Necrotizing Dermatitis: Clinical and Pathogenetic Forms, Differ-Ential Diagnosis and Modern Approaches to Treatment

Аннотация

Necrotizing dermatitis is a heterogeneous group of skin lesions characterized by pro-gressive necrosis of the dermis and/or subcutaneous tissue against the background of infectious, autoimmune or vasculopathic genesis. This condition is associated with a high risk of systemic complications, disability and death, especially with untimely diagnosis and tactical errors in treatment. The article discusses modern clinical and pathogenetic forms of necrotizing dermati- tis, including necrotizing fasciitis, pyoderma gangrenous, necrotizing vasculitis and other rare syndromes. Particular attention is paid to the algorithms of differential diagnosis, the role of laboratory and imaging methods, as well as an interdisciplinary approach to treatment, taking into account the etiology of the disease. The review is based solely on English- language publi-cations of recent years and aims to summarize the most clinically relevant data for dermatolo-gists, surgeons, and intensive care professionals. Keywords: Necrotizing dermatitis; necrotizing fasciitis; pyoderma gangrenous; skin vasculitis; cutaneous necrosis. Introduction: Necrotizing dermatitis is a generalizing clinical and morphological term used to desig-nate a group of skin lesions accompanied by the development International Journal of Medical Science and Public Health Research 78 https://ijmsphr.com/index.php/ijmsphr International Journal of Medical Science and Public Health Research of ischemia, thrombovasculitis, acute inflammation polymicrobial variants of Staphylococcus aureus, and subsequent necrosis of the skin and underlying including MRSA strains, and anaerobic flora tissues. Depending on the etiological factor, this (Bacteroides spp., Clostridium spp., condition can be both an urgent surgical infection (for Peptostreptococcus). example, ne-crotizing fasciitis) and a manifestation of a systemic inflammatory disease of an autoimmune According to D.L. Stevens et al. [1], more than 60% of nature, including necrotizing vasculitis, pyoderma cases of necrotizing fasciitis are streptococcal in nature, gangrenous and other neutrophilic dermato-ses while the production of streptococcal superantigens involving skin vessels. (SpeA, SpeC) initi-ates a massive release of pro- inflammatory cytokines (TNF-α, IL-1β, IFN-γ), inducing a The relevance of the problem of necrotizing dermatitis sys-temic inflammatory response and multi-organ is due to its extremely polymor-phic clinical course, failure. high rate of progression in some cases, as well as difficulties in differential diagnosis with other Infectious forms of necrotizing dermatitis require inflammatory or thrombotic skin lesions. In the initial mandatory bacteriological confirma-tion (cultures, stages, the pathology can be disguised as banal PCR), although in some cases the diagnosis is erysipelas or phlegmon, but within a few hours, deep established mainly clinically due to the rapid course and necrosis of soft tissues develops, accompanied by pain, the inadmissibility of delaying the start of treatment [4]. fever, increasing intoxication and signs of organ dys- function. In such cases, we are talking about a surgical The second major etiological block consists of immune- emergency with a mortality rate of up to 30-40% [1, 2]. dependent necrotic dermatoses, in which the microbial factor is absent or plays a secondary role. These include: On the other hand, immune-dependent forms of pyoderma gan-grenosum; necrotizing cutaneous necrotic dermatoses can debut from sin-gle ulcerative- vasculitis (including ANCA-associated); Sweet syndrome necrotic elements in the complete absence of with necrotic elements; necrotizing erythema nodosum; infectious agents, which requires a radically different drug-induced skin necrosis (for example, with the use of diagnostic approach and the prescription of systemic warfarin, chemotherapy). anti-inflammatory or immunosuppressive therapy. Situations where infectious and immune mechanisms These conditions are based on disorders of are com-bined, intensifying destructive processes in regenerative-inflammatory homeostasis, in which tissues and reducing the effectiveness of standard neutrophil activation, the formation of extracellular treatment algorithms, are particularly difficult. neutrophil traps (NETs), vascular damage, and fibrinoid necrosis of the arterial wall/venules dominate. As MAIN PART emphasized by D. Kohli-Pamnani and A. Saavedra [6], the hyperreactivity of the innate immune response with Etiology and pathogenesis of necrotizing dermatitis dysregulation of IL-8, IL-17, and TNF-α leads to the formation of rapidly spreading ulcerative defects The pathogenesis of necrotizing dermatitis reflects a surrounded by an inflammatory infiltrate zone and a cascade of complex processes lead-ing to damage to lilac-bluish rim. Gupta D. et al. [7] emphasize the skin structures, microcirculatory bed and soft tissues importance of timely exclusion of the infectious nature with the subsequent de