Renal and Retroperitoneal Abscesses
January 6, 2009 1 Comment
Renal and retroperitoneal abscesses are uncommon clinical entities that often pose a significant diagnostic challenge. Nonspecific signs and symptoms frequently lead to a delay in diagnosis and treatment. Consequently, they are associated with significant morbidity, and mortality rates approaching 50% have been reported. An understanding of the anatomy of the retroperitoneal space is essential for classification, diagnosis, and management of renal and retroperitoneal abscesses.
The retroperitoneal space is bounded by the posterior parietal peritoneum and transversalis fascia. . It is divided into the perirenal space and the pararenal space.
The perirenal space surrounds the kidney and is bounded by the renal (Gerota’s) fascia. It contains a lemon-yellow layer of fat, which is thickest posteriorly and laterally. The anterior and posterior leaves of the renal fascia fuse above the adrenal gland, becoming continuous with the diaphragmatic fascia.1 A thinner, more variable layer meets between the adrenal gland and the kidney. Laterally, the fascial layers join to form the lateroconal fascia, which becomes continuous with the posterior parietal peritoneum. Medially, the posterior layer fuses with the psoas muscle fascia, and the anterior layer fuses with the connective tissue surrounding the great vessels and organs of the anterior retroperitoneum (i.e., the pancreas, duodenum, and colon). Because the perirenal space rarely crosses the midline, perirenal abscesses usually remain unilateral.16 Inferiorly, the renal fascial layers do not fuse but, rather, become continuous with the psoas and ureteral coverings.1,11 This opening inferiorly allows spread of perirenal infections to the pararenal space, to the pelvis, to the psoas muscle, and, in some cases, to the contralateral retroperitoneum.
The pararenal space is divided into two compartments: the anterior compartment, which is bounded by the posterior parietal peritoneum and the anterior renal fascia; and the posterior compartment, which is bounded by the posterior renal fascia and transversalis fascia. The pararenal space contains pale adipose tissue, which fills much of the retroperitoneal space. Because the anterior pararenal space extends across the midline, infection arising in one space may become bilateral. The posterior pararenal space does not cross the midline, and infection within it remains unilateral.16
The retrofascial compartment lies posterior to the transversalis fascia. It is important only in development of the rare retrofascial abscess from abscesses of the psoas, iliacus, and quadratus muscles.
Before the advent of antimicrobial therapy, most renal abscesses occurred as a result of hematogenous spread of gram-positive organisms, usually Staphylococcus aureus. These abscesses, which were called renal carbuncles, may still be seen in intravenous drug users and in patients with dermatologic disorders. They may resolve with aggressive antimicrobial therapy if treated before frank suppuration. Presently, most renal and retroperitoneal abscesses are caused by retrograde ascent of gram-negative bacteria from the bladder. The most common organisms include Escherichia coli, Proteus, Klebsiella, and Pseudomonas. Anaerobes may be isolated in abscesses associated with gastrointestinal and respiratory infections. Abscesses caused by opportunistic organisms such as Candida and Aspergillus may occur in immunosuppressed patients. Other uncommon pathogens include Mycobacterium tuberculosis and Echinococcus (see below).
A renal abscess is generally preceded by pyelonephritis, which progresses to abscess formation in the presence of a virulent uropathogen, a damaged or obstructed urinary tract, or a compromised host. Renal abscesses have a predilection for the cortical medullary region and may drain spontaneously through the renal collecting system. When renal infection is complicated by obstruction, a purulent exudate collects in the renal collecting system. Pyonephrosis refers to infected hydronephrosis with suppurative destruction of the parenchyma of the kidney, with total or near total loss of renal function. The most frequent cause of obstruction is calculous disease. A previous history of urinary tract infection or surgery is also common.
Perirenal abscesses usually occur by erosion of abscesses or pyonephrosis into the perirenal space. Because of gravity, the resulting perirenal suppuration tends to localize dorsolaterally to the lower pole of the kidney. Posterior pararenal abscesses may arise from perirenal abscesses or from anterior pararenal abscesses tracking into the pelvis, where the anterior and posterior pararenal spaces communicate. Occasionally they result from hematogenous spread. Anterior pararenal abscesses are rarely urologic in origin. They arise from infection involving the organs within the anterior pararenal space, namely the ascending and descending colon, appendix, duodenal loop, and the pancreas. Abscesses arising from the gastrointestinal tract usually harbor a mixture of microorganisms, of which E. coli is the most prevalent. Extension of anterior pararenal abscesses into the perirenal space is uncommon.
The diagnosis of renal and retroperitoneal abscesses requires a high index of suspicion, as they typically present with insidious, nonspecific signs and symptoms. Presenting symptoms may include fever, chills, abdominal or flank pain, irritative voiding symptoms, nausea, vomiting, lethargy, or weight loss. Symptoms have been present for more than 5 days in the majority of patients with renal and retroperitoneal abscesses, compared with 10% of patients with pyelonephritis. Over one-third of patients may be afebrile. The majority of patients diagnosed with renal and retroperitoneal abscesses have underlying, predisposing medical conditions. These include diabetes mellitus, urinary tract calculi, previous urologic surgery, urinary tract obstruction, polycystic kidney disease, and immunosuppression.
A palpable flank or abdominal mass is present in about half of the cases. The mass may be better appreciated by examination of the patient in the knee–chest position. There may also be signs of psoas muscle irritation with flexion of the thigh.
Laboratory tests are helpful but nondiagnostic. Leukocytosis, elevated serum creatinine, and pyuria are common. Blood and urine cultures are frequently negative; when positive, they usually correlate with culture results from the abscess.
Excretory urography may aid in the diagnosis of renal or retroperitoneal abscesses by showing diminished mobility on inspiratory–expiratory films. A renal abscess causes a decrease in function and enlargement of the nephrogram during the acute phase. Retroperitoneal abscesses may cause displacement of the kidneys or ureters by a mass, scoliosis of the spine, and free air or fluid in the retroperitoneal space. Computed tomography (CT) is highly sensitive for the diagnosis of renal and retroperitoneal abscesses. It precisely localizes and assesses the size of an abscess so that the type of intervention and its anatomic approach can be determined. The presence of gas within a lesion is pathognomonic for an abscess. Additional CT findings characteristic of an abscess include a mass with low attenuation, rim enhancement of the abscess wall after contrast, obliteration of tissue planes, and displacement of surrounding structures. Ultrasonography is less sensitive than CT but useful for monitoring response to therapy. Arteriography and radioisotope scanning rarely add significant information.
INDICATIONS FOR SURGERY
Renal and retroperitoneal abscesses are generally lethal if untreated. Therapeutic options include antimicrobial therapy, percutaneous catheter drainage, and open surgical drainage.
Antimicrobial therapy as the sole treatment is an option, yet most abscesses cannot be cured without drainage. Small renal abscesses may resolve, however, if they are treated early with aggressive antimicrobial therapy. Prolonged antimicrobial therapy without drainage is indicated only if favorable clinical response and radiologic confirmation of abscess resolution indicate that the therapy is effective. If antimicrobial therapy is not effective, prompt percutaneous or open surgical drainage of the pus is mandatory. Progression of a renal abscess leads to perinephric abscess or perforation into the collecting system and results in signs and symptoms of urinary tract infection.
Antimicrobial therapy should be instituted after the urine has been Gram-stained and urine and blood cultures have been obtained. Broad-spectrum coverage should be guided by the presumptive diagnosis and the presumed pathogen. An aminoglycoside for gram-negative rods and ampicillin for gram-positive cocci are preferred. Anaerobic coverage with a drug such as clindamycin is warranted when Gram stain reveals a polymicrobial flora or when a gastrointestinal source is suspected. If the abscess may be of staphylococcal origin, a penicillinase-resistant penicillin, such as nafcillin, should be added. Antimicrobial therapy should be reevaluated when the results of culture and sensitivity tests are available. Unfortunately, urine and blood cultures are frequently sterile, and empirical therapy must be modified on the basis of clinical response and changes in imaging studies.
Most renal and retroperitoneal abscesses are treated with empirical antimicrobial therapy and immediate percutaneous drainage. When successful, minimally invasive therapy minimizes operative morbidity and allows for preservation of renal tissue. The abscess must be confirmed by CT-guided or ultrasonography-guided needle aspiration and must be drainable without injury to other organs. Immediate surgical drainage must be instituted if the procedure fails. After a multiport drainage catheter (8 to 12 Fr) is positioned, the abscess should be drained, and adequate evacuation should be confirmed by CT or ultrasonography. The catheter should then be connected to low intermittent suction, and drainage outputs should be monitored daily. If drainage stops abruptly, occlusion of the catheter should be suspected, and it should be irrigated gently with small amounts of normal saline. Computed tomography or ultrasonography should be performed periodically to monitor catheter position and size of the abscess. Direct instillation of contrast through the drainage tube may be helpful to confirm the catheter position or to rule out a fistula. To avoid bacteremia, prophylactic antimicrobial coverage should be given, and the contrast should be instilled under gravity or by gentle injection. Instillation of 2,500 units of urokinase in 50 ml of normal saline on a daily basis may be successful in evacuating an organizing infected hematoma. Routine abscess irrigation with antimicrobials is of questionable benefit and may promote overgrowth of resistant bacteria. The catheter should be withdrawn gradually as the abscess cavity shrinks and the drainage decreases. The usual duration of drainage is 1 to 3 weeks. The catheter is removed when drainage stops and CT and ultrasonography show complete resolution.
Open Surgical Drainage
The incision should be smaller than that used for routine nephrectomy, and usually a posterior flank muscle-splitting incision below the 12th rib is sufficient. When the retroperitoneal abscess is entered, the pus should be cultured, and the space gently but thoroughly explored to ensure that all loculated cavities are drained. Thorough irrigation of the cavity is essential. Multiple Penrose drains should be inserted into the space through separate stab wounds, and the ends of the drains should be sutured to the skin and tagged with safety pins. Fascial and muscular closure may be performed with chromic catgut suture, but skin and subcutaneous tissue should be left open to prevent the formation of a secondary body wall abscess. The wound can be left to heal from within, or skin sutures may be placed and left untied for dermal approximation 5 to 7 days postoperatively after drainage has ceased. The wound should be packed with gauze, and the packs should be changed daily. The drains should be left in place until purulent drainage has decreased, and then they can be removed slowly over several days.
If a perinephric abscess is due to long-standing obstruction and there is no functioning renal tissue, a nephrectomy at the time of drainage is theoretically attractive. Drainage of a perinephric abscess should usually be performed as a primary procedure, however, with nephrectomy performed at a later date if necessary. Patients are frequently too ill for prolonged general anesthesia and surgical manipulation. Furthermore, nephrectomy is usually difficult to accomplish technically, and preoperative information is usually not sufficient to determine accurately the amount of functioning of salvageable renal tissue. After drainage of the abscess, removal of obstruction, and appropriate antimicrobial therapy, many kidneys may regain sufficient function to obviate future nephrectomy. Nephrectomy, if indicated, can be performed using a standard nephrectomy approach or a subcapsular nephrectomy technique outlined later.
A small renal abscess confined to one pole of the kidney may be managed by partial nephrectomy. If the infection extends beyond the apparent line of cleavage, however, it is essential to remove all infection, and the line of excision should extend through healthy tissue. If multiple abscesses are present, internal drainage is difficult, and nephrectomy may be required.
When a kidney is so adherent to surrounding tissues that dissection is difficult and hazardous, a subcapsular nephrectomy is indicated. These conditions are usually seen after multiple or chronic infections or previous operations have caused scarring to adjacent organs. Blunt dissection results in tearing of structures such as bowel wall. Sharp dissection when there is no definable tissue plane often results in lacerations of the vena cava, aorta, duodenum, spleen, and other structures. In subcapsular nephrectomy, dissection beneath the renal capsule enables one to avoid these vital structures. Subcapsular nephrectomy should not be performed for malignant disease and is undesirable in tuberculosis.
The main difficulty with subcapsular nephrectomy is that the capsule is adherent to the vessels in the hilum, and one usually must go outside the capsule to ligate the renal pedicle. In this setting, the renal hilum usually is involved in the inflammatory reaction, and separate identification of the vessels is difficult.
Kidney exposure is accomplished through the flank using a 12th rib incision. For low-lying kidneys, a subcostal incision may be satisfactory. When the kidney is reached, the capsule is incised and is freed from the underlying cortex. The capsule is stripped from the surface of the kidney, and an incision is made carefully in the capsule where it is attached to the hilum. The vessels may be protected by placing a finger in front of the pedicle when cutting the capsule. The dense apron of capsule can usually be incised best on the anterior aspect. Control of bleeding can be difficult in this procedure. Frequently all landmarks are obscured, and the renal artery and vein cannot be identified. Sharp dissection is usually required, and major vessels may be entered before they are recognized. Fortunately, the dense fibrous tissue tends to prevent their retraction. Frequently, several chromic suture ligatures can be placed through the pedicle between a proximally placed pedicle clamp and the kidney. To avoid damage to the duodenum or major vessels, pieces of capsule may be left behind. However, prolonged drainage can ensue, and as much of the infected tissue should be removed as possible. After ligation and cutting of the pedicle, the ureter is identified and cut, and the distal end is ligated. If distal ureteral obstruction has caused pyonephrosis, a small, 8 to 10 Fr red Robinson catheter may be placed in the distal ureter to allow postoperative antimicrobial irrigation. Multiple drains should be placed and brought through separate stab wounds.
Complications associated with percutaneous drainage include the formation of additional abscesses that communicate with the renal collecting system and may require temporary urinary diversion via percutaneous nephrostomy drainage to affect a cure. Sepsis, the most frequent complication of percutaneous drainage, occurs in fewer than 10% of patients. Other complications, such as transpleural puncture, vascular or enteric injury, and cutaneous fistula, are rare.
Additional complications to open or percutaneous drainage include prolonged purulent drainage, which may indicate a retained foreign body, calculus, or fistula.
Cure rates for percutaneous drainage of renal and retroperitoneal abscesses range from 60% to 90%.8,15 Multiloculated, viscous abscesses and abscesses in immunocompromised hosts are associated with lower cure rates. Large abscesses may require more than one percutaneous access procedure to completely drain them.
In the past, mortality rates were reported to be as high as 50% in patients with retroperitoneal or perinephric abscesses. More recent reports indicate a significant improvement in mortality (approximately 10%), in large part because of more accurate diagnosis from improved imaging techniques, more effective antimicrobial therapy, and better supportive care.
Renal tuberculosis is caused by hematogenous dissemination from an infected source somewhere else in the body. Both kidneys are seeded with tuberculosis bacilli in 90% of cases. Clinically apparent renal tuberculosis is usually unilateral, however. The initial lesion involves the renal cortex, with multiple small granulomas in the glomeruli and in the juxtaglomerular regions. In untreated patients who fail to heal spontaneously, the lesions may progress slowly and remain asymptomatic for variable periods, usually 10 to 40 years. As the lesions progress, they produce areas of caseous necrosis and parenchymal cavitation. Large tumor-like parenchymal lesions or tuberculomas frequently have fibrous walls and resemble solid mass lesions. Once cavities form, spontaneous healing is rare, and destructive lesions result, with spread of the infection to the renal pelvis and development of a parenchymal or peri-nephric abscess.
Indications for Surgery
Surgery was once commonly used in the treatment of renal tuberculosis, but since the advent of effective antituberculosis chemotherapy, it is reserved primarily for management of local complications, such as ureteral strictures, or for treatment of nonfunctioning kidneys. If surgery is warranted, it is wise to precede the operation with at least 3 weeks and preferably 3 months of triple-drug chemotherapy. Use of isoniazid, 300 mg/day; pyrazinamide, 25 mg/kg to a maximum of 2 g, once daily; and rifampicin, 450 mg/day is recommended. If segmental renal damage is obvious and salvage of the kidney is possible, a drainage procedure or cavernostomy can be performed.7 Removal of a nonfunctioning kidney is usually indicated for advanced unilateral disease complicated by sepsis, hemorrhage, intractable pain, newly developed severe hypertension, suspicion of malignancy, inability to sterilize the urine with drugs alone, abscess formation with development of fistula or inability to have appropriate follow-up.
Prophylactic removal of a nonfunctioning kidney to prevent complications, remove a potential source of viable organisms, and shorten the duration of convalescence and requirement for chemotherapy is advocated by some authors.5,19 Others, who followed a large series of patients treated with medical therapy alone, concluded that, because the frequency of late complications is only 6%, routine nephrectomy should not be performed for every nonfunctioning kidney.9 These authors, however, treated patients for at least 2 years. The merits of short-term therapy and prophylactic nephrectomy versus long-term 2-year chemotherapy and selective nephrectomy warrant further study. Modern percutaneous drainage techniques have largely replaced open cavernostomy for treatment of closed pyocalyx.
Renal tuberculosis sometimes results in caliceal infundibular scarring, causing a closed pyocalix. Unroofing of a pyocalix is called cavernostomy. If the calix still communicates with the renal pelvis, or if it is connected to significant functioning parenchyma, a cavernostomy should not be done because a urinary fistula or urinoma may result. To minimize wound contamination and tuberculous spread, thorough needle aspiration of purulent material and saline irrigation of the abscess cavity should be performed using a large-bore needle and syringe . The abscess cavity is then unroofed, and the edge is sutured with a running suture for hemostasis. Any unsuspected connection with the renal pelvis by an open infundibulum must be closed using 5-0 chromic catgut suture to prevent fistula or urinoma formation. After thorough wound irrigation, multiple drains are placed, and closure is undertaken. Drains are managed as previously described for perinephric abscess.
When unilateral tuberculosis causes more extensive parenchymal destruction or nonfunction, a partial or total nephrectomy, respectively, should be performed. For partial nephrectomy, a guillotine incision is made 1 cm beyond the abscess. If the renal pedicle can be freed and polar vessel located and occluded, the incision can be made at the line of demarcation of the ischemia. In partial nephrectomy, it is important to try to save the capsule (if it is not involved with the infection) to cover the raw surface for hemostasis. Alternatively, fat can be used for hemostasis. The amputated calyx is carefully ligated with a 4-0 chromic catgut suture to prevent urinary fistula or urinoma formation.
After nephrectomy, the distal ureter can be ligated and in most cases does not need to be brought to the skin because tuberculosis of the ureter generally heals with chemotherapy after nephrectomy. If renal tuberculosis is associated with severe tuberculosis cystitis, ureteral catheterization for 7 days postoperatively to minimize subsequent ureteral stump abscess formation should be considered.18
Echinococcosis is a parasitic infection caused by the canine tapeworm E. granulosus. Echinococcal or hydatid cysts occur in the kidney in some 3% of patients with this disease. The hydatid cyst gradually develops at a rate of about 1 cm/year and is usually single and located in the cortex.
The symptoms are those of a slowly growing tumor; most patients are asymptomatic or have a dull flank pain or hematuria. Excretory urography typically shows a thick-walled cystic mass, which is occasionally calcified. Ultrasonography and CT usually show a multicystic or multiloculated mass. Confirmation of the diagnosis is most reliably made by diagnostic tests using partially purified hydatid antigens in a double diffusion test.13 Complement fixation and hemagglutination are less reliable. Diagnostic needle puncture is associated with significant risk of anaphylaxis as a result of leakage of toxic cyst contents.
Indications for Surgery
Cyst removal is indicated when an enlarging cyst threatens renal function or produces obstruction.
The cyst should be removed without rupture to reduce the chance of seeding and recurrence. In cases where cyst removal is impossible because of its size or involvement of adjacent organs, marsupialization is required. The contents of the cyst initially should be aspirated, and the cyst should be filled with a scolecidal agent such as 30% sodium chloride, 2% formalin, or 1% iodide for about 5 minutes to kill the germinal portions. Complete evacuation of all hydatid tissue and thorough postmarsupialization irrigation are critical to preventing systemic effects. Penrose drains are left in the cystic cavity until drainage ceases. If large amounts of renal tissue have been damaged, partial or simple nephrectomy may be required.