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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.

• Other pathogens may be present. Proteus. Enterobacteriaceae. Bacteroides. Pseudomonas. cause nonclostridial myonecrosis . Peptostreptococcus. and Klebsiella. • Bacteroides fragilis in combination with E. Clostridium. are frequently the initiating infecting bacteria. coli • Anaerobic streptococci.Bacteria • Group A hemolytic streptococci and Staph aureus. coliforms. occasionally seen in drug addicts. alone or in synergism.

Idiopathic cases are not uncommon. should be sought . • A history of comorbid factors. the local pain progresses to anesthesia. including diabetes mellitus. • Over the next several hours to days. • Fournier gangrene begins with pain and itching of the scrotal skin.History • A history of trauma or a recent surgery to the involved area is often present. • Typically. sudden onset of pain and swelling at the site of trauma or recent surgery.

 Fascial necrosis is typically more advanced than one thinks . the infection begins with an area of erythema that quickly spreads over a course of hours to days.  The normal skin and subcutaneous tissue are loosened a great distance from the initiating wound. • dusky or purplish skin discoloration near the site of insult.  Multiple identical patches develop to produce a large area of gangrenous skin.  The initial necrosis appears as a massive undermining of the skin and subcutaneous layer.Physical • The patient usually appears moderately to severely toxic • Typically. as the erythema continues to spread.

may be present. • secondary involvement of muscle layers may occur. such as fever and severe systemic reactions. resulting in myositis or myonecrosis. Normally.Physical • Anesthesia in the involved region may be detected. the muscular layer remains healthy • intravascular volume loss is detectable • General signs. .

.The most important signs tissue necrosis  putrid discharge Bullae severe pain  gas production  rapid burrowing through fascial planes.  lack of classical tissue inflammatory signs.

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skin is already exhibiting signs of necrosis.  In males. edema.Physical Fournier gangrene begins with local tenderness. .  In 2-7 days. the skin becomes necrotic. this infection may resemble acute orchitis.  crepitus in 50%. or even a strangulated hernia.  continues beyond the penile-scrotal region to the abdomen or the upper legs. epididymitis. torsion. and erythema of the scrotal skin. Fournier gangrene acts more like necrotizing fasciitis.  In women.  This progresses to necrosis of the scrotal fascia. and a characteristic black spot can be seen.  Early on.

Fournier’s gangrene .

• Local ischemia and hypoxia in patients with systemic illnesses as diabetes or cancer in over 90% of cases. intraperitoneal infections and drainage of ischiorectal and perianal abscesses. but pattern changes from hypoxia-induced proliferation of anaerobes.Causes • Surgical procedures. • IM injections and IV infusions • Minor insect bites. Streptococci initially. .

BUN.Lab Studies: • CBC with differential • Electrolytes. glucose. and creatinine • Blood and tissue cultures • Urinalysis • Arterial blood gas .

. Absence of Gadolinium contrast enhancement in T1 images reliably detects fascial necrosis.Imaging Studies • Plain X-rays can reveal the presence of gas in subcutaneous fascial planes. • Magnetic resonance imaging and computerized tomography. • CT scanning demonstrates necrosis with asymmetric fascial thickening and the presence of gas in the tissues.

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.Biopsy • Tissue biopsy is the best method for Dx. • Also to obtain proper cultures for microorganisms.

Finger Test .

• This process may need to be repeated multiple times. Within 12-24 hours.TREATMENT surgical • Aggressive surgical debridement of all necrotic tissue. • Perform fasciotomies in extremities with compromised viability. • Delayed closure is recommended. .

. • Ampicillin may be added if enterococci suspected by Gram stain. • coverage for aerobic and anaerobic bacteria.TREATMENT Antibiotics • If streptococci are the identified major pathogens. metronidazole or third-generation cephalosporins. • Gentamicin. the DOC is penicillin G. combined with clindamycin or chloramphenicol. has been proposed as a standard coverage. with clindamycin as the alternative.

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Adjuvant treatment .

Mortality .

• 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.Mortality/Morbidity • The overall morbidity and mortality is 70-80%. .

Clostridial gas gangrene • highly lethal necrotizing soft tissue infection of skeletal muscle caused by toxin.and gas-producing Clostridium species • synonym clostridial myonecrosis .

cultivated rich soil • isolated from normal human colonic flora. only 6 produce the fulminant clostridial gas gangrene. skin. sporeforming bacilli • found throughout nature esp. anaerobic.Clostridia • Gram-positive. and the vagina • 150 Clostridium species identified. usually more than 1 species .

Pathogenic Clostridia • Clostridium 90% • Clostridium • Clostridium • Clostridium • Clostridium perfringens (welchii) 80novyi (40%) septicum (20%) bifermentans (10%) fallax (5%) .

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 • First. organisms must be inoculated into the tissues • Second.

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 .

and thrombus formation. leukocyte degeneration. . causes lysis of red blood cells. collagenase. hemolysis. produced by C perfringens. and polymorphonuclear cell destruction • Kappa toxin. is a collagenase • Alpha toxin is produced by most clostridia and has phospholipase C activity. fibroblasts. cytolysis. hemagglutinin. fibrinolysin. platelets. It also may decrease cardiac inotropy and trigger histamine release. and leukocytes. myocytes. platelet aggregation. and hemolysin toxins • Theta toxin causes direct vascular injury.Pathophysiology exotoxins • lecithinase. hyaluronidase.

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 .

casts. or dressings applied too tightly . bandages.Causes • Postoperative – Gastrointestinal tract surgery – Genitourinary tract surgery – Abortion – Amputation – Tourniquets.

or metastatic gas gangrene.  The GI is the source. This may result in a more localized infection of the viscera or intraabdominal compartment.Causes • Spontaneous  known as nontraumatic. 40% are hematologic and 34% are colorectal. Of these. The organisms escape the bowel by translocation. and seed distant sites.  It most often is mixed infection caused by C septicum. C perfringens. idiopathic. . enter the bloodstream. and C novyi.  Approximately 80% have an overt or occult malignancy. Several series report a mortality rate that approaches 100%.

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 o o diabetes Steroid use Malnutrition Malignancy Acquired immunodeficiency syndrome (AIDS) .

May have a peculiar. tachycardia. sensorium then may clear as the disease progresses and the . hypotension.Physical • Vital signs .May indicate systemic toxicity and include no or low-grade fever." sweet odor • Crepitus • Mental status . or hypoxia • Edema bullae • Erythema with purplish black discoloration • Extreme tenderness • Brownish skin discoloration (bronzing) with bullae • Profuse. tachypnea. "dish-watery" drainage from ruptured bullae • Discharge . may be depressed early during the disease course.Paradoxically. "mousy.

• An assay for sialidases (neuraminidase). • Elevated liver function test indicate progressive hepatic dysfunction. . • DIC. These tests provide rapid (<2 h) confirmation of Gram stain results. lactate dehydrogenase. • A Gram stain reveals gram-positive rods and an absence of polymorphonuclear cells. potassium.Lab Studies • WBC count may be normal or elevated. • Profound anemia may result from severe intravascular hemolysis. and creatine phosphokinase levels. • Elevated BUN and creatinine • Myonecrosis may elevate serum aldolase. Other organisms also may be present in as many as 75% of cases. • ABGs. metabolic acidosis.

dissecting into the intramuscular fascial planes and muscles. .Imaging Studies • Radiographs reveal fine gas bubbles within the soft tissues. • Intra-abdominal clostridial gas gangrene is evaluated most readily by a computed tomography scan that demonstrates extraluminal gas.

Management • Early surgical debridement. • Make sure tetanus immunity is adequate. • Restore intravenous fluid volume and monitor urine output • Transfer to an intensive care unit. . • Administer supplemental oxygen. • Consider hyperbaric oxygen therapy.

.Antibiotics • Penicillin is the preferred drug for clostridial infections. • Patients allergic to penicillin use clindamycin or chloramphenicol.

• Wound exploration reveals gas. watery discharge.Surgical Care • Prompt aggressive debridement of all involved tissues. • Extensive extremity involvement may require amputation. edematous. and necrotic muscle. Muscle tissue may be pale. and may not bleed when cut nor contract when stimulated with electricity. • The wound may be closed later (secondary closure) . • Daily exploration and further debridement may be necessary.

Mortality/Morbidity • properly treated. the process is 100% fatal. • trunk involvement. • Spontaneous cases have a mortality rate of 67-100%. the overall mortality rate is 20-30% • If untreated. the mortality rate is higher (60%) than of the extremities .

the ideal media are wounds with tissue necrosis. gram-positive bacillus • Lives on soil. • The spores need tissue with the proper anaerobic conditions to germinate. and 10-25% of human GI tracts. . a mobile.Tetanus • infection with Clostridium tetani. dust. anaerobic. skin. manure. clothing. spore-forming.

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 spores of C tetani germinate and produce 2 toxins: • Tetanolysin (a hemolysin) • Tetanospasmin. .Pathophysiology Exotoxins • Under anaerobic conditions. The light chain (50 kd) blocks the release of neurotransmitters. The heavy chain (100 kd) is responsible for specific binding to neuronal cells and for protein transport.

followed by generalized tetanus. .  Once the toxin is synthesized.  When the toxin reaches the spinal cord.Pathophysiology  The toxin binding may be irreversible. localized or cephalic tetanus may occur initially. recovery depends on the sprouting of new axonal terminals. it moves from the contaminated site to the spinal cord in 2-14 days.

.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.

lockjaw). . and sweating. with hypertension and tachycardia alternating with hypotension and bradycardia. • Late in the disease. difficulty swallowing. followed by neck stiffness. rigidity of abdominal muscles. spasms.clinical • Common first signs of tetanus are muscular stiffness in the jaw (ie. • Patients often are afebrile. autonomic dysfunction develops.

• generalized muscle rigidity with intermittent reflex spasms in response to stimuli (ie. resulting from facial muscle involvement. • Nuchal rigidity and dysphagia also are early complaints • Risus sardonicus. extension of the lower extremities). flexion and adduction of the arms. tendon ruptures. . • Tonic contractions cause opisthotonus (ie. The spasms can cause fractures. During these episodes. noise. clenching of the fists.clinical • Approximately 50-75% of patients with generalized tetanus present with trismus secondary to masseter muscle spasm. touch). the ironic smile of tetanus. patients have intact sensorium and feel severe pain. and acute respiratory failure.

source of infection • Wounds (~65%). which often is minor. • Unknown. • Chronic skin ulcers are the source in approximately 5% of cases. .

hysteria.Differential Diagnosis • Strychnine poisoning is the only condition that truly mimics tetanus. • A number of conditions (eg. . encephalitis may cause trismus. dental or other local infections.

• Serum antitoxin levels more than 0. • Blood counts and biochemistry are unremarkable.01 U/mL usually are protective. exclude strychnine poisoning. • Cerebrospinal fluid (CSF) is normal.Lab Studies • Laboratory findings are not diagnostically valuable. except for an increased opening pressure. making the diagnosis less likely .

administer diazepam intravenously. and tetanic seizures. Vecuronium or pancuronium are adequate alternatives. ventilatory support and pharmacologic agents that treat reflex muscle spasms. To prevent spasms that last longer than 5-10 seconds. A dose of 500 U appears as effective as larger doses. • Benzodiazepines are the mainstay of symptomatic therapy.Medical Care • Passive immunization with human tetanus immune globulin (TIG) shortens the course of tetanus and may lessen its severity. . • Supportive therapy . rigidity. typically 10-40 mg every 1-8 hours.

0. neuromuscular blocking agents. and centrally acting muscle relaxants.. .5 g q6h) and penicillin • Sedative hypnotics. inhalational anesthetics. controls muscle rigidity. narcotics.Medical Care • Metronidazole (eg. • Intrathecal baclofen.

• Tetanus booster shot every 10 years. 12-15 months. • TD vaccine to all adults who have not had a booster shot in the last 10 years. • Tetanus and diphtheria (TD) toxoid to children aged 7 years or older. 4 months. adults who have recovered from tetanus and adults who have never received immunization . 6 months. and between 4-6 years.Prevention • Tetanus toxoid in combination with diphtheria toxoid and pertussis vaccine (DTP) to children at ages 2 months.

• Tetanus toxoid is a very effective immunogen that stimulates a protective response in virtually all immunocompetent subjects. or antibiotics if the patient has not been previously immunized with a series of at least 3 doses of toxoid. • administering TIG. If the patient has not had a tetanus toxoid booster in the previous 10 years. • TIG and tetanus toxoid to patients who have had 2 or fewer primary immunizations.Prevention • Clean wounds and remove dead or devitalized tissue. . antitoxin. consider administering a booster if more than 5 years have elapsed since the last dose. • For severe wounds. a single booster.

mortality • mild and moderate tetanus is approximately 6% • severe tetanus. the mortality rate may be as high as 60% .