Psoas Abscess: A Primer for the Internist

, Department of Internal Medicine, Lincoln Health Center and Durham Regional Hospital, Durham, NC

South Med J. 2001;94(1) 

Abstract and Introduction

Psoas abscess is a rare condition with vague clinical presentation. In this article, its epidemiology, etiology, bacteriology, diagnosis, and treatment are discussed. Common diseases that may be erroneously diagnosed in patients with psoas abscess are presented.

Many abdominal conditions are so dramatic in their presentation that patients may go to the emergency room. Psoas abscess has an insidious onset, and patients may be seen by their primary care physician. Because psoas abscess is rare and is uncommonly discussed in primary care medical literature, primary care physicians may miss this diagnosis. Therefore, these practitioners need to be familiar with psoas abscess to prevent delay in diagnosis and treatment. Psoas abscess may be classified as primary or secondary, depending on the presence or absence of underlying disease.

Psoas Muscle Anatomy

The psoas muscle is a retroperitoneal organ that originates from the lateral borders of the 12th thoracic to fifth lumbar vertebrae and inserts on the lesser trochanter of the femur. In 70% of people, it is a single structure (psoas major), but 30% also have a smaller psoas minor muscle, which lies anterior to the psoas major along the same course. It is innervated by branches of L2, L3, and L4, before formation of the femoral nerve. The psoas muscle lies in close proximity to many other organs, including the sigmoid colon, jejunum, appendix, ureters, aorta, renal pelvis, pancreas, iliac lymph nodes, and spine. Thus, infections in these organs can contiguously spread to the psoas muscle. The psoas muscle has a rich vascular supply that is believed to predispose it to hematogenous spread from sites of occult infection.

Epidemiology

In 1992, the worldwide reported occurrence of psoas abscess was 12 cases per year.^[1] This was a significant increase from the calculated occurrence of 3.9 cases per year before 1985. The increase was attributed to improved diagnosis with the widespread use of computed tomography (CT).^[1,2] It is likely that incomplete reporting, particularly in the developing world, spuriously lowered the incidence. Up to 1985, all the cases of psoas abscess reported in developing countries were primary, whereas in the United States and Canada nearly 50% of cases were secondary.^[1] Earlier reports suggested that primary psoas abscess was more common in younger patients, with 83% of cases diagnosed in patients less than age 30. In contrast, up to 40% of secondary psoas abscesses were diagnosed in patients more than 40 years old. Primary and secondary psoas abscesses were relatively rare in the elderly.^[1] This age distribution is different from the findings in a recent series of 18 patients from Johns Hopkins University School of Medicine. In this series, researchers found secondary psoas abscess (age range, 2 to 78 years) to be more prevalent (61%) than primary psoas abscess (age range, 27 to 81 years). It is notable that 28% of the patients were over the age of 65. Of the patients with primary psoas abscess, 86% were intravenous drug users, and 57% were infected with the human immunodeficiency virus (HIV). None of the patients with secondary psoas abscess had HIV infection or a history of intravenous drug abuse. It is possible that the incidence of primary psoas abscess will increase with the HIV pandemic.^[3] Other predisposing conditions include diabetes, immunosupression, and renal failure.^[4] Underlying diseases in patients with secondary psoas abscess are shown in .

Bacteriology

Staphylococcus aureus is the pathogen in 80% of cases of primary psoas abscess.^[2,3] Other pathogens include Serratia marcescens,^[3]Pseudomonas aeruginosa,^[3]Haemophilus aphrophilus,^[5] and Proteus mirabilis.^[1] Secondary psoas abscess is usually caused by enteric bacteria. These include Escherichia coli, Streptococcus species, Enterobacter species, and Salmonella enteritidis.^[3] Methicillin resistant S aureus is also a known pathogen.^[3]Mycobacterium tuberculosis as a cause of psoas abscess is currently rare in the United States. In areas of the world where tuberculosis is still a common disease, it continues to be an important cause of psoas abscess. Nontuberculous mycobacteria are also important, as evidenced by recent case reports of psoas abscess caused by M kansasii^[6] and M xenopi.^[7]

Diagnosis

Symptoms are often nonspecific. Patients may present with fever, flank pain, abdominal pain, or limp. Because of the innervation of the psoas muscle by L2, L3, and L4, pain due to its inflammation sometimes radiates anteriorly to the hip and thigh. Other symptoms are nausea, malaise, and weight loss. These symptoms bring to mind other clinical syndromes that are more commonly seen by primary care physicians ( ).

A good physical examination is critical for the prompt diagnosis of psoas abscess. The diagnosis may be given away, if the patient is noted to favor the position of greatest comfort. This is the supine position, with the knee moderately flexed and the hip mildly externally rotated. Rarely, psoas abscess is associated with painless subinguinal mass. There are well-described signs of psoas inflammation,^[8] which the clinician should look for in every patient suspected of having psoas abscess ( ). The premise of these tests is that the psoas muscle is the primary hip flexor. Flexion and stretching or contraction of the inflamed psoas muscle results in pain.

Laboratory tests are helpful in the evaluation of suspected psoas abscess. Leukocytosis (mean count, 15,900/mm³), elevated erythrocyte sedimentation rate (ESR) (mean, 90 mm/hr), and elevated blood urea nitrogen (BUN) (mean, 30.5 mg/dL) were reported in 100% of patients in the series from Johns Hopkins.^[3] These are not universal findings. Pyuria is sometimes present.^[9] As in most clinical problems, diagnosis is aided by appropriate radiologic testing. Before the availabilty of ultrasonography and CT, many cases of retroperitoneal abscess were diagnosed at autopsy. Whenever psoas abscess is suspected, CT should be done for definitive diagnosis. This has superceded ultrasonography as the radiologic test of choice. Ultrasonography is diagnostic in only 60% of cases of psoas abscess,^[9] compared with 80% to 100% for CT.^[10] Sensitivity and specificity of diagnosing psoas abscess is not improved by magnetic resonance imaging (MRI), and with its higher cost and greater patient discomfort, MRI has no role in the diagnosis of psoas abscess.

Treatment

Treatment involves the use of appropriate antibiotics, as well as drainage of the abscess. Knowledge of common pathogens should guide initial choice of antibiotics. Adjustments should be based on report of abscess fluid culture and sensitivity testing. It has been suggested that in cases of psoas abscess believed to be primary, antistaphylococcal antibiotic therapy should be started before final bacteriologic diagnosis.^[1] However, the identification of nonstaphylococcal organisms in some patients with primary psoas abscess and the identification of staphylococcus in patients with secondary psoas abscess^[3] make it prudent in all cases of psoas abscess to start treatment with broad spectrum antibiotics pending final bacteriologic diagnosis. Coverage should include staphylococcal and enteric organisms, for which agents such as clindamycin, antistaphyloccocal penicillin, and an aminoglycoside may be used.^[11] Less cumbersome regimens can be easily formulated. Drainage of the abscess may be done through CT-guided percutaneous drainage or surgical drainage. Percutaneous drainage is much less invasive and is effective for draining uniloculated and multiloculated psoas abscesses.^[12] It is technically similar to open surgical drainage, and it has been advocated as the drainage method of choice.^[13] Surgical drainage is associated with shorter hospital stay (15.9 vs 28.5 days).^[3] Surgical drainage may be ideal for patients with underlying Crohn's disease or other gastrointestinal diseases. In these patients, performing a single operation to drain abscess and resect diseased bowel is desirable.^[15] An occasional patient will require multiple operations^[15] or repeated percutaneous drainage before the abscess resolves. Abscess drainage needs to be continued until obliteration of the abscess cavity occurs and there is evidence of clinical improvement. Parameters that can be used to determine clinical recovery include defervescence and normalization of the white blood cell (WBC) count, as well as subjective improvement. The duration of antibiotic therapy should be individualized. Antibiotics are sometimes continued up to 2 weeks after complete abscess drainage.

The following report describes a case of psoas abscess in a patient who was also found to have HIV infection.

Case Report

A 51-year-old man without a history of urologic disease went to his primary care physician after 4 days of right flank pain associated with urinary frequency. He denied dysuria, fever, chills, nausea, or vomiting. Physical examination revealed a temperature of 97.8°F and blood pressure of 127/67 mm Hg. There was mild tenderness in the right flank but no pulsatile abdominal mass, bruit, or significant abdominal tenderness. Prostate examination was unremarkable. White blood cell count was 9,400/mm³. Urinalysis showed 5 to 10 WBCs. A 10-day course of trimethoprim/sulfamethoxazole was started for presumed urinary tract infection, and the patient was told to return upon completion of the treatment.

A week after initiating antibiotic therapy, he went to an urgent care clinic because of right hip pain and nausea. He had lost about 4 pounds. Findings on radiography of the hip were negative. No definite diagnosis was made. He was given ibuprofen and discharged home. Three days later, the patient returned to his primary care physician for follow-up. By then, he had severe right hip pain with radiation to the anterior thigh. Temperature was 98.7°F, and total weight loss was 7 pounds. He had physical signs of psoas inflammation in addition to tenderness in the right lower quadrant. Computed tomography of the abdomen and pelvis showed a large right psoas abscess (Figure). The WBC was 7,800/mm³. Liver enzyme, creatinine, and BUN values were normal. The ESR was 87 mm/hr. Broad spectrum antibiotic therapy was started, and percutaneous drainage of the psoas abscess yielded 210 mL of purulent material, which grew E coli and Streptococcus viridans. Urine culture from the initial presentation to his primary care physician also grew E coli. Colonoscopy and upper GI series with small bowel follow-through did not reveal any gastrointestinal disease. Multiple blood cultures were negative, and results of echocardiography were normal. Test for HIV was positive. The patient recovered fully from the abscess after drainage and antibiotic treatment. He is currently receiving care for HIV infection.

Reprint Address

Reprint requests to Babafemi Taiwo, MD, Lincoln Health Center, 1301 Fayetteville St, Durham, NC 27707.

South Med J. 2001;94(1) © 2001  Lippincott Williams & Wilkins

Cite this: Psoas Abscess: A Primer for the Internist - Medscape - Jan 01, 2001.