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Unformatted text preview: Soft tissue infections Soft tissue infections Thomas Genuit, MD,MBA, FACS Sinai Hospital of Baltimore 2006 Definitions and Etiologies Definitions and Etiologies Soft tissue infections were first defined slightly more than a century ago. In 1883, Fournier described a gangrenous infection of the scrotum that continues to be associated with his name. In 1924, Meleney documented the pathogenic role of streptococci in soft tissue infection. Shortly thereafter, Brewer and Meleney described progressive polymicrobial postoperative infection of the muscular fascia with necrosis (the term necrotizing fasciitis was not introduced until the 1950’s). The association between toxic­shock syndrome and streptococcal soft tissue infection was delineated as this disease reemerged in the 1980s. Definitions and Etiologies Definitions and Etiologies Diverse group of diseases that involve the skin and underlying subcutaneous tissue, fascia, or muscle. May be localized to a small area or may involve a large portion of the body. May affect any part of the body, though the lower extremities, the perineum, and the abdominal wall are the most common sites of involvement. Some are relatively harmless if treated promptly and adequately; others can be life­threatening even when appropriately treated. Definitions and Etiologies Definitions and Etiologies Symptoms and signs Pain (localized tendernes) loss of sensation erythema, edema / induration Blisters, crusted plaques (Epi)dermal erosion and necrosis Fluctuation, crepitus Systemic signs of SIRS/Sepsis: fever, tachycardia, hypotension, organ dysfuction Definitions and Etiologies Definitions and Etiologies Simple vs. complex Primary vs. secondary vs. tertiary Cellulitis vs. abscess Superficial vs. deep Necrotizing vs. non­necrotizing Traumatic vs. non­traumatic Dermatitis, fasciitis, myositis ( combinations) Single vs. multiple pathogens Classic syndromes: Rapidly progressive infections toxic shock syndromes Specific etiologies or pathogens Definitions and Etiologies Definitions and Etiologies Non­traumatic ­ “Spontaneous” Glandular infection (folliculitis, furuncle, carbuncle, hidradenitis, perianal­, perineal­, …) Micro­trauma (cuts, insect bites, …) Trauma (wounds ­ including surgical) Clean Wounds: An uninfected operative wound in which no inflammation is encountered and the respiratory, alimentary, genital, or uninfected urinary tracts are not entered. Clean­Contaminated Wounds: Operative wounds in which the respiratory, alimentary, genital, or urinary tracts are entered under controlled conditions and without unusual contamination. Contaminated Wounds: Includes open, fresh, accidental wounds. In addition, operations with major breaks in sterile technique (e.g., open cardiac massage) or gross spillage from the gastrointestinal tract, and incisions in which acute, non­purulent inflammation is encountered are included in this category. Dirty or Infected Wounds: Includes old traumatic wounds with retained or devitalized tissue and those that involve existing clinical infection or perforated viscera. Superficial infections Superficial infections Majority of soft tissue infections Involve epidermis, dermis and/or subcutaneous tissues Pyoderma general term = bacterial infection of the skin. several subcategories Superficial infections Superficial infections Impetigo highly contagious, confined to the epidermis usually face or extremities. most common in infants and preschool children more frequently in patients with preexisting skin conditions (e.g., eczema, atopic dermatitis, varicella, angular cheilitis, scabies). usually in areas of skin breakdown warm and humid weather, crowded living, and poor hygiene contribute dominant pathogen is S. aureus, less common S. pyogenes bullous or a nonbullous form of the disease; Bullous: numerous blisters or bullae that rapidly become pustules ­> rupture within 1 to 2 days ­> thick, honey­colored, crusted plaque remains for days to weeks. Nonbullous: erythema and tiny, less prominent vesicles ­> crusted erosions in the skin. skin lesions are intensely pruritic, local spread as a result of scratching and release of infected fluid; associated regional lymphadenopathy is common. Superficial infections Superficial infections Impetigo Glomerulonephritis may complicate streptococcal­induced impetigo. diagnosis by Gram stain and culture of vesicular fluid or crusted plaque. skin lesions usually resolve spontaneously within 2 to 3 weeks. antibiotic therapy accelerates the resolution Mupirocin ointment (2%) Erythromycin and clindamycin ointments are alternatives with disseminated impetigo, disease of the mouth and in pts in whom topical therapy fails, a 7­day course of oral Abx. Is indicated dicloxacillin, cephalexin, cefadroxil, erythromycin, or clindamycin may be used Superficial infections Superficial infections Erysipelas principally involves the dermis. infection extends through the dermal lymphatic vessels tender, pruritic, intensely erythematous, hyperthermic, sharply demarcated, and raised plaque most cases preceded by influenzalike symptoms pain (local, myalgia) , often high fever, and leukocytosis. lymphangitis and ­adenopathy sometimes present lower leg most common site, followed by face, arms, and upper thighs. predisposing factors: local conditions as athlete's foot, leg ulcers, and venous stasis dermatitis, presence of lymphedema, diabetes mellitus, alcoholism, immunocompromise, and obesity more likely to recur when associated diseases are inadequately treated (10% within 6 months, 30% within 3 years) almost invariably caused by S. pyogenes. Superficial infections Superficial infections Erysipelas antibiotic treatment uncomplicated erysipelas: penicillin, amoxicillin effective in at least 80% of cases. Oral and intravenous antibiotic regimens are equally efficacious. patients with erysipelas of the lower extremity should be placed on bed rest, and the involved leg should be elevated once the patient is able to resume normal activities, he or she should be fitted with elastic stockings, to help reduce the recurrence of edema and lower the risk of lymphedema. For patients with tinea pedis, a topical antifungal agent is used to treat the infection and prevent recurrence. Superficial infections Superficial infections Folliculitis infection of the hair follicle painful, tender, erythematous papule with a central pustule single or multiple lesions in the skin of any hair­bearing area Predisposing factors: shaving, plucking, waxing, heat and humidity, the use of corticosteroids or antibiotics, immunosuppression, and occlusion of the skin by clothing, adhesives, etc. typically caused by S. aureus. It is characterized by a. In rare cases, Pseudomonas aeruginosa, Klebsiella species, Enterobacter species, Proteus species, yeasts, and fungi. Pseudomonas folliculitis: exposure to inadequately chlorinated water (swimming pools, hot tubs, or whirlpools); folliculitis with fever and malaise appearing 6 hours to 3 d p. exposure. Klebsiella, Enterobacter, and Proteus species:in patients receiving long­ term Abx. therapy for acne vulgaris. Yeast folliculitis and fungal folliculitis occur in immunocompromised pts. Superficial infections Superficial infections Folliculitis most resolve spontaneously within 7 to 10 days. topical therapy: clindamycin, erythromycin, or mupirocin ointments chlorhexidine or benzoyl peroxide + warm soaks may accelerate resolution Isotretinoin can be used to treat gram­negative folliculitis. Gentamicin cream may be helpful in Pseudomonas folliculitis with refractory or disseminated follicular infections: oral antibiotics S. aureus: dicloxacillin, erythromycin, cephalexin, cefadroxil, or clindamycin (cave: up to 20­30% prevalence of MRSA in certain pts.) Gram neg: oral ciprofloxacin; more aggressive therapy with systemic symptoms of sepsis Elimination of predisposing factors to reduce likelihood of recurrence. Superficial infections Superficial infections Furuncles and carbuncles deeper infections of the hair follicle that extend into the subcutaneous tissue. furuncle, or boil: small abscess firm, tender, erythematous nodule occurs in skin areas exposed to friction ( inner thighs and the axilla). also face, neck, upper back, and buttocks. predisposing factors: increased friction and perspiration (obese individuals or athletes), corticosteroid use, diabetes mellitus, and inherited or acquired defects in neutrophil function Initial treatment: warm compresses to help promote drainage oral antimicrobial agent effective against S. aureus incision­and­drainage necessary when lesions do not drain spontaneously. Failure to drain these lesions adequately may result in recurrence, as well as in progression to a more serious infection. “Superficial” infections Carbuncle: deep cutaneous infection involving multiple hair follicles characterized by destruction of fibrous tissue septa and formation of a series of interconnected abscesses. Patients commonly present with relatively large skin lesions (confluence) associated with chronic drainage, sinus tracts, and scarring typically painful, red, tender, indurated area of skin with multiple sinus tracts. Systemic manifestations (e.g., fever and malaise) are common. occurs most frequently on nape of the neck, upper part of the back, or the posterior thigh. Therapy: incision­and­drainage w. thorough search for loculated areas should be undertaken Wide local excision of the involved skin and subcutaneous fat is often necessary to prevent recurrent disease. oral antistaphylococcal agent Bites Bites ~ 50% of all Americans bitten by animal or human during lifetime ~ 1% of all emergency department visits. soft tissue infection is the most common complication risk of infection depends on type of bite, site of injury, time elapsed, host factors, and management of the wound hand or foot or over a major joint scalp or the face of an infant puncture wound delay in treatment > 12 hr immunosuppression, chronic alcoholism, diabetes mellitus corticosteroid use, preexisting edema in affected extremity overall risk of infection 5% ­ 15%; patients who seek medical attention 2% ­ 20% for dog bites, 30% to > 50% for cat bites, 10% ­ 50% for human bites. Bites Bites Animal bites dog 80% to 90%, cat 3% to 15%, non­domestic animals 1% to 2% Aerobes Anaerobes Pasteurella multocida Corynebacterium species Staphylococcus species Streptococcus species Capnocytophaga canimorsus (rare) Bacteroides species Prevotella species Porphyromonas species Peptostreptococci Fusobacterium species Bacteroides fragilis Veillonella parvula Infection: typically significant pain, soft tissue swelling, and tenderness; associated injuries to nerves, tendons, bones, joints, or blood vessels. Hand bites associated with an increased risk of tenosynovitis, septic arthritis, and abscess formation. Infections are usually polymicrobial, aerobes and anaerobes. P. multocida 50% to 80% cat bites and 25% dog bites.Infection with acute severe pain, tenderness, and swelling, within 12 to 18 hours Capnocytophaga canimorsus in immunocompromized pts. can be serious, w. overwhelming sepsis; associated mortality is 25% to 30%. Bites Bites Therapy: Immediate wound toilet: wash w. soap and water, irrigate, debride devitalized tissue close < 6 hours older than 12 hours, cat bites, and bites on the hand should be left open. In all cases of infection: get aerobic and anaerobic cultures Determine tetanus immune status and immunize when appropriate. non­domestic carnivore bites (e.g., bats, skunks, raccoons, foxes, or coyotes): irrigate with povidone­iodine and immunize against rabies w. established soft tissue infection and/or risk factors: Abx effective against aerobic and anaerobic organisms Amoxicillin­clavulanate , trimethoprim­sulfamethoxazole, doxycycline, and/or ciprofloxacin P. multocida : penicillin V, amoxicillin, cefuroxime, or ciprofloxacin C. canimorsus: pcn, ampicillin, cipro, erythromycin, or doxycycline. Bites Bites Human bites occlusional bites (teeth puncture the skin) or clenched­fist injuries (contact with teeth). occlusional bites carry same risk of infection as animal bites, clenched­fist injuries and all hand injuries are associated with higher risk of infection. Soft tissue infections are polymicrobial, mixture of aerobes and anaerobes. On avg. five different microorganisms isolated concentration of bacteria in the oral cavity is higher in humans bacteroides species are more common and often produce b­lactamases. predominant aerobic organisms are S. aureus, Staphylococcus epidermidis, a­ and b­hemolytic streptococci and corynebacteria contact with blood or saliva may transmit hepatitis B and C, Mycobacterium tuberculosis, and HIV. Bites Bites Therapy thorough high­pressure irrigation, with 1% povidone­iodine (bactericidal & viricidal). aerobic and anaerobic cultures debride devitalized tissue leave wound should open, infected or not. extremity should be immobilized and elevated. Abx for all infected & hand wounds: amoxicillin­clavulanate or doxycycline Assess tetanus status and immunize as appropriate Admit and IV Abx w. systemic signs of infection , severe cellulitis, compromised immune status diabetes mellitus; significant associated joint, nerve, bone, or tendon involvement infection refractory to oral Abx. therapy Superficial infections Superficial infections Cellulitis acute bacterial infection of the dermis and subcutaneous tissues primarily lower extremities ­ can affect all other areas common causes: puncture wounds from injection of illicit drugs, foreign bodies or bites secondary infection of preexisting skin lesions (eczema; tinea pedis; decubitus, venous stasis, or ischemic ulcers) Less common: extension of a subjacent infection (e.g., osteomyelitis) bacteremia from a remote site of infection. Predisposing factors: lymphatic disruption or lymphedema, interstitial edema, previous irradiation of soft tissue, peripheral vascular disease diabetes mellitus, malnutrition, immunocompromise Superficial infections Superficial infections Cellulitis Nonnecrotizing Form = overwhelming majority typically pain, soft tissue erythema, and constitutional symptoms (e.g., fever, chills, or malaise) erythema with advancing borders, skin warmth, tenderness, edema. +/­Lymphangitis or ­adenitis usually single aerobic pathogen In otherwise healthy adults S. pyogenes and S. aureus S. pyogenes ­ more common (esp w. lymphangitis) S. aureus ­ often w. underlying chronic skin disease. Other: H. influenzae ­ children or adults infected with HIV S. pneumoniae ­ pts with diabetes mellitus, alcoholism, nephr. syndrome, SLE, or hematol. malignancies. P. multocida ­ dog or cat bites. S. epidermidis ­ immunocompromised pts, (incl. HIV txplants) V. vulnificus ­ pts who ingested raw seafood or who had soft tissue trauma and sea water exposure A. hydrophila ­ w. soft tissue trauma fresh water exposure Superficial infections Superficial infections Cellulitis Nonnecrotizing Form Gram negatives and anaerobes in decubital ulcers, diabetic, perianal/perineal infections Therapy: empirical antibiotic regimen attempts to isolate pathogen are usually unsuccessful; needle aspiration / skin biopsy at advancing margin positive < 15% / 40% bacteremia is uncommon: blood cultures positive < 2% to 4% unless Sx of sepsis In an otherwise healthy adult, uncomplicated cellulitis w/o systemic manifestations: oral antibiotic on an outpatient basis Superficial infections Superficial infections Cellulitis Nonnecrotizing Form Therapy: majority of Strep and Staph are PCNase + dicloxacillin, augmentin, cephalexin, cefadroxil, erythromycin, or clindamycin margins of erythema should be marked reduced activity and elevation appropriate analgesic agents should be given. diabetic or immunocompromised pts. and w. high fever or rapidly spreading cellulitis / cellulitis refractory to oral Abx (>48 h): admission for I.V. Abx. Nafcillin, Cefazolin or ampicillin­sulbactam Clindamycin for suspected MRSA and PCN allergies; Vancomycin, other Abx. and combination regimen Deep infections Deep infections Cellulitis Necrotizing form: superficial vs. deep “Superficial” necrotizing cellulitis similar etiology and pathogenesis to nonnecrotizing cellulitis Predominantly in PVD, diabetes, pressure ulcer, venostasis, lymphedema or neglected primary cellulitis more serious and often progressive pathogens similar + anaerobes clostridia, peptostreptococcus, bacteroides, … Therapy: broad­spectrum Abx. urgent operative debridement is indicated +/­ hyperbaric O2 therapy Deep infections Deep infections Cellulitis Necrotizing form: Deep necrotizing cellulitis: Necrotizing dermatitis, fasciitis, myositis extension of superficial infection or primary deep space infection crush / penetration / neglect / hematogenous does not have to have skin necrosis often lack of specific early signs & Sx, delayed diagnosis host and pathogen factors most are polymicrobial early: localized pain, tenderness, mild edema / erythema may be subtle ­> cave: systemic illness > local signs Later: bullae, intense erythema, skin necrosis, crepitus Deep infections Deep infections Cellulitis Necrotizing form: Deep necrotizing cellulitis: Necrotizing fasciitis angiothrombotic microbial invasion and liquefactive necrosis of deep subqutaneous tissues, fascia +/­ muscle Hallmark: dishwater tissue fluid, thrombosis of vessels frank necrosis occurs later initially, tissue invasion proceeds horizontally, Myonecrosis rapidly progressive life­threatening infection indicates involvement of Clostridium species. gas formation common but not sine qua non short incubation: severe progressive disease in < 24 h acute severe pain, often minimal physical findings systemic signs of toxicity/ sepsis Deep infections Deep infections Cellulitis Necrotizing form: Deep necrotizing cellulitis: Therapy: broad­spectrum Abx to include MRSA, Gr. Neg and Clostridia bacteriocidal agents! when clostridia suspected or confirmed, penicillin G, 2 to 4 million U every 4 hours immediately; clindamycin, 900 mg every 8 hours, should be added. hyperbaric O2 therapy operative debridement. Special infections Special infections Rapidly progressive Cellulitis = “flesh eating bacteria” Strep. And Staph with Hyaluronidase, elastase, … Other exotoxins: hemolysins, fibrinolysins, and streptolysins cause severe SIRS, hemolysis, intravascular thrombosis ­> DIC Often extremely short progression time to MOF Therapy as with deep necrotizing infections broad­spectrum Abx to include MRSA, Gr. neg and Clostridia bacteriocidal agents! – cave: Eagle effect and toxin production during lag phase hyperbaric O2 therapy wide operative debridement. Special infections Special infections Streptococcal Toxic­Shock Syndrome hemolytic streptococci of group A (S. Pyogenes) more than 60% of patients with STSS have bacteremia. current incidence 1.5 per 100,000 ­ STSS 10% to 15%, necrotizing fasciitis in 6%. typically extremity infection only 50% have a demonstrable portal of entry severe pain is the most common initial symptom sudden onset / generally precedes physical findings –> rapid progression. hypotension invariably develops within 4 to 8 hours after presentation ­> Shock, ,MOF, ARDS Hemoglobinuria and an elevated serum creatinine, even w. adequate resuscitation Special infections Special infections Streptococcal Toxic­Shock Syndrome S. pyogenes classified into > 80 different strains, or M types M proteins impede phagocytosis and induce vascular leakage by forming complexes with fibrinogen. They cleave (NAD), interrupting elemental cellular processes. The M proteins M1 and M3 are associated with the majority of streptococcal necrotizing soft tissue infections. Streptococcal pyrogenic exotoxins (SPEs) produced by most streptococci cause severe soft tissue infection; can be transmitted by bacteriophages to different M types. They are the cause of the fever, shock, and tissue injury; SPE­A and SPE­B induce synthesis of TNF­a, IL­1b, and IL­6. M proteins or SPEs may act as superantigens. stimulate T cell responses direct binding to the Vb region of the T cell receptor, bypassing the normal antigen presentation pathway; they do not undergo phagocytosis; this pathway can stimulate more than a thousand times more T cells than the conventional antigen pathway and trigger a massive release of cytokines. Special infections Special infections Streptococcal Toxic­Shock Syndrome clinical treatment failure sometimes w. penicillin alone attributable to the large inoculum size = Eagle effect: large inocula reach the stationary growth phase very quickly. Penicillin and other b­lactam antibiotics are ineffective in the stationary growth phase because of the reduced expression of penicillin­binding proteins) toxin production is not inhibited by b­lactam antibiotics during the stationary growth phase. ­> add Abx. that inhibit protein synthesis Clindamycin is more effective than b­lactam agents it suppresses bacterial toxin synthesis and inhibits M­protein synthesis, Clindamycin also suppresses synthesis of penicillin­binding proteins, and it can act synergistically with penicillin. Surgical Site Infections Surgical Site Infections NNIS data on nosocomial infections Surgical site infection 37% Urinary tract infection 27% Pneumonia (NP, VAP) 15% Primary BSI All other sites 15% 7% VA NSQIP data on nosocomial infections Surgical site infections 5.1% Pneumonia Urinary tract infection 3.5% Sepsis/systemic BSI 3.6% 2.1% Surgical Site Infections Surgical Site Infections SSI impact Procedures SSI No. deaths Cost (M$) Cardiac Surgery 383,000 15,000 11,000 83.5 Colorectal Surgery 250,000 15,500 11,500 127.0 Other Surgery >500,000 7,900 4,500 63.0 In 2002 CDC and CMS initiated Surgical Infection Prevention Project (SIPP) – now core benchmark for hospital performance, monitored by JCHAO and other organizations (WWW.SURGICALINFECTIONPREVENTION.ORG) Natl. Acad. Sciences Research Council Natl. Acad. Sciences Research Council Classification of wounds Clean Class I Nontraumatic, No inflammation encountered No break in technique Respiratory, GI, or GU tract not entered Clean­contaminated Class II GI or respiratory tract entered w/o significant spillage Appendectomy; Oropharynx, Vagina entered GU or biliary tract entered in absence of infection Contaminated Class III Minor break in technique Major break in technique; Gross spillage from GI tract Traumatic wound, fresh Entrance of GU or biliary tracts in presence infection Dirty and infected Class IV Acute bacterial infection encountered Transection of "clean" tissue for surgical access to pus Traumatic wound with devitalized tissue, foreign bodies, fecal contamination, delayed treatment, or all of these; or from dirty source NNIS risk factors for SSI NNIS risk factors for SSI risk factors in addition to wound class: location of operation (abdomen or chest) duration of operation condition of wound at end of case American Society of Anesthesiologists (ASA) class III, IV or V patient clinical status (three or more diagnoses on discharge). Endogenous bacteria are more important source of SSI than exogenous pathogens Personnel is the most important source for exgenous bacteria Surgical Site Infections Surgical Site Infections SSI: prevention is key! Avoid elective surgery in the presence of remote infection Proper selection and timing of peri­op Abx. Strict adherence to infection control Facilities, instruments, practices Providers: Hands, protection, … Modification of host factors Nutrition, tight diabetic control Immunosuppressants … Parenteral Antibiotics Recommended Parenteral Antibiotics Recommended for Prophylaxis of SSI For coverage against aerobic gram­pos +/­ gram­neg organisms Cefazolin 1g I.V. or I.M. (I.V. preferred) If patient allergic to cephalosporins or if MRSA suspected Vancomycin 1g I.V. Clindamycin 600 mg I.V. or Combination regimens for gram­neg aerobes and anaerobes Metronidazole 500 mg I.V. plus Aminoglycoside) 1.5 mg/kg I.V. For single­agent coverage against gram­neg aerobes and anaerobes Cefoxitin 1–2 g I.V. or Cefotetan 1–2 g I.V. Must be given ½ to 1 hour prior to incision! Surgical Site Infections Surgical Site Infections SSI: prevention is key! Modification of host factors Bowel preparation – mechanic vs. SGD ? Antimicrobial shower / baths (chlorhexidine) ? Preoperative skin decontamination ! Clip rather than shave ! Preoperative nutritional optimization ?! Peri­op tight diabetic control – esp. week one ! Post operative O2 therapy ! Smoking cessation ! … Surgical Site Infections Surgical Site Infections SSI: prevention is key! Modification operative factors Decrase duration of OR ?! Avoid hypotension/hypoxia ?! Minimize use of Electrocautery ! Reduce talking ! Reduce tension on wound edges ! Reduce ischemia reperfusion ! Post operative O2 therapy ! Reduce need for blood transfusion ?! Avoid drains ?! … Surgical Site Infections Surgical Site Infections SSI: Therapy Open the wound Culture the wound Ampiric Abx. therapy if significant cellulitis ...
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This note was uploaded on 01/12/2012 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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