Bursitis

Morphology and pathways of infection

Synovial bursae (bursae) are circumscribed connective tissue sacs with a smooth inner surface. They are lined with endothelium and normally secrete a small amount of synovial fluid. When pus accumulates in such a cavity, acute purulent bursitis develops.

The main causative agents of the purulent process are pyogenic microbes (primarily staphylococci and streptococci). Specific pathogens are significantly less common: gonococci, tubercle bacilli, Escherichia coli, and pneumococci.

Infection enters the cavity through several pathways:

• Lymphogenous. Bacteria spread from nearby purulent foci (erysipelas, carbuncle, furuncle, phlegmon, or osteomyelitis).
• Hematogenous. Inflammation becomes a complication of general systemic infections (influenza, tonsillitis, rheumatism).
• Contact and traumatic. Constant mechanical trauma causes reactive inflammation with the release of serous or serosanguineous exudate. If this is compounded by a breach of skin integrity (microtrauma) and local pyoderma, infection joins in, and the process rapidly transforms into a purulent one.

Clinical presentation

The symptoms of purulent bursitis are divided into local and general manifestations. The most typical localization of the pathology is the bursae of the elbow, knee, and shoulder joints.

The local signs include:

• A rounded, tumor-like protrusion of significant size in the projection of the affected bursa.
• Sharp pain upon palpation.
• Pronounced edema and hyperemia (redness) of the skin over the swelling.
• Local increase in temperature.
• The fluctuation sign (sensation of fluid movement), which is detected when there is a significant accumulation of exudate.
• Limb function is only mildly impaired.

General symptoms are typical of intoxication syndrome: the patient complains of general weakness, body temperature rises to 38–38.5 °C, and leukocytosis is recorded in the complete blood count.

If the purulent process extends beyond the walls, it can spread to the surrounding soft tissues. As a result of partial necrosis of the bursa, pus ruptures through, leading to the development of subcutaneous and intermuscular phlegmons. In advanced cases, long-standing, non-healing fistulas form.

Diagnostics and differential diagnosis

The baseline diagnosis is established based on classic visual signs of acute purulent inflammation. To confirm the diagnosis and determine the management tactics, a puncture of the bursa cavity is mandatory.

During the puncture, the surgeon aspirates the contents and sends the pus for bacteriological examination. This is necessary to identify specific pathogens (e.g., Brucella or gonococcus) and select adequate antibiotic therapy.

The main objective in making a diagnosis is to differentiate bursitis from arthritis. In joint inflammation, movements are sharply restricted due to pain within the joint cavity itself. In bursitis, the range of motion in the joint is completely preserved, as the inflammatory process is strictly localized within the synovial bursa and does not affect the articular surfaces.

Principles of treatment and prevention

In the early stages, as well as in protracted courses of the acute process, a conservative approach is used. The cavity is punctured, pus is completely aspirated, and antibiotics are injected inside (often in combination with procaine solution). Frequently, this leads to complete recovery.

If punctures are unsuccessful, treatment proceeds to surgical intervention: the bursa is opened, all pus is removed, and the wound is subsequently managed according to the rules of purulent surgery (regular drainage, dressings).

In recurrent purulent bursitis, a radical measure is indicated — extirpation. This is a procedure in which the synovial bursa is completely removed under local anesthesia without opening its lumen. The technique involves an incision to the side of the bursa and careful dissection of the formation. Finally, the wound is either left open or sutured tightly after local administration of antibiotics.

There are also methods of chemical obliteration: the cavity is opened, partially excised, and treated with chemical agents (5% phenol solution, alcoholic iodine solution) to accelerate fusion.

For the prevention of purulent forms, it is critically important to treat acute serous bursitis promptly and actively. The basis of such treatment is mandatory immobilization: the upper limb is fixed with a sling bandage, and a hardening plaster cast or splint is applied to the lower limb.

Class and exam questions

What else to study on this topic

• Features of specific bursitis (gonococcal, tuberculous, brucellar).
• Technique for performing punctures of the elbow and knee synovial bursae.
• Mechanism of development of reactive inflammation in constant mechanical trauma.
• Methodology of cavity chemical obliteration: indications and drugs used.
• Rules for managing a postoperative wound after opening an acute purulent focus.

Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.