necrotizing infections

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 dischargeBullaesevere pain gas production rapid burrowing through fascial planes, lack of classical tissue inflammatory signs.

PhysicalFournier 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.

Fournier’s 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, spore-forming 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 perfringens (welchii) 80-90% • Clostridium novyi (40%) • Clostridium septicum (20%) • Clostridium bifermentans (10%) • Clostridium 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

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

• 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 intra-abdominal 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 diabetes o Steroid useo Malnutritiono Malignancyo 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 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 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.

PathophysiologyExotoxins

• 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 151-kd

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%