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Psoas abscess

Psoas abscess
Literature review current through: Jan 2024.
This topic last updated: Oct 25, 2022.

INTRODUCTION — Psoas (or iliopsoas) abscess is a collection of pus in the iliopsoas muscle compartment [1]. It may arise via contiguous spread from adjacent structures or by the hematogenous route from a distant site. The incidence is rare, but the frequency of this diagnosis has increased with the use of computed tomography, prior to which most cases were diagnosed at postmortem [2]. The anatomy, pathogenesis, microbiology, clinical manifestations, diagnosis, treatment, and outcome of psoas abscess will be reviewed here.

ANATOMY — Understanding the clinical manifestations, complications, and management of psoas abscess requires knowledge of the anatomy of the psoas muscle and its adjacent structures.

The psoas muscle arises from the transverse processes and the lateral aspects of the vertebral bodies between the 12th thoracic and the 5th lumbar vertebrae. From this origin, it courses downward across the pelvic brim, passes deep to the inguinal ligament and anterior to the hip joint capsule to form a tendon that inserts into the lesser trochanter of the femur. The iliacus muscle joins the psoas to insert via the same tendon. The iliacus and psoas muscles are the main hip flexors.

The psoas and iliacus are sometimes considered together as the iliopsoas muscle, located in an extraperitoneal space called the iliopsoas compartment. The tendon is separated from the hip capsule by the iliopsoas bursa. This bursa is in communication with the hip joint space in up to 15 percent of persons, which may facilitate spread of infection between these sites.

The psoas muscle is situated near a number of important anatomical structures including the vertebral bodies, the abdominal aorta, the sigmoid colon, the appendix, the hip joint, and iliac lymph nodes. Infection may spread directly between these structures and the psoas muscle.

PATHOGENESIS — Psoas abscesses may be divided into primary and secondary abscesses according to the pathogenesis.

Primary abscess — Primary psoas abscess occurs as a result of hematogenous or lymphatic seeding from a distant site (which may be occult) [2-4]. Risk factors include diabetes, intravenous drug use, human immunodeficiency virus (HIV) infection, renal failure, and other forms of immunosuppression [1,2]. Trauma and hematoma formation can predispose to development of psoas abscess [3]. Psoas abscess has been reported as a complication of epidural anesthesia [5]. Migration of an ingested toothpick to the psoas muscle has also resulted in psoas abscess [6].

Primary psoas abscesses tend to occur in children and young adults [2,3,7]. They are more common in tropical and resource-limited settings. In Asia and Africa, 99 percent of iliopsoas abscesses are primary; in Europe and North America, 17 to 61 percent are primary [3]. It may be difficult to distinguish between primary and secondary abscesses in some circumstances [8].

Secondary abscess — Secondary psoas abscess occurs as a result of direct spread of infection to the psoas muscle from an adjacent structure. It may be uncertain whether involvement of a contiguous structure is a cause or a consequence of the psoas muscle abscess [9].

Risk factors for secondary abscess include trauma and instrumentation in the inguinal region, hip region, and lumbar spine, including facet joint injection [9-13].

Adjacent structures — Involved structures may include the vertebral bodies and discs, the hip joint, the gastrointestinal tract, the genitourinary tract, vascular structures, and other sites [2,9].

Vertebrae – Bony sites are the most frequent contiguous infected site (39.5 percent in one report) [7]. Vertebral osteomyelitis or discitis can give rise to psoas abscess when infection spreads from bone and perforates the psoas sheath. Psoas abscess may be accompanied by involvement of the epidural space with epidural abscess formation due to spread of infection from the vertebral body [14]. Vertebral osteomyelitis with a psoas abscess has been reported as a complication of epidural catheter use [15]. Demonstration of a psoas abscess should prompt investigation for a possible vertebral source [16]. (See "Vertebral osteomyelitis and discitis in adults".)

Hip arthroplasty – Psoas abscess can occur in association with total hip arthroplasty [9]. In one series of 106 patients admitted with hip arthroplasty infection, psoas abscess was observed in 12 percent of cases. Hematogenous infection and history of neoplasm were predictors of psoas abscess [17]. However, the frequency of associated psoas infections is probably much lower in situations where the diagnosis of hip arthroplasty infection is promptly identified and treated.

Gastrointestinal tract – Hip pain in patients with Crohn's disease should prompt consideration of psoas abscess, particularly in the setting of severe ileocolitis [1,18]. The incidence of psoas abscess in Crohn's disease has been estimated to be between 0.4 and 4.3 percent [19]. Diagnosis can be delayed if hip pain is initially attributed to arthritis (a well-described extraintestinal manifestation of Crohn's disease).

Psoas abscess has also been described in the setting of appendicitis, colorectal cancer, ulcerative colitis, and following abdominal surgery [2,3,7,20].

Aorta – Psoas abscess can occur in patients with an infected aortic aneurysm; this may be complicated by aortic rupture [21,22]. In a series of 40 cases of infected aortic aneurysms, 20 percent were complicated by psoas abscess [21]. Psoas abscess has also been described in the setting of aorto-duodenal fistula and infected stent graft material [22-24].

Genitourinary tract – Psoas abscess can occur as a complication of renal surgery, extracorporeal shock wave lithotripsy, and nephrectomy [25]. Ruptured renal abscess has also been associated with psoas abscess. Among Klebsiella pneumoniae psoas abscesses reported from Taiwan, 43 percent had concurrent urinary infection. Xanthogranulomatous pyelonephritis, an uncommon form of pyelonephritis, has also been associated with psoas abscess [26]. (See "Invasive liver abscess syndrome caused by Klebsiella pneumoniae" and "Xanthogranulomatous pyelonephritis".)

Other sites – A ruptured abscess of the pancreas can result in psoas abscess. Instrumentation involving the inguinal or lumbar region can also be complicated by psoas abscesses [1].

MICROBIOLOGY — The microbiology of psoas abscess varies with geography and pathogenesis of infection (eg, whether the process is primary or secondary to infection at an adjacent site).

Primary psoas abscesses are most frequently due to infection with a single organism [14]. The most common bacterial cause is Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA); in one study, S. aureus was implicated in 88 percent of cases (followed by streptococci and Escherichia coli; 4.9 and 2.8 percent, respectively) [3,7,20,27-29]. Mycobacterium tuberculosis is a frequent cause of psoas abscess in regions where tuberculosis is common [1,2,30]. Psoas abscess has also been described as a complication of Brucella spondylodiscitis [31]. (See "Bone and joint tuberculosis".)

Secondary psoas abscess may be monomicrobial or polymicrobial; in one report of psoas abscesses due to bacterial infection, 55 percent were polymicrobial, and 82 percent of these contained enteric organisms [3]. In another report of psoas abscesses, 21 percent of psoas abscesses reflected polymicrobial infection, including enteric organisms (particularly in the setting of abscesses with gastrointestinal tract origin). Anaerobes were isolated from 15 percent of psoas abscesses in one report [7].

Klebsiella pneumoniae is an important cause of psoas abscess in Taiwan, especially in patients with diabetes [32]. There are reports of psoas abscess caused by Streptococcus pneumoniae [33], Streptobacillus moniliformis [34], Staphylococcus lugdunensis [35], Actinomyces israelii [36], and disseminated nocardiosis [37]. Psoas abscess due to Salmonella (mostly non-typhi Salmonella) has also been reported [38,39]. Psoas abscess due to Candida albicans has also been described, although rarely [14]. Brucella infection should be considered as a possible cause of psoas abscess in endemic regions [40]. Psoas abscess has also been reported as a manifestation of chronic Q fever infection [41], disseminated blastomycosis [42], and as a complication following bladder instillation of Bacille Calmette-Guérin (BCG) for therapy of bladder cancer [43]. Non-tuberculosis Mycobacterium have also been described especially in immunocompromised hosts [44]. (See "Invasive liver abscess syndrome caused by Klebsiella pneumoniae" and "Nocardia infections: Epidemiology, clinical manifestations, and diagnosis".)

CLINICAL MANIFESTATIONS — Psoas abscesses are more common in males than females [3,7]. The median age of patients is 44 to 58 years in developed countries. However, psoas abscesses tend to occur more frequently among patients <20 years in resource-limited settings than in North America (81 versus 48 percent) [3,7,20]. Psoas abscess has also been diagnosed in a neonate in whom the initial diagnosis was a femoral hernia [45].

Psoas abscess occurs on the right and left sides with roughly equal frequency. Bilateral psoas abscesses are uncommon. In most case series, the frequency of bilateral abscesses is 1 to 5 percent; however, some authors have reported bilateral abscesses in up to 30 percent of cases [3,14,20,46,47].

Symptoms and signs — Symptoms and signs of psoas abscess include back or flank pain, fever, inguinal mass, limp, anorexia, and weight loss [1-3,7]. Pain is present in up to 91 percent of cases with localization to the back, flank, or lower abdomen, with or without radiation to the hip and/or the posterior aspect of the thigh [1,3,7,14,25]. Fever is present in up to 75 percent of cases, and a psoas abscess may manifest as a fever of unknown origin [25,46].

Psoas abscesses occasionally extend distally and present as a painful or painless mass below the inguinal ligament [25]. When an inguinal mass in a patient with a psoas abscess is painless (ie, a cold abscess), tuberculosis is a more likely cause than another bacterial infection [48]. The mass may rarely mimic inguinal lymphadenopathy or a femoral hernia.

Lower abdominal pain is often exacerbated when performing movements in which the psoas muscle is stretched or extended; the "psoas sign" is pain brought on by extension of the hip. Limitation of hip movement is common, and patients frequently prefer to be in a position of less discomfort that includes hip flexion and lumbar lordosis [48]. Unlike septic arthritis, hip pain in patients with psoas abscesses is usually diminished with hip flexion [49].

The presenting symptoms may be nonspecific, and the onset is often subacute; symptoms may be present for a few weeks and up to six months [14]. However, patients may also present with septic shock with only nonspecific clinical features [50]. Symptoms may have features suggesting other diagnoses such as septic hip arthritis or gastrointestinal or renal tract pathology, leading to delayed diagnosis [2]. In one study, the median time between the onset of symptoms and diagnosis was 22 days; the interval was >42 days for one-third of patients [7].

Laboratory tests — Leukocytosis (>10,000/mL) is observed in up to 83 percent of cases; anemia <11 g/L is frequent (42.6 percent in one series) [7,14,32]. Thrombocytosis is observed less frequently (27 percent of cases) [7]. An elevated erythrocyte sedimentation rate may be observed (>50 in 73 percent of cases); the C-reactive protein is often elevated and averaged 189.8 in one series [2,32]. Elevated aspartate aminotransferase has also been described (>40 in 38 percent of cases) [7] and in one study, elevated aminotransferase was more frequently associated with gram-negative rod etiology [51].

Complications — Complications of psoas abscess include:

Septic shock (about 20 percent of cases in two series) [32,46]

Deep venous thrombosis due to extrinsic compression of the iliac and femoral vein has also been described, as has paralytic bowel ileus [52,53]

Hydronephrosis due to ureteric compression [1]

Bowel ileus [2]

Hip septic arthritis including prosthetic joint infection [54]

DIAGNOSIS — The diagnosis of a psoas abscess may be suspected on clinical grounds and confirmed on imaging studies. Identification of the etiological organism requires culture of blood or aspirated pus or, rarely, surgically obtained tissue.

Imaging — Computed tomography (CT) is the optimal radiographic modality to evaluate for psoas abscess (image 1), though sensitivity may be limited early in the course of disease [1,7,8,55,56]. In most cases, an abscess is obvious; other findings may include a focal hypodense lesion, infiltration of surrounding fat, and gas or an air fluid level within the muscle [22,55]. Magnetic resonance imaging (MRI) may allow improved definition of soft tissues and adjacent structures, especially visualization of the vertebral bodies [1,2,57]. Evidence of bony spinal infection should increase suspicion for tuberculosis in the appropriate epidemiologic circumstances.

Abdominal plain radiographs may suggest loss of psoas muscle definition, abnormal soft tissue shadows, and the presence of gas, but such findings are often not consistent or definitive [2]. In one study, routine abdominal radiography was a poor diagnostic tool in that psoas muscle involvement was indicated in only 14.4 percent of cases [7]. Chest radiograph may demonstrate elevation of the diaphragm or a pleural effusion [8].

Although CT is the modality of choice when a psoas abscess is suspected clinically, a psoas abscess may also be visualized on nuclear imaging used to identify occult foci of infection [18,58]. (See "Approach to imaging modalities in the setting of suspected nonvertebral osteomyelitis", section on 'Nuclear modalities'.)

Ultrasound has low sensitivity and specificity; bowel gas and the pelvic bone may make ultrasound diagnosis difficult [25]. Although ultrasound imaging may be diagnostic in up to 50 percent of cases, this modality may miss a diffuse phlegmon or small lesions [7,17,25,46].

There are limited reports of the use of positron emission tomography (PET)-CT. In one report, PET-CT was useful in the follow-up assessment of a patient with a tuberculous psoas abscess [59].

Culture — Both blood cultures and abscess material should be obtained in all cases and sent to the microbiology laboratory for Gram stain and bacterial culture. Acid-fast bacilli (AFB) smear and mycobacterial culture should also be performed when tuberculosis is suspected or when routine Gram staining is negative. These specimens should be obtained when a diagnosis of psoas abscess is confirmed and before initiation of antimicrobial therapy, if feasible, to optimize the culture yield. (See "Diagnosis of pulmonary tuberculosis in adults".)

Blood cultures are positive in 41 to 68 percent of cases; the most frequent blood culture isolate is S. aureus [3,16]. Psoas abscess with or without vertebral osteomyelitis can be a presentation of endocarditis. Therefore, if there is any supportive evidence for this diagnosis, then echocardiography should be considered. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

Histopathology — Biopsy material should be sent for histopathology evaluation as this may be useful for identification of mycobacterial infection as well as an alternative diagnosis such as tumor [60].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of psoas abscess includes:

Psoas muscle hematoma – This occurs most often in the setting of anticoagulation or a bleeding disorder. Psoas abscess and psoas hematoma present with similar clinical manifestations, including back or flank pain and fever; they may be distinguished radiographically.

Retrocecal appendicitis – Patients with retrocecal appendicitis may not exhibit marked localized tenderness in the right lower quadrant since the appendix does not come into contact with the anterior parietal peritoneum. Rather, retrocecal appendicitis may be associated with a "psoas sign" (right lower quadrant pain with passive hip extension). The inflamed appendix may lie against the right psoas muscle, causing the patient to shorten the muscle by drawing up the right knee. Patients with retrocecal appendicitis typically have pain in the retrovesical pouch during a rectal exam, whereas those with a psoas abscess do not. (See "Acute appendicitis in adults: Clinical manifestations and differential diagnosis".)

Iliopsoas bursitis – Iliopsoas bursitis can occur in the setting of rheumatoid arthritis, trauma, or overuse injuries. Infection generally occurs as a result of hematogenous or contiguous spread of infection or, in rare cases, direct inoculation in the setting of corticosteroid injection. In a minority of patients, the iliopsoas bursa is in direct communication with the hip joint. Therefore, in this setting, infection at one of these sites can easily extend to the other. The diagnosis is suggested in the setting of normal psoas muscle imaging and presence of localized hip pain. Deep septic bursitis is confirmed by bursa aspiration. (See "Septic bursitis".)

Septic hip arthritis – Patients with septic hip arthritis present with joint pain, swelling, and restricted movement. The diagnosis is established by joint aspiration with findings of leukocytosis and positive bacterial culture results. (See "Septic arthritis in adults".)

Metastatic disease – There are reports of metastatic disease mimicking a psoas abscess, including a poorly differentiated carcinoma [61] and a mucinous adenocarcinoma [62]. In both, the diagnosis was confirmed by tissue biopsy.

Other pathologies – Other mimickers of psoas abscess include calcium pyrophosphate deposition pseudo-abscess [63], herniated disc fragments [64], and pseudomyxoma retroperitonei [65].

TREATMENT — Management of psoas abscess consists of drainage and prompt initiation of appropriate antibiotic therapy. Secondary abscess also requires management of the adjacent infected focus (such as ruptured viscus, fistula, or infected aortic aneurysm).

Drainage — Abscess drainage may be achieved with percutaneous or surgical intervention. Percutaneous drainage (by ultrasound or computed tomographic guidance) is an appropriate initial approach; in one study, this technique was successful in 90 percent of cases [1,2,20,60,66]. Following needle aspiration, a pigtail catheter may be placed in situ to allow further drainage. The percutaneous catheter may be removed when drainage has ceased, the patient's condition has improved, and repeat imaging demonstrates that the drainage has been satisfactory.

Surgical drainage may be warranted in the setting of percutaneous drainage failure; there are no studies directly comparing open and percutaneous approaches. Indications for surgical drainage include multiloculated abscesses and significant involvement of an adjacent structure requiring surgical management [2,46]. Options for surgical drainage include laparoscopic and open surgical drainage. Advantages of laparoscopy include the extraperitoneal nature of the procedure, the capability to break down loculations, and rapid postoperative recovery [67].

Open drainage via an extraperitoneal approach was previously the surgical intervention of choice; in one series, successful outcomes were described in 97 percent of patients [3]. Open surgical drainage may be warranted in the setting of a multiloculated psoas abscess, an abscess secondary to bowel disease (eg, Crohn's disease) in which bowel resection may be necessary [1], or a psoas abscess with a gas-forming organism [68].

Antibiotics — In general, directed antimicrobial therapy (based on the results of cultures and smears) is preferable to empiric therapy. It is preferable to attempt to make definitive diagnosis before initiating antibiotic therapy. For circumstances in which prompt microbial diagnosis is not feasible, empiric antibiotic therapy should include activity against S. aureus (including activity against methicillin-resistant S. aureus in regions where prevalence is substantial) and enteric organisms (both aerobic and anaerobic enteric flora) (table 1) [46].

Antimicrobial therapy should be tailored to culture and susceptibility results. Evidence of mycobacterial infection should prompt management as described in detail separately. (See "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults with HIV infection: Initiation of therapy" and "Treatment of drug-susceptible pulmonary tuberculosis in nonpregnant adults without HIV infection".)

Parenteral antibiotics should be administered in conjunction with psoas abscess drainage. Antibiotics alone are unlikely to be curative, although some success with antibiotic therapy alone has been reported in a small number of patients with abscesses <3 cm [20,46]. (See 'Drainage' above.)

The optimal duration of antibiotics is uncertain; three to six weeks of therapy following adequate drainage is likely appropriate; the decision on duration of therapy may be impacted by the presence of osteomyelitis, for example [25,46]. Follow-up imaging should be performed near the end of the planned course of antimicrobial therapy to ensure satisfactory response to therapy. Most, if not all, cases of tuberculous psoas abscesses have associated vertebral osteomyelitis. (See "Bone and joint tuberculosis".)

OUTCOME — Psoas abscess can portend significant morbidity and mortality. In one series, mortality due to primary and secondary abscess was 2.4 and 19 percent, respectively; in untreated cases, mortality may approach 100 percent [1]. Risk factors for mortality include delayed or inadequate treatment, advanced age, the presence of bacteremia, cardiovascular disease, and infection due to E. coli [7,46,51].

Relapse can occur up to one year after initial presentation; this outcome has been reported in 15 to 36 percent of cases [7,32,69]. Recurrence may be associated with inadequate drainage or inadequate antimicrobial therapy [14]. In addition, presence of hip flexion deformity at clinical presentation may not completely resolve as a result to fibrosis within the iliopsoas sheath [48].

SUMMARY AND RECOMMENDATIONS

A psoas (or iliopsoas) abscess is a collection of pus in the iliopsoas muscle compartment [1]. It may arise via contiguous spread from adjacent structures (secondary abscess) or by the hematogenous route from a distant site (primary abscess). (See 'Pathogenesis' above.)

Primary psoas abscesses are most frequently due to infection with a single organism. In regions where Mycobacterium tuberculosis is endemic, this is a frequent cause of psoas abscess. The most common bacterial cause is Staphylococcus aureus, including methicillin-resistant S. aureus (MRSA). Secondary psoas abscess may be monomicrobial or polymicrobial and frequently consist of enteric organisms (both aerobic and anaerobic bacteria). (See 'Microbiology' above.)

Symptoms and signs of psoas abscess include back or flank pain, fever, inguinal mass, limp, anorexia, and weight loss. Pain may localize to the back, flank, or lower abdomen, with or without radiation to the hip and/or the posterior aspect of the thigh. Limitation of hip movement is common, and patients frequently prefer to be in a position of less discomfort that includes hip flexion and lumbar lordosis. Pain is exacerbated when performing movements in which the psoas muscle is stretched or extended; the "psoas sign" is pain brought on by extension of the hip. (See 'Clinical manifestations' above.)

The diagnosis of a psoas abscess may be suspected on clinical grounds and confirmed on imaging studies. Computed tomography (CT) is the optimal radiographic modality to evaluate for psoas abscess. Blood samples and abscess material should be sent to the microbiology lab for Gram stain and bacterial culture. Acid-fast bacilli smear and mycobacterial culture should also be performed in the setting of risk for tuberculosis. (See 'Diagnosis' above.)

Management of psoas abscess consists of drainage and prompt initiation of appropriate antibiotic therapy. We suggest initial management with percutaneous drainage (by ultrasound or CT guidance) (Grade 2C). Following needle aspiration, a pigtail catheter may be placed in situ to allow further drainage. (See 'Drainage' above.)

Empiric antibiotic therapy should include activity against S. aureus (including activity against MRSA in regions where prevalence is substantial) and enteric organisms (both aerobic and anaerobic enteric flora) (table 1). Antimicrobial therapy should be tailored to culture and susceptibility results. Evidence of mycobacterial infection should prompt management as described in detail separately. (See 'Antibiotics' above.)

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