Knee bursitis

INTRODUCTION — Bursae are synovial-lined virtual cavities that facilitate the interplay between tendon and bone, such as the anserine bursa and the deep infrapatellar bursa; between muscle and muscle, such as the gastrocnemius-semimembranosus bursa; between fascia and fascia, such as some bursal structures present in the prepatellar region; and between skin and deep fascia, such as the subcutaneous prepatellar bursa, the subcutaneous pre-tendinous (patellar tendon) bursa, and the olecranon bursa.

The term bursitis should only be used to describe the inflammation of bursae. In this context, inflammation refers to bursal swelling with or without tenderness, redness, compression of neighboring structures, or documented rupture. However, some knee pain syndromes that have been commonly labeled "bursitis" are unrelated to bursae. One such example is that of pes anserine pain syndrome (PAPS), which was formerly referred to as anserine bursitis. This topic will review the diagnosis and management of PAPS, prepatellar and superficial infrapatellar bursitis, and other pain syndromes related to other bursae around the knee. A discussion on septic bursitis is presented separately. (See "Septic bursitis".)

PES ANSERINUS PAIN SYNDROME (FORMERLY ANSERINE BURSITIS) — Pes anserinus pain syndrome (PAPS), previously known as "anserine bursitis," is a common, clinically defined condition that features pain around the medial knee and tenderness over the upper medial tibia. "Pes anserinus" refers to the insertional footprint of the conjoined tendons of sartorius, gracilis, and semitendinosus, which is said to resemble the footprint of a goose ("anser" in Latin and old Spanish). Local swelling is rarely present [1,2].

The pathophysiology, treatment, and long-term course of PAPS are not well-defined. Ultrasonography (US) studies in PAPS have only rarely shown bursitis or tendonitis; therefore, PAPS should no longer be classified as a bursitis. However, there are rare cases of true anserine bursitis in which localized swelling, rather than pain, is the chief complaint [3]. The anserine bursa may also be the site of proliferative and inflammatory conditions, which are described below [4,5]. (See 'Differential diagnosis' below.)

Epidemiology — In a large, population-based study in Mexico with almost 13,000 surveyed individuals, PAPS had a prevalence of 0.34 percent [6]. In another study of 4240 subjects from three indigenous peoples from Mexico and one from Argentina, the prevalence of PAPS was 0.54 percent of males and 0.7 percent of females [7]. Estimates of PAPS among patients with knee osteoarthritis (OA) are higher, as there appears to be an association between PAPS and knee OA. As an example, in a small observational study including 37 patients with PAPS, 93 percent also had knee OA, the majority of whom were obese women [8]. In another observational study of 50 patients with 90 symptomatic osteoarthritic knees, PAPS was present in 73 knees (83 percent) [9].

Risk factors — There is an established association of PAPS with diabetes. In one study, PAPS was present in 34 (36 percent) of 94 non-insulin-dependent diabetics, while there were no cases of PAPS among the 57 non-diabetic controls [10]. This finding was confirmed in another study of 100 diabetic patients and 102 matched controls, which found PAPS among 38 diabetic patients compared with 17 controls [11].

Based upon clinical experience and limited available evidence, other risk factors for PAPS include female sex, obesity, knee OA, and knee malalignment [8,9,12]. Additional, larger studies of risk factors for PAPS in which the precise site of tenderness is determined clinically or by US are needed.

Etiopathogenesis — The pathophysiology of PAPS remains speculative, as inflammation is rarely present in the anserine bursa or the pes anserinus in patients with PAPS. The frequent association of PAPS with knee OA, obesity, and angular deformity of the knee strongly suggest that a mechanical derangement within the medial knee joint causes referred pain experienced at the upper medial tibia.

The low incidence of inflammation around the anserine bursa and surrounding tendons has been demonstrated in several US studies of patients with PAPS. In one study of 37 patients with PAPS, only one patient had US evidence of pes anserine bursitis, and two patients had pes anserinus tendinitis [8]. In a subsequent US study including 73 knees with PAPS among 50 patients with symptomatic knee OA, there was no ultrasound evidence of anserine bursitis or pes anserinus tendinopathy [9]. However, PAPS was frequently associated with a medial meniscus protrusion and displacement of the medial collateral ligament (also referred to as the tibial collateral ligament). In a study in which 85 patients had PAPS and symptomatic knee OA, 20 percent had ultrasound evidence of anserine bursitis based upon a bursal thickness of ≥2 mm [13]. However, the study did not evaluate the local tendons, ligaments, or menisci. Finally, in a study of 348 Korean subjects with a mean age of 72, 50.6 percent of whom were females, 120 had OA and 146 had knee pain. By magnetic resonance imaging (MRI), anserine bursitis was present in 17.5 and 2.2 percent of subjects with and without OA, respectively, and in 14.4 and 2.5 percent of subjects with and without knee pain, respectively. The presence of PAPS, which is a clinical diagnosis, cannot be determined in this study. Also, MRI may be more sensitive than US to detect effusions around the anserine bursa [14].

Based on US data, a protruded medial meniscus may cause PAPS either directly or by stretching the medial collateral ligament in patients with knee OA [9]. A valgus knee angulation creating excessive traction forces on the medial collateral ligament may explain PAPS in other patients [12]. In the author's opinion, PAPS is not a condition per se, but rather a red flag that points to some articular or periarticular derangement in the medial knee that warrants further investigation.

Relevant anatomy — The medial aspect of the knee is a multilayered, complex restraining structure in which the individual components slide upon each other during knee flexion and extension [15]. Pertinent structures described from internal to external are as follows: the medial meniscus; the medial (tibial) collateral ligament that is adherent to the meniscus in its midportion; several bursae, including the anserine bursa (figure 1 and figure 2 and figure 3) [16], a bursa between the superficial and deep layers of the proximal medial collateral ligament [17,18], and a bursa partially tucked under the posterior medial collateral ligament that is saddled on an anterior reflection of the semimembranosus tendon [19,20]; the pes anserinus; and the subcutaneous fat pad.

The anserine bursa is a large (about 7 cm in length), roughly oval synovial sac that extends from the tibial joint line to the insertion of pes anserinus. Its long diameter lies beneath the anterior medial collateral ligament in knee extension [16] and is uncovered and at a 90-degree angle in knee flexion. This angular motion may be facilitated by internal gliding between the bursal walls. The lubrication of the anserine bursa has not been studied; however, the viscous fluid aspirated from cystic distensions suggests that there is a high hyaluronate content in the normal state [3].

The semimembranosus bursa may facilitate the interplay between the posterior medial collateral ligament, the anterior reflection of the semimembranosus tendon insertion, and the posterior osseous corner of the joint [19,20] and prevent friction between these structures in the normal state.

The pes anserinus tendons are arranged in two layers: the sartorius is superficial, and the partially overlapping gracilis and semitendinosus tendons are beneath the sartorius tendon. The combined width of these tendons is approximately 4.5 cm. The saphenous nerve, which contributes to the innervation of the medial and anterior knee, descends along the medial side of the knee behind the sartorius.

Diagnosis — There are no established diagnostic criteria for PAPS. We diagnose PAPS in patients with the following symptoms and signs (see 'Differential diagnosis' below):

●Medial knee pain

●Tenderness over the upper medial tibia between the pes anserinus and the tibial joint line

●Absence of local swelling or induration

In patients with symmetric pain, tenderness due to fibromyalgia should be excluded. (See "Clinical manifestations and diagnosis of fibromyalgia in adults".)

Evaluation — PAPS should be suspected in patients who seek medical attention for one of the following three reasons:

●Medial knee pain with activities such as rising from a chair, ascending or descending stairs, or lying in bed with one knee pressing on the other (which may disturb sleep)

●Rapidly mounting knee pain in a patient with knee OA

●The transition of pain with activity to pain at night in a patient with known knee OA

More often than not, patients with PAPS also have knee OA. Patients are also often obese, and a knee valgus or varus deformity is common.

Patients suspected of having PAPS should have a detailed history, physical examination, and, in most cases, imaging to diagnose coexisting OA.

Physical examination — The patient with suspected PAPS should be examined supine with the knees initially in extension. If the pain is unilateral, the unaffected knee should be examined first to establish a baseline. The physical examination in patients with medial knee pain due to suspected PAPS should include attention to the following:

●Assessment of knee alignment – Assessment of knee alignment may reveal a valgus or varus deformity (figure 4). (See "Physical examination of the knee", section on 'Alignment'.)

●Palpation around the pes anserine insertion site – With the patient supine and the legs in extension, tenderness to palpation around the pes anserine insertion site, including the bursa, may be found anywhere in the proximal, medial tibia from the medial joint line to the pes anserinus.

More precise information about the location of the tender site may be obtained by examining the knee at 90 degrees flexion (picture 1A-B). With the patient supine, and the knees flexed 90 degrees, the patient is asked to press their heels against the examining table. Two of the pes anserinus tendons should be prominent in the medial popliteal fossa. The medial tendon is the gracilis, and 1 to 2 cm lateral to it is the prominent and sharp semitendinosus tendon. An imaginary line that follows these tendons intersects the tibia at the pes anserinus enthesis (picture 2). Then, several structures may be palpated in the following sequence: the pes anserinus enthesis, the anserine tendons (that have now moved posterior to the bursa), the upper medial tibia, and the joint line down to its posteromedial corner. It is at this site where the semimembranosus reaches the tibia. This cylindrical, nontendinous, fleshy structure runs anterior and parallel to the gracilis tendon and should be a helpful landmark to identify tenderness in cases of semimembranosus-tibial collateral ligament bursitis [19,20].

●Medial joint line palpation – Tenderness at the medial joint line (picture 2) may suggest a meniscal tear, protrusion, or cyst; bursitis in one of the regional bursae; a tender osteophyte at the femoral condylar rim; subcutaneous fat pad tenderness; or fibromyalgia. (See 'Differential diagnosis' below.)

The complete physical examination of the knee is presented separately. (See "Physical examination of the knee".)

Imaging — Although imaging is generally not necessary to diagnose PAPS, conventional knee radiographs may be obtained to detect underlying OA if the patient has no prior radiograph and has risk factors for OA (eg, age >50, overweight or obesity, varus or valgus malalignment). If local swelling or induration is present, US or MRI should be obtained to exclude alternative diagnoses. (See 'Differential diagnosis' below.)

●Conventional radiography – A standing anteroposterior film of the knees can be useful to confirm the presence of OA if it is suspected based on symptoms and physical examination. (See "Radiologic evaluation of the chronically painful knee in adults", section on 'Osteoarthritis'.)

●Ultrasonography – If available, US can be used to obtain more detailed anatomic information and guide a therapeutic injection. As discussed above, US findings are usually unremarkable (see 'Etiopathogenesis' above). However, if a bulge or induration is present in the medial aspect of the knee, US evaluation may reveal a fluid collection within the anserine bursa. Interestingly, longstanding cases of anserine bursitis have been described with cortical bone scalloping and even intra-osseous extension [21]. Other solid lumps in the anserine bursa area have included lesions such as synovial chondromatosis [4], giant cell tumors of the tendon sheath [22], angioleiomyoma [23], tuberculosis, and other lesions described below [22] (see 'Differential diagnosis' below), or, in the worst scenario, a sarcoma. The evaluation of these lesions is discussed elsewhere.

●Magnetic resonance imaging – MRI can also be useful in the assessment of knee OA and is important when a bulge is palpated and an US study reveals a solid lesion.

Differential diagnosis

●True anserine bursitis – Patients with true anserine bursitis present with localized swelling, with or without fluctuation, and little pain. If acute pain, swelling, and redness over the bursa are also present, a diagnosis of bursal gout and/or septic bursitis should be considered. Gouty involvement of the bursa has been reported [24] but is very rare. Occasional cases of cystic or proliferative lesions of the anserine bursa, with bone erosion and intraosseous progression, have been described [21]. The saphenous nerve, and in particular, its infrapatellar branch that lies in close association with pes anserinus, may be damaged when tendon in harvested for anterior cruciate ligament repair, or may be compressed by bursal swelling, causing pain and hypesthesia in the pes anserinus region [25,26].

●Other bursitis in the medial knee – Other bursae around the medial knee can cause localized swelling and tenderness at the medial joint line. These include the medial (tibial) collateral ligament bursa lateral to the femoral condyle [17] or the semimembranosus bursa in the posteromedial knee (figure 2) [19]. This condition, also known as semimembranous tenosynovitis, features a slowly developing localized pain and tenderness at the posteromedial corner of the knee, exacerbated by physical activity. A boggy swelling may be felt around the tendon [27]. (See 'Medial collateral ligament bursitis' below and 'Semimembranosus-tibial collateral ligament bursitis' below.)

●Proliferative synovial conditions – Proliferative synovial conditions such as synovial chondromatosis [4] and tenosynovial giant cell tumor (formerly pigmented villonodular synovitis) may occur in the anserine bursa [22], which is enlarged with a variable degree of pain and tenderness. (See "Radiologic evaluation of knee tumors in adults", section on 'Synovial (osteo)chondromatosis' and "Radiologic evaluation of knee tumors in adults", section on 'Tenosynovial giant cell tumor'.)

●Other masses in medial knee – These include hemangioma, lipoma, myxolipoma, myxoid liposarcoma, neurilemoma, bursal cysts, and tuberculosis [28].

●Snapping pes anserinus and medial friction syndrome – Snapping of the pes anserinus tendons upon knee flexion and extension is a clinically obvious cause of medial knee pain [29]. In this friction syndrome, while snapping may occur, the main symptom is pain. In these patients, the distance between sartorius, gracilis, and semitendinosus tendons and the posterior medial condyle may be shortened and cause intervening edema [30]. In other cases, a prominent tibial crest impinges on the neighboring soft tissues [31]. It has also been described following unicompartmental knee arthroplasty [32].

●Medial meniscus tear – Medial knee pain upon standing and a "catching" sensation suggest a meniscal tear. Popliteal pain may be present. The most frequent finding is tenderness with digital pressure at the joint line. The applied force should be sufficient to blanch the nail of the examining finger. Another useful maneuver is the McMurray test (picture 3) [33]. Reproducible acute pain in the medial knee at a given angle of extension, with or without a palpable click, is highly indicative of a medial meniscus tear. (See "Meniscal injury of the knee", section on 'Provocative testing'.)

●Medial meniscus cyst – A medial meniscus cyst causes an aching pain that is exacerbated by activity. A smooth, tense lump is felt at the medial joint line of the knee. The lump should be more apparent in full extension as a result of increased pressure within the joint [33]. These cysts are caused by leakage of synovial fluid through a horizontal meniscal tear.

●Medial collateral ligament sprain – Patients with a medial (tibial) collateral ligament sprain have a history of trauma with swelling and ecchymosis in the medial knee. On knee examination, there is pain and/or evidence of joint instability with valgus stress testing (picture 4).

●Tibial stress fracture – A tibial stress fracture should be suspected in athletes or military recruits with medial knee pain on weightbearing and on activities. Depending on the slope and intensity of training, the condition may occur in as many as 25 percent of trainees [34]. The upper tibia is most frequently involved. Focal tenderness, sometimes with swelling, may be present. The knee should be examined in flexion to confirm bone tenderness. (See "Stress fractures of the tibia and fibula".)

●Femoral or tibial osteonecrosis – An older person, or a person receiving long-term oral glucocorticoids who develops medial knee pain with weightbearing and activity should be suspected of having osteonecrosis. Focal tenderness is usually present. Initial radiographs of the knee may be normal. In such cases, an MRI of the knee should be obtained [35]. (See "Treatment of nontraumatic hip osteonecrosis (avascular necrosis of the femoral head) in adults".)

●Tibial osteomyelitis – Brodie's abscess is a type of subacute osteomyelitis seen predominantly in adolescence. It may cause pain as well as bone swelling in the medial tibia. Pathologically, there is a metaphyseal abscess with sclerotic walls. Staphylococcus aureus is the most commonly isolated organism. The young age of the patient should make the clinician consider this lesion as well as a malignancy [36]. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

●Fat pad tenderness – A tender, thick medial fat pad is commonly seen in overweight women. The prominence of this fat pad may be accentuated by genu valgum. Pinching the fat pad between the thumb and index triggers severe pain. The absence of generalized tenderness can help distinguish this condition from fibromyalgia. Gross, symmetrical fat swelling in the medial knees, known as "symmetric lipomatosis," is quite rare [37] and should be distinguished from adiposis dolorosa (Dercum disease) in which there are multiple fat nodules that are small (<2 cm diameter), tender, and have characteristic features on US or MRI [38]. (See "Clinical manifestations and diagnosis of fibromyalgia in adults".)

●Fibromyalgia – Fibromyalgia must be distinguished from PAPS, particularly in patients with bilateral symptoms. The tender points that have been described in fibromyalgia patients included the medial fat pad proximal to the joint line, which is located superior to the tenderness associated with PAPS [39]. However, in both conditions, the tenderness may involve an area rather than a discrete point. Physical examination should include that of the contralateral medial knee as well as other areas commonly tender in patients with fibromyalgia. Since fibromyalgia and PAPS may coincide, a gross discrepancy in tenderness between both knees should make the clinician consider an overlap. An immediate, complete, and lasting response to a lidocaine/steroid infiltration can also help identify PAPS in the setting of fibromyalgia. (See "Clinical manifestations and diagnosis of fibromyalgia in adults".)

Treatment

Initial therapy — The initial treatment of PAPS includes a weight-reduction program, quadriceps-strengthening exercises, wearing a soft knee brace, and the use of an analgesic and/or short-term nonsteroidal antiinflammatory drugs (NSAIDs), unless contraindicated by gastrointestinal, renal, or heart disease. Strengthening exercises are reviewed below. Soft-knee braces have reduced pain and decreased dynamic instability in knee OA [40]. Weight-reduction programs and the use of analgesics are reviewed separately (see "Obesity in adults: Overview of management" and "Initial treatment of rheumatoid arthritis in adults", section on 'NSAIDs'). Since PAPS is thought to be related to an underlying knee condition such as OA or an angulation deformity (eg, valgus or varus), local treatment measures typically provide only transient relief. Exercises are a possible exception, as they reduce pain, strengthen the muscles acting on the knee, and improve the patient's overall fitness. However, no long-term studies of exercise or use of a brace in OA have focused on the effects of medial knee pain.

Of the quadriceps-strengthening exercises, the author prefers isometric quadriceps setting exercises performed with the legs in extension. In this position, the quadriceps-patella-tibial spine pull is parallel to the femoral condyles, thereby avoiding the patellofemoral stress that would occur with knee flexion [41]. Although ideally a physical therapist should instruct and supervise the strengthening exercises, a simple exercise that may help patients if added to their daily routines is as follows [41]:

●While lying supine in bed with both legs in extension, the patient concentrates on the anterior thigh in the unaffected leg and contracts the quadriceps (front thigh muscles) maximally. The contraction is held for six seconds, counting aloud while watching a clock, and then the muscle is allowed to relax. The quadriceps contraction is then attempted on the affected side. Initially, it is sometimes necessary to have someone else (eg, spouse, child) ascertain that the muscle actually contracts. This may be difficult at first when knee pain is severe. A modest twitch of contraction may be all that can be achieved at first, but with practice, a full contraction will later appear.

●The isometric contraction is repeated, alternating sides, for an increasing number of times as tolerated.

●These exercises are performed twice a day and are most convenient when performed before getting up in the morning and upon retiring at night, with an increasing number of maximal contractions to a target number of 10 six-second contractions on each side.

Approximately 30 percent of patients improve, although it is uncertain as to whether it can be entirely attributed to the regimen described above since many mechanically determined conditions improve spontaneously. If after one month there is no improvement, it is unlikely that this strengthening regimen will relieve pain.

As mentioned previously, many patients with PAPS may also have underlying knee OA, which requires concomitant therapy. The management of OA is discussed in detail separately (see "Management of knee osteoarthritis" and "Management of moderate to severe knee osteoarthritis"). Treating PAPS in a patient with advanced knee OA offers the possibility of a rapid, and at times major, improvement of pain and sleep.

Although unproven, a heel wedge may also be beneficial and at no risk to the patient in those with an angular deformity of the knee. An inner heel wedge may be used in the patient in genu valgum, and a lateral heel wedge in genu varum [42]. Although a glucocorticoid injection typically is reserved for persistent symptoms, it may be given as part of initial therapy in patients who have night pain that disrupts sleep, with remarkable success. (See 'Persistent symptoms' below.)

Persistent symptoms — For the approximately 70 percent of patients who do not improve with initial therapy, a local glucocorticoid injection is typically administered (picture 5 and picture 6) [43]. The author would repeat the injection up to three times if needed, three weeks apart. A failure to improve after three injections, in addition to continuing the exercises and wearing the soft brace, should prompt an orthopedic evaluation.

The author's approach to injecting for PAPS is to first identify and mark the area of maximal tenderness (picture 5) with the knee extended. The area is cleansed with iodine prep and then injected. The author uses both an anesthetic injection (2 mL of 1 percent lidocaine) followed by 40 mg of methylprednisolone mixed with 1 mL of 1 percent lidocaine. A single injection of lidocaine and glucocorticoid is acceptable as well; the initial anesthetic injection is useful because it makes the second painless. A 25-gauge needle is comfortable for the patient and adequate as no aspiration occurs. The author directs the needle perpendicular to the tibial surface until the needle hits the tibia. Then the author backs off by 1 mm and empties the syringe, moving the needle a few mm in all directions to affect an area approximately 1 cm in diameter.

The evidence supporting the efficacy of glucocorticoid injections in PAPS is limited and inconsistent. Glucocorticoid injections have traditionally been considered useful in PAPS [44], at least in the short term, and this has been consistent with the author's experience. However, a randomized controlled trial comparing the injection of 40 mg of methylprednisolone acetate mixed with lidocaine and lidocaine mixed with water in patients with PAPS showed a 60 percent improvement in both treatment groups at four weeks [45]. In another study, 60 PAPS patients with knee OA were randomized to receive a local injection of 40 mg of triamcinolone acetonide in the most tender point or a two-week course of physical therapy consisting of hot packs, ultrasound, and transcutaneous electrical nerve stimulation (TENS) to the pes anserinus [46]. Both groups improved similarly after eight weeks. No sham-treated patients were included. It is therefore possible that the time-honored efficacy of glucocorticoid injections and physical therapy modalities in PAPS may have been a placebo effect. An additional study of OA patients with PAPS compared sodium diclofenac 25 mg in 1 mL given as mesotherapy, three times per week for three weeks, with oral sodium diclofenac 50 mg given daily for three weeks. Both groups improved similarly at the end of therapy, 30 days and 90 days. Once again, no sham-controlled group was included [47]. Additional controlled studies are needed in PAPS comparing US-guided versus blind injections with the knee at 90-degree flexion to better define the pain-generating structure.

PREPATELLAR AND SUPERFICIAL INFRAPATELLAR BURSITIS — Prepatellar and superficial infrapatellar bursitis are common conditions presenting as localized tenderness and swelling anterior to the patella or patellar tendon. The prepatellar and superficial infrapatellar bursae may be affected by, in decreasing order of frequency, infection, chronic or acute trauma, gout, and rheumatoid arthritis.

Epidemiology and risk factors — Few studies, all in the field of occupational medicine, have addressed the epidemiology and risk factors of prepatellar or superficial infrapatellar bursitis. Penetrating trauma and jobs that require prolonged kneeling, such as mining [48], carpet laying [49], and the clergy, are known causes of this condition. Kneeling affects the patellar tendon and the tibial tubercle, rather than the patella [48,50]. In addition, the exposed nature of the prepatellar region is a prime site for blunt and shear trauma, affecting the bursae or the surrounding subcutaneous tissue [51-53].

Pathogenesis — Several factors may determine the development of prepatellar or superficial infrapatellar bursitis. One is the thinness of the skin over these bursae, which both chronic glucocorticoid therapy and old age accentuate. Another factor is the sparse innervation of the acral skin. Pinch as hard as you can the skin in front of your patella or at the tip of your elbow and little pain will occur. The acral exposure of subcutaneous bursae also renders them vulnerable to occupational and recreational trauma. It is of interest that tophi and rheumatoid nodules, that are known to occur at pressure points, grow in the superficial bursal wall and move freely with the skin, whereas the hard pebbles that are palpable in traumatic bursitis are fixed at the bottom of the bursal sac. Finally, due to their location in the convex side of a joint, in a fluid-distended bursa, flexion of the joint further increases the intrabursal pressures, sometimes to the point of rupture [54].

Etiology — Acute causes of bursitis are usually septic (from common skin bacteria) and less frequently due to gout, but they can also be due to trauma (eg, a hemobursa). Chronic bursitis, on the other hand, is generally traumatic, but may also be due to gout, rheumatoid arthritis, and, rarely, a fastidious infection.

Immunosuppressed hosts are also prone to subcutaneous bursitis. Other predisposing factors for acute bursitis include diabetes, human immunodeficiency virus (HIV), metastatic cancer, hemodialysis, emphysema and glucocorticoid use. Hemobursa is a rare cause of acute prepatellar or superficial infrapatellar bursitis, except in cases of occupational exposure or anticoagulation [48,55].

Relevant anatomy — There are few data on the anatomy of the superficial infrapatellar bursa. The anatomy of the prepatellar bursae, on the other hand, has been studied in great detail (picture 7) [56,57]. There are three overlapping bursae beneath the prepatellar skin. A subcutaneous bursa lies between the deep dermis and a tenuous fascial plane derived from the fascia lata. This bursa appears to be most frequently involved in prepatellar bursitis. There is also an intermediate bursal space between the fascial plane and oblique fibers derived from the muscles vastus medialis and vastus lateralis. Finally, a third bursal space separates the latter from vertical fibers of rectus anterior layered on, and firmly attached to, the patella. Based upon clinical observations, the latter two bursae are rarely involved in disease.

The superficial infrapatellar (or pretendinous) bursa is a subcutaneous bursa distal to the prepatellar bursa and anterior to the patellar tendon. The deep infrapatellar bursa, which is located at the insertional angle between the patellar tendon and the upper tibia, is distal to the superficial infrapatellar bursa (picture 8).

Clinical features — Patients with bursitis of the prepatellar or the superficial infrapatellar bursae may present with either acute or chronic symptoms.

●Acute bursitis – Patients with acute prepatellar or superficial infrapatellar bursitis present with localized redness, swelling, and marked tenderness anterior to the patella or patellar tendon. A history of fever may be present in approximately 30 percent of patients. There may be evidence of puncture wound, skin abrasion, fissured dermatitis, or psoriasis overlying the patella or patellar tendon [58-61]. A sympathetic knee effusion may be observed in approximately 30 percent of cases. In patients with a bursal rupture, extensive cellulitis may be observed.

●Chronic bursitis – Patients with chronic prepatellar or superficial infrapatellar bursitis present with a soft, non-tender, globular fluid-filled lump in front of the patella or patellar tendon. The lump may be cold or slightly warm to touch. There is generally little to no tenderness to palpation. Lumps on the superficial bursal wall suggest tophaceous gout or rheumatoid arthritis. The skin inflammation is typically mild, except for cases in which chronic dermatitis preceded the bursitis. Indolent surrounding inflammation may suggest a mycobacterial infection or fungal etiology.

Clinical findings that may accompany acute prepatellar or superficial infrapatellar bursitis include the following:

●Sympathetic knee effusion – Sympathetic effusions are common in septic prepatellar or superficial infrapatellar bursitis [62,63]. The synovial fluid is typically non- or minimally inflammatory (leukocyte counts ≤3000/mm³, predominance of mononuclear cells, and negative culture results). The patient is usually able to fully extend the knee without added discomfort. (See "Monoarthritis in adults: Etiology and evaluation", section on 'Joint aspiration'.)

●Diffuse knee swelling – Acute bursitis, usually septic, may cause a severe inflammatory reaction around the knee closely resembling septic arthritis. A sympathetic joint effusion may be present and further suggest this condition. However, if the patient is able to keep the leg fully extended without discomfort, acute bursitis becomes a more likely diagnosis [54,59]. This useful clinical sign derives from the fact that in a conscious patient, acute knee and elbow arthritis automatically bring the joint to semiflexion, a position in which, for a given volume of effusion, intraarticular pressures are lowest [64]. The opposite findings were recorded in patients with olecranon or prepatellar bursitis. The lowest pressures occurred from full extension to 30- to 40-degree flexion, and further flexion led to an exponential rise in pressure.

●Bursal rupture – The high cavitary tension generated by an effusion, plus an effort in flexion which further increases the intrabursal pressures, may rupture the bursal sac. Bursal rupture causes a rapidly extending cellulitis to the sides of the knee and along the leg [59]. A preceding prepatellar or pretendinous swelling, which vanishes as cellulitis extends, supports the diagnosis of septic bursal rupture.

Other possible features of the bursitis include bacteremia in up to 20 percent of septic cases [65]. Septic shock is extremely rare. Fistula formation can also occur either spontaneously, or following aspiration through the bursal apex where the skin has no recoil. Compartment syndrome can sometimes occur.

Diagnosis — Prepatellar and superficial infrapatellar bursitis are usually diagnosed based upon clinical history and physical examination.

●Acute bursitis – In patients with acute prepatellar or superficial infrapatellar bursitis, localized redness, swelling and marked tenderness in the prepatellar or pretendinous region is present. A history of trauma, microcrystalline disease, immunosuppression, or infection may be elicited.

●Chronic bursitis – In patients with chronic bursitis, a soft, non-tender, globular fluid-containing mass is present in front of the patella or the patellar tendon. A history of trauma or repetitive overuse is usually present. A nodular surface suggests tophaceous gout or nodular rheumatoid arthritis.

Once the presence of bursitis is confirmed, diagnostic testing is usually necessary to determine the etiology.

Diagnostic testing — Diagnostic testing for acute or chronic prepatellar or superficial infrapatellar bursitis includes laboratory testing, bursal fluid analysis, and imaging. A key component of the evaluation of knee bursitis is the exclusion of septic bursitis, which requires bursal aspiration and analysis with a white cell count and differential, glucose content, crystal identification, Gram stain, and culture. (See 'Bursal fluid aspiration and analysis' below.)

Physical examination — The physical examination in patients with knee swelling anterior to the patella or patellar tendon should include inspection of the overlying skin for evidence of redness or breakdown suggestive of cellulitis or an infectious cause of bursitis. Occasionally, indolent peribursal inflammation and thickened surrounding tissues suspicious for a tuberculous, brucellar, or fungal etiology is present. In these cases, aspiration of bursal fluid is required.

Patients with knee bursitis may have a sympathetic knee effusion or diffuse knee swelling (see 'Clinical features' above). A complete examination of the knee is presented separately. (See "Physical examination of the knee".)

Laboratory testing — A complete blood cell count and differential, serum glucose, C-reactive protein, erythrocyte sedimentation rate, and serum uric acid should be obtained in all patients with prepatellar or pretendinous bursitis. If the patient is febrile, appears toxic, or reports having had fever or chills, blood cultures should also be obtained.

Bursal fluid aspiration and analysis — In acute bursitis, as well as in protracted cases with indolent peribursal inflammation, aspiration of the bursal sac should always be performed. (See "Septic bursitis", section on 'Obtaining bursal samples'.)

Aspiration technique of the prepatellar for pretendinous bursae and handling of small samples. — Aspiration of the prepatellar or pretendinous bursa should be performed with the limb in extension to avoid compression of the bursa by the skin, which tightens in flexion. The skin overlying and surrounding the involved bursa is thoroughly cleansed, and four or five layers of an antiseptic solution are applied. The skin in front of the knee (and also in the olecranon region) has little pain perception, and local anesthesia is usually unnecessary. A 20- or 18-gauge needle may be used, the latter being preferable when the process appears septic and symptoms have been present for several days. The aspiration of the prepatellar or the pretendinous bursa is generally more difficult than the aspiration of the olecranon bursa, as effusions are often smaller. Due to this inherent difficulty, no tap should be considered dry until air is blown through the needle aiming to a microscope slide. The spot may be examined for crystals with a polarizing microscope or, if unavailable, with a regular microscope with the condenser in a low position, and then Gram stained. To obtain a culture, the needle may be washed with nonbacteriostatic saline or broth. If a larger volume is obtained (ie, enough to fill the needle hub), a drop may be placed onto a microscope slide and aspirated with a white blood cell pipette for a white and red blood cell count. The remaining material is covered with a cover slide for a thorough crystal search. Then, slide and cover slide are separated; the former is Gram stained and the latter stained with Wright-Giemsa for a differential count. Any material remaining in the needle is used for culture. Larger bursal fluid volumes lend themselves to a routine fluid analysis, as described separately (see "Synovial fluid analysis"). Occasionally the clinician may be surprised by the aspiration of pure blood. An early hemobursa may give no clue as to the nature of the effusion, although in a few days, a large ecchymosis will appear. If ultrasonography (US) is available, small effusions that may be inapparent on palpation may be identified and aspirated under direct observation. In early septic and gouty bursitis, the bursal fluid white cell count may be only mildly elevated, but a high percentage of neutrophils is a telltale sign of one of these diagnoses [59,66]. A crystal search under the polarizing microscope should be exhaustive, particularly when the Gram stain reveals no microorganisms.

In chronic bursitis, which usually results from recurrent microtrauma, the bursal fluid on aspiration is not purulent and may be slightly blood-tinged. The white cell count is usually less than 2000 cells/mm³, with 80 percent or more of these cells mononuclear cells. On occasion, monosodium urate crystals are present. Cultures are usually negative in such cases. As described above, indolent peribursal inflammation may suggest a mycobacterial or fungal infection, in which case bursal fluid aspiration and analysis is required. A detailed discussion of bursal fluid aspiration and analysis in septic bursitis can be found elsewhere. (See "Septic bursitis", section on 'Obtaining bursal samples'.)

Imaging — Imaging studies of the knee are rarely necessary for cases of prepatellar and superficial infrapatellar bursitis that lack signs of local (eg, redness, increased temperature) or systemic (eg, chills, fever, malaise) inflammation. However, when septic bursitis or gout are suspected, and if physical examination does not clearly identify an effusion, a US-guided aspiration would be far more likely than a blind aspiration to yield a diagnostic sample. Uncertainty about the presence of bursitis can be frequent in patients with prepatellar and pretendinous (patellar tendon) subcutaneous bursitis. MRI is rarely necessary for diagnostic purposes; however, such advanced imaging would be appropriate in cases of chronic bursitis in which underlying osteomyelitis or malignancy were suspected. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Clinical approach' and "Approach to imaging modalities in the setting of suspected nonvertebral osteomyelitis".)

Treatment — Treatment of prepatellar or superficial infrapatellar bursitis is guided by the underlying cause. With the exception of septic and gouty knee bursitis, isolated bursitis of the prepatellar or superficial infrapatellar bursa is usually a self-limited condition. Therefore, the goal of treatment is to relieve the immediate symptoms and prevent repetitive trauma. Traumatic effusions resolve slowly, typically within a few weeks to three months. We do not administer a local glucocorticoid injection in the prepatellar or pretendinous bursae due to the risk of promoting an infection. The use of protective knee pads or knee braces, as developed for the prevention of knee injuries in high risk occupations, is important when kneeling cannot be avoided. Chemical ablation has also been used in refractory cases [67].

Patients with septic bursitis are managed with transient immobilization of the knee in the neutral position with a posterior plaster or other splint, antibiotics, and re-aspirations as needed [68,69]. The treatment of septic bursitis is discussed in detail separately. (See "Septic bursitis" and "Septic bursitis", section on 'Treatment'.)

If gout is proven by crystal identification and the Gram stain of the bursal fluid is negative, immobilization is unnecessary and patients should be treated for gout (see "Treatment of gout flares"). If there are no crystals and the Gram stain is negative, very symptomatic patients may be treated with full doses of a nonsteroidal antiinflammatory drug (NSAID), with attention to age and comorbidities. (See "NSAIDs: Therapeutic use and variability of response in adults".)

OTHER TYPES OF KNEE BURSITIS

Biceps femoris bursitis — Biceps femoris bursitis is a rare type of bursitis that causes a cystic-like growth near the proximal fibular head. Patients can present with lateral knee pain aggravated by palpation [70]; in the author's experience, biceps femoris bursitis has been observed in competitive volleyball and basketball players. Because of this location of the bursa, the common peroneal nerve may be compressed.

Semimembranosus-tibial collateral ligament bursitis — The semimembranosus bursa is located at the posteromedial aspect of the knee, at the medial aspect of the semimembranosus tendon (image 1) [19,20]. The semimembranosus bursa can be identified by palpation with the patient in the sitting position. Semimembranosus, which is muscle almost to its insertion site, is often felt as a thin cylinder (about 2 cm in diameter) that runs above gracilis, meets the tibia, and contracts with resistance of internal rotation of the foot. The semimembranosus bursa (not to be confused with the semimembranous-gastrocnemius bursa, which is the substrate of the Baker cyst) is present at this site. Semimembranosus bursitis has been documented anatomically by MRI [70], and its clinical syndrome, under the name of semimembranosus tenosynovitis, has been described [27]. Semimembranosus bursitis or tenosynovitis (figure 2) may be suspected in patients with pain, tenderness, and localized swelling at the posterior medial knee.

The frequency of semimembranosus-tibial collateral ligament bursitis is not known. In the author's opinion, cases of semimembranosus-tibial collateral ligament bursitis may be overlooked in patients thought to have pes anserine pain syndrome (PAPS) diagnosed by palpation, and injected, in knee extension.

Deep infrapatellar bursitis — The deep infrapatellar bursa (DIB), which is homologous to the retrocalcaneal bursa [71,72], is wedged between the patellar tendon and the anterior upper tibia. Rather than contributing to tissue gliding, these bursae allow a more distal and mechanically advantageous insertion of the patellar tendon and the Achilles tendon, respectively, at their insertion sites. The spacer that allows such action is the anterior-inferior corner of the infrapatellar fat pad (Hoffa's fat), a fat wedge that enters the DIB in knee extension, and the retrocalcaneal bursa in foot plantar flexion, as the insertional angles open [73]. The intermittent wall-on-wall pressure that occurs when the foot is dorsally flexed in the retrocalcaneal bursa, and the knee is flexed in the DIB, leads to fibrocartilage formation in the opposing walls. The DIB and the retrocalcaneal bursa and related tissues are prototypical target organs in spondyloarthritis [71,74]. There are also occasional cases described of DIB due to infection and gout [75].

The differential diagnosis of deep infrapatellar bursitis includes Osgood-Schlatter (OS) disease and Sinding-Larsen-Johansson (SLJ) disease. Both are overload syndromes in adolescents who are active in sports [76]. Pain, tenderness, and swelling occur at the lower pole of the patella in SLJ, and at the tibial tuberosity in OS. The distinction between OS or SLJ disease from DIB may be difficult (see "Approach to chronic knee pain or injury in children or skeletally immature adolescents", section on 'Osgood-Schlatter disease (tibial tubercle apophysitis)' and "Approach to chronic knee pain or injury in children or skeletally immature adolescents", section on 'Sinding-Larsen-Johansson disease (patellar apophysitis)'). An associated Achilles tendon enthesitis, lower-extremity arthritis, and an increased level of acute phase reactants all suggest the presence of spondyloarthritis. (See "Treatment of peripheral spondyloarthritis", section on 'Enthesitis'.)

The treatment of DIB is guided by the underlying etiology. Transient knee immobilization with a posterior plaster splint helps with pain control in most cases.

Medial collateral ligament bursitis — The medial collateral ligament (MCL) bursa is located between the MCL and the joint capsule (figure 3). This bursitis presents with tenderness over the medial aspect of the knee joint and is seldom associated with a demonstrable effusion. It may also be a component of any inflammatory joint disease.

Differential diagnosis includes MCL injury, bony pathology of the tibia, and medial meniscal tear. In MCL injury, patients should have pain when applying valgus stress to the knee; in MCL bursitis, this maneuver does not accentuate the pain. Tibial pathology such as avascular necrosis of the tibia or a medial tibia plateau fracture may be evident on plain radiographs, should be visible on MRI, and is typically associated with pain over the bone and not the joint line. With medial meniscal tear, patients often have medial joint line tenderness and sometimes worse pain with the McMurray maneuver, in which the tibia is rotated upon the femur (picture 3). (See "Approach to the adult with unspecified knee pain" and "Meniscal injury of the knee" and "Meniscal injury of the knee", section on 'Provocative testing'.)

As is the case with pes anserinus pain syndrome, the patient may respond dramatically to a local injection of an anesthetic with a steroid, a result that tends to confirm the diagnosis of bursitis [77,78].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Knee pain".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (See "Patient education: Bursitis (The Basics)" and "Patient education: Knee pain (The Basics)".)

●Beyond the Basics topic (See "Patient education: Knee pain (Beyond the Basics)".)

SUMMARY AND RECOMMENDATIONS

●Pes anserine pain syndrome

•Definition – Pes anserinus pain syndrome (PAPS), previously known as "anserine bursitis," is a common, clinically defined condition that features pain around the medial knee and tenderness over the upper medial tibia. Ultrasonography (US) studies in PAPS have only rarely shown bursitis or tendonitis; therefore, PAPS should no longer be classified as a bursitis. However, there are rare cases of true anserine bursitis in which localized swelling, rather than pain, is the chief complaint. (See 'Introduction' above and 'Pes anserinus pain syndrome (formerly anserine bursitis)' above.)

•Risk factors – Risk factors for PAPS include knee osteoarthritis (OA), obesity, female sex, knee malalignment and diabetes. (See 'Risk factors' above.)

•Diagnosis – There are no established diagnostic criteria for PAPS. We diagnose PAPS in patients with medial knee pain, tenderness over the upper medial tibia between the pes anserinus and the tibial joint line, and without local swelling or induration. In patients with symmetric pain, tenderness due to a tender, thick medial fat pad, and fibromyalgia should be excluded. (See 'Diagnosis' above.)

•Evaluation – PAPS should be suspected in patients who seek medical attention for one of the following three reasons (see 'Evaluation' above):

-Medial knee pain with activities such as rising from a chair, ascending or descending stairs, or lying in bed with one knee pressing on the other (which may disturb sleep).

-Rapidly mounting knee pain in a patient with knee OA.

-The transition of pain with activity to pain at night in a patient with known knee OA.

•Physical examination – The physical examination in patients with medial knee pain due to suspected PAPS should include attention to knee alignment and areas of focal tenderness around the medial joint. (See 'Physical examination' above.)

•Imaging – Although imaging is generally not necessary to diagnose PAPS, conventional knee radiographs may be obtained to detect underlying OA if the patient has no prior radiograph and has risk factors for OA (eg, age >50, overweight or obesity, varus or valgus malalignment). If local swelling or induration is present, US or MRI should be obtained to exclude alternative diagnoses. (See 'Imaging' above.)

•Differential diagnosis – The differential diagnosis includes a variety of other conditions that can lead to medial knee pain. (See 'Differential diagnosis' above.)

•Treatment – The initial treatment of PAPS includes a weight-reduction program, quadriceps strengthening exercises, and the use of an analgesic and/or short term nonsteroidal antiinflammatory drugs (NSAIDs). For patients who do not improve with initial therapy, a local glucocorticoid injection typically is administered (picture 5 and picture 6). Occasionally a glucocorticoid injection may be given as part of the initial therapy in patients who have night pain that disrupts sleep. (See 'Initial therapy' above and 'Persistent symptoms' above.)

●Prepatellar and superficial infrapatellar bursitis

•Definition – Prepatellar and superficial infrapatellar bursitis present as localized tenderness and swelling anterior to the patella or patellar tendon. The prepatellar and superficial infrapatellar bursae may be affected by, in decreasing order of frequency, infection, chronic or acute trauma, gout, and rheumatoid arthritis. (See 'Clinical features' above.)

•Diagnosis and evaluation – Once the presence of bursitis is confirmed by clinical history and physical examination, diagnostic testing for acute or chronic prepatellar or superficial infrapatellar bursitis includes laboratory testing, bursal fluid analysis, and imaging. A key component of the evaluation is the exclusion of septic bursitis, which requires bursal aspiration and analysis with a white cell count and differential, glucose concentration, crystal identification, Gram stain, and culture. (See 'Diagnosis' above and 'Diagnostic testing' above.)

•Treatment – Treatment of prepatellar or superficial infrapatellar bursitis is guided by the underlying cause. With the exception of septic bursitis, isolated bursitis of the prepatellar or superficial infrapatellar bursa is usually a self-limited condition. Patients with septic bursitis, in addition to the antibiotic treatment, are locally managed with transient immobilization of the knee and re-aspirations as needed. If gout is proven by crystal identification and the Gram stain of the bursal fluid is negative, patients should be treated for gout. (See 'Treatment' above.)

●Other types of knee bursitis – Other types of knee bursitis include biceps femoris bursitis, semimembranosus-tibial collateral ligament bursitis, deep infrapatellar bursitis, and medial collateral ligament bursitis. (See 'Other types of knee bursitis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Juan J Canoso, MD, MACR, who contributed to earlier versions of this topic review.