Necrotizing fasciitis

Etiology and predisposing factors

The disease is distinctly polyetiological in nature. The inflammatory process can be caused by both aerobic and anaerobic microorganisms.

• Streptococcal fasciitis is caused by $\beta$-hemolytic streptococcus (Streptococcus pyogenes).
• Other pathogens: bacteroids, various species of Enterobacteriaceae, Peptococcus, Peptostreptococcus, and other streptococcal strains frequently participate in the pathological process.
• Specific pathogen: Erysipelothrix rhusiopathiae. Infection occurs via contact through microtraumas of the skin during the dressing of contaminated meat.
• Exception: clostridial infection is not included in this group, as clostridial necrotizing fasciitis is considered separately as one of the forms of gas gangrene.

The development of the infection is promoted by debilitating diseases that reduce the body's resistance: diabetes mellitus, tuberculosis, severe hypovitaminosis, and substance abuse. The pathogen penetrates either through traumatic injuries to the skin and deep tissues or as a complication of existing purulent diseases such as mastitis, erysipelas, or hidradenitis. In the case of Erysipelothrix rhusiopathiae, there is a clear occupational risk factor: workers in the meat, fish, canning, and leather industries, as well as housewives handling raw meat, fish, or game, are susceptible to the disease.

Pathogenesis of the disease

The mechanism of development is based on progressive necrosis of the superficial (subcutaneous) fascia. Skin lesions are exclusively secondary in nature.

Skin necrosis occurs under the influence of two key factors: direct toxic damage to tissue structures and thrombosis of the supplying blood vessels. An important role in the pathogenesis is played by the allergic component, which develops by the type of the Sanarelli-Shwartzman phenomenon.

From a pathomorphological perspective, serous inflammation of all skin layers, concomitant lymphangitis, pronounced edema of adjacent tissues, and a massive accumulation of mast cells directly in the inflammation zone are observed in the focus.

Clinical manifestations of Erysipelothrix rhusiopathiae infection

This form of infection often has an incubation period lasting 3–7 days. The process is localized predominantly on the fingers (especially their dorsal surface).

Dynamics of the development of local symptoms:

1. First day: a painful, itchy pink-red spot forms on the dorsum of the finger. The spot rises slightly above the level of healthy skin and has sharp borders.
2. Height of the disease: over the next few days, the intensity of itching increases significantly.
3. Resolution period: occurs after 2–3 weeks. Edema gradually subsides, itching stops completely, and hyperemia disappears. Characteristic skin peeling remains at the site of inflammation.

The process can spread to the dorsum of the hand and neighboring fingers, accompanied by lymphangitis and lymphadenitis. Complications may include the development of acute arthritis of the interphalangeal joints. It is important to note that the patient's general condition is little affected, and body temperature usually does not rise. High fever is observed only when a mixed infection joins. Due to the mild general presentation, the disease is often misdiagnosed as finger erysipelas, simple dermatitis, felon, or isolated lymphangitis.

Primary necrotizing fasciitis

The primary form is characterized by the fact that inflammation begins directly with damage to fascial structures. Early symptoms are isolated pain, local swelling, edema, and skin hyperemia over the focus. The clinical presentation strongly depends on the type of pathogen.

In streptococcal fasciitis: Local manifestations develop extremely rapidly. Dark spots appear on the skin, then vesicles filled with dark exudate form. Soon, areas of superficial necrosis appear, which rapidly merge into extensive full-thickness skin necrosis.

In non-streptococcal fasciitis: The disease develops more gradually, and local symptoms are less pronounced. The appearance of "woody" density of the skin against the background of edema is characteristic. The color of the affected areas varies: pale or erythematous spots against the background of a dense infiltrate. If there is an open wound, the fascia in it acquires a dirty gray color, and a turbid, sometimes brown exudate is released. A specific instrumental sign is that the subcutaneous adipose tissue separates extremely easily from the underlying fascia.

Secondary necrotizing fasciitis

The secondary form occurs as a severe complication against the background of existing, neglected purulent skin diseases.

The clinical picture of secondary fasciitis is superimposed on the symptoms of the primary pathology. There is a sharp and pronounced deterioration in the patient's general condition. Local necrotic changes begin to develop rapidly in the localization of the primary purulent focus, indicating the involvement of the fascia in the destructive process.

Class and exam questions

What else to study on this topic

• Pathophysiology of the Sanarelli-Shwartzman phenomenon in surgical infections
• Differential diagnosis of necrotizing fasciitis, felon, and finger erysipelas
• Features of microthrombosis of supplying vessels in purulent-necrotic processes
• Specifics of the immune response and the role of mast cells in the zone of serous inflammation
• Management tactics for patients with purulent complications against the background of debilitating diseases (diabetes mellitus)

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

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