DECEMBER 2013

WHAT IS NECROTIZING FASCIITIS? WHAT ARE ITS CAUSES? HOW WILL YOU
MANAGE SUCH A CASE?

Formerly called streptococcal gangrene. This is a dangerous and rapidly spreading

infection of the fascial planes leading to necrosis of the subcutaneous tissues and
overlying skin.

Term Necrotizing soft tissue infections (NSTIs) is now a day's used that covers
necrotizing fasciitis. They typically involve deep subcutaneous tissue, superficial or
deep fascia, or muscle, or any combination of the three.

Deep soft-tissue infections are classified as either necrotizing fasciitis or necrotizing

myositis. Necrotizing fasciitis represents a rapid, extensive infection of the fascia
deep to the adipose tissue. Necrotizing myositis primarily involves the muscles but
typically spreads to adjacent soft tissues.

It is termed Fourniers gangrene when it affects the perineal area and Meleneys
synergistic gangrene when it involves the abdominal wall.

Lower limb is most commonly affected (60%)

CAUSES:
Polymicrobial infections tend to be more common than single organism
The most common organisms isolated from patients presenting with necrotizing
soft-tissue infections include the gram-positive organisms:

Group A streptococci

Enterococci

Coagulase-negative staphylococci

S. aureus

S. epidermidis

Clostridium species
Gram-negative species frequently associated with necrotizing infections include
Escherichia coli
Enterobacter
Pseudomonas species
Proteus species
Serratia species
Bacteroides

Clostridial infections are worth special mention. They are typically monomicrobial,
although they can be seen in combination with other bacteria. They are often
characterized by infection and necrosis of muscles (myonecrosis) and are
associated with a significantly worse prognosis. Clostridial infections are more
common in patients with intravenous drug use and are accompanied by a very high
white blood cell count.

Clinical risk factors for necrotizing soft-tissue infection include

Trauma is most common precipitating factor (80%)
 Old age
Smoking
Diabetes mellitus
Malnutrition
Obesity
Chronic alcoholism
Peripheral vascular disease
Chronic lymphocytic leukemia
Immunosuppressed state: HIV
Steroid use
Renal failure
Cirrhosis
Autoimmune deficiency syndrome

CLINICAL FEATURES:

The diagnosis is usually made on clinical grounds.

1. Extensive necrosis, oedema and thrombosis of the microvasculature.

2. The area becomes oedematous, painful and very tender with discoloration,
ulceration and necrotic associated with ecchymoses or blistering of the skin,
or both.
3. The area may develop bullae and progress to overt cutaneous gangrene with
subcutaneous emphysema. It spreads to contiguous areas but occasionally
also produces skip lesions
4. The presence of gas detected either by physical examination (crepitus) or by
radiographs
5. Foul smelling discharge
6. It is accompanied by toxemia, high grade fever with chills
7. Renal failure as a result of hypovolaemia and cardiovascular collapse caused
by septic shock may occur.
8. Features of SIRS and MODS

INVESTIGATIONS:

Creatinine kinase levels may show enormous elevation

Leukocytosis greater than 15,400/Ml
serum sodium level less than 135 mEq/L
Imaging with either computed tomography (CT) or magnetic resonance
imaging may be helpful. However, imaging studies, though sensitive, are
nonspecific
Biopsy of the fascial layers can confirm the diagnosis.

TREATMENT:
Patients are admitted to ICU and treated aggressively with careful monitoring of
volume derangements and cardiac status.

1. Oxygen supplementation is advantageous and endotracheal intubation is

required in patients unable to maintain their airway.
2. Aggressive fluid replacement is typically needed to offset acute renal
failure from ongoing sepsis.
3. Control of diabetes
4. Electrolyte monitoring and balance
5. Catheterization to monitor urine output
6. Use of antibiotic depends of culture and sensitivity. High-dose penicillin G
along with broad-spectrum antibiotics such as third-generation
cephalosporins and metronidazole should be given intravenously until the
patients toxicity abates
7. The cornerstone of management is surgical excision of the necrotic
tissue. The fascial planes are opened with ease as the infection produces
inflammatory degloving and the yellowish green necrotic fascia is visible.
Devitalised tissue should be removed generously, preferably going beyond
the area of induration. This can lead to profuse bleeding and it is wise to have
blood already cross-matched. The wound is lightly packed with fluffed gauze
and dressed. This process should be continued on a daily basis as the
necrosis is prone to spread beyond the edges of the excised wound. In
patients who survive, this results in a large wound, which will require skin
grafting or flap coverage.
8. Vacuum assisted dressing (VAC device) is better than plain dressing
9. Recently, the role of hyperbaric oxygen (HBO) has become more
established. It is claimed that it is bactericidal, improves neutrophil function
and promotes wound healing. The patient is placed in a high-pressure
chamber and 100% oxygen administered at a pressure of 23 atmospheres.