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INTRARENAL AND PERINEPHRIC ABSCESSES


INTRARENAL AND PERINEPHRIC ABSCESSES
Kidney abscesses can be located either within the renal parenchyma (intrarenal abscess) or between the renal capsule and renal fascia (perinephric abscess). Intrarenal abscesses may be present in the cortex or medulla. Perinephric abscesses are generally confined to the renal fascia but may extend into the retroperitoneum.


PATHOPHYSIOLOGY
The most common cause of both intrarenal and perinephric abscesses is ascending pyelonephritis in the presence of a urinary tract obstruction. The flushing effect of urine plays an important role in the clearance of bacteria. Hence, an obstruction to the flow of urine with subsequent urinary stasis produces a milieu favorable to infection. In addition, the forniceal rupture that can occur secondary to obstruction can release infected urine into the perinephric space. These infections typically involve gram negative pathogens (such as E. coli, Klebsiella, Pseudomonas), although polymicrobial infections are also seen and may involve fungal organisms such as Candida spp.
A smaller number of abscesses result from hematogenous seeding of the renal parenchyma in the setting of systemic bacteremia. In these cases, the abscesses are typically intrarenal rather than perinephric. In addition, gram positive organisms (e.g., Staphylococcus aureus) are usually responsible.
In both ascending and hematogenous infection, there is tissue necrosis and subsequent sequestration of the phlegmon into an abscess.

INTRARENAL AND PERINEPHRIC ABSCESSES

PRESENTATION AND DIAGNOSIS
Patients with an intrarenal or perinephric abscess typically have signs and symptoms of acute pyelonephritis (see Plate 5-5) but fail to improve after several days of appropriate antimicrobial therapy (e.g., persistent fever, persistently positive cultures, and no resolution in elevated white blood cell count). In some cases, physical examination may reveal a palpable mass or overlying inflammatory skin changes.
When an abscess is suspected, the basic tests for evaluation of upper UTI should and often already have been performed, including urine and blood cultures. In patients with hematogenously seeded abscesses, a urine culture may reveal organisms not usually found in the urinary tract, such as gram-positive organisms, and the same organism may be identified on a blood culture.
Once an abscess is suspected, abdominal images should be obtained. Computed tomography (CT) is the study of choice, and renal abscesses have the same characteristics as abscesses located elsewhere. The pus- filled central portions are lucent and do not enhance, while the inflamed walls are thicker than those of cysts, have indistinct borders, and do enhance. Ultrasonography may reveal fluid-containing, masslike structures with flow in the walls seen on Doppler imaging.

TREATMENT
Empiric intravenous antibiotic treatment should include broad-spectrum agents that can penetrate walled-off infections. Options include piperacillintazobactam, cefepime, and carbapenems. These agents will target gram-negative and most susceptible gram positive pathogens that can cause an abscess, with the exception of resistant organisms such as methicillin-resistance Staphylococcus aureus or vancomycin-resistant Enterococcus. The choice of antimicrobial agent can be refined once blood or urine culture results are obtained. Percutaneous or surgical drainage should be performed for abscesses that are more than 3 to 5 cm in diameter. Gram stain and culture of the aspirate may facilitate identification of the causative pathogen and its susceptibilities. Percutaneous drainage, which can be performed under CT or ultrasound guidance, carries less risk than an open surgical procedure. In the case of a large abscess that cannot be drained with a single aspiration, an indwelling catheter is appropriate. The combination of percutaneous drainage and appropriate antibiotic treatment has been shown to clear more than 90% of infections. When this approach fails, open drainage may become necessary.
The duration of antibiotic therapy depends on the size of the abscess and the extent of drainage. Generally, it is continued for 2 to 3 weeks following successful drainage. The response to antibiotics can be slow, and the patient should be monitored closely for improvement in symptoms and laboratory markers of inflammation, such as leukocyte count, C-reactive protein, and erythrocyte sedimentation rate. Follow-up imaging is recommended after treatment to document resolution, especially in patients with diabetes or other causes of immune compromise.