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Psoas abscess

Author Section Editor Deputy Editor


Denis Spelman, MBBS, FRACP, Daniel J Sexton, MD Elinor L Baron, MD, DTMH
FRCPA, MPH

Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Dec 2013. | This topic last updated: Sep 24, 2012.

INTRODUCTION — 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 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 (CT), prior
to which most cases were diagnosed at post mortem [2]. The anatomy, pathogenesis, microbiology, clinical
manifestations, diagnosis, and treatment 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
twelfth thoracic and the fifth 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].

Primary psoas abscesses tend to occur in children and young adults [2,3,5]. They are more common in tropical
and developing countries. 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 [6].

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
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a consequence of the psoas muscle abscess [7].

Risk factors for secondary abscess include trauma and instrumentation in the inguinal region, lumbar spine, or hip
region [7-10].

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 [2,7].

● Vertebrae — Bony sites are the most frequent contiguous infected site (39.5 percent in one report) [5].
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 [11]. Vertebral osteomyelitis with
a psoas abscess has been reported as a complication of epidural catheter use [12]. Demonstration of a psoas
abscess should prompt investigation for a possible vertebral source [13]. (See "Vertebral osteomyelitis and
discitis" and "Hematogenous osteomyelitis in adults".)

● Hip arthroplasty — Psoas abscess can occur in association with total hip arthroplasty [7]. 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 [14]. 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 [1,15]. The incidence of psoas abscess in Crohn's
disease has been estimated to be between 0.4 and 4.3 percent [16]. 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 [2,3,5,17].

● Aorta — Psoas abscess can occur in patients with an infected aortic aneurysm; this may be complicated by
aortic rupture [18,19]. In a series of 40 cases of infected aortic aneurysms, 20 percent were complicated by
psoas abscess [18]. Psoas abscess has also been described in the setting of aorto-duodenal fistula and
infected stent graft material [19-21].

● Genitourinary tract — Psoas abscess can occur as a complication of renal surgery, extracorporeal shock
wave lithotripsy, and nephrectomy [22]. 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 [23]. (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 [11]. Mycobacterium
tuberculosis is a frequent cause of psoas abscess in regions where tuberculosis is common [1,2]. The most
common bacterial cause is Staphylococcus aureus, including methicillin-resistant Staphylococcus aureus (MRSA);
in one study, S. aureus was implicated in 88 percent of cases (followed by streptococci and E. coli; 4.9 and 2.8
percent, respectively) [3,5,17,24,25]. (See "Skeletal 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
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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 [5].

Klebsiella pneumoniae is an important cause of psoas abscess in Taiwan, especially in patients with diabetes [26].
There are reports of psoas abscess caused by S. pneumoniae [27] and Streptobacillus moniliformis [28], and in
disseminated nocardiosis. Psoas abscess due to Salmonella (mostly non-typhi Salmonella) has also been reported
[29]. Candida albicans has also been described, although rarely [11]. (See "Invasive liver abscess syndrome
caused by Klebsiella pneumoniae" and "Clinical manifestations and diagnosis of nocardiosis".)

CLINICAL MANIFESTATIONS — Psoas abscesses are more common in males than females [3,5]. 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 developing countries than in North America (81 versus 48 percent) [3,5,17].

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 [3,11,17,30,31].

Signs and symptoms — Signs and symptoms of psoas abscess include back or flank pain, fever, inguinal mass,
limp, anorexia, and weight loss [1-3,5]. 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 [1,3,5,11,22].
Fever is present in up to 75 percent of cases and a psoas abscess may manifest as a fever of unknown origin
[22,30].

Psoas abscesses occasionally extend distally and present as a painful or painless mass below the inguinal
ligament [22]. When an inguinal mass in a patient with a psoas abscess is painless (ie, a cold abscess),
tuberculosis is a more likely cause than a bacterial infection [32]. The mass may rarely mimic inguinal
lymphadenopathy or a femoral hernia.

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. 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 [32]. Unlike septic arthritis,
hip pain in patients with psoas abscesses is usually diminished with hip flexion [33].

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 [11]. 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 [5].

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) [5,11,26]. Thrombocytosis is observed less frequently (27 percent of cases)
[5]. 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 [2,26]. Elevated aspartate aminotransferase has also
been described (>40 in 38 percent of cases) [5].

Complications — Complications of psoas abscess include:

● Septic shock (about 20 percent of cases in two series) [26,30]


● Deep venous thrombosis due to extrinsic compression of the iliac vein has also been described, as has
paralytic bowel ileus [34]
● Hydronephrosis due to ureteric compression [1]
● Bowel ileus [2]

Differential diagnosis — Retroperitoneal and intraperitoneal lesions including inflammation, hematoma, or tumor
of the psoas muscle can mimic a psoas abscess, as may retrocecal appendicitis [35]. However, patients with

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retrocecal appendicitis typically have pain in the retrovesical pouch during a rectal exam, whereas those with a
psoas abscess do not.

Enlargement of the iliopsoas bursa (which can communicate with the hip joint) can be difficult to distinguish from a
psoas abscess. Infection of adjacent structures not involving the psoas muscle (eg, septic hip arthritis) can also
mimic a psoas abscess.

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; it
provides definitive diagnosis in almost all cases (image 1) [1,5,6,36]. 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 [19,36]. Magnetic resonance imaging (MRI) may allow improved definition of soft tissues and adjacent
structures, especially visualization of the vertebral bodies [1,2,37]. 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 [5]. Chest x-ray may demonstrate elevation of the diaphragm or a pleural effusion [6].

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 [15,35]. (See "Approach to imaging
modalities in the setting of suspected osteomyelitis", section on 'Nuclear modalities'.)

Ultrasound has low sensitivity and specificity; bowel gas and the pelvic bone may make ultrasound diagnosis
difficult [22]. Although ultrasound imaging may be diagnostic in up to 50 percent of cases, this modality may miss
a diffuse phlegmon or small lesions [5,14,22,30].

Culture — Blood samples and abscess material should be sent to the microbiology lab for Gram stain and
bacterial culture. AFB smear and mycobacterial culture should also be performed when tuberculosis is suspected
or when routine Gram staining is negative. (See "Diagnosis of pulmonary tuberculosis in HIV-negative patients".)

Blood cultures are positive in 41 to 68 percent of cases; the most frequent blood culture isolate is S. aureus [3,13].
Culture of abscess material is frequently needed to identify the causative organism. If feasible this material should
be obtained prior to initiation of antimicrobial therapy to optimize the culture yield.

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 [38].

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 CT guidance) is an appropriate initial approach; in one study this technique successful in
90 percent of cases [1,2,17,38]. 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 [2,30]. Options for surgical
drainage include laparoscopic and open surgical drainage. Advantages of laparoscopy include the extraperitoneal
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nature of the procedure, the capability to break down loculations, and rapid postoperative recovery [39].

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 or an abscess secondary to bowel disease (eg, Crohn's Disease) in
which bowel resection may be necessary [1].

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 MRSA in regions where prevalence is substantial) and enteric
organisms (both aerobic and anaerobic enteric flora) (table 1) [30].

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 pulmonary tuberculosis in the
HIV-infected patient" and "Treatment of pulmonary tuberculosis in HIV-negative patients".)

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 [17,30]. (See 'Drainage' above.)

The optimal duration of antibiotics is uncertain; three to six weeks of therapy following adequate drainage is likely
appropriate [22,30]. Followup imaging should be performed near the end of the planned course of antimicrobial
therapy to ensure satisfactory response to therapy. Tuberculous abscesses are normally treated for six months.

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, and infection due to E. coli [5,30].

Relapse can occur up to one year after initial presentation; this outcome has been reported in 15 to 36 percent of
cases [5,26,40]. Recurrence may be associated with inadequate drainage or inadequate antimicrobial therapy [11].
In addition, presence of hip flexion deformity at clinical presentation may not completely resolve as a result to
fibrosis within the iliopsoas sheath [32].

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 Staphylococcus aureus (MRSA).
Secondary psoas abscess may be monomicrobial or polymicrobial and frequently consist of enteric
organisms (both aerobic and anaerobic bacteria). (See 'Microbiology' above.)

● Signs and symptoms 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 is the optimal radiographic modality to evaluate for psoas abscess. Blood samples
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and abscess material should be sent to the microbiology lab for Gram stain and bacterial culture. AFB 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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REFERENCES

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4. Santaella RO, Fishman EK, Lipsett PA. Primary vs secondary iliopsoas abscess. Presentation,
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10. Lin SS, Vaccaro AR, Reisch S, et al. Low-velocity gunshot wounds to the spine with an associated
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abscess after epidural catheter use. Acta Orthop Belg 2007; 73:670.
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abscesses: case report. Spine (Phila Pa 1976) 2006; 31:E561.
14. Dauchy FA, Dupon M, Dutronc H, et al. Association between psoas abscess and prosthetic hip infection: a
case-control study. Acta Orthop 2009; 80:198.
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the literature. Rev Infect Dis 1983; 5:1003.
16. Ogihara M, Masaki T, Watanabe T, et al. Psoas abscess complicating Crohn's disease: report of a case.

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Surg Today 2000; 30:759.


17. Yacoub WN, Sohn HJ, Chan S, et al. Psoas abscess rarely requires surgical intervention. Am J Surg 2008;
196:223.
18. Hsu RB, Lin FY. Psoas abscess in patients with an infected aortic aneurysm. J Vasc Surg 2007; 46:230.
19. Inufusa A, Mikawa Y, Morita I, Fujiwara T. Ruptured abdominal aortic aneurysm associated with a psoas
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20. Sharif MA, Lee B, Lau LL, et al. Prosthetic stent graft infection after endovascular abdominal aortic aneurysm
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and grave prognosis in gas-forming cases. J Microbiol Immunol Infect 2001; 34:201.
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world literature. Isr J Med Sci 1996; 32:771.
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and psoas abscess after rooster scratches. J Clin Microbiol 2008; 46:2820.
29. Heyd J, Meallem R, Schlesinger Y, et al. Clinical characteristics of patients with psoas abscess due to non-
typhi Salmonella. Eur J Clin Microbiol Infect Dis 2003; 22:770.
30. Huang JJ, Ruaan MK, Lan RR, Wang MC. Acute pyogenic iliopsoas abscess in Taiwan: clinical features,
diagnosis, treatments and outcome. J Infect 2000; 40:248.
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32. Stefanich RJ, Moskowitz A. Hip flexion deformity secondary to acute pyogenic psoas abscess. Orthop Rev
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33. Fish DE, Middleton K, Gluzman A. Atypical presentation of osteomyelitis, discitis, epidural, and iliopsoas
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35. Kao PF, Tzen KY, Tsui KH, et al. The specific gallium-67 scan uptake pattern in psoas abscesses. Eur J
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38. Kishi Y, Kajiwara S, Seta S, et al. Retroperitoneal schwannoma misdiagnosed as a psoas abscess: report of
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Topic 7652 Version 8.0

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GRAPHICS

Psoas abscess on CT scan

An axial CT scan through the upper pelvis (A) shows a gas containing abscess (arrow) in the
left psoas muscle. A coronal reconstruction (B) shows the ovoid shaped abscess extending
into the iliacus muscle (arrow).

CT: computed tomography.

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Empiric antiobitic therapy for psoas abscess in adults*

Empiric therapy with activity against methicillin-resistant S. aureus


Preferred Vancomycin (30 mg/kg IV every 24 h in 2 equally divided doses)

Alternatives Daptomycin (6 mg/kg IV once daily)

Linezolid (600 mg IV or orally twice daily)

PLUS

Empiric therapy with activity against gram-negative and anaerobic


pathogens
Monotherapy with a beta-lactam/beta-lactamase inhibitor, such as one of the following:
Ampicillin-sulbactam (3 g every 6 hours)

Piperacillin/tazobactam (3.375 g every 6 hours)

Ticarcillin-clavulanate (3.1 g every 4 to 6 hours)

A third generation cephalosporin such as ceftriaxone (1 g IV every 24 hours) PLUS


metronidazole (500 mg IV every 8 hours)

A fluoroquinolone (eg, ciprofloxacin 400 mg IV every 12 hours or levofloxacin 500 mg IV daily)


PLUS metronidazole (500 mg IV every 8 hours)

Monotherapy with a carbapenem• such as one of the following:


Imipenem (500 mg every 6 hours)

Meropenem (1 g every 8 hours)

Ertapenem (1 g daily)

* Antibiotic therapy should be tailored to culture and sensitivity data when available.
• Carbapenems should not be used for patients with history of immediate-type hypersensitivity to
beta-lactams.

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