Necrotizing fasciitis is a rapidly progressive inflammatory infection of the fascia, with

secondary necrosis of the subcutaneous tissues. The speed of spread is directly

proportional to the thickness of the subcutaneous layer. Necrotizing fasciitis moves
along the fascial plane. [1, 2]
Necrotizing fasciitis has also been referred to as hemolytic streptococcal gangrene,
Necrotizing fasciitis may occur as a complication of a variety of surgical
procedures or medical conditions, including cardiac catheterization, [3] vein
sclerotherapy, [4] and diagnostic laparoscopy, It may also be idiopathic,
The causative bacteria may be aerobic, anaerobic, or mixed flora.  [13] A few distinct
necrotizing fasciitis syndromes should be recognized. The 3 most important are as
follows:
 Type I, or polymicrobial
 Type II, or group A streptococcal
 Type III gas gangrene, or clostridial myonecrosis
 A variant of necrotizing fasciitis type I is saltwater necrotizing fasciitis, in which an
apparently minor skin wound is contaminated with saltwater containing a Vibrio
species.
 Because of the presence of gas-forming organisms, subcutaneous air is
classically described in necrotizing fasciitis. This may be seen only on
radiographs or not at all.
 The frequency of necrotizing fasciitis has been on the rise because of an
increase in immunocompromised patients with diabetes mellitus, cancer,
alcoholism, vascular insufficiencies, organ transplants, HIV infection, or
neutropenia.
The mean age of a patient with necrotizing fasciitis is 38-44 years. 

Patopysioloy

Historically, group A beta-hemolytic Streptococcus (GABS) has been

identified as a major cause of this infection. This monomicrobial infection is
usually associated with an underlying cause, such as
diabetes, [25] atherosclerotic vascular disease, or venous insufficiency with
edema. GABS usually affects the extremities; approximately two thirds of the
GABS infections are located in the lower extremities. [26]
Anaerobic bacteria are present in most necrotizing soft-tissue infections, usually in
combination with aerobic gram-negative organisms. Anaerobic organisms proliferate in
an environment of local tissue hypoxia in those patients with trauma, recent surgery, or
medical compromise.
Facultative aerobic organisms grow because polymorphonuclear neutrophils (PMNs)
exhibit decreased function under hypoxic wound conditions. This growth further lowers
the oxidation/reduction potential, enabling more anaerobic proliferation and, thus,
accelerating the disease process.
Carbon dioxide and water are the end products of aerobic metabolism. Hydrogen,
nitrogen, hydrogen sulfide, and methane are produced from the combination of aerobic
and anaerobic bacteria in a soft tissue infection. These gases, except carbon dioxide,
accumulate in tissues because of reduced water solubility.
In necrotizing fasciitis, group A hemolytic streptococci and Staphylococcus
aureus, alone or in synergism, are frequently the initiating infecting bacteria. However,
other aerobic and anaerobic pathogens may be present, including the following:
 Bacteroides
 Clostridium
 Peptostreptococcus
 Enterobacteriaceae
 Coliforms (eg, Escherichia coli)
 Proteus
 Pseudomonas
 Klebsiella
 Organisms spread from the subcutaneous tissue along the superficial and deep
fascial planes, presumably facilitated by bacterial enzymes and toxins. This deep
infection causes vascular occlusion, ischemia, and tissue necrosis. Superficial
nerves are damaged, producing the characteristic localized anesthesia.
Septicemia ensues with systemic toxicity.
 Important bacterial factors include surface protein expression and toxin
production. M-1 and M-3 surface proteins, which increase the adherence of the
streptococci to the tissues, also protect the bacteria against phagocytosis by
neutrophils.
 Streptococcal pyrogenic exotoxins (SPEs) A, B, and C are directly toxic and tend
to be produced by strains causing necrotizing fasciitis. These pyrogenic
exotoxins, together with streptococcal superantigen (SSA), lead to the release of
cytokines and produce clinical signs such as hypotension. The etiological agent
may also be a Staphylococcus aureus isolate harboring the enterotoxin gene
cluster seg, sei, sem, sen, and seo, but lacking all common toxin genes,
including Panton-Valentine leukocidin.  [30]
 Surgical procedures may cause local tissue injury and bacterial invasion,
resulting in necrotizing fasciitis. These procedures include surgery for
intraperitoneal infections and drainage of ischiorectal and perianal abscesses.
Intramuscular injections and intravenous infusions may lead to necrotizing
fasciitis.
 Minor insect bites may set the stage for necrotizing infections. Streptococci
introduced into the wounds may be prominent initially, but the bacteriologic
pattern changes with hypoxia-induced proliferation of anaerobes.
 Local ischemia and hypoxia can occur in patients with systemic illnesses (eg,
diabetes). Host defenses can be compromised by underlying systemic diseases
favoring the development of these infections. Illnesses such as diabetes or
cancer have been described in over 90% of cases of progressive bacterial
gangrene.
Types

n type I necrotizing fasciitis, anaerobic and facultative bacteria work synergistically to

cause what may initially be mistaken for a simple wound cellulitis. A variant of type I
necrotizing fasciitis is saltwater necrotizing fasciitis in which an apparently minor skin
wound is contaminated with saltwater containing a Vibrio species.
In type II necrotizing fasciitis, varicella infection and the use of nonsteroidal anti-
inflammatory drugs may be predisposing factors.
Type III necrotizing fasciitis is usually caused by Clostridium perfringens. When type III
necrotizing fasciitis occurs spontaneously, C septicum is more likely to be the etiologic
agent; these cases usually occur in association with colon cancer or leukemia.

Symptoms

severe pain

fever, malaise, and myalgias.

Typically, the infection begins with an area of erythema that quickly spreads
over a course of hours to days. The redness quickly spreads, and its margins
move out into normal skin without being raised or sharply demarcated. As the
infection progresses, the skin near the site of insult develops a dusky or
purplish discoloration. Multiple identical patches expand to produce a large
area of gangrenous skin, as the erythema continues to spread.

 necrosis appears as a massive undermining of the skin and subcutaneous

layer

yellowish-green necrotic fascia

Anesthesia in the involved region

caused by thrombosis of the subcutaneous blood vessels, leading to necrosis

of nerve fibers.
Without treatment, secondary involvement of deeper muscle layers may occur, resulting
in myositis or myonecrosis. Normally, however, the muscular layer remains healthy red
with normal bleeding muscle under the yellowish-green fascia.
Usually, the most important signs are tissue necrosis, putrid discharge, bullae, severe
pain, gas production, rapid burrowing through fascial planes, and lack of classical tissue
inflammatory signs.
Usually, some degree of intravascular volume loss is detectable on clinical examination.
Other general signs, such as fever and severe systemic reactions, may be present.
Local crepitation can occur in more than one half of patients. This is an infrequent
finding, specific but not sensitive, particularly in cases of nonclostridial necrotizing
fasciitis.

Complications
Complications may include the following:
 Renal failure
 Septic shock with cardiovascular collapse
 Scarring with cosmetic deformity
 Limb loss
 Sepsis
 Toxic shock syndrome

Investiations

 Complete blood count with differential

 Serum chemistry studies
 Arterial blood gas measurement
 Urinalysis
 Blood and tissue cultures
Deeper tissue samples, obtained at the time of surgical debridement, are
needed to obtain proper cultures for microorganisms.
New techniques include rapid streptococcal diagnostic kits and a polymerase chain
reaction (PCR) assay for tissue specimens that tests for the genes for streptococcal
pyrogenic exotoxin (SPE; eg, SPE-B) produced by group A streptococci.
B-mode and possibly color Doppler ultrasonography, contrast-enhanced computed
tomography (CT) scanning, or magnetic resonance imaging (MRI) can promote early
diagnosis of necrotizing infections. [53] In addition, these studies permit visualization of
the location of the rapidly spreading infection. More importantly, MRI or CT scan
delineation of the extent of necrotizing fasciitis may be useful in directing rapid surgical
debridement.
plain radiographs, often obtained to detect soft-tissue gas that is sometimes
present in polymicrobial or clostridial necrotizing fasciitis, are of no value in
the diagnosis of necrotizing infections.

Sonography may reveal subcutaneous emphysema spreading along the deep

fascia, swelling, and increased echogenicity of the overlying fatty tissue with
interlacing fluid collections, allowing for early surgical debridement and
parenteral antibiotics
CT scanning can pinpoint the anatomic site of involvement by demonstrating
necrosis with asymmetric fascial thickening and the presence of gas in the
tissues.

Finger Test and Biopsy

The finger test should be used in the diagnosis of patients who present with
necrotizing fasciitis. [72, 73] The area of suspected involvement is first infiltrated
with local anesthesia. A 2-cm incision is made in the skin down to the deep
fascia. Lack of bleeding is a sign of necrotizing fasciitis. On some occasions, a
dishwater-colored fluid is noticed seeping from the wound.
A gentle, probing maneuver with the index finger covered by a sterile powder-
free surgical double glove puncture indication system is then performed at the
level of the deep fascia. If the tissues dissect with minimal resistance, the
finger test is positive.
Tissue biopsies are then sent for frozen section analysis. The characteristic
histologic findings are obliterative vasculitis of the subcutaneous vessels,
acute inflammation, and subcutaneous tissue necrosis. 

Tissue stainin

gRams staing

hpe

Sections from necrotizing fasciitis tissue show superficial fascial necrosis with
blood vessels occluded by thrombi. A dense infiltration of neutrophils may be
observed in deeper parts of the subcutaneous tissue and fascia.
Subcutaneous fat necrosis and vasculitis are also evident. Eccrine glands and
ducts may be necrotic

Treatment

A regimen of surgical debridement is continued until tissue necrosis ceases

and the growth of fresh viable tissue is observed.

Amputation

Antibiotic therapy is a key consideration. Possible regimens include a

combination of penicillin G and an aminoglycoside (if renal function permits),
as well as clindamycin (to cover streptococci, staphylococci, gram-negative
bacilli, and anaerobes).