Suppurative bursitis

Etiology and main developmental mechanisms

The development of the inflammatory process can be triggered by various factors, which are globally divided into infectious and aseptic.

In the former case, a key role is played by pyogenic microflora. Its penetration into tissues occurs via several pathways:

• Hematogenous pathway — microorganisms are carried by the bloodstream, directly entering the vascular or tissue wall.
• Lymphogenous pathway — the pathogen migrates from a pre-existing primary purulent focus along lymphatic vessels.
• Contact pathway — inflammation spreads from adjacent affected tissues, for example, in the presence of phlegmon, abscess, or osteomyelitis.

In addition to infectious inflammation, it can be aseptic in nature. It occurs without the involvement of bacteria as a result of mechanical irritation of the internal membranes (for example, with a prolonged presence of a catheter in the lumen) or due to chemical tissue damage, which may be caused by the administration of concentrated solutions or certain antibiotics.

Pathogenesis and conditions for the development of thrombophlebitis

For thrombophlebitis to form within the vascular bed, a combination of specific conditions is required. These include:

1. Significant deceleration of blood flow velocity.
2. Qualitative changes in the composition of the blood itself.
3. Physical or chemical damage to the vessel wall.
4. Presence of an infectious agent.
5. Various neurotrophic disorders, endocrine disruptions, or allergic reactions of the organism.

The pathophysiological mechanism is based on initial endothelial damage. This triggers a cascade activating the blood coagulation system. Concurrently, a critical decrease in the activity of the anticoagulation system occurs: the body reduces the synthesis of heparin sodium, fibrinolysis inhibitors, and fibrinolysis activators.

The situation is aggravated by concomitant pathologies and risk factors, among which hemorrhoids and varicose veins, neoplasms, past traumas and injuries, and the postoperative period (especially after pelvic organ surgeries) are highlighted.

Pathomorphology of venous wall inflammation

Depending on where the inflammatory process originates and how it spreads, three main pathomorphological forms of venous involvement are distinguished:

• Endophlebitis (endophlebitis). Inflammation starts from the inner lining of the vessel. The endothelial layer is actively infiltrated by polymorphonuclear leukocytes, and thrombotic masses begin to adhere tightly to it. Meanwhile, the outer coat of the vein remains intact (undamaged).
• Periphlebitis (periphlebitis). The process proceeds in the opposite direction — from the surrounding affected tissues. First and foremost, the outer coat of the vessel and the so-called vasa vasorum (vasa vasorum) suffer, undergoing thrombosis.
• Panphlebitis (panphlebitis). Represents total involvement of the entire thickness of the venous wall.

Of particular concern is suppurative thrombophlebitis. In this form, entire colonies of microorganisms are found directly within the vein wall and inside the thrombotic masses. This creates an extremely high risk of infection generalization: the pathogen spreads throughout the body, forming secondary abscesses in internal organs, which ultimately leads to the development of sepsis (sepsis).

Treatment tactics: conservative and surgical approaches

In the acute period of the disease, competent conservative therapy is of paramount importance. The patient is prescribed strict rest with the mandatory elevation of the affected limb. Medical treatment includes the administration of anti-inflammatory and anticoagulant drugs (acetylsalicylic acid, rutoside, troxerutin, phenylbutazone). Locally, dressings with rutoside or heparin ointment are applied. To relieve pronounced symptoms, procaine blockades in combination with heparin sodium are used.

Among physiotherapeutic methods, UHF and electrophoresis (with potassium iodide or trypsin) are indicated. As acute manifestations subside, moderate mobilization of the patient is indicated — dosed walking, strictly under the condition of obligatory elastic bandaging of the limb.

In some cases, conservative measures are insufficient, and indications for surgery arise. Surgical intervention is absolutely necessary in the development of suppurative thrombophlebitis due to the direct threat of sepsis, as well as when thrombosis is localized directly in the area of the saphenous vein ostium (due to the high risk of thrombus extension into deep veins and the development of Pulmonary Thromboembolism — PE). The main types of surgeries include complete excision of the thrombosed vein or ligation of its ostium at the site of entry into the deep venous trunk.

Purulent hand infections

A separate large group of inflammatory diseases in outpatient surgery comprises upper extremity lesions. They are classified according to the exact localization of the purulent focus:

1. Panaritium (panaricium). This is an acute inflammatory lesion of the finger tissues.
2. Hand phlegmon. Represents diffuse purulent inflammation of the tissues of the hand proper. Depending on the anatomical zone of involvement, phlegmons are distinguished in:
3. The thenar eminence (thenar);
4. The hypothenar eminence (hypothenar);
5. The midpalmar space;
6. The dorsal surface of the hand.

Class and exam questions

What else to study on this topic

• Mechanisms of formation and clinical consequences of pulmonary thromboembolism (PTE)
• Differences in the course of inflammation in the thenar and hypothenar spaces
• Mechanisms of action of direct and indirect anticoagulants in the treatment of venous pathologies
• Technique and indications for procaine blockades with heparin
• Prevention of aseptic inflammation during prolonged vascular catheterization

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.