Bursitis is the swelling or inflammation of a synovium-lined sac-like structure called a bursa. These are found throughout the body near bony prominences and between bones, muscles, tendons, and ligaments.[1] They function to reduce friction between these structures. Inflammation of the bursa around large joints like the shoulder, knee, hip, and elbow may prompt patient visits to healthcare providers. There are four major bursae associated with the knee joint: suprapatellar, infrapatellar, pes anserine, and prepatellar. This article will focus on the prepatellar bursa and, specifically, prepatellar bursitis. This bursa is present between the patella and the overlying subcutaneous tissue. It represents the most commonly affected bursae of the knee and the second most commonly affected bursa overall, following the olecranon bursa. The location makes it a target during repetitive kneeling and has led to it being colloquially referred to as housemaid's, carpet layers, and carpenter's knee.
The thin walls present within bursae allow for them to become easily inflamed when they become irritated. This may be produced by acute direct trauma or, more commonly, as repetitive trauma from kneeling. Much less frequently, prepatellar bursitis may be caused by gout, rheumatoid arthritis, or infections. Conditions causing immunosuppression lead to an increased risk for developing bursitis, such as diabetes mellitus, chronic steroid use, and hemodialysis. Chronic bursitis may also develop from repetitive trauma, although it occurs less frequently in the prepatellar when compared to olecranon bursa.
The incidence of prepatellar bursitis is difficult to accurately assess, as a large percentage of cases that actually reach the point of presentation to a healthcare setting are likely to be septic, while the mild cases may never seek care. However, it is believed to have an annual incidence of 10/100,000, with more than 80% of all bursitis patients being males aged 40–60 years.[2] It is important to recognize that while the majority of these cases are non-septic, up to 1/3 may present as septic bursitis and have an associated increase in morbidity.[2] Any age group can be affected by prepatellar bursitis, but septic bursitis appears more likely to occur in children. People with chronic immunosuppressive conditions (e.g., diabetes mellitus) are at an increased risk of developing bursitis.
Trauma to the bursa increases blood flow, migration of leukocytes into the bursa, and fluid production from within the synovial cells of the bursa, providing the foundation of the inflammatory response seen in bursitis. Trauma itself, direct inoculation, presence of overlying skin and soft tissue infections, or hematogenous spread can lead to septic bursitis. Direct microscopy examination of the synovial fluid of the bursa may reveal a source of inflammation, including gout or calcium pyrophosphate dihydrate crystals or bacteria. Molecular examination of fluid is likely to reveal elevated inflammatory mediators such as tumor necrosis factor-alpha, various interleukins, and cyclooxygenases.
Bursitis may present acutely or chronically, with wide variation in symptoms and presentation. A detailed history focusing on medical and social histories will assist the clinician in differentiating. Important historical factors include the presence of immunosuppression (e.g., diabetes, chronic steroid use) and hobbies or occupation (e.g., housemaid, carpentry, roofing, gardening). Acute bursitis more commonly arises from trauma, infection, or crystalline joint disease, whereas chronic bursitis tends to be the result of inflammatory arthropathies and repetitive pressure or overuse. The physical examination findings also vary. Acute bursitis generally presents with erythema, warmth, and tenderness on palpation of the bursa, and possibly decreased range-of-motion in certain planes secondary to discomfort. Contrarily, chronic bursitis is often painless - the bursa has had time to expand and to accommodate for the increased fluid. In either scenario, it is important to assess the area for signs of overlying trauma, erythema, and warmth. One study suggested that an increase in the surface temperature of just 2.2 degrees centigrade between the skin overlying the affected bursa and the unaffected, contralateral bursa was highly sensitive and specific for septic bursitis.[3] The bursa may be warm during an episode of acute bursitis, highlighting the importance of additional diagnostic studies, particularly in those individuals without similar prior episodes.
The diagnosis of bursitis is primarily clinical. Routine lab work is not likely to be beneficial. However, imaging may be a useful adjunct to a thorough history and physical examination to help narrow the differential diagnosis. Plain film x-rays may be considered when acute trauma produces a concern for fracture or foreign body. Ultrasound may be helpful in differentiating between an inflamed bursa and the presence of cobblestoning in cellulitis. It is also likely to be useful to observe changes with range of motion, which help to rule out tendonous injury, and provides an added benefit when obtaining needle aspirates.[4] While unlikely to be necessary for diagnosis, MRI may be obtained to rule out other differential diagnoses. Prepatellar bursitis appears as an oval fluid-signal-intensity lesion between the subcutaneous tissue and the patella on MRI.[5]
Needle aspiration of bursal fluid is crucial in differentiating between causes. Aspirated bursal fluid should be sent for cell count, gram stain and culture, glucose, and analysis for crystals. The presence of negatively-birefringent crystals rules in gout, whereas positively-birefringent crystals suggest pseudogout (calcium pyrophosphate dihydrate deposition disease). A predominance of polymorphonuclear leukocytes suggests septic causes, while a predominance of mononuclear cells suggests non-infectious etiologies. While fluid leukocytes are non-specific, bursal leukocytosis >2000/mm had a sensitivity and specificity for septic bursitis of 94 and 79 percent, respectively.[6] Aspirate fluid should be tested for glucose as lower levels suggest an infectious process. The sensitivity of gram staining is widely variant, ranging from 15 to 100%.[7][8] Obtaining a culture of the bursal fluid is the gold standard for the diagnosis of septic bursitis.[9]
Prepatellar bursitis may present acutely or chronically. The underlying causes should also be addressed, such as with medical therapies for gout and antimicrobial therapy for septic bursitis. The general approach to the treatment of bursitis should be focused on conservative therapies of rest, ice, activity modification, nonsteroidal anti-inflammatory medications, and aspiration.[10] Most acute cases will respond to conservative measures. In chronic cases, similar therapies are pursued, but occasionally, corticosteroid injection may be considered. Early differentiation between septic and non-septic bursitis is a key factor in management and improving patient outcomes, although the conservative measures above are beneficial for both groups.[2] A structured approach to managing patients, including frequent, close follow-up, is likely to prevent the need for hospital admission and lessens the frequency of long-term complications.[11] Incision and drainage are rarely needed but may be indicated in traumatic or septic cases that don't respond to conservative measures.[12] Based on several studies, oral and intrabursal, antimicrobial therapies are unlikely to be beneficial for the treatment of septic infrapatellar bursitis, therefore hospitalization, needle aspiration, and intravenous antibiotics are indicated.[12][13] Sclerotherapy (using polidocanol, hypertonic saline, or others) and bursectomy may be considered for recalcitrant cases.[14] In cases of traumatic bursitis, intractable to initial conservative therapies, consider endoscopic therapies.[15][16]
The possible differential diagnosis for acute knee pain vary somewhat by age group but remain extensive regardless of age or gender. A thorough examination can help differentiate prepatellar bursitis from patellar subluxation/dislocation, tibial apophysitis, patellar tendonitis, and patellofemoral tracking syndrome. Osteoarthritis of the knee is a common cause of discomfort, while reactive and rheumatoid arthritis may also cause knee pain. Septic arthritis will also produce discomfort. Radiation of pain from hip fracture, osteoarthritis of the hip, slipped capital femoral epiphysis (SCFE), and other disorders of the hip may refer pain to the knee. It is important to assess for cellulitis or other skin, and soft tissue infections as these can present similarly to prepatellar bursitis. Other common causes of knee pain include ligamentous and meniscal injuries within the knee joint itself. Fractures of the tibial plateau also produce discomfort within the knee. Inflammation of a bursa other than the prepatellar may produce knee discomfort.
The overall prognosis of bursitis is excellent. However, complications, such as infection, increase the morbidity, and it is important to recognize these early.
The primary complication of prepatellar bursitis is the development of infection. Other complications are more likely to be secondary to management options, including infection due to the inoculation of bacteria from needle aspiration, a fistula between the skin surface and bursa after needle aspiration, subcutaneous atrophy as a result of corticosteroid injections, bleeding after injections, and even patellar tendon rupture.
Treatment-resistant cases of prepatellar bursitis may require orthopedic surgery consultation in order to arrange definitive surgical management.
Patient education will revolve around prevention. Appropriate precautions to avoid trauma to the knee, avoid frequent kneeling, whenever possible, or to use protective equipment, such as bulky knee pads, for those who cannot. In the less common episodes caused by sports-related trauma, knee pads may also be beneficial in prevention.
The majority of simple, acute cases of prepatellar bursitis may be appropriately managed by a primary care provider, and the majority cared for in the outpatient setting. The presence of septic bursitis, severe sepsis, or septic shock is likely to require inpatient therapies and possibly infectious disease consultation, dependent on the microbial pathology. Referral to an orthopedic surgeon may be required when surgical excision of the bursa is being considered. [Level 5]
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