Renal Corticomedullary Abscess 

Updated: Aug 18, 2021
Author: Aaron Benson, MD; Chief Editor: Edward David Kim, MD, FACS 

Overview

Practice Essentials

Renal corticomedullary abscess is a term used to describe a spectrum of diseases that encompass various intrarenal infectious processes, such as acute focal bacterial nephritis (eg, lobar nephronia, focal pyelonephritis), acute multifocal bacterial nephritis, emphysematous pyelonephritis, and xanthogranulomatous pyelonephritis (XGP). Renal corticomedullary abscess is caused by ascending spread of bacteria; in contrast, renal cortical abscess (ie, renal carbuncle) is caused by hematogenous spread of bacteria.

The most common predisposing risk factors for renal abscesses in adults are diabetes mellitus, nephrolithiasis, and ureteral obstruction. In the pediatric population, urological abnormality (vesicoureteral reflux [VUR], ureteropelvic junction obstruction, and calyceal diverticulum) and urolithiasis are the most important predisposing risk factors.[1]

Although kidney and perirenal space infections are uncommon, they can exact significant morbidity and carry a risk of mortality, especially if diagnosis is delayed. However, the diagnosis is not easy to make without imaging studies. The clinical presentation of renal abscess may be nonspecific, and can include fever, nausea/vomiting, flank pain, and abdominal pain. Laboratory findings include elevated erythrocyte sedimentation rate, leukocytosis, and positive blood/urine cultures.

CT shows specific findings in cases of renal abscess and it remains the best choice for diagnosis. In addition, CT has the advantage of providing a distinction between renal and perirenal abscesses.[1] See Workup.

In most patients with suspected corticomedullary abscess, a prompt attempt at treatment with intravenous antibiotics directed against culture-specific bacteria in addition to intravenous fluid resuscitation may be used. See Treatment and Medication.

For patient education information, see Urinary Tract Infections and Antibiotics, as well as the Infections Center.

Pathophysiology

Renal cortical abscess results from hematogenous spread of bacteria from a primary extrarenal focus of infection. The source is not apparent in up to one third of cases at the time of diagnosis. Staphylococcus aureus is the etiologic agent in 90% of cortical abscess cases. In contrast, renal corticomedullary abscess develops as an ascending infection by organisms in the urine. Severe renal parenchymal involvement in combination with corticomedullary abscess is more likely to extend to the renal capsule and perforate, thus forming a perinephric abscess. Renal corticomedullary infections include the acute and chronic infectious processes of the kidney described below.

Acute focal bacterial nephritis

Acute focal bacterial nephritis (eg, lobar nephronia, focal pyelonephritis) is a well-localized renal infection without frank abscess formation. This form of bacterial interstitial nephritis 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, acute focal bacterial nephritis represents an early phase that eventually progresses to the more severe acute multifocal bacterial nephritis. In these more severe cases, a heavy polymorphonuclear infiltrate is present throughout the kidney, with areas of liquefaction and abscess formation.

In children with acute focal bacterial nephritis, which is commonly caused by infection with Escherichia coli[2, 3] or Klebsiella pneumoniae, a 3-week course of appropriate antibiotic therapy is recommended.[4, 5] This treatment duration precludes failure or relapse and, thereby, subsequent complications such as renal abscess.

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, which is located within the renal parenchyma rather than the collecting system, suggests infection with 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. Emphysematous pyelonephritis carries an overall mortality rate of approximately 45%.[6]

Xanthogranulomatous pyelonephritis

Xanthogranulomatous pyelonephritis (XGP) is a chronic destructive granulomatous inflammation that is characterized by urinary tract obstruction, urinary calculi, and invasion of the renal parenchyma.[7]   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 contains lipid-laden macrophages (ie, foam cells) and replaces the renal parenchyma.

XGP can be found in 2 forms: the diffuse form comprises 85% of cases and the focal (localized, segmental) comprises the remaining 15%.[8]  

Most persons (75%) with XGP have accompanying renal calculi, and approximately 34% of those are staghorn calculi.[8] Proteus mirabilis is the most common bacteria associated with XGP, but E coli is also common. A pathologic classification system based on the amount of renal and perirenal involvement stratifies XGP into the following 3 stages[9] :

  • Stage I XGP (nephritic) - Characteristic xanthogranulomatous infection in the kidney
  • Stage II XGP (perinephric involvement) - Involvement of renal parenchyma and Gerota fascia
  • Stage III XGP (paranephric) - Widespread extension into the retroperitoneum

XGP has clinical, radiologic, and pathologic similarities to renal tumors. XGP is occasionally associated with renal cell carcinoma,[10]  transitional cell carcinoma, and squamous cell carcinoma.

Relevant anatomy

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 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 ureterovesical junction (UVJ). These are sites where a ureteral calculus is likely to become obstructed. Of these 3 locations, ureteral obstruction is most likely to occur at the UVJ, followed by the UPJ and the crossing of the iliac vessels.

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. Occlusion of the main renal artery leads to infarction of the entire kidney.

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.

Intrarenal abscesses develop within the renal capsule. Untreated and fulminant infections can rupture through the capsule and can involve the perinephric space and retroperitoneum. Because the kidneys are positioned retroperitoneally, 3 areas are of considerable importance when discussing infections in this area:

  • Anterior perirenal space - Contains portions of the pancreas, bowel, and colon
  • Perinephric space - Contains Gerota fascia and the adrenals
  • Intrarenal space - Contains renal parenchymal tissue

Spread of infection can adversely affect 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.

Etiology

Renal corticomedullary abscess is caused by infection with enteric gram-negative bacilli, often coupled with urinary tract abnormalities. E coli is responsible for 75% of these infections. Approximately 15-20% of cases are caused by Klebsiella, Proteus, Enterobacter, and Serratia species. The few remaining cases of renal corticomedullary abscess are caused by gram-positive bacteria, including Streptococcus faecalis and, less commonly, S aureus.

Renal corticomedullary abscesses are usually associated with an underlying urinary tract abnormality (eg, vesicoureteral reflux [VUR], urinary tract obstruction). Renal corticomedullary abscesses most commonly occur in individuals with diabetes mellitus with or without urinary tract obstruction.[11]  Several risk factors, described below, may contribute to upper urinary tract infections and possible subsequent renal corticomedullary abscess.

Recurrent urinary tract infections

Enteric gram-negative bacteria are the usual infecting organisms among all age groups. Approximately 66% of patients with renal corticomedullary abscess have a history of recurrent urinary tract infections. Bacterial pathogens causing cystitis ascend to the upper tract and 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.

Renal calculi

Approximately 30% of patients with corticomedullary abscess have nephrolithiasis.[12]  These patients often have associated urinary tract infections that may result in bacterial seeding of the renal calculi. Longer-standing infections with urea-splitting bacteria (eg, Proteus, Pseudomonas, and Klebsiella species) may lead to the formation of struvite stones (magnesium-ammonium-phosphate). In the presence of an infection nidus such as a renal calculus, the urinary environment may facilitate an ascending infection.

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 UVJ should allow urine to enter the bladder but prevent urine from refluxing back into the kidney. This protects the kidney 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 to intrarenal abscess among patients with diabetes mellitus include diabetic neuropathy, diabetic cystopathy, and impaired leukocyte function.

Splenectomy

Splenectomy is associated with renal and perinephric abscesses, particularly comorbid with diabetes mellitus.  A population-based retrospective cohort study of 16,426 patients who underwent splenectomy found the overall incidence rate of renal and perinephric abscesses was 2.14-fold greater in the splenectomy group compared to a sex-matched, age-matched, and comorbidity-matched, randomly selected nonsplenectomy group. In further analysis, the adjusted hazard ratio (HR) markedly increased from 2.24 to 7.69 for those comorbid with splenectomy and diabetes mellitus (95% confidence index 3.31–17.9).[13]

Epidemiology

The incidence of renal corticomedullary abscess ranges from 1-10 cases per 10,000 hospital admissions. Pyelonephritis that leads to corticomedullary abscess is rare. Although approximately 75% of renal cortical abscesses occur in males, renal corticomedullary abscess is equally common in males and females. However, renal corticomedullary abscess is rare in the absence of risk factors; thus, the likelihood of infection may be influenced by predisposing factors.

Prognosis

Renal corticomedullary abscess carries a mortality rate of 1.5-15%. Prognosis improves with early recognition of symptoms and early aggressive therapy. Factors associated with poor prognosis include the following:

  • Advanced age
  • Urosepsis
  • Anatomic abnormalities
  • Advanced disease
  • Impaired renal function at presentation

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 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.

When treated with antibiotics alone, emphysematous pyelonephritis (EPN) has a mortality rate as high as 80%.[6]

 

Presentation

History

Common signs and symptoms in patients with renal corticomedullary abscess include fever, chills, nausea/vomiting, and flank or abdominal pain. Some individuals with renal corticomedullary abscess develop dysuria and other urinary tract symptoms.

Nonspecific constitutional symptoms (eg, malaise, fatigue, weight loss) may occur in patients with xanthogranulomatous pyelonephritis (XGP). Besides abscess formation, other rare complications have included reno-cutaneous fistula, reno-colonic fistula, and reno-bronchial fistula.[7]

Obtaining a thorough medical history is important in evaluating patients with a possible renal corticomedullary abscess. Patients with this infection frequently have long-standing (approximately 14 d) symptoms such as fever, back pain, and/or abdominal discomfort. Unfortunately, these symptoms may be vague and do not always reflect the severity of the infection. In addition, various host factors influence the development and severity of renal infection (see Overview/Etiology). Most patients with renal corticomedullary abscess have a history of recurrent urinary tract infections, renal calculi, and/or prior genitourinary tract instrumentation. Urinary tract obstruction is an important predisposing factor.

Physical Examination

Signs that accompany renal corticomedullary abscess vary greatly and are nonspecific. However, the physical examination findings usually indicate significant infection, including ill appearance, fever, and hemodynamic instability. In patients with accompanying sepsis, the hemodynamic and overall instability may be more pronounced, with tachycardia, hypotension, and tachypnea. In addition, many patients with renal corticomedullary abscess have palpable masses. Costovertebral angle tenderness is almost uniformly present with each type of corticomedullary infection.

 

DDx

Diagnostic Considerations

Diagnosis of acute focal bacterial nephritis (AFBN) is often delayed because of the similarity in presentation to acute pyelonephritis (APN).  AFBN can be differentiated by its higher and more persistent fever, peri-umblical pain, pain in the right or left quadrant and the presence of Murphy's sign during an abdominal examination.[14]

Differential Diagnoses

 

Workup

Approach Considerations

Laboratory test results are not specific for the diagnosis of renal abscess. Renal ultrasonography and computed tomography (CT) are the fundamental tests for diagnosing corticomedullary abscesses. CT scanning is the study of choice in evaluating intrarenal abscesses. Ultrasonographic findings are less specific than findings on CT scanning. Magnetic resonance imaging (MRI) usually offers no additional information beyond that yielded by CT scanning.

Laboratory Studies

Complete blood count with differential and basic metabolic panel

Elevated peripheral leukocytosis with a left shift is a common finding in patients with renal corticomedullary abscess. Anemia may be present in patients with xanthogranulomatous pyelonephritis (XGP).

Blood urea nitrogen (BUN) and creatinine levels are often elevated, usually secondary to prerenal azotemia. Hypovolemic states are caused by vomiting with gastrointestinal fluid loss or decreased renal perfusion, which is observed in patients with sepsis. Patients who develop acute kidney injury, as demonstrated by rising BUN and creatinine levels, show altered renal resorptive capabilities.

Calculate the fractional excretion of sodium (FENa) and measure urinary electrolyte levels to aid in diagnosis. The following formula is used to calculate the FENa:  FENa (%) = (urinary sodium × plasma creatinine)/(plasma sodium × urine creatinine) × 100.

The calculated FENa is less than 1% in prerenal azotemia. If the FENa is greater than 1%, acute tubular necrosis is more likely. 

Urinalysis and urine culture

Pyuria and proteinuria are common features of renal corticomedullary abscess. However, bacteria and pyuria may be absent if the ureter and/or collecting system is completely obstructed.

Although urine culture results are often positive, cultures may fail to grow a causative organism. In emphysematous pyelonephritis and XGP, approximately 75% of urine cultures are positive. The most common pathogens recovered are Escherichia coli, Proteus mirabilis, and Klebsiella species.

Blood cultures

Blood cultures are positive in more than 50% of patients with renal corticomedullary abscess and are particularly useful in patients with urosepsis. The organisms isolated are usually the same gram-negative microbes isolated from the urine.

Imaging Studies

Radiography 

This modality is often unhelpful in identifying intrarenal abscess; however, it may show radiopaque stones in patients with emphysematous pyelonephritis who have calculus-induced obstruction or intraparenchymal gas.

Intravenous pyelography

Intravenous pyelography (IVP) provides only limited characterization of acute renal parenchymal infections. Although IVP is inexpensive and can provide functional assessment of the kidneys, the risks associated with patient exposure to intravenous contrast and radiation outweigh the benefits, as this study offers low sensitivity in the detection of renal abscesses.

Ultrasonography

Ultrasonography is a readily accessible, rapid, and relatively inexpensive initial screening tool that reveals renal lesions and anatomic abnormalities. The disadvantages of ultrasonography include the following:

  • Operator dependence
  • Limited imaging capability in patients with a large body habitus
  • Lower sensitivity than CT
  • Inability to assess renal function

Ultrasonographic findings that suggest renal abscess include an ill-defined renal mass (either hyperechoic or hypoechoic) with low-amplitude internal echoes and disruption of the corticomedullary junction, possible posterior acoustic enhancement, and lack of vascularity on Doppler imaging (to distinguish a complex abscess from malignancy).

CT scanning

This is the most useful modality in diagnosing intrarenal abscess and planning operative procedures for treatment. Noncontrast CT scans may demonstrate renal enlargement, inflammatory changes, and variable attenuation, but poorly demonstrate intrarenal abscesses. When renal abscess is suspected, obtain both contrast and noncontrast images for comparison.

Contrasted CT scan that demonstrates a corticomedu Contrasted CT scan that demonstrates a corticomedullary abscess in a 27-year-old patient with diabetes mellitus who has a history of multiple urinary tract infections. Note the heterogeneous hypodense lesion in the right kidney. Extracapsular extension is not present.

CT scanning is extremely useful to characterize renal infections as diffuse or focal, to detect the presence of gas, and to help the clinician evaluate for perinephric extension. Disadvantages of CT scanning include high cost, radiation exposure, and the use of iodinated contrast.

Findings suggestive of renal abscess include a poorly defined, wedge-shaped, hypodense area that may involve liquefaction and focal renal involvement. The characteristic appearance consists of a low-attenuation (0-20 Hounsfield units), distinctly marginated, parenchymal lesion that fails to enhance after contrast administration. Other features may include perirenal fluid and inflammatory stranding with thickening of Gerota fascia.

MRI

MRI is highly sensitive in demonstrating renal abnormalities that may contribute to renal corticomedullary abscess but does not offer information in addition to that obtained with CT scanning. Advantages of MRI include no ionizing radiation or iodinated contrast exposure. Disadvantages of MRI include high cost, low availability, longer imaging times, motion artifacts, and a lower sensitivity for renal calculi than CT scanning.

Other Tests

Lipid-containing foam cells (xanthoma cells) observed on a renal biopsy specimen establishes a definite diagnosis of XGP.[8, 7]

 

Treatment

Medical Care

In most patients with acute focal or multifocal pyelonephritis, treatment with appropriate antibiotics should produce a clinical response within 1 week of initiating therapy. However, well-established large abscesses are often difficult to treat with antibiotics alone, with most studies limiting treatment of renal abscesses with antibiotics alone to lesions smaller than 3 cm.

In most patients with suspected corticomedullary abscess, a prompt attempt at treatment with intravenous antibiotics directed against culture-specific bacteria in addition to intravenous fluid resuscitation may be used. Medical treatment alone should be limited to hemodynamically stable patients with small (< 3 cm) corticomedullary abscesses. Patients with signs of hemodynamic instability due to sepsis or with large renal abscesses (≥3 cm) should undergo percutaneous or surgical drainage for abscess management (see Surgical Care). Moreover, medical therapy alone in the treatment of perinephric abscesses is inappropriate, as the risk of mortality associated with perinephric abscess treated with antibiotics alone is upward of 33%.

Comploj et al treated 6 pediatric patients conservatively with broad-spectrum antibiotics. None of the abscesses were treated surgically or percutaneously drained. In all 6 cases, the abscess was successfully resolved.[15]

A penicillin derivative, a cephalosporin, an aminoglycoside, or a fluoroquinolone, administered intravenously, is the appropriate initial antibiotic. For combination therapy, a beta-lactam antibiotic plus an aminoglycoside should be administered intravenously. Administer this line of therapy until culture and sensitivity results are received and then modify the regimen to the most appropriate agent.

The duration of therapy is not well defined. Continue parenteral antibiotics for at least 24-48 hours after symptoms have improved and the fever resolves. Then, switch to a suitable oral antibiotic and continue treatment for an additional 2-4 weeks, until complete clinical and radiographic resolution of the intrarenal process has occurred.

Factors that may contribute to medical treatment failure include elderly age, diabetes mellitus, large abscesses, obstructive uropathy, and urosepsis.

Antimicrobial therapy alone is not indicated for patients with xanthogranulomatous pyelonephritis (XGP). Nephrectomy is required.

Surgical Care

Surgical debridement, drainage, and nephrectomy were once widely used to treat corticomedullary abscesses. However, since the advent of effective antibiotics along with percutaneous techniques, the open surgical approach is now reserved for more severe, refractory cases. Indications to intervene aggressively include persistent infection unresponsive to appropriate antibiotics, impending sepsis, and ongoing hemodynamic instability.

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.

Abscess drainage

In general, large intrarenal abscesses require drainage if the patient has persistent fever and no clinical improvement after 1 week of appropriate antimicrobial therapy. Percutaneous drainage plus parenteral antibiotics is indicated as the initial treatment for abscesses 3-5 cm in size. Renal abscesses may be drained percutaneously under CT or ultrasonographic guidance.

In cases that involve perirenal abscess or infected urinoma, also place a percutaneous perirenal drain. Drainage via the percutaneously placed tube should continue at least until the patient is afebrile and stable, and then until drain output is minimal.

Surgical therapy

If surgical intervention is indicated, the abscess should be explored and drained. Copious irrigation of the infected renal fossa with an antibiotic irrigant along with placement of perirenal drains should follow. Reserve nephrectomy for patients with diffusely damaged renal parenchyma or patients who are septic and require urgent intervention for survival.

Nephrectomy

Simple nephrectomy is usually adequate.

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).

Nephrectomy is often required for patients with symptomatic XGP. Following nephrectomy, the prognosis is excellent in patients without other urinary tract pathology. The xanthogranulomatous process does not recur after excision.

Preoperative details

A thorough workup that involves screening for risk factors that predispose to intrarenal abscess is necessary. This workup should include preoperative imaging to define the extent of the parenchymal process (see Imaging Studies). Contrast CT scanning is the standard imaging modality and allows greatest definition of the patient’s anatomy, degree of abscess extension, and associated conditions (eg, obstructive uropathy). Moreover, if surgical intervention is necessary, CT imaging can be used to help determine the optimal surgical approach.

Intraoperative details

Either supine or flank positions may be used. Usually, the flank position is preferred because of ease of establishing a drainage tract and prevention of possible peritoneal exposure to infected material.

Postoperative details

Postoperative parenteral antibiotic therapy should continue following surgery, with subsequent conversion to oral administration when the patient is able to tolerate a diet. Antibiotic therapy is generally continued for at least 2 weeks.

Discharge patients under the following conditions:

  • Tolerating diet
  • Ambulating
  • Afebrile
  • Adequate pain control on oral analgesics

Inform the patient that normal activities can resume in 4-6 weeks.

Follow-up

Patient should return to the clinic in 1-2 weeks for follow-up examination, which includes the following:

  • Checking the wound for signs of surgical-site infection
  • Removal of staples or sutures
  • Contrast CT scan to ensure resolution of renal parenchymal abnormalities

Complications

The most feared complication of corticomedullary abscess is 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 challenging because adjacent organs, such as the pancreas and bowel, may be involved.

 

Medication

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications. Initial empirical choices for intravenous antibiotic therapy include a penicillin derivative, a cephalosporin, an aminoglycoside, or a fluoroquinolone; for combination therapy, a beta-lactam antibiotic plus an aminoglycoside can be given.

Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Piperacillin and tazobactam sodium (Zosyn)

Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during active multiplication stage.

Ticarcillin and clavulanate (Timentin)

Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active growth. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive organisms, most gram-negative organisms, and most anaerobes.

Nafcillin (Nafcil, Nallpen, Unipen)

Initial therapy for suspected penicillin G–resistant streptococcal or staphylococcal infections.

Use parenteral therapy initially in severe infections. Change to PO therapy as condition warrants.

Because of thrombophlebitis, particularly in the elderly, administer parenterally only for short term (1-2 d); change to PO route as clinically indicated.

Ceftazidime (Fortaz)

Third-generation cephalosporin with broad-spectrum, gram-negative activity, including Pseudomonas species; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibit the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis. The condition of the patient, severity of the infection, and susceptibility of the microorganism should determine the proper dose and route of administration.

Cefepime (Maxipime)

Fourth-generation cephalosporin. Gram-negative coverage comparable to that of ceftazidime but has better gram-positive coverage (comparable to ceftriaxone). Cefepime is a zwitter ion; rapidly penetrates gram-negative cells. Best beta-lactam drug for IM administration. Poor capacity to cross blood-brain barrier precludes use for treatment of meningitis.

Ciprofloxacin (Cipro)

Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.

Levofloxacin (Levaquin)

For pseudomonal infections and infections due to multidrug-resistant gram-negative organisms.

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage bacteria, including Pseudomonas species. Synergistic drug with beta-lactamase against enterococci. Interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.

Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as body space into which agent needs to distribute. Dose of gentamicin may be given IV/IM. Each regimen must be followed by at least trough level drawn on third or fourth dose, 0.5 h before dosing; may draw peak level 0.5 h after 30-min infusion.

Amikacin (Amikin)

Irreversibly binds to 30S subunit of bacterial ribosomes; blocks recognition step in protein synthesis; causes growth inhibition. For gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against Pseudomonas aeruginosa.

Use patient's IBW for dosage calculation. The same principles of drug monitoring for gentamicin apply to amikacin.

Tobramycin (Nebcin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes.