Imaging-negative psoas abscess

Abstract

In April, 2012, a 55-year-old man came to our emergency department with acute-onset left lower abdominal pain that had persisted for 12 h. He had been on haemodialysis for 20 years because of diabetic nephropathy. On examination, his temperature was 37·8°C and other vital signs were normal. The patient dragged his left leg when walking. His pain was relieved by lying on his back with the left knee fl exed. The left lower quadrant of the abdomen was tender and the psoas sign (pain on hip extension) was positive on the left. His white cell count was normal, but C-reactive protein was slightly raised. Although psoas abscess was suspected, neither enhanced CT (fi gure) nor plain MRI detected any lesion. Orthopaedic and radiological consultation suggested that psoas abscess was excluded by negative imaging studies. However, no other diagnosis was more compatible with this patient’s condition, and he had multiple risk factors for psoas abscess. Therefore, we made a provisional diagnosis of early imaging-negative psoas abscess (an infl ammatory process before overt abscess formation). The patient was admitted and treated with IV vancomycin (500 mg every 48 h) after two sets of blood cultures were obtained. On the third hospital day, repeat enhanced CT showed multiple hypodense foci with ring enhancement in the left psoas muscle, confi rming the diagnosis of psoas abscess (fi gure). Blood cultures grew meticillin-sensitive Staphylococcus aureus. Because other investigations, including transoesophageal echocardiography, revealed no source of infection, the patient’s arteriovenous fi stula was judged the probable source. He responded to treatment with IV cefazolin (2 g after dialysis thrice weekly for 6 weeks). In June, 2013, he was well without relapse. Psoas abscess is rare, although identifi cation has increased with widespread availability of imaging studies. It is classifi ed as primary or secondary. Primary psoas abscess occurs because of haematogenous or lymphatic spread of infection from a distant site, whereas secondary psoas abscess is caused by direct extension of infection from adjacent structures. The most common bacterial pathogen in primary abscess is Staphylococcus aureus, whereas mixed enteric fl ora predominate in secondary psoas abscess. Risk factors for primary abscess include diabetes, intravenous drug use, HIV infection, renal failure, and other causes of immunosuppression. There have been several case reports of primary psoas abscess in dialysis patients with haemodialysis access septicaemia. The clinical presentation is variable, with the classic triad of fever, back pain, and limp in only 30% of patients. Hyperextension of the hip causes pain because of stretching of the aff ected psoas muscle. CT almost always provides a defi nite diagnosis and is regarded as the so-called gold standard, although some authors report that MRI is more sensitive. In our patient, neither modality revealed abnormalities initially, suggesting that very early psoas abscess might be undetectable by these methods. A case report has suggested the limitations of plain CT for diagnosing early psoas abscess, but none has reported on the limitations of enhanced CT and MRI to our knowledge. Treatment of psoas abscess requires prompt initiation of antibiotic therapy and drainage. The mortality rate of primary psoas abscess is 2·4%, but it rises to 18·9% for secondary abscess and approaches 100% in untreated cases. The main cause of death is delayed or inadequate treatment. Therefore, correct diagnosis and early initiation of appropriate treatment are essential. If early psoas abscess is suspected, timely initiation of antibiotic therapy is recommended even if imaging studies are negative.