American Journal of Physical Medicine & Rehabilitation:
De Mesa, Charles DO, MPH; Dajoyag-Mejia, Maria A. MD
From the Department of Physical Medicine and Rehabilitation, Baylor College of Medicine (CDM, MAD-M), and Spinal Cord Injury Care Line, Michael E. DeBakey VA Medical Center, Houston, Texas (MAD-M).
All correspondence and requests for reprints should be addressed to: Charles De Mesa, DO, MPH, BCM/UT Houston PM&R Alliance, 1333 Moursund Avenue Suite # A-220 Houston, TX 77030.
Baylor College of Medicine Institutional Review Board and the Baylor College of Medicine were granted exemption for this activity (reference H-29581). Signed consent for release of de-identified information was obtained.
Financial disclosure statements have been obtained, and no conflicts of interest have been reported by the authors or by any individuals in control of the content of this article.
A 54-yr-old man with an L1 AIS D (American Spinal Injury Association Impairment Scale) spinal cord injury (SCI) secondary to epidural and bilateral psoas abscesses 6 mos before presented for evaluation of left knee pain and swelling (Fig. 1). He reported a grinding pain of his knee, made worse with movement. He also described a red, swollen, and tender calf muscle. A nonhealing ischial pressure ulcer on the affected limb prompted him to seek medical attention. He had no other associated symptoms.
On physical examination, he had a 3 × 4 cm mass on the lateral aspect of the popliteal fossa, which was smooth, fluctuant, and tender. Additional palpation revealed warmth and edema extending to the lateral and posterior compartments of his lower limb, with exquisite tenderness of the calf.
An ultrasound was negative for deep vein thrombosis and revealed a ruptured Baker’s (popliteal) cyst. Despite conservative management, the patient continued to have low-grade fevers and persistent leukocytosis. A white blood cell scan demonstrated infected ruptured Baker’s cyst (Fig. 2). Soft tissue aspiration caused immediate pain relief, and he was started empirically on intravenous Vancomycin. Cultures returned positive for Methicillin-sensitive Staphylococcus aureus, and he was switched to intravenous Cefazolin.
Baker’s cysts are usually painless swellings accompanying noninfectious knee joint effusions. The synovial fluid is typically sterile, and rupture does not commonly result in infection. Treatment is conservative. In contrast, infected ruptured Baker’s cyst may present with painful limb swelling, fever, and persistent leukocytosis. Because there is extrusion of fluid down the leg between the calf muscles, it can be confused clinically with deep vein thrombosis or cellulitis. Such conditions may co-exist. Furthermore, SCI patients, depending on the nature of injury, may present with insensate limbs, making the diagnosis more challenging.
Careful evaluation of thromboembolic disease is critical, particularly in acute SCI patients. Data suggest that in such patients who are less than 1-yr postinjury, the risk for deep vein thrombosis and pulmonary embolus is significantly greater than chronic SCI patients.1 Pulmonary embolus is the leading cause of death in acute SCI and is tied for second as the leading cause of death in neurologically incomplete lesions.2 Case reports of infected popliteal cysts are rare, with one literature review revealing only 18 cases during a 32-yr period.3 S. aureus was the most common organism.
In summary, infected ruptured Baker’s cysts are rare but are important to be distinguished from thromboembolic disease. It should be suspected in patients with a history of intravenous drug abuse, local inflammation, and systemic infection to provide appropriate management.
1. Paralyzed Veterans of America/Consortium for Spinal Cord Medicine. Prevention of thromboembolism in spinal cord injury. Washington, DC: Paralyzed Veterans of America (PVA), 1999, pp. 4–5
2. Suárez JI. Critical Care Neurology and Neurosurgery. Totowa, New Jersey, Humana Press Inc., 2004, p. 204
3. Drees C, Lewis T, Mossad S: Baker’s cyst infection: Case report and review. Clin Infect Dis 1999; 29: 276–8
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