Olecranon Bursitis

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Chapter 36 Olecranon Bursitis

Introduction

A bursa either communicates with a joint space/tendon sheath or forms in response to friction in order to facilitate movement. There are approximately 140 bursae throughout the body,1 with 50 named and in constant positions.2 Most are deep and are found between tendon and other tendons, ligaments or bone. A small number are subcutaneous, being located between bone and skin. Their walls consist of cellular or collagenous connective tissue and are lined with synovium.3 There are 11 in the vicinity of the elbow of which the olecranon bursa, situated between skin and the posterior aspect of the olecranon process is most frequently affected by inflammation. The normal olecranon bursa contains very little fluid but significant amounts are produced when it is inflamed and this can result in substantial swelling.

An anatomical study of 20 full-term foetuses found that eight had olecranon bursae.4 In contrast, a similar study, based on the dissection of 63 cadavers of varying ages, noted that (i) no olecranon bursae occurred in those under the age of 7, which is consistent with the low incidence of olecranon bursitis in children, (ii) their volume increased with age and (iii) the bursa on the right was larger than that on the left in all those over the age of 10.

A study comparing elbow effusions with olecranon bursitis5 found that the lowest pressure in an elbow joint effusion occurred at 30–40° of flexion and then rose rapidly with further flexion. Baseline pressure within olecranon bursal fluid, however, persisted until approximately 60° of elbow joint flexion and then rose exponentially with further flexion, although this did not cause pain. It was felt more likely that pain arose in receptors in the area between the bursa and the underlying osteo-tendinous structures. It was also noted that, as flexion progressed, the olecranon process including the triceps insertion, moved distally under the bursa. Another difference between joint and bursal fluid is that bursal fluid has poor mucin clot and a lower white cell count, glucose and complement.

Background/aetiology

There are a variety of synonyms for olecranon bursitis:

Most of these relate to activities involving repetitive elbow movements, leaning on the point of the elbow or to the clinical appearance of the bursa. Although a significant number of patients with olecranon bursitis are encountered in primary care, the majority of the literature is based on cases requiring hospital admission, and as such the true incidence of this condition is unknown.

Clinical Pearl 36.1

Most cases of olecranon bursitis are caused by low level trauma or repetitive elbow movements. Other predisposing factors include conditions causing systemic inflammation or impaired immunity (Table 36.1). There is also an increased incidence in patients on maintenance haemodialysis.

Table 36.1 Factors predisposing to olecranon bursitis

Traumatic Repetitive low level trauma, e.g. in miners, mechanics, carpet-layers, book-keepers, wrestlers, gymnasts, gardeners, those with spinal cord injury, those with tardive dyskinesia (by causing involuntary movements while leaning on elbows)
Single direct impact
Penetrating injury, e.g. laceration, surgical incision, intrabursal steroid injection, internal fracture fixation
Distal triceps tendon injury
Systemic inflammation Rheumatoid arthritis
Gout
Calcium pyrophosphate deposition (pseudogout)
Systemic lupus erythematosus
Pigmented villonodular synovitis
Impaired immunity Diabetes
Steroid therapy
Malignancy
Human immune deficiency syndrome
Immunosuppressive drugs
Uraemia
Monoclonal gammopathy
Myelodysplasia
Alcoholism
Intravenous drug abuse
Miscellaneous Adjacent internal fixation metalwork maintenance haemodialysis
Chronic obstructive pulmonary disease
Psoriasis
Scleroderma
Sunitinib therapy (used in treatment of renal cell carcinoma)

A study of mononuclear cells in the fluid from aseptic olecranon bursitis has revealed ‘a preponderance of activated T cell subpopulations and monocyte/macrophages’ suggesting that there is ‘an immunologic role in the development and perpetuation’ of this condition.6 The authors proposed that trauma to the bursa caused synovial damage, increasing permeability and exposing the vascular endothelium.

Aseptic olecranon bursitis

In most, but not all, cases of aseptic bursitis the history suggests a predisposing cause. The most common is low level trauma such as occurs when repeatedly leaning on the elbow (Table 36.1). Other cases are associated with more substantial trauma including direct impact, a laceration and surgery. It has also been reported in association with a distal triceps tendon injury but whether this is cause or effect is unclear. Integrity of the distal triceps tendon should, however, always be tested. Systemic inflammatory conditions, impaired immunity and miscellaneous other conditions are also associated with this condition.

Rheumatoid synovitis can affect the olecranon bursa and may predate a more generalized manifestation of the disease.3 Rheumatoid nodules and gouty tophi in this area may form within the bursa or be extra-bursal. Calcium pyrophosphate crystal deposition (pseudogout) can also occur and give rise to bursitis.

Inflammation of the serous membranes (pericardium, pleura and peritoneum), i.e. serositis, is known to occur in uraemic patients and this may explain the increased incidence of olecranon bursitis in those receiving haemodialysis. The condition nearly always occurs in the same limb as the vascular access and the possibility of it being caused by repeated low level trauma to this area has also been raised. In most reported cases the elbow has rested on the arm of a chair and it is suggested that prolonged pressure over the olecranon with small movements during the few hours of dialysis is the cause of the bursitis. However, one group reported three cases despite the practice of performing the procedure with the patient in bed and with padding behind the elbows.1

Septic olecranon bursitis

Approximately one-third of cases of olecranon bursitis are septic and yet clinically distinguishing them from non-septic cases is difficult. The portal of entry for the infecting organism is usually the skin. The haematogenous route is rare. A past history of septic bursitis and the presence of rheumatoid nodules or gouty tophi are associated with an increased risk of infection.7

Although Staphylococcus aureus is the commonest cause of infection numerous other organisms have been reported (Table 36.2) many of them as single case reports. Some infections are caused by mixed flora. There is a significant association with conditions or therapy that impair immunity (Table 36.1). In all rheumatoid patients with septic olecranon bursitis the possibility of septic arthritis of the elbow should be considered.8

Table 36.2 Organisms reported to cause septic olecranon bursitis

Gram-positive Staphylococcus aureus
Group A streptococci (Streptococcus pyogenes)
Staphylococcus epidermidis
Enterococcus
Gram-negative Enterobacter
Serratia marcescens
Escherichia coli
Haemophilus influenzae
Brucella abortus
Neisseria
Atypical Mycobacterium tuberculosis
Atypical mycobacteria
Nocardia
Achlorophyllic algae (Prototheca species)
Fungi Candida
Phaeoacremonium species
Cryptococcus neoformans
Anthopsis deltoidea

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