retroperitoneally, 3 areas are of considerable importance when discussing infections in this area:
Spread of infection can adversely impact these vital structures. Once infection spreads to the perinephric spaces, percutaneous or open surgical drainage is required. Identifying and treating an intrarenal abscess before capsular invasion occurs can prevent perinephric and retroperitoneal spread of infection to avoid further complications. CONTRAINDICATIONSSection 5 of 12
Contraindications regarding medical therapy deal primarily with adverse reactions to antibiotics. If a patient has a known hypersensitivity or allergy to a medication, an alternative should be used. A coagulopathy is the main contraindication to percutaneous drainage or surgical intervention. In most cases, the coagulopathy can be corrected so that the appropriate therapy can be delivered. WORKUPSection 6 of 12
Lab Studies
Imaging Studies
TREATMENTSection 7 of 12
Medical therapyTreatment of acute focal and multifocal pyelonephritis with appropriate antibiotics should produce a clinical response within 1 week of initiating therapy in most patients. However, well-established large abscesses are often difficult to treat with antibiotics alone. In most patients, attempt an intensive trial of appropriate antibiotics directed against culture-specific bacteria before attempting surgical drainage. If corticomedullary abscess is suspected, promptly administer parenteral antibiotics and intravenous hydration. Consider administering a penicillin derivative, a cephalosporin, an aminoglycoside, or a fluoroquinolone. If choosing a combination therapy, use a beta-lactam antibiotic administered intravenously with an aminoglycoside. Administer this line of therapy until culture and sensitivity results are received and then modify the antimicrobial therapy to the most appropriate agent. Drug Category: Antibiotics -- Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Duration of therapy is not well defined. Continue parenteral antibiotics for at least 24-48 hours after patient symptoms clinically improve and the fever resolves. Then, administer a suitable oral agent and continue for an additional 2-4 weeks, as determined by complete clinical and radiographic resolution of the intrarenal process. Predisposing factors for patients in whom antibiotic therapy fails include elderly age, diabetes mellitus, large abscesses, obstructive uropathy, and urosepsis. Antimicrobial therapy alone does not cure patients with xanthogranulomatous pyelonephritis (XGP). Nephrectomy is required. Surgical therapyHistorically, surgical debridement, drainage, and nephrectomy were widely used to treat corticomedullary abscesses. With the advent of effective antibiotics along with percutaneous techniques, the open surgical approach is now reserved for more severe, refractory cases. Abscess drainage Generally, large intrarenal abscesses require drainage if the patient has persistent fever and absence of clinical improvement after 1 week of appropriate antimicrobial therapy. Renal abscesses may be drained percutaneously under CT or ultrasonographic guidance. If perirenal abscess or infected urinoma is present, also place a percutaneous perirenal drain. Leave the drainage tube in place until the patient is afebrile and stable. Leave the drain in situ until the output from the drain becomes minimal. If the patient requires open surgical drainage, proceed with exploration and drainage. Irrigate the infected renal fossa copiously with antibiotic irrigant and leave perirenal drains. Reserve nephrectomy for patients with diffusely damaged renal parenchyma or patients who are septic and require urgent intervention for survival. Nephrectomy is often required for patients with symptomatic XGP. Following nephrectomy, prognosis is excellent in patients without other urinary tract pathology. Nephrectomy Simple nephrectomy often suffices. Partial nephrectomy may be possible in patients with focal disease confined to the kidney (stage I) or perinephric fat (stage II); however, the more common presentation is diffuse disease involving most of the kidney and extending to the perirenal fat (stage II) and beyond (stage III). The xanthogranulomatous process does not recur after excision. Preoperative detailsConduct a thorough workup that involves screening for risk factors that predispose patients to intrarenal abscess. Perform preoperative imaging to define the extent of the parenchymal process. Contrast CT scanning is the standard imaging and allows greatest definition of patient anatomy, degree of abscess extension, and associated conditions (eg, obstructive uropathy). Moreover, if surgical intervention is necessary, CT imaging helps the surgeon dictate the surgical approach. Intraoperative detailsEither supine or flank positions may be used. Usually, the flank position is preferred because of ease of establishing a drainage tract and avoiding possible peritoneal exposure to infected material. If possible, remain extraperitoneal. Postoperative detailsAdminister postoperative antibiotic therapy parenterally following surgery and then convert to oral administration when patient is eating. Antibiotic therapy is generally continued for at least 2 weeks. Discharge patients under the following conditions:
Follow-up
For excellent patient education resources, visit eMedicine's Infections Center and Kidneys and Urinary System Center. Also, see eMedicine's patient education articles Urinary Tract Infections and Antibiotics. COMPLICATIONSSection 8 of 12
The most feared complication of corticomedullary abscess is potential extension of the abscess through the renal capsule, resulting in a perinephric abscess. Gerota fascia usually contains the abscess within the perinephric space, but the process may extend into the retroperitoneum to infect adjacent structures. In these situations, simple nephrectomy is quite challenging because adjacent organs, such as the pancreas and bowel, may be involved. OUTCOME AND PROGNOSISSection 9 of 12
Acute focal bacterial nephritis usually responds to antimicrobial therapy alone. Follow-up radiographic studies typically show complete resolution of the intrarenal lesion. Conversely, patients with acute multifocal bacterial nephritis take longer to improve with antibiotics alone. Occasionally, patients may require some form of a drainage procedure. In most situations, patients with large abscesses or xanthogranulomatous disease who require open surgical procedure fully recover, albeit with a higher degree of morbidity. Prognosis improves with early recognition of symptoms and early aggressive therapy. Poor prognosis factors include patients who are elderly and patients with urosepsis, anatomic abnormalities, advanced disease, and impaired renal function at presentation. FUTURE AND CONTROVERSIESSection 10 of 12
MULTIMEDIASection 11 of 12
REFERENCESSection 12 of 12
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