{"id":1761,"date":"2024-05-07T15:43:34","date_gmt":"2024-05-07T19:43:34","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=1761"},"modified":"2025-10-17T19:31:06","modified_gmt":"2025-10-17T23:31:06","slug":"bursitis","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/bursitis\/","title":{"raw":"Bursitis","rendered":"Bursitis"},"content":{"raw":"<h3><strong>Bursa<\/strong><\/h3>\r\nBursa are sac-like structures found between tendons, ligaments, bone, and skin that provide protection and cushioning while allowing structures to move in relation to each other.\u00a0 Amazingly, humans have over 150 bursae, many of which are lined with synovial membranes that produce and absorb the <strong>bursal fluid<\/strong> that is rich in collagen and proteoglycans.\u00a0 These bursae are termed <strong>constant bursae<\/strong> and form during embryonic development.\u00a0 Bursal fluid is similar in composition to synovial fluid and contains the oily hyaluronic acid, which helps to create a slippery fluid with low coefficient of friction.\r\n\r\nSome bursae (termed <strong>adventitial bursae<\/strong>) form later in life in response to repetitive microtraumas and these bursae lack synovial endothelial cells and do not contain fluid.\u00a0 Examples include those that develop over bunions.\r\n\r\nBoth types of bursae (constant and adventitial) can become inflamed when irritate or infected resulting in bursitis.\r\n<h3><strong>Risk Factors - Bursitis<\/strong><\/h3>\r\nRisk factors include repetitive physical activity and sedentary behaviour that prolongs stress on load-bearing bursae.\u00a0 The highest incidence of bursitis occurs in runners, followed by occupations that involve heavy workload or frequent kneeling.\u00a0 The wearing of tight high-heeled shoes is a risk factor for developing <strong>bunions<\/strong> (a deformity of the metatarsophalangeal joint and bone of the big toe, as well as inflammation of the bursal sac in that region).\r\n\r\n<strong>Genetics<\/strong> and <strong>rheumatoid arthritis<\/strong> increase the risk of bunions, and bursitis in general, as does <strong>diabetes mellitus<\/strong> and <strong>HIV.<\/strong>\r\n\r\nUric acid crystal deposition associated with <strong>gouty arthritis<\/strong> (gout) can lead to bursitis, and is sometimes accompanied by kidney stones.\r\n\r\nRunning and <strong>rheumatoid arthritis<\/strong> as well as <strong>osteoarthritis<\/strong> are risk factors for developing bursitis associated with the anterior hip, knee, ankle and heel.\r\n\r\n&nbsp;\r\n\r\n&nbsp;\r\n\r\nCommon examples:\r\n\r\nBursa associated with rotator cuff muscles can become inflamed with overuse of the muscles and tendons in this region (e.g., <strong>subacromial bursitis<\/strong>).\r\n\r\nElbow bursa can become inflamed due to microtraumas accumulating from activities such as swimming, skiing, gymnastics and\/or weightlifting giving rise to <strong>olecranon bursitis<\/strong>.\r\n\r\n<strong>Ischiogluteal bursitis<\/strong> can occur due to excessive sitting (e.g., resulting in so called \"weaver's bottom\").\r\n\r\nFrequent kneeling is linked to the development of what used to be called \u201chousemaid's knee\u201d (<strong>prepatellar bursitis<\/strong>) or \u201cclergyman\u2019s knee\u201d <strong>(infrapatellar bursitis).<\/strong>\r\n\r\n&nbsp;\r\n\r\nBursitis can also be caused by infections or acute trauma of the bursa.\u00a0 Open wounds carry the risk of <strong>septic bursitis<\/strong> (bursitis caused by infection).\u00a0 Infections of bursa with bacteria or fungi can also result from blood infections, or through the spread of cellulitis (most often caused by <em>Staphylococcus aureus<\/em> bacteria).\r\n\r\n&nbsp;\r\n<h3><strong>Pathogenesis - Bursitis<\/strong><\/h3>\r\nIrritation of the bursa often by repetitive movements or stresses can lead to microtrauma of bursa inducing inflammation.\u00a0 Acute trauma, infection, or autoimmune dysfunction (e.g., rheumatoid arthritis, systemic lupus erythematosus, and gout) can also cause bursitis.\u00a0 If bursitis does not resolve, it may lead to irritation and inflammation of surrounding tissues (e.g., tendons, muscles, ligaments, skin) which may increase pain, swelling and deterioration of tissues.\r\n\r\nObesity, smoking, fibromyalgia, hypothyroidism, alcoholism, diabetes mellitus, arthritis, and emotional stress correlate with slower and reduced healing and recovery.\r\n\r\n<strong>Complications<\/strong> can involve an increased risk of <strong>deterioration<\/strong> of surrounding tissues, that are slow to heal and may not be able to fully regenerate (e.g., ligaments, tendons, muscles).\u00a0 Potential complications include <strong>scarring<\/strong> that can impede range of motion.\r\n<h3><strong>Signs and Symptoms - Bursitis<\/strong><\/h3>\r\nBursitis that is caused by repetitive movements or prolonged weight-bearing may develop insidiously and give rise to <strong>inflammation<\/strong> (swelling, redness, pain, warmth), <strong>tenderness,<\/strong> and <strong>impaired function<\/strong>.\u00a0 Acute bursitis caused by trauma will also result in inflammation, and is often associated with damage to surrounding tissues and risk of infection.\u00a0 Infections and septic bursitis may cause a <strong>fever<\/strong> to develop. Range of motion may decrease due to pain or swelling.\u00a0 Chronic bursitis can lead to irritation, inflammation, and deterioration of surrounding tissues (e.g., tendons, ligaments, muscles) as well.\r\n<h3><strong>Diagnostic Tests - Bursitis<\/strong><\/h3>\r\nPhysical examination and imaging may be used to diagnose bursitis and determine the extent of inflammation and\/or damage to the bursa as well as any deterioration of surrounding structures.\r\n\r\nAspiration of the fluid and blood tests can be analyzed for the presence of infectious agents, crystals, and cell count.\u00a0 Removal of exudate fluid can also be therapeutic reducing the debris, inflammation, pain and assisting in the healing process.\r\n\r\nImaging (e.g., ultrasound, x-ray) can be helpful in ruling out other causes and assessing the level of inflammation and damage.\r\n<h3><strong>Treatment - Bursitis<\/strong><\/h3>\r\nTreatment depends on the extent of the damage, but can involve surgery (e.g., bursectomy), orthotics, RICE, NSAIDs, acetaminophen, and topical anesthetics.\u00a0 Infections require the use of antibiotics.\u00a0 At times aspiration and\/or corticosteroids are used.\r\n\r\nMost often bursitis resolves without surgery, however surgical drainage and excision may be necessary, particularly with chronically inflamed bursae.\r\n\r\nTreatment of severe bunions often require surgery to correct joint deformity, remove bony prominences, and reducing pain.\r\n\r\nProgressive rehabilitative strategies (e.g., stretching and strength training that are gradually increased) are recommended to reduce chances of excess scarring and loss of ROM (e.g., adhesive capsulitis also known as frozen shoulder).","rendered":"<h3><strong>Bursa<\/strong><\/h3>\n<p>Bursa are sac-like structures found between tendons, ligaments, bone, and skin that provide protection and cushioning while allowing structures to move in relation to each other.\u00a0 Amazingly, humans have over 150 bursae, many of which are lined with synovial membranes that produce and absorb the <strong>bursal fluid<\/strong> that is rich in collagen and proteoglycans.\u00a0 These bursae are termed <strong>constant bursae<\/strong> and form during embryonic development.\u00a0 Bursal fluid is similar in composition to synovial fluid and contains the oily hyaluronic acid, which helps to create a slippery fluid with low coefficient of friction.<\/p>\n<p>Some bursae (termed <strong>adventitial bursae<\/strong>) form later in life in response to repetitive microtraumas and these bursae lack synovial endothelial cells and do not contain fluid.\u00a0 Examples include those that develop over bunions.<\/p>\n<p>Both types of bursae (constant and adventitial) can become inflamed when irritate or infected resulting in bursitis.<\/p>\n<h3><strong>Risk Factors &#8211; Bursitis<\/strong><\/h3>\n<p>Risk factors include repetitive physical activity and sedentary behaviour that prolongs stress on load-bearing bursae.\u00a0 The highest incidence of bursitis occurs in runners, followed by occupations that involve heavy workload or frequent kneeling.\u00a0 The wearing of tight high-heeled shoes is a risk factor for developing <strong>bunions<\/strong> (a deformity of the metatarsophalangeal joint and bone of the big toe, as well as inflammation of the bursal sac in that region).<\/p>\n<p><strong>Genetics<\/strong> and <strong>rheumatoid arthritis<\/strong> increase the risk of bunions, and bursitis in general, as does <strong>diabetes mellitus<\/strong> and <strong>HIV.<\/strong><\/p>\n<p>Uric acid crystal deposition associated with <strong>gouty arthritis<\/strong> (gout) can lead to bursitis, and is sometimes accompanied by kidney stones.<\/p>\n<p>Running and <strong>rheumatoid arthritis<\/strong> as well as <strong>osteoarthritis<\/strong> are risk factors for developing bursitis associated with the anterior hip, knee, ankle and heel.<\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>Common examples:<\/p>\n<p>Bursa associated with rotator cuff muscles can become inflamed with overuse of the muscles and tendons in this region (e.g., <strong>subacromial bursitis<\/strong>).<\/p>\n<p>Elbow bursa can become inflamed due to microtraumas accumulating from activities such as swimming, skiing, gymnastics and\/or weightlifting giving rise to <strong>olecranon bursitis<\/strong>.<\/p>\n<p><strong>Ischiogluteal bursitis<\/strong> can occur due to excessive sitting (e.g., resulting in so called &#8220;weaver&#8217;s bottom&#8221;).<\/p>\n<p>Frequent kneeling is linked to the development of what used to be called \u201chousemaid&#8217;s knee\u201d (<strong>prepatellar bursitis<\/strong>) or \u201cclergyman\u2019s knee\u201d <strong>(infrapatellar bursitis).<\/strong><\/p>\n<p>&nbsp;<\/p>\n<p>Bursitis can also be caused by infections or acute trauma of the bursa.\u00a0 Open wounds carry the risk of <strong>septic bursitis<\/strong> (bursitis caused by infection).\u00a0 Infections of bursa with bacteria or fungi can also result from blood infections, or through the spread of cellulitis (most often caused by <em>Staphylococcus aureus<\/em> bacteria).<\/p>\n<p>&nbsp;<\/p>\n<h3><strong>Pathogenesis &#8211; Bursitis<\/strong><\/h3>\n<p>Irritation of the bursa often by repetitive movements or stresses can lead to microtrauma of bursa inducing inflammation.\u00a0 Acute trauma, infection, or autoimmune dysfunction (e.g., rheumatoid arthritis, systemic lupus erythematosus, and gout) can also cause bursitis.\u00a0 If bursitis does not resolve, it may lead to irritation and inflammation of surrounding tissues (e.g., tendons, muscles, ligaments, skin) which may increase pain, swelling and deterioration of tissues.<\/p>\n<p>Obesity, smoking, fibromyalgia, hypothyroidism, alcoholism, diabetes mellitus, arthritis, and emotional stress correlate with slower and reduced healing and recovery.<\/p>\n<p><strong>Complications<\/strong> can involve an increased risk of <strong>deterioration<\/strong> of surrounding tissues, that are slow to heal and may not be able to fully regenerate (e.g., ligaments, tendons, muscles).\u00a0 Potential complications include <strong>scarring<\/strong> that can impede range of motion.<\/p>\n<h3><strong>Signs and Symptoms &#8211; Bursitis<\/strong><\/h3>\n<p>Bursitis that is caused by repetitive movements or prolonged weight-bearing may develop insidiously and give rise to <strong>inflammation<\/strong> (swelling, redness, pain, warmth), <strong>tenderness,<\/strong> and <strong>impaired function<\/strong>.\u00a0 Acute bursitis caused by trauma will also result in inflammation, and is often associated with damage to surrounding tissues and risk of infection.\u00a0 Infections and septic bursitis may cause a <strong>fever<\/strong> to develop. Range of motion may decrease due to pain or swelling.\u00a0 Chronic bursitis can lead to irritation, inflammation, and deterioration of surrounding tissues (e.g., tendons, ligaments, muscles) as well.<\/p>\n<h3><strong>Diagnostic Tests &#8211; Bursitis<\/strong><\/h3>\n<p>Physical examination and imaging may be used to diagnose bursitis and determine the extent of inflammation and\/or damage to the bursa as well as any deterioration of surrounding structures.<\/p>\n<p>Aspiration of the fluid and blood tests can be analyzed for the presence of infectious agents, crystals, and cell count.\u00a0 Removal of exudate fluid can also be therapeutic reducing the debris, inflammation, pain and assisting in the healing process.<\/p>\n<p>Imaging (e.g., ultrasound, x-ray) can be helpful in ruling out other causes and assessing the level of inflammation and damage.<\/p>\n<h3><strong>Treatment &#8211; Bursitis<\/strong><\/h3>\n<p>Treatment depends on the extent of the damage, but can involve surgery (e.g., bursectomy), orthotics, RICE, NSAIDs, acetaminophen, and topical anesthetics.\u00a0 Infections require the use of antibiotics.\u00a0 At times aspiration and\/or corticosteroids are used.<\/p>\n<p>Most often bursitis resolves without surgery, however surgical drainage and excision may be necessary, particularly with chronically inflamed bursae.<\/p>\n<p>Treatment of severe bunions often require surgery to correct joint deformity, remove bony prominences, and reducing pain.<\/p>\n<p>Progressive rehabilitative strategies (e.g., stretching and strength training that are gradually increased) are recommended to reduce chances of excess scarring and loss of ROM (e.g., adhesive capsulitis also known as frozen shoulder).<\/p>\n","protected":false},"author":1370,"menu_order":20,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"Pictures coming soon!","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[48],"contributor":[60],"license":[57],"class_list":["post-1761","chapter","type-chapter","status-web-only","hentry","chapter-type-standard","contributor-zoe-soon","license-cc-by-nc-sa"],"part":41,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1761","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":6,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1761\/revisions"}],"predecessor-version":[{"id":1769,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1761\/revisions\/1769"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/41"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/1761\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=1761"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=1761"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=1761"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=1761"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}