Version July 2025
INTRODUCTION —
Psoas (or iliopsoas) abscess is a collection of pus in the iliopsoas muscle compartment [1]. Psoas pyomyositis is a purulent infection of the iliopsoas muscle, which may or may not be accompanied by a psoas abscess.
Infection of the iliopsoas muscle may arise via contiguous spread from adjacent structures or by the hematogenous route from a distant site. The frequency of this diagnosis has increased with the use of advanced imaging techniques [2]. The anatomy, pathogenesis, microbiology, clinical manifestations, diagnosis, treatment, and outcome of psoas abscess and pyomyositis will be reviewed here.
A general overview of pyomyositis is found separately. (See "Primary pyomyositis".)
ANATOMY —
Understanding the clinical manifestations, complications, and management of psoas infection 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 (figure 1 and figure 2 and figure 3).
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, the kidneys and ureters, and iliac lymph nodes. Infection may spread directly between these structures and the psoas muscle.
PATHOGENESIS AND RISK FACTORS —
Psoas infections may be divided into primary and secondary infections according to the pathogenesis.
It may be difficult to distinguish between primary and secondary abscesses in some circumstances [3-8].
Primary infection — Primary psoas infection occurs as a result of hematogenous or lymphatic seeding from a distant site; in some cases, the distant source is never identified [2,9,10].
Risk factors include diabetes, intravenous drug use, renal failure, and human immunodeficiency virus (HIV), as well as other forms of immunosuppression [1,2]. Focal trauma and hematoma formation can predispose patients to the development of psoas infection [9]. Iatrogenic psoas infection has been reported as a complication of epidural anesthesia [11,12]. Migration of an ingested toothpick to the psoas muscle has also resulted in a psoas abscess [13].
Primary psoas infections tend to occur in children and young adults [2,9,14].
Secondary infection — Secondary psoas infection occurs as a result of direct spread of infection to the psoas muscle from an adjacent structure. It may be unclear whether the involvement of a contiguous structure is a cause or consequence of the psoas muscle abscess [4-8,15].
The primary risk factor for secondary psoas infection is infection in an adjacent anatomical structure. Other risk factors include trauma and instrumentation in the inguinal region, hip region, and lumbar spine, including facet joint injection [15-19].
Adjacent structures — Spread of infection to the psoas muscle may occur from infections of the vertebral bodies and discs, the hip joint, the gastrointestinal tract, the genitourinary tract, vascular structures, and other sites [2,15,20].
●Vertebrae – The spine is the most frequent contiguous infected site (39.5 percent in one report) [14]. Vertebral osteomyelitis or discitis can give rise to psoas infection when the vertebral infection spreads to and perforates the psoas sheath.
In addition to causing psoas infection, vertebral infections may also involve the epidural space with epidural abscess formation in addition to psoas infection [21]. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)
●Prosthetic hip – Psoas abscess can occur in association with total hip arthroplasty [15]. In one series of 106 patients admitted with hip arthroplasty infection, psoas abscess was observed in 12 percent of cases [22]. Hematogenous infection and history of neoplasm were predictors of psoas abscess.
●Gastrointestinal tract – Hip pain in patients with Crohn disease should prompt consideration of psoas abscess, particularly in the setting of severe ileocolitis [1,23,24]. The incidence of psoas abscess in patients with Crohn disease has been estimated to be between 0.4 and 4.3 percent [25].
Diagnosis can be delayed if hip pain is initially attributed to noninfectious inflammatory arthritis (a well-described extraintestinal manifestation of Crohn disease).
Psoas abscess has also been described in the setting of appendicitis, colorectal cancer, ulcerative colitis, and following abdominal surgery [2,9,14,26].
●Aorta – Psoas abscess can occur in patients with an infected aortic aneurysm; this may be complicated by aortic rupture [27,28]. In a series of 40 cases of infected aortic aneurysms, 20 percent were complicated by psoas abscess [27]. Psoas abscess has also been described in the setting of aortoduodenal fistula and infected stent graft material [28-30].
●Genitourinary tract – Health care-associated psoas abscess can occur as a complication of renal surgery, extracorporeal shock wave lithotripsy, and nephrectomy [31].
Urinary tract infections can also be associated with psoas infection. Ruptured renal abscess, xanthogranulomatous pyelonephritis, emphysematous cystitis, and emphysematous pyelonephritis have also been associated with psoas abscess [32]. (See "Invasive liver abscess syndrome caused by Klebsiella pneumoniae" and "Xanthogranulomatous pyelonephritis".)
●Other sites – Other reported sources of psoas infection include ruptured pancreatic abscesses and instrumentation of the inguinal or lumbar region [1].
MICROBIOLOGY —
The microbiology of psoas abscesses varies with geography and pathogenesis of infection (eg, whether the process is primary or secondary to infection at an adjacent site).
●Primary infection – Primary psoas abscesses are most frequently due to infection with a single organism [21]. The most common bacterial cause is Staphylococcus aureus, including methicillin-resistant S. aureus; 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) [9,14,20,26,33-36].
●Secondary infection – A secondary psoas abscess may be monomicrobial, especially if associated with vertebral osteomyelitis and discitis. Mycobacterium tuberculosis is a frequent cause of vertebral osteomyelitis and secondary psoas abscess in regions where tuberculosis is common [1,2,37]. Psoas abscesses have also been described as a complication of Brucella spondylodiscitis in endemic regions [38,39]. (See "Bone and joint tuberculosis".)
Secondary psoas abscesses due to gastrointestinal sources are often polymicrobial [20]. In one report of psoas abscesses due to bacterial infection, 55 percent were polymicrobial, and 82 percent of these contained enteric organisms [9]. In another report of psoas abscesses, 21 percent of psoas abscesses reflected polymicrobial infection, including enteric and anaerobic organisms, particularly in the setting of abscesses with gastrointestinal tract origin [14].
Numerous other pathogens have been implicated [20,21,40-49]. Unique examples include Salmonella spp in association with aortitis and hypervirulent Klebsiella pneumoniae in southeast Asia [50-52]. Psoas abscesses have also occurred as a complication following bladder instillation of Bacille Calmette-Guérin as therapy for bladder cancer [53].
CLINICAL MANIFESTATIONS —
Psoas abscesses occur on the right and left sides with roughly equal frequency. Bilateral psoas abscesses are uncommon, occurring in 1 to 5 percent of patients in most case series, although some authors have reported bilateral abscesses in up to 30 percent of patients [9,21,24,26,54-56].
Psoas abscesses are more common in males than females [9,14,56].
Symptoms — The clinical presentation of psoas infection is variable and nonspecific. Historically, psoas abscesses have been thought to present with a classic "triad" of symptoms: fever, back pain, and limp. However, this triad only occurs in approximately 30 percent of patients [20].
Clinical onset of symptoms is typically subacute, and the diagnosis is often delayed for days to weeks because of the overlap of symptoms with benign musculoskeletal etiology [20,21,57].
Like other forms of pyomyositis, psoas infection progresses in three consecutive clinical stages [20,57] (see "Primary pyomyositis", section on 'Course of illness'):
●Stage 1 – This stage is characterized by insidious onset of pain. Flank or low back pain is the most common complaint. Pathologically, this stage correlates with the beginning of pyomyositis prior to the development of an abscess. Unless the muscle is diffusely infected, few patients present in this stage.
●Stage 2 – Most patients present in this stage. Pain is more prominent and localized due to formation of an abscess.
Common complaints include flank pain, low back pain, vague abdominal pain, and/or hip pain. The hip pain is characterized by pain with hip movement, and patients may be unable to walk without a limp.
Groin pain and/or posterior thigh pain are other possible complaints during this stage. This pain is due to referred pain from nerve roots L2, L3, and L4, which innervate these anatomical sites as well as the psoas muscle [20].
In total, 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 [1,9,14,21,31].
During this stage, many patients also develop systemic symptoms, such as fever (present in up to 75 percent of cases), malaise, anorexia, and weight loss [1,2,9,14,21,31,54]. Rarely, patients may report a painful or painless mass below the inguinal ligament.
●Stage 3 – The third stage is characterized by systemic toxic symptoms, including high fever or even septic shock [20,58]. Patients may rapidly deteriorate at this stage. (See 'Outcome' below.)
Physical examination — A thorough physical examination should be performed with a focus on the location of patients' pain. However, physical examination findings are often nonspecific.
Given the deep anatomical location of the iliacus and psoas muscles, the muscles are rarely palpable on examination.
During examination, most patients will prefer to lay still and will maintain the hip in a flexed and externally rotated position [59]. In some patients, the examiner can elicit a positive "psoas sign" by passively extending the hip; if passive hip extension causes pain and hip flexion relieves pain, the psoas sign is positive. During this procedure, pain may localize to the flank, low back, hip, or lower abdomen.
Rarely, examination may reveal a painful or painless mass below the inguinal ligament [20]. If the mass is painless (ie, a cold abscess), tuberculosis is a more likely cause than another bacterial infection [59].
Careful examination may help differentiate psoas pathology from other causes of pain, such as septic arthritis of the hip, an intra-abdominal or urologic process, or inguinal hernia or lymphadenopathy. (See 'Differential diagnosis' below.)
Laboratory tests — Laboratory abnormalities are typically consistent with an infectious process.
Specific laboratory findings include the following:
●Leukocytosis (>10,000/mL) is observed in up to 83 percent of cases [14,21,50].
●Anemia (42.6 percent in one series) [14,21,50].
●Thrombocytosis (27 percent of cases) [14].
●An elevated erythrocyte sedimentation rate (>50 mm/hr in 73 percent of cases) and/or C-reactive protein [2,50].
●Elevated aspartate aminotransferase (>40 units/L in 38 percent of cases) [14,60].
Complications — Psoas infections may be associated with other adjacent focal infections, including vertebral osteomyelitis, spinal epidural abscess, and/or septic arthritis of the hip. In these cases, it is difficult to ascertain whether the psoas infection led to these other conditions or vice versa, or whether underlying bacteremia caused simultaneous infections in these adjacent anatomical sites.
Other possible complications of a psoas abscess include:
●Septic shock (approximately 20 percent of cases in two series) [20,50,54]
●Deep venous thrombosis due to extrinsic compression of the iliac and femoral vein [61,62]
●Hydronephrosis due to ureteric compression [1]
●Bowel ileus [2,61,62]
●Hip septic arthritis, including prosthetic joint infection [63]
DIAGNOSIS
When to suspect psoas infection — Psoas abscess should be suspected in patients with a compatible clinical syndrome (eg, fever, flank or back pain, positive psoas sign), particularly in patients with risk factors (eg, recent bacteremia, adjacent infection). (See 'Pathogenesis and risk factors' above and 'Clinical manifestations' above.)
Prompt diagnosis is associated with improved outcomes in patients with psoas infection. (See 'Outcome' below.)
Because psoas infection has an insidious onset, and symptoms and signs are nonspecific, many patients do not immediately seek clinical care. Furthermore, the diagnosis may be delayed because clinicians often initially suspect other diagnoses (eg, septic hip arthritis or gastrointestinal or urologic pathology) [2,13,21]. 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 [14]. In another, the absence of fever led to delayed diagnosis [20]. (See 'Differential diagnosis' below.)
Confirming the diagnosis — The diagnosis of psoas infection is confirmed by imaging studies and positive culture results.
Imaging — Imaging is the primary method for diagnosing psoas infection.
●Computed tomography – Computed tomography (CT) with intravenous contrast is the most common radiographic modality used to evaluate for psoas abscess (image 1) [24,56]. Intravenous contrast enhances contrast between the muscle and the abscess (the abscess may be identified by its enhancing rim).
Early in the course of psoas infection (ie, when pyomyositis is present but an abscess has not yet formed), the sensitivity of CT may be limited [1,3,14,64,65]. However, once an abscess is present, sensitivity of CT with intravenous contrast approaches 100 percent [24].
Besides an abscess, other findings that may be visible on CT include a focal hypodense lesion, infiltration of surrounding fat, and gas or an air fluid level within the muscle [28,64]. Evidence of bony spinal infection should increase suspicion for tuberculosis in the appropriate epidemiologic circumstances.
●Magnetic resonance imaging – Compared with CT, magnetic resonance imaging (MRI) with and without intravenous contrast (eg, gadolinium) can improve definition of soft tissues and adjacent structures, especially visualization of early pyomyositis or vertebral osteomyelitis [1,2,24,56,66]. The addition of intravenous contrast provides more detailed visualization of the muscle and abscess.
●Other imaging modalities
•Ultrasound is rarely used for the diagnosis of psoas infection, including abscess, because it has low sensitivity and specificity. It may be diagnostic in up to 50 percent of cases but may miss a diffuse phlegmon or small lesions [14,22,24,31,54,56]. Bowel gas and the location of the pelvic bone can alter ultrasound visualization of the psoas muscle [31].
•Abdominal radiographs have poor sensitivity and specificity for psoas infection [24]. Clues to psoas abscess that may be present on plain radiographs include loss of psoas muscle definition, abnormal soft tissue shadows, gas in the psoas region, elevated diaphragm, or pleural effusion [2,3,14].
•Other imaging modalities that have been used to detect psoas infection include nuclear imaging (eg, gallium scan, positron emission tomography [PET]-CT) [23,67]. In one report, PET-CT was useful in the follow-up assessment of a patient with a tuberculous psoas abscess [68].
Cultures and histopathology — Blood cultures and tissue/abscess sampling help to confirm the diagnosis and guide antimicrobial therapy.
●Cultures – Blood cultures should be obtained in all patients; fluid from abscess material should be obtained and sent for microbiologic study if the pathogen is unknown or in the setting of large abscess size in need of drainage for treatment. Acid-fast bacilli smear and mycobacterial culture should also be performed when tuberculosis is suspected or if routine Gram staining is negative.
In stable patients, it is preferable to obtain samples prior to antibiotic administration to optimize culture yield, although the impact of prior antibiotics on culture results is not known. Antibiotics should be administered immediately in patients who are unstable or septic.
Blood cultures are positive in 41 to 68 percent of cases; the most frequent blood culture isolate is S. aureus [9,69].
●Histopathology – If there is suspicion for tuberculosis or noninfectious etiology, histopathology may be useful for identification [70].
Additional studies to assess for complicated infection — As described above, psoas abscesses often coexist with other infections. (See 'Pathogenesis and risk factors' above.)
Structures adjacent to the psoas muscle should be considered as possible sources or concomitant areas of infection:
●We perform dedicated spine imaging to assess for vertebral osteomyelitis or epidural abscess in any patient with psoas abscess [69]. (See "Vertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Imaging studies'.)
●Some experts suggest psoas imaging in all patients with prosthetic hip infection. We obtain CT in such patients if there are clinical features suggestive of psoas infection [22].
●All patients with psoas infection in whom imaging raises concerns for aortic infection should undergo urgent evaluation for aortic infection, including vascular consult [27,28]. Psoas infection with associated aorta infection may result in aortic rupture. (See "Overview of infected (mycotic) arterial aneurysm", section on 'Other presentations'.)
In patients with bacteremia and psoas abscess, endocarditis should be considered, especially for patients with S. aureus bacteremia. If there is any evidence suggestive of endocarditis, echocardiography should be considered. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis" and "Clinical approach to Staphylococcus aureus bacteremia in adults".)
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 or by biopsy.
●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 examination, 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. Unlike psoas infection, hip pain in patients with septic hip infection is usually increased with hip flexion [71]. 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 [72] and a mucinous adenocarcinoma [73]. In both, the diagnosis was confirmed by tissue biopsy.
●Inguinal hernia or lymphadenopathy – Like inguinal hernia or lymphadenopathy, psoas abscess may rarely present as a painful or painless mass below the inguinal ligament [31]. Imaging and/or biopsy can differentiate these diagnoses. (See "Overview of treatment for inguinal and femoral hernia in adults", section on 'Inguinal hernia' and "Evaluation of peripheral lymphadenopathy in adults", section on 'Inguinal'.)
●Other pathologies – Other mimickers of psoas abscess include calcium pyrophosphate deposition pseudoabscess [74], herniated disc fragments [75], and pseudomyxoma retroperitonei [76].
TREATMENT —
Management of psoas infection consists of drainage of any abscess (if feasible), prompt initiation of appropriate antibiotic therapy, and management of any adjacent or concomitant infections (eg, vertebral osteomyelitis, abdominal pathology, infected aortic aneurysm, endocarditis).
Drainage — We suggest that all abscesses be drained, if feasible. Drainage is an integral component of management of psoas abscess, although some success with antibiotic therapy alone has been reported in a small number of patients with abscesses <2 to 3 cm [26,54,77,78]. Abscess drainage may be achieved with either percutaneous or surgical intervention.
●Percutaneous drainage – Percutaneous drainage (by ultrasound or CT guidance) is an appropriate initial approach for many patients [1,2,26,70,79]. 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.
In one study, CT-guided drainage was successful in 90 percent of cases [26]. In a systematic review of 20 studies of 338 patients with psoas abscess, CT-guided drainage was highly successful, while outcomes varied with ultrasound guidance [56].
Despite high success rates of percutaneous drainage, surgical drainage may be more appropriate for certain patients, as described below.
●Surgical drainage – Historically, surgical drainage and debridement via an open retroperitoneal approach was the standard for draining a psoas abscess. More recently, laparoscopic drainage is another surgical option [80].
Despite frequent use of percutaneous drainage, surgical drainage (open or laparoscopic) is often preferred in patients with certain characteristics [1,2,54,56]:
•Concomitant infection requiring surgical intervention (eg, spinal epidural abscess, bowel disease requiring resection, appendicitis)
•Multiloculated abscess
•Thick viscous fluid in abscess
•Extensive necrosis or phlegmon
•Gas-forming organism [81]
Surgical drainage is often required in patients whose abscesses fail to drain after percutaneous drainage.
There are no studies directly comparing surgical and percutaneous approaches. In the aforementioned systematic review, there was a trend toward surgical drainage achieving a higher likelihood of complete drainage compared with percutaneous [56].
Antibiotics — Along with drainage of an abscess (if present), antibiotic therapy is a mainstay of treatment of psoas infection.
●Empiric antibiotic regimens – 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) [54]. An example regimen is intravenous vancomycin plus ceftriaxone plus metronidazole.
We do not include empiric coverage for Pseudomonas spp, except in patients with recent pseudomonal infection or recent bacteremia due to a multidrug-resistant gram-negative infection. Pseudomonas spp rarely cause psoas abscess, as discussed above. (See 'Microbiology' above.)
In general, it is preferable to defer empiric antimicrobial therapy until after draining abscess fluid (see 'Drainage' above). However, immediate empiric antibiotic coverage should be provided for some patients, including those with sepsis or a concomitant infection requiring immediate antibiotic treatment (eg, appendicitis).
While awaiting culture results, antibiotic regimens can be tailored based on Gram stain results once available.
●Subsequent antibiotic regimens – Once culture and susceptibility results are available, antibiotic therapy should be tailored.
Oral antibiotic regimens can be used to complete therapy for susceptible organisms, unless there is a concomitant infection that requires prolonged intravenous therapy. Depending on culture results, oral options include beta-lactams, doxycycline, trimethoprim-sulfamethoxazole, and fluoroquinolones, among others (fluoroquinolones should not be used as monotherapy for staphylococcal infections).
For culture-negative infection, an oral option with the same spectrum of coverage as the empiric intravenous therapy is appropriate; an example regimen is doxycycline plus amoxicillin-clavulanate.
Evidence of mycobacterial infection should prompt management as described in detail separately. (See "Bone and joint tuberculosis".)
●Duration of therapy – The optimal duration of antibiotics is uncertain. Two to three weeks of therapy is generally adequate following adequate drainage, unless a concomitant infection is present that requires a longer duration of therapy (eg, vertebral osteomyelitis, endocarditis, S. aureus bacteremia) [31,54]. For patients whose abscess was not drained, it is reasonable to extend therapy to three to four weeks. Follow-up imaging should be performed near the end of the planned course of antimicrobial therapy to ensure satisfactory response to therapy.
OUTCOME —
Psoas infection can cause significant morbidity and mortality.
●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 [1,20,36].
Risk factors for mortality include delayed diagnosis, inadequate drainage or antibiotic therapy, advanced age, the presence of bacteremia, cardiovascular disease, and infection due to E. coli [14,20,54,57,60].
●Relapse – Relapses can occur up to one year after initial presentation; this outcome has been reported in 15 to 36 percent of cases [14,20,36,50,82]. Recurrence may be associated with inadequate drainage or inadequate antimicrobial therapy [21].
●Morbidity – Hip flexion abnormalities may persist after cure of infection as a result of fibrosis within the iliopsoas sheath [59].
SUMMARY AND RECOMMENDATIONS
●Anatomy – The iliacus and psoas muscles are the main hip flexors; together, they are often called the iliopsoas muscle (figure 1 and figure 2 and figure 3).
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, the kidneys and ureters, and iliac lymph nodes. (See 'Anatomy' above.)
●Pathogenesis and microbiology – Psoas abscesses occur either via primary or secondary infection.
•Primary infection – Primary psoas infection occurs from hematogenous or lymphatic seeding from a distant site. The most common bacterial cause is Staphylococcus aureus, including methicillin-resistant S. aureus. (See 'Primary infection' above and 'Microbiology' above.)
•Secondary infection – Secondary psoas infection occurs as a result of direct spread of infection to the psoas muscle from an adjacent structure. A secondary psoas abscess may be monomicrobial, especially if associated with vertebral osteomyelitis and discitis. Polymicrobial infection is common if the source is an adjacent gastrointestinal infection. (See 'Secondary infection' above and 'Microbiology' above.)
●Clinical manifestations
•Symptoms – The classic "triad" of symptoms for psoas abscess are fever, back pain, and limp; however, this triad only occurs in approximately 30 percent of patients.
Clinical onset of symptoms is typically subacute, and the diagnosis is often delayed for days to weeks because of the overlap of symptoms with benign musculoskeletal etiology. (See 'Symptoms' above.)
•Physical examination – Given the deep anatomical location of the iliacus and psoas muscles, the muscles are rarely palpable on examination.
During examination, most patients will prefer to lay still and will maintain the hip in a flexed and externally rotated position. In some patients, the examiner can elicit a positive "psoas sign" by passively extending the hip; if passive hip extension causes pain and hip flexion relieves pain, the psoas sign is positive. (See 'Physical examination' above.)
●Diagnosis
•Imaging – CT or MRI with intravenous contrast are the most common radiographic modality used to evaluate for psoas abscess (image 1). (See 'Imaging' above.)
In patients with confirmed psoas abscess, we often obtain dedicated spine imaging to assess for spine infection or epidural abscess. (See 'Additional studies to assess for complicated infection' above.)
•Cultures – Blood cultures should be obtained in all patients; fluid from abscess material should be obtained and sent for microbiologic study if the pathogen is unknown or in the setting of large abscess size in need of drainage for treatment. (See 'Cultures and histopathology' above.)
●Treatment – Management of psoas infection consists of drainage of any abscess (if feasible), prompt initiation of appropriate antibiotic therapy, and management of any adjacent or concomitant infections. (See 'Treatment' above.)
•Drainage – We suggest drainage of all abscesses, if feasible (Grade 2C). In abscesses <2 to 3 cm in size, antibiotic therapy alone has been successful in a small number of patients.
Abscess drainage may be achieved with either percutaneous or surgical intervention. (See 'Drainage' above.)
•Antibiotics
-Empiric antibiotic therapy – We suggest empiric antibiotic therapy that includes 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) (Grade 2C). An example regimen is intravenous vancomycin plus ceftriaxone plus intravenous metronidazole; other regimens are listed in the table (table 1).
In general, it is preferable to defer empiric antimicrobial therapy until after culturing abscess fluid. However, immediate empiric antibiotic coverage should be provided for some patients, including those with sepsis or a concomitant infection requiring immediate antibiotic treatment (eg, appendicitis). (See 'Antibiotics' above.)
-Subsequent antibiotic regimens – Once culture and susceptibility results are available, antibiotic therapy should be tailored.
Oral antibiotic regimens can be used to complete therapy for susceptible organisms, unless there is a concomitant infection that requires prolonged intravenous therapy. For culture-negative infection, an oral option with the same spectrum of coverage as the empiric intravenous therapy is appropriate. (See 'Antibiotics' above.)
-Duration of therapy – The optimal duration of antibiotics is uncertain. Two to three weeks of therapy is generally adequate following adequate drainage, unless a concomitant infection is present that requires a longer duration of therapy (eg, vertebral osteomyelitis, endocarditis, S. aureus bacteremia). For patients whose abscess was not drained, it is reasonable to extend therapy to three to four weeks. Follow-up imaging should be performed near the end of the planned course of antimicrobial therapy to ensure satisfactory response to therapy. (See 'Antibiotics' above.)
