Prepatellar Bursitis

Etiology

Bursae's thin walls make them susceptible to inflammation once triggered by acute direct trauma or repetitive trauma from frequent kneeling. Additionally, prepatellar bursitis may arise from underlying factors such as gout, rheumatoid arthritis, or infections. Conditions causing immunosuppression lead to an increased risk of developing bursitis, such as diabetes mellitus, chronic steroid use, and hemodialysis. Chronic bursitis may also develop from repetitive trauma, although this occurs less frequently in the prepatellar when compared to the olecranon bursa.

Epidemiology

The incidence of prepatellar bursitis is challenging to assess, as many cases reaching the point of clinical presentation are likely to be septic. In contrast, patients with mild cases may never seek care. However, prepatellar bursitis is estimated to have an annual incidence of 1 in 10,000 individuals—with more than 80% of all patients with bursitis being men 40 to 60 years.[2] Although the majority of these cases are non-septic, up to one-third may present as septic and have an associated increase in morbidity.[2] Any age group can be affected by prepatellar bursitis; however, septic bursitis is more likely to occur in children. People with chronic immunosuppressive conditions (eg, diabetes mellitus) also have an increased risk of developing bursitis.

Pathophysiology

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, direct inoculation, overlying skin, soft tissue infections, or hematogenous spread can lead to septic bursitis. Direct microscopy examination of the bursa's synovial fluid may reveal a source of inflammation, including gout, calcium pyrophosphate dihydrate crystals, or bacteria. Molecular fluid analysis will likely show elevated inflammatory mediators such as tumor necrosis factor-alpha, interleukins, and cyclooxygenases.[3]

History and Physical

Bursitis may present acutely or chronically, with a wide variation in symptoms and presentation. A detailed history focusing on medical and social histories will assist the clinician with diagnosis. Important historical factors include the presence of immunosuppression (eg, diabetes, chronic steroid use) and hobbies or occupation (eg, housekeeping, carpentry, roofing, gardening). Acute bursitis more commonly arises from trauma, infection, or crystalline joint disease, whereas chronic bursitis tends to result from inflammatory arthropathies and repetitive pressure or overuse. 

The physical examination findings also vary. Acute bursitis generally presents with erythema, warmth, 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 accommodate the increased fluid. In either scenario, assessing the affected area for signs of overlying trauma, erythema, and warmth is essential. Results from a study suggested that an increase in the surface temperature of just 2.2 °C between the skin overlying the affected bursa and the unaffected contralateral bursa was susceptible and specific for septic bursitis.[4] The bursa may be warm during an episode of acute bursitis, highlighting the importance of additional diagnostic studies, particularly in individuals without similar prior episodes.

Evaluation

The diagnosis of bursitis is primarily clinical. Routine lab work is not likely to be beneficial. However, imaging may be a valuable adjunct to a thorough history and physical examination to help narrow the differential diagnoses. Plain film x-rays may be considered when acute trauma produces a concern for fracture or foreign body. Ultrasound may help differentiate between an inflamed bursa and the presence of cobblestoning in cellulitis. Ultrasound may also help observe changes in the range of motion, which helps to rule out tendonous injury and provides an added benefit when obtaining needle aspirates.[5] While unlikely to be necessary for diagnosis, magnetic resonance imaging (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.[6] 

Needle aspiration of bursal fluid is crucial in differentiating between causes. Aspirated bursal fluid should be sent to the lab for cell count, gram stain and culture, glucose, and crystal analysis. Negative birefringent crystals rule 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/mm³ had a sensitivity and specificity for septic bursitis of 94% and 79%, respectively.[7] 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%.[8][9] Obtaining a culture of the bursal fluid is the gold standard for diagnosing septic bursitis.[10]

Treatment / Management

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 treating bursitis should focus on conservative therapies of rest, ice, activity modification, nonsteroidal anti-inflammatory medications, and aspiration.[11] Most acute cases will respond to conservative measures. Similar therapies are pursued in chronic cases, but corticosteroid injections may be considered. Early differentiation between septic and nonseptic bursitis is a key factor in managing and improving patient outcomes; however, the conservative measures above benefit both groups.[2] A structured approach to patient care, including frequent, close follow-up, is likely to prevent the need for hospital admission and reduce the frequency of long-term complications.[12] Incision and drainage are rarely needed but may be indicated in traumatic or septic cases that do not respond to conservative measures.[13] Based on several studies, oral and intrabursal antimicrobial therapies are unlikely to be beneficial for treating septic infrapatellar bursitis. Therefore, hospitalization, needle aspiration, and intravenous antibiotics are indicated.[13][14] Sclerotherapy (polidocanol, hypertonic saline, or others) and bursectomy may be considered for recalcitrant cases.[15] In cases of traumatic bursitis, intractable to initial conservative therapies, consider endoscopic therapies.[16][17](A1)

Aspiration Technique

Mark the bursa's site of maximum fullness on the skin so that a needle may be inserted in that location. Use an antiseptic solution to clean the area. Anesthetize the local skin with a freezing spray or inject a local anesthetic (less than 1 mL) into the skin. At the point of maximal fluctuance, insert the needle through the skin with a continuous gentle pull back on the plunger. Retract, then advance the needle at a different angle if a bone is struck. Aspirate the bursa's fluid by milking the liquid toward the needle tip. To reduce the risk of reaccumulation, fenestrate the bursal sac by multiple needle passages through the bursa. Fluid reaccumulation in traumatic bursitis may be avoided using a protective compression bandage. The patient is commenced on exercise, ice, elevation, and oral NSAIDs. Bursal aspiration is not recommended if there is a nearby acute fracture, osteomyelitis, skin ulcer, bacteremia, or osteochondral fracture.[15] 

Endoscopic Excision

An open bursectomy is a common surgical procedure in which the infected bursa is removed through a transverse/longitudinal incision in the skin. This area of the skin has a very precarious blood supply, which leads to a high risk of wound-healing complications, including necrosis and wound dehiscence. The endoscopic procedure irrigates the prepatellar bursa with a drug, drains the suppurative material, and excisions the chronically thickened bursa. After injecting the local anesthetic, 2 mm anteromedial and anterolateral portals are made around the patella. A 2.7 mm, 30-degree endoscope and a motorized shaver will remove the bursal sac. After surgical debridement and excision, the portal site is approximated with adhesive tape, and a loose bandage is applied.[16] 

Hospitalization is advised in systemic infection or immunocompromised individuals, and intravenous antibiotic therapy for 7 to 10 days should be followed by oral antibiotic therapy for up to 2 weeks. Antibiotics are administered orally for 2 weeks as an outpatient treatment for mild to moderate septic bursitis. The afflicted bursa should be surgically removed in situations of refractory or recurrent septic bursitis, unsuccessful drainage, immunocompromised individuals, and critical illness.[2](A1)

Differential Diagnosis

The possible differential diagnosis for acute knee pain varies somewhat by age group but remains 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. Knee osteoarthritis 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, hip osteoarthritis, slipped capital femoral epiphysis, and other hip disorders may refer to knee pain. Assessing for cellulitis or other skin and soft tissue infections (as these can present similarly to prepatellar bursitis) is essential. Other common causes of knee pain include ligamentous and meniscal injuries within the knee joint. Fractures of the tibial plateau also produce discomfort within the knee. Inflammation of a bursa other than the prepatellar may cause knee discomfort.[18]

Prognosis

The overall prognosis of bursitis is excellent. However, complications such as infection increase morbidity; therefore it is important to recognize these signs early.

Complications

The primary complication of prepatellar bursitis is 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 patellar tendon rupture.