NECROTIZING SOFT TISSUE
INFECTIONS
Gangrenous erysipelas
Necrotizing erysipelas
Hemolytic streptococcal gangrene
Nonclostridial crepitant cellulitis
Nonclostridial gas gangrene
Synergistic necrotizing cellulitis
Bacterial synergistic gangrene
Necrotizing fasciitis
Necrotizing cellulitis
Fournier's gangrene
Necrotizing fasciitis
Is a progressive, rapidly spreading,
infection located in the deep fascia,
with secondary necrosis of the
subcutaneous tissues
Bacteria may be aerobic, anaerobic,
or mixed flora, and the expected
clinical course varies
Necrotizing fasciitis
occur after trauma or around foreign
bodies in surgical wounds, or idiopathic,
as in scrotal necrotizing fasciitis.
hemolytic streptococcal gangrene,
Meleney ulcer, acute dermal gangrene,
hospital gangrene, suppurative fascitis,
and synergistic necrotizing cellulitis.
Fournier gangrene
Pathophysiology
Most have anaerobic bacteria
present, usually in combination with
aerobic gram-negative organisms.
They proliferate in an environment of
local tissue hypoxia in those patients
with trauma, recent surgery, or
medical compromise.
Pathophysiology
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.
Bacteria
Group A hemolytic streptococci and Staph
aureus, alone or in synergism, are frequently
the initiating infecting bacteria.
Other pathogens may be present;
Bacteroides, Clostridium, Peptostreptococcus,
Enterobacteriaceae, coliforms, Proteus,
Pseudomonas, and Klebsiella.
Bacteroides fragilis in combination with E. coli
Anaerobic streptococci, occasionally seen in
drug addicts, cause nonclostridial
myonecrosis
History
A history of trauma or a recent surgery to
the involved area is often present.
Idiopathic cases are not uncommon.
Typically, sudden onset of pain and
swelling at the site of trauma or recent
surgery.
Over the next several hours to days, the
local pain progresses to anesthesia.
Fournier gangrene begins with pain and
itching of the scrotal skin.
A history of comorbid factors, including
diabetes mellitus, should be sought
Physical
The patient usually appears moderately to
severely toxic
Typically, the infection begins with an area of
erythema that quickly spreads over a course of
hours to days.
dusky or purplish skin discoloration near the
site of insult.
Multiple identical patches develop to produce a
large area of gangrenous skin, as the erythema
continues to spread.
The initial necrosis appears as a massive
undermining of the skin and subcutaneous layer.
The normal skin and subcutaneous tissue are
loosened a great distance from the initiating wound.
Fascial necrosis is typically more advanced than one
thinks
Physical
Anesthesia in the involved region may be
detected.
secondary involvement of muscle layers
may occur, resulting in myositis or
myonecrosis. Normally, the muscular layer
remains healthy
intravascular volume loss is detectable
General signs, such as fever and severe
systemic reactions, may be present.
The most important signs
tissue necrosis
putrid discharge
Bullae
severe pain
gas production
rapid burrowing through fascial
planes,
lack of classical tissue inflammatory
signs.
Physical
Fournier gangrene
begins with local tenderness, edema, and
erythema of the scrotal skin.
This progresses to necrosis of the scrotal fascia.
crepitus in 50%.
continues beyond the penile-scrotal region to the
abdomen or the upper legs,
In males, skin is already exhibiting signs of necrosis.
In 2-7 days, the skin becomes necrotic, and a
characteristic black spot can be seen.
Early on, this infection may resemble acute orchitis,
epididymitis, torsion, or even a strangulated hernia.
In women, Fournier gangrene acts more like
necrotizing fasciitis.
Fourniers gangrene
Causes
Surgical procedures. intraperitoneal
infections and drainage of ischiorectal and
perianal abscesses.
IM injections and IV infusions
Minor insect bites. Streptococci initially,
but pattern changes from hypoxia-induced
proliferation of anaerobes.
Local ischemia and hypoxia in patients
with systemic illnesses as diabetes or
cancer in over 90% of cases.
Lab Studies:
CBC with differential
Electrolytes, glucose, BUN, and
creatinine
Blood and tissue cultures
Urinalysis
Arterial blood gas
Imaging Studies
Plain X-rays can reveal the presence of
gas in subcutaneous fascial planes.
CT scanning demonstrates necrosis with
asymmetric fascial thickening and the
presence of gas in the tissues.
Magnetic resonance imaging and
computerized tomography. Absence of
Gadolinium contrast enhancement in T1
images reliably detects fascial necrosis.
Biopsy
Tissue biopsy is the best method for Dx.
Also to obtain proper cultures for
microorganisms.
Finger Test
TREATMENT
surgical
Aggressive surgical debridement of all
necrotic tissue.
This process may need to be repeated
multiple times. Within 12-24 hours.
Delayed closure is recommended.
Perform fasciotomies in extremities
with compromised viability.
TREATMENT
Antibiotics
If streptococci are the identified major pathogens,
the DOC is penicillin G, with clindamycin as the
alternative.
coverage for aerobic and anaerobic bacteria;
metronidazole or third-generation cephalosporins.
Gentamicin, combined with clindamycin or
chloramphenicol, has been proposed as a
standard coverage.
Ampicillin may be added if enterococci suspected
by Gram stain.
Adjuvant treatment
Mortality
Mortality/Morbidity
The overall morbidity and mortality is
70-80%.
Fournier gangrene has a reported
mortality as high as 75%.
The mean age of survivors is 35
years.
The mean age of nonsurvivors is 49
years.
Clostridial gas gangrene
highly lethal necrotizing soft tissue
infection of skeletal muscle caused
by toxin- and gas-producing
Clostridium species
synonym clostridial myonecrosis
Clostridia
Gram-positive, anaerobic, sporeforming bacilli
found throughout nature esp.
cultivated rich soil
isolated from normal human colonic
flora, skin, and the vagina
150 Clostridium species identified, only
6 produce the fulminant clostridial gas
gangrene, usually more than 1 species
Pathogenic Clostridia
Clostridium
90%
Clostridium
Clostridium
Clostridium
Clostridium
perfringens (welchii) 80novyi (40%)
septicum (20%)
bifermentans (10%)
fallax (5%)
Pathophysiology
First, organisms must be inoculated
into the tissues
Second, oxygen tension must be low
enough for the organisms to
proliferate; they are not strict
anaerobes
Incubation period ranges from 12-24
hours but can vary from 1 hour or as
long as several weeks
Pathophysiology
Infections are characterized by a
very low level of host inflammation
Purulence is often absent
Myonecrosis can spread as fast as 2
cm/h
systemic toxicity and shock can be
fatal within 12 hours
Pathophysiology
exotoxins
lecithinase, collagenase, hyaluronidase,
fibrinolysin, hemagglutinin, and hemolysin
toxins
Theta toxin causes direct vascular injury,
cytolysis, hemolysis, leukocyte degeneration,
and polymorphonuclear cell destruction
Kappa toxin, produced by C perfringens, is a
collagenase
Alpha toxin is produced by most clostridia and
has phospholipase C activity, causes lysis of
red blood cells, myocytes, fibroblasts,
platelets, and leukocytes. It also may decrease
cardiac inotropy and trigger histamine release,
platelet aggregation, and thrombus formation.
Causes
Trauma
Compound fractures
Foreign bodies
Frostbite
Thermal or electrical burns
Subcutaneous or intravenous injection
of medications or illicit drugs
Pressure sores
Motor vehicle crashes
Causes
Postoperative
Gastrointestinal tract surgery
Genitourinary tract surgery
Abortion
Amputation
Tourniquets, casts, bandages, or
dressings applied too tightly
Causes
Spontaneous
known as nontraumatic, idiopathic, or metastatic
gas gangrene.
It most often is mixed infection caused by C
septicum, C perfringens, and C novyi. Several
series report a mortality rate that approaches
100%.
The GI is the source. The organisms escape the
bowel by translocation, enter the bloodstream,
and seed distant sites. This may result in a more
localized infection of the viscera or intraabdominal compartment.
Approximately 80% have an overt or occult
malignancy. Of these, 40% are hematologic and
34% are colorectal.
History
Prior trauma or surgery
Pain
Increasing pain after surgery or trauma out of proportion
to physical findings
Sudden onset
May be quite severe
Peripheral vascular disease
Alcoholism or drug abuse
Chronic debilitating disease(s)
Immunocompromised state
o
o
o
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diabetes
Steroid use
Malnutrition
Malignancy
Acquired immunodeficiency syndrome (AIDS)
Physical
Vital signs - May indicate systemic toxicity and
include no or low-grade fever, tachycardia,
tachypnea, hypotension, or hypoxia
Edema bullae
Erythema with purplish black discoloration
Extreme tenderness
Brownish skin discoloration (bronzing) with bullae
Profuse, "dish-watery" drainage from ruptured
bullae
Discharge - May have a peculiar, "mousy," sweet
odor
Crepitus
Mental status - Paradoxically, may be depressed
early during the disease course; sensorium then
may clear as the disease progresses and the
Lab Studies
WBC count may be normal or elevated.
Elevated liver function test indicate progressive
hepatic dysfunction.
Elevated BUN and creatinine
Myonecrosis may elevate serum aldolase, potassium,
lactate dehydrogenase, and creatine phosphokinase
levels.
Profound anemia may result from severe intravascular
hemolysis.
ABGs; metabolic acidosis.
DIC.
A Gram stain reveals gram-positive rods and an
absence of polymorphonuclear cells. Other organisms
also may be present in as many as 75% of cases.
An assay for sialidases (neuraminidase). These tests
provide rapid (<2 h) confirmation of Gram stain results.
Imaging Studies
Radiographs reveal fine gas bubbles
within the soft tissues, dissecting into
the intramuscular fascial planes and
muscles.
Intra-abdominal clostridial gas
gangrene is evaluated most readily by
a computed tomography scan that
demonstrates extraluminal gas.
Management
Early surgical debridement.
Administer supplemental oxygen.
Restore intravenous fluid volume and
monitor urine output
Transfer to an intensive care unit.
Make sure tetanus immunity is
adequate.
Consider hyperbaric oxygen therapy.
Antibiotics
Penicillin is the preferred drug for
clostridial infections.
Patients allergic to penicillin use
clindamycin or chloramphenicol.
Surgical Care
Prompt aggressive debridement of all
involved tissues.
Extensive extremity involvement may
require amputation.
Daily exploration and further debridement
may be necessary.
Wound exploration reveals gas, watery
discharge, and necrotic muscle. Muscle
tissue may be pale, edematous, and may
not bleed when cut nor contract when
stimulated with electricity.
The wound may be closed later (secondary
closure)
Mortality/Morbidity
properly treated, the overall mortality
rate is 20-30%
If untreated, the process is 100% fatal.
Spontaneous cases have a mortality
rate of 67-100%.
trunk involvement, the mortality rate
is higher (60%) than of the extremities
Tetanus
infection with Clostridium tetani, a
mobile, spore-forming, anaerobic,
gram-positive bacillus
Lives on soil, manure, dust, clothing,
skin, and 10-25% of human GI tracts.
The spores need tissue with the proper
anaerobic conditions to germinate; the
ideal media are wounds with tissue
necrosis.
Pathophysiology
Exotoxins
Under anaerobic conditions, the spores of C
tetani germinate and produce 2 toxins:
Tetanolysin (a hemolysin)
Tetanospasmin, which is responsible for
tetanus
Tetanospasmin is synthesized as a single 151kd chain and is cleaved to generate toxins
with 2 chains joined by a single disulfide bond.
The heavy chain (100 kd) is responsible for
specific binding to neuronal cells and for
protein transport. The light chain (50 kd)
blocks the release of neurotransmitters.
Pathophysiology
The toxin binding may be irreversible;
recovery depends on the sprouting of
new axonal terminals.
Once the toxin is synthesized, it moves
from the contaminated site to the spinal
cord in 2-14 days.
When the toxin reaches the spinal cord,
localized or cephalic tetanus may occur
initially, followed by generalized
tetanus.
History
Symptoms usually begin 8 days after
the infection, but range from 3 days to
3 weeks.
Patients may report a sore throat with
dysphagia
Localized tetanus causes muscle
rigidity at the site of spore inoculation.
clinical
Common first signs of tetanus are
muscular stiffness in the jaw (ie,
lockjaw), followed by neck stiffness,
difficulty swallowing, rigidity of
abdominal muscles, spasms, and
sweating.
Patients often are afebrile.
Late in the disease, autonomic
dysfunction develops, with hypertension
and tachycardia alternating with
hypotension and bradycardia.
clinical
Approximately 50-75% of patients with generalized
tetanus present with trismus secondary to
masseter muscle spasm.
Nuchal rigidity and dysphagia also are early
complaints
Risus sardonicus, the ironic smile of tetanus,
resulting from facial muscle involvement.
generalized muscle rigidity with intermittent reflex
spasms in response to stimuli (ie, noise, touch).
Tonic contractions cause opisthotonus (ie, flexion
and adduction of the arms, clenching of the fists,
extension of the lower extremities). During these
episodes, patients have intact sensorium and feel
severe pain. The spasms can cause fractures,
tendon ruptures, and acute respiratory failure.
source of infection
Wounds (~65%), which often is
minor.
Chronic skin ulcers are the source in
approximately 5% of cases.
Unknown.
Differential Diagnosis
Strychnine poisoning is the only
condition that truly mimics tetanus.
A number of conditions (eg, dental or
other local infections, hysteria,
encephalitis may cause trismus.
Lab Studies
Laboratory findings are not diagnostically
valuable, exclude strychnine poisoning.
Blood counts and biochemistry are
unremarkable.
Cerebrospinal fluid (CSF) is normal, except
for an increased opening pressure.
Serum antitoxin levels more than 0.01
U/mL usually are protective, making the
diagnosis less likely
Medical Care
Passive immunization with human tetanus
immune globulin (TIG) shortens the course of
tetanus and may lessen its severity. A dose of
500 U appears as effective as larger doses.
Supportive therapy ; ventilatory support and
pharmacologic agents that treat reflex
muscle spasms, rigidity, and tetanic seizures.
Benzodiazepines are the mainstay of
symptomatic therapy. To prevent spasms that
last longer than 5-10 seconds, administer
diazepam intravenously, typically 10-40 mg
every 1-8 hours. Vecuronium or pancuronium
are adequate alternatives.
Medical Care
Metronidazole (eg, 0.5 g q6h) and
penicillin
Sedative hypnotics, narcotics,
inhalational anesthetics,
neuromuscular blocking agents, and
centrally acting muscle relaxants.
Intrathecal baclofen. controls muscle
rigidity..
Prevention
Tetanus toxoid in combination with diphtheria
toxoid and pertussis vaccine (DTP) to children
at ages 2 months, 4 months, 6 months, 12-15
months, and between 4-6 years.
Tetanus and diphtheria (TD) toxoid to children
aged 7 years or older.
Tetanus booster shot every 10 years.
TD vaccine to all adults who have not had a
booster shot in the last 10 years, adults who
have recovered from tetanus and adults who
have never received immunization
Prevention
Clean wounds and remove dead or devitalized
tissue. If the patient has not had a tetanus toxoid
booster in the previous 10 years, a single booster.
For severe wounds, consider administering a
booster if more than 5 years have elapsed since the
last dose.
administering TIG, antitoxin, or antibiotics if the
patient has not been previously immunized with a
series of at least 3 doses of toxoid.
TIG and tetanus toxoid to patients who have had 2
or fewer primary immunizations.
Tetanus toxoid is a very effective immunogen that
stimulates a protective response in virtually all
immunocompetent subjects.
mortality
mild and moderate tetanus is
approximately 6%
severe tetanus, the mortality rate
may be as high as 60%
