Bursitis is an inflammation or degeneration of the sac-like structures that protect the soft tissues from underlying bony prominences. Bursitis may result from a local insult or be a manifestation of a systemic disease. Examples of the latter include rheumatoid arthritis, tophaceous gout, and sepsis. Adjacent tenosynovitis and calcium apatite deposition disease commonly coexist.
More than 140 bursae have been described in the human body. The clinically important bursae are the trochanteric, subdeltoid, ischiogluteal, pes anserine, iliopsoas, retrocalcaneal and olecranon bursae.
Ischial bursitis is characterized by pain over the center of the buttock and along the hamstring muscles in the leg. Most patients can be managed conservatively though in some cases injection treatments may be needed. Surgical excision of the bursa is reserved for those with frequent relapses and those who are unresponsive to conservative treatments.
The ischiogluteal bursa is an inconstant anatomical finding located between the gluteus maximus and the ischial tuberosity. While standing, the bursa is covered by the gluteus maximus; however, while sitting the muscle contracts and slides upwards leaving only fibrous tissue between bursa and skin. Ischiogluteal bursitis, sometimes called ‘weaver’s’ or ‘lighterman’s bottom’, is a rare disorder. Historically, ischiogluteal bursitis was frequently encountered in weavers, because of irritation or intermittent pressure upon the ischial tuberosity from prolonged sitting. As the bursa lies in close contact with the sciatic and posterior femoral cutaneous nerve, ischiogluteal bursitis can mimic the symptoms of radiculopathy.
Two types of bursae are described in the human body: constant and adventitial. Constant bursae, which are formed during normal embryologic development, are saclike structures lined with endothelial cells. They are generally located between tendon and bone or between tendon and skin. Some of them may communicate with a nearby joint. Adventitial bursae, on the other hand, form later in life through a process of myxoid degeneration of fibrous tissue in response to stress at the site of friction between adjacent structures. These bursae do not have an endothelial lining and will therefore not produce or contain synovial fluid; the fluid in adventitial bursitis appears after repetitive injury, leading to vasodilatation and increased vascular permeability, with extravasation of serum proteins and extracellular fluid into the bursa. The ischiogluteal bursa is an example of an adventitial bursa.
Many causes of bursitis have been described, the most common of which are trauma (hemorrhagic bursitis), inflammation (rheumatoid arthritis and spondyloarthropathies), infection and crystal deposition. There are three basic crystal-induced arthropathies: monosodium urate crystal deposition disease(gout); calcium pyrophosphate dihydrate (CPPD) crystal deposition disease (pseudogout and other clinical presentation); and calcium hydroxy-apatite (HA) crystal deposition disease.
Ischiogluteal bursitis is clinically characterized by pain over the centre of the buttock and along the hamstring muscles of the leg. Pain is exacerbated by sitting down and may be relieved to some extent on standing. Differential diagnosis include disc herniation in the lumbar spine, piriformis syndrome and radiculopathy.
Imaging studies are helpful in evaluating the nature and extent of the bursa and in differentiating the mass from ganglion cyst, schwannoma in the sciatic nerve, and other benign and malignant neoplasms with cystic changes.
Treatment of nonseptic bursitis should include patient education and relief of the acute symptoms of inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs) are generally used initially and steroid injections are reserved for patients who do not respond to simple analgesics. Surgical excision of the bursa is reserved for those with frequent relapses and those who are unresponsive to conservative treatment.
The patient should be educated in the recognition of aggravating factors such as direct pressure on the painful area. Obesity, compression injury or other minor local trauma may be additional factors.
Ice, heat, and rest should be recommended until acute pain has subsided.
NSAIDs, either selective cyclooxygenase 2 inhibitors (coxibs) or nonselective agents, are effective in treating episodes of nonseptic bursitis. It is prudent to avoid use of NSAIDs and coxibs in patients with known coronary artery or cerebrovascular disease, or those with multiple risk factors for cardiovascular disease, those with renal disease, and edematous states due to the increased risk of adverse cardiovascular side effects and/or the risk of acute renal failure. NSAIDS should also be avoided in patients with history of gastric ulcers and gastro intestinal bleeding.
Injection of local anaesthetic and steroids can be effective in management of nonseptic bursitis.
Diagnostic local anesthetic injections into the ischial bursa can potentially be helpful when the diagnosis is uncertain.
Corticosteroids are often injected into the bursa when other conservative measures are unsuccessful.
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