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Surgical Infections Revised 2008
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Surgical Infections Revised 2008

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Surgical Infections Revised 2008 Surgical Infections Revised 2008 Presentation Transcript

  • Surgical Infections Lu Ning, MD Assistant Professor of Surgery
  • Introduction
    • Unlikely to respond to nonsurgical treatment ( it must be excised or drained )
    • Occurs in operated site
  • Introduction
    • Surgery, trauma, non-trauma local invasion can lead to bacterial insult.
    • Once present, bacteria, initiate the host defense processes.
    • Inflammatory mediators (kinins, histamine, etc.) are released, compliment and plasma proteins are released, PMN’s arrive, etc.
  • Introduction
    • Surgical infections may arise in the surgical wound itself or in other systems in the patient.
    • They can be initiated not only by “damage” to the host but also by changes in the host’s physiologic state.
  • Risk
    • Many established factors have a role in infection.
    • These can be either surgical factors or patient-specific factors.
    • Patient-specific factors can be further defined as either local or systemic.
  • Surgical Risk Factors
    • Type of procedure
    • Degree of contamination
    • Duration of operation
    • Urgency of operation
  • SPREAD OF SURGICAL INFECTIONS
    • NECROTIZING INFECTION
    • ABSCESSES
    • PHLEGMONS AND SURPERFICIAL INFECTIONS
    • SPREAD OF INFECTIONS VIA THE LYMPHATIC SYSTEM
    • SPREAD OF INFECTION VIA BLOODSREAM
  • COMPLICATIONS OF SURGICAL INFECTION
    • Fistulas and sinus tract
    • Suppressed wound healing
    • Immunosuppression and superinfection
    • Bacteremia
    • Organ dysfunction, sepsis, and systemic inflammatory response syndrome
  • CLINICAL FINDIINGS AND DIAGNOSIS
    • Physical examination
      • Warmth, erythema, induration, tenderness, splinting
    • Laboratory findings
      • General findings: leucocytosis, acidosis, and signs of disseminated intravascular coagulation
      • Cultures:
    • Imaging studies
    • Source of infection
  • TREATMENT
    • Incision and drainage
    • Excision
    • Circulatory enhancement
    • Antibiotics
    • Nutritional support
  • Infections
    • Two main types
      • Community-Acquired
      • Hospital-Acquired
  • Community-Acquired
    • Skin/soft tissue
      • Cellulitis: Group A strep
      • Carbubcles/furuncle: Staph aureus
      • Necrotizing: Mixed
      • Hiradenitis suppurativa: Staph aureus
      • Lymphangitis: Staph aureus
  • Cellulitis
  • Cellulitis
    • Appears on an extremity as a brawny red or reddish-brawn area of edematous skin
    • It advances very rapidly from its starting point, and the advancing edge may be vague or sharply defined (erysipelas facialis)
    • Portal of entry: surgical wound, puncture, skin ulcer, patch of dermatitis (tinea pedis)
    • Most cases are caused by streptococci or staphylococci.
    • A moderate or high fever is almost always present.
    • Lymphangitis arising from cellutitis produces red, warm, tender streaks 3-4 mm wide leading from the infetion along lymphatic vessels to the regional lymph nodes.
  • Treatment
    • Rest , elevation, warm packs, and an oral or intravenous antibiotics
    • There is no suppuration. There is no needs of incision and drainadge.
    • Semi-synthetic penicillins or first-generation cephalosporins are usually effective.
    • If clear response has not occurred in 12-24 hours, on should suspect an abscess or consider the possibility that the causative agent is a gram-negative rod or resistant organism.
  • FURUNCLES AND CARBUNCLES
    • Furuncles and carbuncles are cutaneous abscess that begin in skin glands and hair follicles.
    • If the pilosebaceous apparatus becomes obstructed at the skin level, the development of a funruncle can be anticipate.
    • A carbuncle is a deep –seated mass of fistulous tracts between infected hair follicles.
    • Funruncles are the most common surgical infections, but carbuncles are rare.
  • Furuncle
  • Carbuncle
  • HIDRADENITIS
    • Serious skin infection of the axillae or groin
    • Consisting of multiple abscesses of the apocrine sweat glands.
    • The condition often becomes chronic and disabling.
    • The cause is unknown but may involve a defect of terminal follicular epithelium
  • Hiradenitis
  • TREATMENT
    • The classic therapy of furuncle is drainage, not antibiotics.
    • Invasive carbuncles must be treated by excision and antibiotics.
    • Hidradenitis is usually treated by drainage of the individual abscess and followed by careful hygeine
  • Lymphangitis
  • Community-Acquired
    • Breast Abcess
      • Staphylococcal infection
      • Usually post-partum
      • Treatment
      • MRSA is uncommon
  • Breast Abscess
  • Community-Acquired
    • Peri-rectal abcess
      • Results from infection of the anal crypts
      • Can be extensive
      • Can result in bacteremia
      • Treatment
  • Peri-rectal abscess
  • Community-Acquired
    • Hand Infections
      • Paronychia
        • Usually staph
        • Where?
        • Treatment
      • Felon
        • Where?
        • Treatment
      • Both can lead to tenosynovitis
  • Paronychia An inflammatory reaction involving the folds of the skin surrounding the fingernail. It is characterized by acute or chronic purulent, tender, and painful swellings of the tissues around the nail, caused by an abscess of the nail fold. The pathogenic yeast causing paronychia is most frequently Candida albicans. Saprophytic fungi may also be involved. The causative bacteria are usually Staphylococcus, Pseudomonas aeruginosa, or Streptococcus.
  • Felon
  • Community-Acquired
    • Diabetic foot infection.
  • DIFFUSE NECROTIZING INFECTIONS
  • Diffuse necrotizing infections
    • Particular dangerous
    • Difficult to diagnose, extremely toxic, spread rapidly, often leading to limb amputation
    • Popular press characterize the causative bacteria as “ flesh-eating ” or “ meat-eating ”
  • Pathogenic factors
    • Anaerobic wound
    • Bacterial exotoxins
    • Bacterial synergy
    • Thrombosis of nutrient bridging vessels
  • Classification of diffuse necrotizing infections
    • Clostridial
      • Necrotizing cellulitis
      • Myositis
    • Nonclostridial
      • Necrotizing fasciitis
      • Streptococcal gangrene
  • Clostridial Infections
    • Clostridia are saprophytes . vegetative and spore forms are widespread in soil, sand, clothing and feces.
    • The are fastidious anaerobes
    • On gram-stain they appear as relatively large, gram-positive, rod-shaped bacteria.
    • A broad spectrum of disease is caused by clostridia, ranging from negligible surface contamination through invasive cellulitis of connective tissue to invasive anaerobic infection of shock.
  • Clinical Findings
    • Crepitant abscess or cellulitis
    • Brown seropurulent exudate and mousy odor
    • Invasion is usually superficial to the deep fascia and may spread very quickly, producing discoloration.
    • Delayed debridement of injured tissue after devascularizing injury is the common setting.
  • Gas Gangrene
  • Clinical Findings
    • Severe pain suggests extension into muscle compartments ( myositis).
    • The disease progresses rapidly, with loss of blood supply to the infected tissue.
    • Profound shock can appear early, rapidly leading to organ dysfunction.
    • Air bubbles often visible on plain radiograph
    • Crepitus may be present, but not reliable to differentiation .
  • Nonclostridial Infections
    • Caused by multiple nonclostridial bacterial pathogens
    • Microaerophilic streptococci, staphyloccci, aerobic gram-negative bacteria, and anaerobes, especially peptostreptococci and bacteroides.
  • Necrotizing
  • Clinical Findings
    • Usually begins in a localized area such as a puncture wound, leg ulcer, or surgical wound.
    • Spread along the relatively ischemic facial plains, leading to thrombosis of penetrating vessels.Overlying subcutaneous tissue and skin are thus devascularized.
    • Externally, hemorrhgic bullae are usually the first sign of skin death
    • The skin is anesthetic and crepitus is occasionally present.
    • The fascial necrosis is usually wider than the skin appearance indicates.
    • The patient often seems alert and unconcerned but appears toxic.(“dyscrasia”)
    • At operation, the finding of edematous, dull-gray, and necrotic fascia and subcutaneous tissue confirm the diagnosis.
  • Streptococcal gangrene
    • Group A streptococcus is a bacterium frequently found in in the skin and throat.
    • Streptococcal gangrene is uncommon
    • The sudden onset of severe pain is the most common presenting symptom, usually in an extremity associated with a wound.
    • Fever and other signs of systemic infection are frequently present at the time of presentation.
    • Shock and renal dysfunction are usually present within 24 hours.
    • Invasion of deeper layers, especially muscle, is uncommon.
  • TREATMENT
    • The major emphasis is inevitable sugical.
    • Suspicion should be directed toward and wound incurred out of doors and contaminated with a foreign body , soil , or feces and any wound in which tissue has been extensively injured.
    • Complete debridement and depress tight fascial compartment.
    • Amputation.
  • TREATMENT
    • Broad-spectrum antibiotic therapy
    • Resuscitative therapy
    • Treat diabetes mellitus aggressively
    • Hyperbaric oxygenation inhibit bacterial invasion but does not eliminate the focus of infection. It is only reported anecdotally.
  • Community-Acquired
    • Biliary Tract
      • Usually result from obstruction
      • Usual suspects:
        • E. coli, Klebsiella, Enterococci
      • Acute Cholecystitis
        • GB empyema
      • Ascending cholangitis
        • Diagnosis
        • Treatment
  • Community-Acquired
    • Peritonitis
      • Causes
      • Diagnosis
      • Treatment
  • Community-Acquired
    • Viral
      • Hepatitis
      • HIV/AIDS
  • Community-Acquired
    • Tetanus
      • C. tetani infection
      • “ lock-jaw”
      • Caused by exotoxin
      • Treatment
  • TETANUS
  •  
  • Tetanus
    • Specific anaerobic infection mediated by a neurotoxin that causes nervous irritability and tetanic muscular contraction.
    • Causative organism: clostridium tetani
    • Tetanus-prone wound: puncture wound or one containing devitalized tissue or a foreign body
  • Clinical Findings and Diagnose
    • Tetanus is a clinical diagnose, as confirmatory laboratory tests are not routinely available.
    • Symptoms may occur as soon as 1 day following exposure or as long as several months later, the median incubation period is 7 days.
  • Clinical Findings and Diagnose
    • The first symptoms are usually pain or tingling in the area of injury, limitation of movement of the jaw (“lockjaw”), and spasms of the facial muscles (risus sardonicus)
    • Following presents: stiffness of the neck, dysphagia, and laryngospasm.
    • In more severe cases, spasm of the muscls of the back produce opisthotonos.
    • As chest and diaphgram spasms occur, longer and longer apnea floow.
  • Risus sardonicus
  • Courtesy: Google image on tetanus L ockjaw’s opisthotonos
  • PREVENTION
    • Each person should be actively immunized with tetanus toxoid, beginning with routine childhood immunization and continuing with booster injection every 10 years.
    • All patients with traumatic wounds should be queried regarding previous tetanus prophylaxis.
    • Active Immunization
    • Passive Immunization
    • Active and passive Immunization
    • Antibiotics
    PREVENTION
  • Active Immunization
    • 1 st dose - 6 th week
    • 2 nd dose - 10 th week
    • 3 rd dose - 14 th week
    • 1 st booster - 18 th month
    • 2 nd booster - 6 th year
    • 3 rd booster - 10 th year
  • Passive Immunization
    • ATS(equine) Ig- 1500 IU/s.c after sensitivity test
    • (or)
    • 2. ATS(human) Ig- 250-500 IU, no anaphylactic shock, very safe and costly.
  • Immunization requires at least three doses of Td. 1 st dose should be administered on the First visit 2 nd dose 4 – 8 weeks after the first dose of Td and 3rd dose after 6 months of the second Td. A booster dose of Td should be repeated every 10 years throughout life Persons Seven Years of Age or Older Who Have Not Been Immunized
  •  
  • TREATMENT
    • Neutralization of the toxin with TIG
    • Excision and debridement of the suspected wound.
    • Intravenous high-dose penicillin
    • Ventilator support if indicated
    • Protection from sudden stimuli
  • Prognosis
    • Mortality rate : 18%
    • An attack of tetanus does not confer lasting immunity.
  • Hospital-Acquired
    • Post-operative
    • The “5 W’s” (of fever)
  • Hospital-Acquired
    • Pulmonary
      • Pneumonia
        • Non-ventilator associated
          • Cause
          • Treatment
        • Ventilator associated
          • Cause
          • Treatment
        • Aspiration
          • Actually more a pneumonitis
          • Cause(s)
          • Treatment
  • Hospital-Acquired
    • Urinary Tract
      • Diagnosis
      • Usual suspects
        • Pseudomonas, Serratia, other GM-
      • Prevention?
      • Treatment
  • Hospital-Acquired
    • Wound infection
      • Self-explanatory
      • Diagnosis
      • Treatment
  • Hospital-Acquired
    • Intra-abdominal
      • Usually post-op
      • Causes?
      • Diagnosis
      • Treatment
  • Hospital-Acquired
    • Empyema
      • Infection-related
      • Iatrogenic
    • 3 phases
      • Acute:
      • Fibrinopurulent:
      • Organizing:
    • Treatment(s)
  • Hospital-Acquired
    • Foreign-body associated
      • Sites
        • Catheters
        • Lines
        • Prosthetics/grafts
      • Treatment
  • SURGICAL SITE INFECTIONS
  • GENERAL CONCIDERATIONS
    • Previously called postoperative wound infection
    • Result from bacterial contamination during or after a surgical procedure
    • The third most frequently reported nosocomial infection (14-16%)
    • Most frequent causes of infection in surgical patients ( 38%)
  • Types of surgical site infections(SSIs)
    • Incisioal SSIs
      • Superficial incisional (skin and subcutaneous tissues)
      • Deep incisional ( deeper soft tissue of the incision)
    • Organ/space SSIs
      • Any part of the anatomy other than body wall layers that was manipulated during the precedure
  • Wound Classification
  • Patient Factors
    • Local:
      • High bacterial load
      • Wound hematoma
      • Necrotic tissue
      • Foreign body
      • Obesity
    • Systemic:
      • Advanced age
      • Shock
      • Diabetes
      • Malnutrition
      • Alcoholism
      • Steroids
      • Chemotherapy
      • Immuno-compromise
  • Surgical Site Infections (SSI)
    • Third most common nosocomial infection (14%–16%)
    • Most common nosocomial infection among surgical patients (38%)
      • 2/3 incisional
      • 1/3 organs or spaces accessed during surgery
    • 7.3 additional postoperative days at cost of $3,152 in extra charges
    Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278.
  • Colonization vs Contamination – Definitions
    • Colonization
      • Bacteria present in a wound with no signs or symptoms of systemic inflammation
      • Usually less than 10 5 cfu/mL
    • Contamination
      • Transient exposure of a wound to bacteria
      • Varying concentrations of bacteria possible
      • Time of exposure suggested to be < 6 hours
      • SSI prophylaxis best strategy
  • SSI – Definitions
    • Infection
      • Systemic and local signs of inflammation
      • Bacterial counts ≥ 10 5 cfu/mL
      • Purulent versus nonpurulent
      • LOS effect
      • Economic effect
    • Surgical wound infection is SSI
    LOS=length of stay.
  • Superficial Incisional SSI
    • Infection occurs within 30 days after the operation and involves only skin or subcutaneous tissue of the incision
    Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278. Subcutaneous tissue Skin Superficial incisional SSI
  • Deep Incisional SSI
    • Infection occurs within 30 days after the operation if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operation and the infection involves the deep soft tissue (e.g., fascia and muscle layers)
    Superficial incisional SSI Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278. Deep soft tissue (fascia & muscle) Deep incisional SSI
  • Organ/Space SSI
    • Infection occurs within 30 days after the operation if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operation and the infection involves any part of the anatomy, other than the incision, which was opened or manipulated during the operation
    Deep incisional SSI Superficial incisional SSI Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278. Organ/space SSI Organ/space
  • SSI – Risk Factors Operation Factors
    • Duration of surgical scrub
    • Maintain body temp
    • Skin antisepsis
    • Preoperative shaving
    • Duration of operation
    • Antimicrobial prophylaxis
    • Operating room ventilation
    • Inadequate sterilization of instruments
    Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278.
    • Foreign material at surgical site
    • Surgical drains
    • Surgical technique
      • Poor hemostasis
      • Failure to obliterate dead space
      • Tissue trauma
  • SSI – Risk Factors Patient Characteristics
    • Age
    • Diabetes
      • HbA 1C and SSI
      • Glucose > 200 mg/dL postoperative period (<48 hours)
    • Nicotine use: delays primary wound healing
    • Steroid use: controversial
    • Malnutrition: no epidemiological association
    • Obesity: 20% over ideal body weight
    Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278.
    • Prolonged preoperative stay: surrogate of the severity of illness and comorbid conditions
    • Preoperative nares colonization with Staphylococcus aureus : significant association
    • Perioperative transfusion: controversial
    • Coexistent infections at a remote body site
    • Altered immune response
  • Bacterial dose Virulence Impaired host resistance Risk of Infection
  • Bacterial dose Virulence Impaired host resistance Risk of Infection
  • Virulence Impaired host resistance Risk of Infection Bacterial dose Virulence Impaired host resistance Risk of Surgical Infection Bacterial dose
  • SSI – Wound Classification
    • Class 1 = Clean
    • Class 2 = Clean contaminated
    • Class 3 = Contaminated
    • Class 4 = Dirty infected
    Mangram AJ et al. Infect Control Hosp Epidemiol. 1999;20:250-278. Prophylactic antibiotics indicated Therapeutic antibiotics
  • SSI – Risk Stratification NNIS Project
    • 3 independent variables associated with SSI risk
      • Contaminated or dirty/infected wound classification
      • ASA > 2
      • Length of operation > 75th percentile of the specific operation being performed
    NNIS=National Nosocomial Infections Surveillance. NNIS. CDC. Am J Infect Control. 2001;29:404-421.
  • SSI – Wound Class vs NNIS Class NNIS. CDC. Am J Infect Control. 2001;29:404-421. Wound Class All NNIS 0 NNIS 1 NNIS 2 NNIS 3 Clean 2.1% 1.0% 2.3% 5.4% N/A Clean contaminated 3.3% 2.1% 4.0% 9.5% N/A Contaminated 6.4% N/A 3.4% 6.8% 13.2% Dirty infected 7.1% N/A 3.1% 8.1% 12.8% All 2.8% 1.5% 2.9% 6.8% 13.0%
  • CLINICAL FINDINGS
    • Usually appear between the 5th and 10th days of surgery
    • The first sign is fever
    • The patient may complain of wound pain
    • Wound edema may be obvious
    • Palpation: firm and fluctuation, crepticus, or tenderness
  • PREVENTION
    • Careful, gentle, clean surgery
    • Reduction of contaminations
    • Support of patient’s defenses, including use of prophylactic antibiotics.
  • TREATMENT
    • Open the wound and allow it to drain
    • Antibiotics are not necessary unless the infection is invasive, manifested by surrounding zone of soft tissue inflammation
    • Cultures should be performed
  • Questions?????