Girl, 5, With Fever and Hip Pain

DISCUSSION
Psoas abscess is a collection of pus in the iliopsoas compartment, an extraperitoneal space containing the psoas and iliacus muscles.² It can be life-­threatening if the infection progresses to septic shock. Historically, psoas abscesses were a frequent complication of tuberculosis (TB) of the spine; but with modern TB treatment, these abscesses have become rare.² Paradoxically, increased utilization of CT to evaluate sepsis of unknown etiology has led to a recent increase in the frequency of psoas abscess diagnosis.³

Psoas abscesses are categorized as either primary or secondary, with primary infections originating in the psoas muscle and secondary infections spreading from adjacent organs.² In 42% to 88% of cases (depending on the study), primary psoas abscesses are caused by the hematogenous spread of Staphylococcus aureus from distant infection sites.^2,4,5 The psoas muscle is particularly susceptible to this mode of infection because of its rich vascular supply.⁶ Children, immunosuppressed adults (ie, patients with diabetes, HIV/AIDS, or renal failure), IV drug users, and patients with a history of trauma to the muscle are most susceptible to developing a primary psoas abscess.^2,5

Secondary psoas abscesses are caused by infections involving adjacent structures of the gastrointestinal, urinary, and skeletal systems. They are most frequently associated with intra-abdominal inflammatory processes, with the most common etiology being Crohn disease.⁵ Secondary psoas abscesses, though more diverse in their bacterial flora, tend to follow certain microbiologic patterns based on the inoculating source; Escherichia coli is the most common pathogen in secondary abscesses caused by gastrointestinal (42%) and urinary (61%) sources, and S aureus the most common (35%) from skeletal origins (ie, osteomyelitis).^4,5Mycobacterium tuberculosis is the more frequently found cause in developing countries but should be considered if the patient has recently travelled outside the United States.

Review of the literature suggests that the incidence of methicillin-resistant S aureus (MRSA) as the causative agent of psoas abscesses may be increasing. However, there is a wide variance in the incidence reported, ranging from 1.1% to 12% of confirmed microbial infections.^5,7,8

The classic historical presentation of psoas abscess has been described as the triad of back pain, fever, and limp^5,6; however, this triad has only been described in approximately 30% of cases.⁵ The typical presentation consists of flank or lower limb pain (91%), fever (75%), anorexia (46%), and/or weakness (43%).⁴ Laboratory abnormalities include leukocytosis (67%) and elevated markers of inflammation (eg, erythrocyte sedimentation rate, seen in 73% of cases).⁴

Imaging via abdominal ultrasound may be helpful to screen for psoas abscess; however, its utility is limited by a low diagnostic yield of 60% or less.^2,4 Direct visualization of the retroperitoneal structures, for example, can be problematic due to the presence of bowel gas.⁹ Abdominal CT is considered the gold standard for the definitive diagnosis of psoas abscess due to its high sensitivity (100%) and specificity (77%); it can also be used simultaneously to guide percutaneous drainage to treat the abscess if needed.⁷ However, some clinicians prefer abdominal MRI because of its ability to enhance soft-tissue visualization without requiring use of IV contrast.^2,4

The approach to treating psoas abscess varies from a strictly antibiotic regimen to percutaneous drainage, and in rare circumstances, open surgical drainage. Antibiotic therapy without drainage or surgical intervention is a sufficient starting point for treatment of abscesses less than 3 cm in size.³

The antibiotic regimen choice depends on the suspected pathogen. In cases of suspected S aureus, empiric antistaphylococcal antibiotics should be initiated while culture results are pending.^2,4 Secondary psoas abscesses thought to be derived from a urinary or gastrointestinal source should prompt use of a broader spectrum antibiotic due to the higher probability of gram-negative, anaerobic, or polymicrobial involvement.^2,4

Once final culture and sensitivity results are obtained, antibiotic therapy should be modified to target the isolated pathogen(s). Treatment duration is typically six weeks but may vary, depending on serial culture results and the inoculating source.⁴ Review of the literature reveals that abscesses resulting from skeletal sources have traditionally been treated longer, usually with antibiotics alone, than those from urinary or gastrointestinal sources, which are often treated with the combination of antibiotics and percutaneous drainage.⁴

In cases of psoas abscesses larger than 3 cm, management should include both appropriate antibiotics and percutaneous drainage of the abscess.² Percutaneous drainage is preferred to open surgical drainage because outcomes are similar, it is less invasive, and there is less risk of spreading abscess contents.^2-4 In a retrospective analysis by Dietrich et al, 50% of patients treated with antibiotics and percutaneous drainage responded after one drainage, but the success rate increased to 100% after a second drainage.⁷ In addition, percutaneous drainage was associated with a lower mortality rate and a shorter hospital stay when compared to open surgical drainage.⁷

Open surgical drainage is rarely performed and usually only considered if the patient is not responding to a combination of focused antibiotic treatment and percutaneous drainage or has associated comorbidities, such as Crohn ileocolitis.^2-4 In a retrospective analysis by Tabrizian et al, percutaneous drainage served as a bridge to open surgical drainage in nearly all patients with a gastrointestinal origin, such as Crohn disease, diverticulitis, appendicitis, and/or pancreatitis.⁶

Treatment of psoas abscesses has an overall failure rate of 15.8%, with an associated mortality rate of less than 7%.⁴ Overall prognosis is good, but outcomes can be negatively affected by such factors as advanced age, delay in diagnosis, bacteremia, and other comorbidities.⁴

Next page: Outcome for the case patient >>