International Journal of Medical Science and Public Health Research
78
https://ijmsphr.com/index.php/ijmsphr
TYPE
Original Research
PAGE NO.
98-102
DOI
10.37547/ijmsphr/Volume06Issue05-08
OPEN ACCESS
SUBMITED
23 March 2025
ACCEPTED
19 April 2025
PUBLISHED
30 May 2025
VOLUME
Vol.06 Issue05 2025
CITATION
Okhunov Alisher Oripovich, & Erkulov Abbosjon Sherali ugli. (2025).
Necrotizing Dermatitis: Clinical and Pathogenetic Forms, Differ-Ential
Diagnosis and Modern Approaches to Treatment. International Journal of
Medical Science and Public Health Research, 6(05), 98
–
102.
https://doi.org/10.37547/ijmsphr/Volume06Issue05-08
COPYRIGHT
© 2025 Original content from this work may be used under the terms
of the creative commons attributes 4.0 License.
Necrotizing Dermatitis:
Clinical and Pathogenetic
Forms, Differ-Ential
Diagnosis and Modern
Approaches to Treatment
Okhunov Alisher Oripovich
Professor, Doctor of Medical Sciences, Head of the De-partment of General
and Pediatric Surgery No1 of the Tashkent State Medical University, Tash-
kent, Uzbekistan
Erkulov Abbosjon Sherali ugli
Assistant Professor, Department of General and Pedi-atric Surgery,
Tashkent State Medical University, Tashkent, Uzbekistan
Abstract:
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
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of ischemia, thrombovasculitis, acute inflammation
and subsequent necrosis of the skin and underlying
tissues. Depending on the etiological factor, this
condition can be both an urgent surgical infection (for
example, ne-crotizing fasciitis) and a manifestation of
a systemic inflammatory disease of an autoimmune
nature, including necrotizing vasculitis, pyoderma
gangrenous and other neutrophilic dermato-ses
involving skin vessels.
The relevance of the problem of necrotizing dermatitis
is due to its extremely polymor-phic clinical course,
high rate of progression in some cases, as well as
difficulties in differential diagnosis with other
inflammatory or thrombotic skin lesions. In the initial
stages, the pathology can be disguised as banal
erysipelas or phlegmon, but within a few hours, deep
necrosis of soft tissues develops, accompanied by pain,
fever, increasing intoxication and signs of organ dys-
function. In such cases, we are talking about a surgical
emergency with a mortality rate of up to 30-40% [1, 2].
On the other hand, immune-dependent forms of
necrotic dermatoses can debut from sin-gle ulcerative-
necrotic elements in the complete absence of
infectious agents, which requires a radically different
diagnostic approach and the prescription of systemic
anti-inflammatory or immunosuppressive therapy.
Situations where infectious and immune mechanisms
are com-bined, intensifying destructive processes in
tissues and reducing the effectiveness of standard
treatment algorithms, are particularly difficult.
MAIN PART
Etiology and pathogenesis of necrotizing dermatitis
The pathogenesis of necrotizing dermatitis reflects a
cascade of complex processes lead-ing to damage to
skin structures, microcirculatory bed and soft tissues
with the subsequent de-velopment of ischemic and
inflammatory necrosis. Despite the variety of clinical
forms, three main etiopathogenetic categories can be
distinguished: infectious, autoimmune, and toxico-
ischemic. Each of them is characterized by its own
spectrum of triggers and mechanisms, but
intersections are often observed between them.
The most well-known representative of infectious
necrotizing dermatitis is necrotizing fasciitis - an acute
polyetiological disease in which necrosis spreads at a
high rate through the fascial spaces, involving the skin
and subcutaneous tissue. In the vast majority of cases,
the dis-ease is caused by gro
up A β
-hemolytic
streptococcus (Streptococcus pyogenes), as well as in
polymicrobial variants of Staphylococcus aureus,
including MRSA strains, and anaerobic flora
(Bacteroides
spp.,
Clostridium
spp.,
Peptostreptococcus).
According to D.L. Stevens et al. [1], more than 60% of
cases of necrotizing fasciitis are streptococcal in nature,
while the production of streptococcal superantigens
(SpeA, SpeC) initi-ates a massive release of pro-
inflammatory cytokines (TNF-
α, IL
-
1β, IFN
-
γ), inducing a
sys-temic inflammatory response and multi-organ
failure.
Infectious forms of necrotizing dermatitis require
mandatory bacteriological confirma-tion (cultures,
PCR), although in some cases the diagnosis is
established mainly clinically due to the rapid course and
the inadmissibility of delaying the start of treatment [4].
The second major etiological block consists of immune-
dependent necrotic dermatoses, in which the microbial
factor is absent or plays a secondary role. These include:
pyoderma gan-grenosum; necrotizing cutaneous
vasculitis (including ANCA-associated); Sweet syndrome
with necrotic elements; necrotizing erythema nodosum;
drug-induced skin necrosis (for example, with the use of
warfarin, chemotherapy).
These conditions are based on disorders of
regenerative-inflammatory homeostasis, in which
neutrophil activation, the formation of extracellular
neutrophil traps (NETs), vascular damage, and fibrinoid
necrosis of the arterial wall/venules dominate. As
emphasized by D. Kohli-Pamnani and A. Saavedra [6],
the hyperreactivity of the innate immune response with
dysregulation of IL-8, IL-17, and TNF-
α leads to the
formation of rapidly spreading ulcerative defects
surrounded by an inflammatory infiltrate zone and a
lilac-bluish rim. Gupta D. et al. [7] emphasize the
importance of timely exclusion of the infectious nature
of lesions before the ini-tiation of immunosuppression,
since mixed forms are increasingly common in clinical
practice.
A separate category is ischemic forms of necrotizing
dermatitis that occur as a result of coagulopathies,
disseminated intravascular coagulation syndrome, the
use of anticoagulants, or antiphospholipid syndrome.
These conditions can manifest themselves with the
development of skin necrosis, especially in areas of
increased vascular resistance (thigh, abdomen, gluteal
re-gion).
Thus, necrotizing dermatitis is a syndromic clinical
phenomenon that unites diverse in origin, but
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pathogenetically similar processes of cutaneous
necrosis. Its successful diagnosis and treatment
require an accurate understanding of the etiological
profile and an assessment of the systemic disorders
underlying the lesion.
Clinical manifestations and differential diagnosis
The clinical picture of necrotizing dermatitis varies
significantly depending on the etio-logical variant, the
depth of tissue damage, the patient's immune status
and the timing of treat-ment. Nevertheless, there are
a number of common signs that make it possible to
suspect a ne-crotic process in the skin and
subcutaneous structures. Classically, the course is
characterized by progressive pain syndrome, the
appearance of a dark purple or cyanotic focus, the
formation of blisters with hemorrhagic or serous-
purulent contents, and the subsequent development
of black, dry or wet necrosis.
The most acute form of infectious necrotizing
dermatitis. At the onset, moderate ery-thema, swelling
and pain on palpation are possible, but after 12-24
hours, a pronounced edema develops with areas of
cyanosis, then blisters, hemorrhagic impregnation and
areas of the skin with darkening. A distinctive feature
is pain, disproportionate to external manifestations. In
some patients, "skin anesthesia" is observed over the
areas of necrosis due to ischemia of skin nerve endings.
Clinically important indicator is the rate of spread: the
lesion increases by 2-3 cm per hour. It is often
accompanied by tachycardia, fever, hypotension, and
other signs of sep-sis [1].
An immune-dependent form often associated with
inflammatory bowel diseases (Crohn's disease,
ulcerative
colitis),
rheumatoid
arthritis
and
hematologic pathologies. It begins with the
appearance of an inflammatory nodule or pustule,
which soon ulcerates and turns into a deep, painful,
undermined necrotic defect with a purple border.
Peripheral ulcer progression is a char-acteristic sign.
Unlike infectious forms, the general condition of the
patient can remain stable, and the cultures of the
contents are sterile. As emphasized by D. Kohli-
Pamnani and A. Saa-vedra [6], surgical debridement in
pyoderma gangrenous can aggravate the course.
As L. Lancerotto et al. emphasize. [3], a comprehensive
approach is important for ne-crotizing dermatitis:
assessment of the clinic, anamnesis, laboratory
parameters
(including
leu-
kocytosis
>15×10⁹/l,
creatinine >1.6 mg/dl, C-reactive protein level >150
mg/l), as well as the calculation of the LRINEC index
(Laboratory Risk Indicator for Necrotizing Fasciitis) [4].
Thus, timely differential diagnosis allows not only to
prevent complications, but also to choose the right
tactics: from urgent surgery to the prescription of
immunosuppressive drugs. Mistakes at this stage are
often fatal.
Treatment tactics
Therapy of necrotizing dermatitis is determined by its
etiopathogenesis, clinical form, rate of progression and
severity of systemic manifestations. Conventionally, all
cases can be di-vided into two groups: infectious forms
that require urgent surgical and antimicrobial therapy,
and immune-dependent forms, in which the key link in
treatment is the suppression of the pathological
inflammatory response. The third, intermediate group
consists of combined or un-clear forms that require an
interdisciplinary approach with the parallel application
of several strategies.
It has been established that early surgical intervention
in necrotizing fasciitis (within 6-12 hours from diagnosis)
reduces mortality by 20-40% [1]. The basic principles of
surgical treatment: immediate radical necrectomy with
excision of all necrotically altered tissues up to viable
borders; repeated revisions every 24-48 hours until the
necrosis zone is completely stabi-lized; possible use of
vacuum therapy (VAC) after primary debridement.
Lancerotto L. et al. [3] emphasize that even in the
absence of visual necrosis, suspected fascial
involvement requires surgery to confirm and prevent
progression.
Empirical antibiotic therapy should be initiated
immediately and include drugs active against: β
-
hemolytic
streptococcus;
methicillin-resistant
Staphylococcus aureus (MRSA); an-aerobic flora and
gram-negative
bacteria.
After
obtaining
the
microbiological analysis data, sensitivity therapy is de-
escalated.
Regardless of the form, patients with necrotizing
dermatitis are indicated: infusion ther-apy with
correction of water-electrolyte and acid-base balance;
maintenance of adequate tissue perfusion (mean BP
>65 mm Hg); glycaemic control (stress-hyperglycaemia
reduces repair); prevention of thrombosis and stress
ulcers;
protein-enriched
diet,
especially
with
pronounced catabolism.
Promising areas are: VAC therapy (vacuum-assisted
closure): reduces the risk of second-ary infection and
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stimulates granulation; collagen and silicone coatings;
PRP therapy (platelet-rich plasma) - as an additional
stimulator of regeneration; biologics (anti-TNF, IL-1
inhibitors) with a resistant immune component.
Thus, the treatment of necrotizing dermatitis requires
a personalized approach, in which etiological
differentiation is crucial. Delay in surgical debridement
in infectious forms is fatal, as well as excessive
intervention in autoimmune lesions. The work of a
multidisciplinary team is optimal: a surgeon, a
dermatologist,
an
intensivist
and
a
clinical
immunologist.
Prognosis and complications
The prognosis for necrotic skin lesions directly depends
on the etiology, the timeliness of treatment, the
presence of systemic diseases and the extent of tissue
damage. The most unfavor-able course is characteristic
of necrotizing fasciitis, especially with late diagnosis,
concomitant diabetes mellitus, immunosuppression
and generalized sepsis. On the other hand, immune-
dependent forms, with correct differentiation and
timely therapy, usually have a more favorable
outcome.
According to M.S. Dworkin et al. [5], the most
significant prognostic factors associated with mortality
in necrotizing skin and soft tissue infections are:
delayed surgical debridement (>24 hours from the
onset of symptoms); age >60 years; concomitant
diabetes, chronic renal failure, immunodeficiency;
hypotension, lactic acidosis, acute renal failure at the
time of hospi-talization; widespread tissue damage
(>5% of the div surface); the presence of gas
formation in the tissues according to computed
tomography or revision. The mortality rate in
necrotizing fasciitis ranges from 20 to 40%, reaching
60% in septic shock [1].
The most common systemic complications include:
sepsis and septic shock, the most common cause of
death; multiple organ failure (acute kidney injury,
respiratory failure, DIC syndrome); inhibitory
hyperglycemic response in severe infections in
patients with diabetes; immunodepression secondary
to sepsis, increasing the risk of secondary infections.
Local complications: deep scars and deformities,
especially in areas with a small soft tissue reserve
(lower legs, hands, face); impaired function of the limb
with the involvement of fascia, muscles, joints;
repeated purulent-inflammatory processes with
incomplete sanitation or residual pockets; the need for
skin grafting or reconstructive interventions.
Long-term consequences: psychological disorders: post-
traumatic stress disorder, anxie-ty, depression
especially after extensive lesions and amputations; the
formation of chronic ul-cers in persistent autoimmune
forms; Recurrences are more common in pyoderma
gangrenous and vasculitis, especially with insufficient
immunosuppression.
Gupta D. et al. emphasize that about 30% of patients
with necrotizing dermatoses re-quire rehospitalization
within 6 months, mainly due to relapses or
complications of therapy [7].
Successful recovery from necrotizing dermatitis
requires long-term monitoring and re-habilitation,
including: dynamic assessment of immune and
metabolic status; control over tissue repair and
prevention of trophic disorders; psychological and social
support; provision of ade-quate nutrition, especially in
catabolic syndrome.
In patients with immune-dependent forms, it is
important to maintain supportive immu-nosuppression
under the supervision of a rheumatologist or
immunologist to minimize the risk of recurrence [8-10].
Thus, the prognosis of necrotizing dermatitis is
multifactorial and requires clear risk stratification, early
aggressive intervention in infectious forms, and rational
use of immunosup-pression in autoimmune variants.
Particular attention should be paid not only to the acute
peri-od, but also to the rehabilitation stage, including
the restoration of the skin and the general con-dition of
the patient.
CONCLUSION AND PROSPECTS
Necrotizing dermatitis is a clinical syndrome combining
a wide range of cutaneous and subcutaneous lesions
with a common morphological outcome of tissue
necrosis, but different etiology, pathogenesis, and
therapeutic approaches. The leading threat to the
patient's life is in-fectious forms, primarily necrotizing
fasciitis, which require immediate diagnosis and radical
surgery. However, immune-dependent necrotizing
dermatoses, including pyoderma gangrenous and
cutaneous vasculitis, can also lead to significant
destructive lesions, requiring accurate dif-ferential
diagnosis and systemic immunosuppression.
Current evidence suggests the need for a
multidisciplinary approach that includes a sur-geon,
dermatologist,
infectious
disease
specialist,
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resuscitator, and immunologist. The key to successful
treatment is early risk stratification and the selection
of appropriate therapeutic tac-tics based on the clinical
presentation, laboratory findings, microbiological
analysis and, if nec-essary, histological confirmation.
Promising areas of scientific and clinical development
remain: the introduction of bi-omarkers of progression
and prognosis of necrotic skin lesions (for example,
neutrophil
cyto-kines,
NETs,
levels
of
pro-
inflammatory mediators); development of molecularly
targeted ther-apies (anti-TNF, IL-1/IL-17 blockers) for
resistant immune forms; Improvements in early warn-
ing systems and imaging techniques (e.g., contrast-
enhanced computed tomography combined with
modern analytics); optimization of rehabilitation
protocols, including skin restoration, psycho-
emotional health and functional adaptation.
Thus, necrotizing dermatitis is not only a
dermatological or surgical problem, but also a clinical
challenge that requires comprehensive diagnosis,
rapid reactivity and personalized medicine. Only if
these principles are followed, it is possible to achieve a
favorable outcome and reduce mortality in this
category of patients.
Conflict of Interest
- The authors declare that there is
no conflict of interest in the prepa-ration and writing
of this article.
Funding
- The authors did not receive external funding
for this review.
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