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 fasciitisIs 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.
PathophysiologyHydrogen, 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.
BacteriaGroup 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
HistoryA 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
The patient usually appears moderately to severely toxicTypically, 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
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 healthyintravascular volume loss is detectable General signs, such as fever and severe systemic reactions, may be present.
The most important signs
tissue necrosis putrid dischargeBullaesevere pain gas production rapid burrowing through fascial planes, lack of classical tissue inflammatory signs.
PhysicalFournier gangrenebegins 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.
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 differentialElectrolytes, glucose, BUN, and creatinineBlood and tissue culturesUrinalysisArterial blood gas
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.
Tissue biopsy is the best method for Dx.
Also to obtain proper cultures for microorganisms.
TREATMENTsurgicalAggressive 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.
AntibioticsIf 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.
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, spore-forming bacilli found throughout nature esp. cultivated rich soilisolated 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 ClostridiaClostridium perfringens (welchii) 80-90% Clostridium novyi (40%) Clostridium septicum (20%) Clostridium bifermentans (10%) Clostridium fallax (5%)
PathophysiologyFirst, 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 inflammationPurulence is often absent Myonecrosis can spread as fast as 2 cm/h systemic toxicity and shock can be fatal within 12 hours
Pathophysiologyexotoxins 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 TraumaCompound fracturesForeign bodiesFrostbiteThermal or electrical burnsSubcutaneous or intravenous injection of medications or illicit drugsPressure soresMotor vehicle crashes
Causes PostoperativeGastrointestinal tract surgeryGenitourinary tract surgeryAbortionAmputationTourniquets, casts, bandages, or dressings applied too tightly
Causes Spontaneousknown 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 intra-abdominal compartment.Approximately 80% have an overt or occult malignancy. Of these, 40% are hematologic and 34% are colorectal.
History Prior trauma or surgeryPainIncreasing pain after surgery or trauma out of proportion to physical findingsSudden onsetMay be quite severePeripheral vascular diseaseAlcoholism or drug abuseChronic debilitating disease(s)Immunocompromised statediabetes Steroid useMalnutritionMalignancyAcquired immunodeficiency syndrome (AIDS)
Physical Vital signs - May indicate systemic toxicity and include no or low-grade fever, tachycardia, tachypnea, hypotension, or hypoxiaEdema bullaeErythema with purplish black discolorationExtreme tendernessBrownish skin discoloration (bronzing) with bullaeProfuse, "dish-watery" drainage from ruptured bullaeDischarge - May have a peculiar, "mousy," sweet odorCrepitusMental status - Paradoxically, may be depressed early during the disease course; sensorium then may clear as the disease progresses and the patient is near death
- 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