Infection and Microbiology
Infection and Microbiology
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Musculoskeletal infections overview
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Treatment overview
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Empirical treatment: based on the presumed type of infection as determined from clinical findings and symptoms. Staphylococcus and Streptococcus are the most common organisms infecting skin, soft tissue, and bone.
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Definitive treatment: based on final culture and sensitivity results when available
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Surgical treatment: draining of contained infections, débridement of dead tissue, restoration of vascularity
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Bacterial virulence
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Antibiotic resistance—plasmid
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β-Lactamase (bla gene)—makes staphylococci resistant to penicillin
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Penicillin-binding protein 2a (mecA gene)—makes
Staphylococcus aureus MRSA
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Increased surface adhesion
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Fnb gene—fibronectin in S. aureus
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Increases adhesion to titanium
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Glycocalyx-biofilm-slime-polysaccharide capsule
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Improves attachment to inert surfaces
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Protects bacteria from desiccation
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Cell protection from phagocytosis
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Toxins
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Glycocalyx-biofilm-slime-polysaccharide capsule
—inhibits phagocytosis
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Hides PAMPs
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Protects bacteria from toxic enzymes/chemicals
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Protein A: S. aureus—inhibits phagocytosis
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Binds immunoglobulins (Fc region of IgG)
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M protein: group A Streptococcus pyogenes— inhibits phagocytosis
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Inhibits activation of alternative complement pathway on cell surface
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Endotoxin: gram-negative lipopolysaccharide capsules
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Exotoxin
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Clostridium perfringens: lecithinase— tissue-destroying alpha toxin
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Myonecrosis and hemolysis of gangrene
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Clostridium tetani: tetanospasmin— blocks inhibitory nerves
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“Lockjaw” or muscle spasms
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Clostridium botulinum: botulism— blocks acetylcholine release
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“Floppy” baby (also wrinkle relaxers and antispasmodic for cerebral palsy)
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Community-associated MRSA: Panton-Valentine leukocidin (PVL) cytotoxin
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Superantigens
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Pore-forming toxin specific to neutrophils
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Activate approximately 20% of T cells
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Trigger cytokine release
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Systemic inflammation; appears as septic shock
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S. pyogenes (group A streptococci): M protein
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S. aureus: TSS toxin-1 causes toxic shock syndrome
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Acute febrile illness with a generalized scarlatiniform rash
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Hypotension (shock) with organ system failure
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Desquamation of palmar/plantar skin lesions (if the patient lives)
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Treatment:
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Removal of foreign object (retained sponge or tampon)
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Supportive care with fluids and anti-Staphylococcus antibiotics
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Staphylococcus: roughly 80% of orthopaedic infections
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Antibiotic resistance
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Penicillin (β-lactam antibiotic)—inhibits peptidoglycan bonds of bacterial cell walls
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β-Lactamases are enzymes produced by bacteria that provide resistance by breaking down the antibiotic structure.
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MRSA
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mecA gene
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Community versus hospital
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Located on staphylococcal chromosome cassette mobile element–carrying IV (SCCmecIV)
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Encodes for penicillin-binding protein 2A, which has a low affinity for β-lactam antibiotics
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Hospital-acquired MRSA (HA-MRSA) or health care–acquired (HC-MRSA)
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Seen in patients from nursing homes, those with recent bacteria have larger SCCmec genetic elements
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Multiple antibiotic
resistance genes
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More drug resistance; known as “super bugs”
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Community-acquired MRSA (CA-MRSA)
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Bacteria have smaller SCCmec genetic elements
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Infection by tissue type
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Less drug resistance
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Almost all have PVL cytotoxin
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γ-Hemolysin: a pore-forming toxin that can lyse PMNs
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Seen in young adults with recurrent boils and severe hemorrhagic pneumonia
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At-risk groups: athletes, IV drug abusers, homeless persons, military recruits, prisoners
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Risk factors
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Previous antibiotic use within 1 year
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Frequent skin-to-skin contact with others
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Frequent sharing of personal items
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Compromised skin integrity
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Soft tissue infections: superficial to deep (Table 1.32)
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Erysipelas: infection of dermis and lymphatics—group A streptococci
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Painful raised lesion with a red, edematous, indurated (peau d’orange) appearance and an advancing raised border
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Treatment: penicillins or erythromycin
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Cellulitis: subcutaneous infection most commonly group A streptococci or S. aureus
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Acute spreading infection with pain, erythema, and warmth, with or without lymphadenopathy; may develop into abscess (may surround abscess or ulcer)
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Treatment: routine for cellulitis—penicillin, dicloxacillin; but IV cefazolin or nafcillin if systemic systems prominent or patient is at high risk (asplenia, neutropenia, immunocompromise, cirrhosis, cardiac or renal failure, local trauma, or
preexisting edema)
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Abscess: pus-filled inflammatory subcutaneous nodule (furuncle = “boil”) that may be multiple and may coalesce (carbuncle): almost always S. aureus. Small lesions sometimes mistaken as spider bites.
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Painful pus under pressure
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Treatment: incision and drainage (I&D), then left open, with culture and sensitivity testing to select antibiotics.
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For simple abscesses, addition of systemic antibiotics has not been shown to improve cure rate or decrease recurrence above I&D alone.
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Systemic antibiotics only for (Infectious Disease Society of America Guidelines):
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Severe or extensive disease
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Rapid progression in the presence of associated cellulitis
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Signs and symptoms of systemic illness
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Associated comorbidities or immunosuppression, extremes of age
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Abscess in an area difficult to drain
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Associated septic phlebitis
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Lack of response to incision and drainage
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Empirical antibiotics selected should aim at MRSA.
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Necrotizing fasciitis
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Rare, rapidly progressive, life-threatening infection of the fascia and subcutaneous tissue
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Causes liquefactive necrosis with thrombosis of the cutaneous microcirculation
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Most commonly polymicrobial, but group A β-hemolytic (“flesh-eating”) streptococci the most common monomicrobial cause (i.e., S. pyogenes).
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Risk factors: diabetes, peripheral vascular disease, liver failure
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Death most related to delay in treatment for more than 24 hours
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Fascial infection spreads faster than the observed skin changes.
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Skin microcirculation thrombosis and later necrosis
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Early—pain out of proportion, swelling and edema
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Late
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Blisters/bullae
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Skin that does not blanch (skin is dying)
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Skin becomes numb (nerves are dying)
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Difficult diagnosis—paucity of cutaneous findings so high clinical suspicion needed
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Less than one-fifth of cases diagnosed at admission; preadmission antibiotics mask severity
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Repeated examinations noting margins that migrate quickly despite antibiotic treatment
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Surgical findings
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Grayish necrotic fascia
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Lack of normal muscular fascial resistance to blunt dissection
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Lack of bleeding of the fascia during dissection
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Foul-smelling “dishwater ” pus
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Treatment: broad-spectrum antibiotics
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Early operative débridement of all necrotic tissue—level selected should be ahead of the infection
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Amputation/disarticulation should be considered.
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Second-look procedure should be performed 24 hours later for reevaluation.
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Gas gangrene
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C. perfringens (obligate anaerobe) most common organism that produces gas and toxins in subcutaneous tissues and muscle
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Dirty wound managed with primary closure: war wounds, tornado, lawn mower
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Inadequate débridement of more severe devitalizing injuries
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Clostridial dermonecrotizing exotoxin lecithinase
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Crepitance of soft tissue, air in soft tissues on x-rays, foul “sweet”-smelling discharge
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Early, adequate, and thorough surgical débridement
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Delayed closure and second-look procedure 24 hours later for reevaluation
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High-dose IV penicillin and hyperbaric oxygen can help if available.
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Surgical site infection
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Infections are the product of bacteria that take hold in a favorable wound environment in a host with a susceptible immune system.
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Bacterial issues
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Load
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Prevention
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More than 10 5 colony-forming units (CFUs) needed in normal host to cause infection
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Need only about 100 CFUs if foreign object present
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Prophylactic antibiotics
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Given from less than 1 hour before until 24 hours after procedure
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Repeated if preceding time is more than 4 hours (longer than half-life of antibiotic selected)
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Repeated if blood loss more than 1000 mL
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Doubled if patient weighs more than 80 kg (>176 lb)
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Avoidance of hematogenous seeding
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No active infections in elective cases
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—legs, feet, toes checked preoperatively
Table 1.32
Soft Tissue Infections
Type Affected Tissues Clinical Findings
Cellulitis,
erysipelas
Superficial, subcutaneous
Erythema; tendern warmth; lymphangitis;
Aggressive, life threatening may be associated an underlyi vascular dis (particularl diabetes)
Commonly occ after surger trauma, or streptococc skin infecti
Progressive, se pain; edem (distant fro the wound) foul-smellin serosanguin discharge; h fever; chills tachycardia confusion
Clinical finding consistent toxemia
Radiographs typically sh widespread in the soft tissues (facilitates r spread of th infection)
Staphylococcal
Toxemia, not septicemia
In orthopaedics, TSS is secondary to colonization of surgical or
Fever, hypoten an erythemato macular ras with a sero exudate (gr positive coc
Tox shock
syndrome:
Muscle; commonly in grossly contaminated, traumatic wounds, particularly those that are closed primarily
Gas gangrene
Muscle fascia
Necrotizing fasciitis
lymphadenopa
traumatic wounds (even after minor trauma)
TSS can be
associated with tampon use through colonization of the vagina with toxin-producing S. aureus
Similar to
staphylococcal
Marine injuries Varies
History of fishi (or other m activity) inj with signs o infection
Culture specim at 30°C (60
organisms take several weeks to gr on culture media
Varies
Surgical wound infection
Toxemia, not septicemia
Commonly
associated with erysipelas or necrotizing fasciitis
Streptococcal
are present)
The infected wound ma look benign which may the seriousn of the underlying condition
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If urologic symptoms: urinalysis and culture
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Postpone surgery if:
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Over 103 CFUs and dysuria/frequency
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Symptoms of urinary obstruction
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Reduced force, hesitancy, straining
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Foley catheterization should be discontinued as soon as possible after surgery.
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MRSA: carrier screening and eradication, “active detection and isolation (ADI)”
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Nasal carriage—important risk factor, with some controversy; if patient part of high-risk population
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Screening
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Swab culture versus PCR
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If positive screen result: postoperative infection rates are two to nine times higher
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Use
vancomycin 1 g every 12 hours
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2% intranasal mupirocin ointment twice daily × 5 days
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2%
chlorhexidine showers daily × 5 days
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Nutrition (malnutrition associated with wound dehiscence and infection)
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Clinical evaluation
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History of weight loss (10% over 6 months or
5% over 1 month)
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Albumin value less than
3.5 g/dL, total lymphocyte count less than 1500 cells/µL, transferrin level less than 200 mg/dL
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Obesity—body mass index (BMI)
more than 30 kg/m2; higher numbers
= more wound problems
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Bariatric consultation should be considered early in course for patient likely to progress to need large elective procedure.
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Smoking: two to four times more infections/osteomyelitis
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Hypoxia—CO binds to Hb = carboxyhemoglobin (HbCO)
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Nicotine—microvascular vasoconstriction
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Reduced bone, skin, soft tissue healing
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Cessation of smoking 4 to 6 weeks preoperatively leads to decreased complications.
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Alcohol: heavy alcohol use (blood alcohol >200 mg/dL) increases rate of infections 2.6 times
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Reduced fibroblast production of collagen type I
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Inhibits osteoblasts: reduced osteocalcin, inhibits Wnt/β-catenin pathway
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Diabetes
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Special soft tissue infections
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Impairs fracture healing
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Associated with “bad behaviors,” cirrhosis, and liver failure
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Chronic issues well known: cardiac, renal, peripheral vascular, neuropathy
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Best measured with HbA1c—goal is less than 6.9% of total hemoglobin
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Acute hyperglycemia is also a threat
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Collagen synthesis suppressed at blood glucose value of 200 mg/dL—impaired wound healing
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WBC phagocytosis impaired at blood glucose value of 250 mg/dL—decreased ability to fight infection
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Bite infections (Table 1.33)
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Initial treatment: exploration of wound, removal of foreign objects, débridement, and irrigation
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Consider delayed primary closure at 48–72 hours
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Antibiotic prophylaxis controversial
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Should be considered for bites to hands, feet, face
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Wounds hard to clean—deep punctures, edema/crush injury
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Bites involving tendon, cartilage, or bone
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Bites in immunocompromised or asplenic host
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Bite prophylaxis antibiotics: amoxicillin-clavulanate
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For penicillin-allergic patient, trimethoprim-sulfamethoxazole plus clindamycin
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Antibiotic treatment: oral unless infection rapidly spreads or patient is febrile or high risk; then IV
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Bite organisms
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Most oral flora is polymicrobial in nature. Some bacteria are more specific to source of “bite.”
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Human bites: Streptococcus viridans common,
Eikenella corrodens
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“Fight bite” x-rays for cartilage divots, broken teeth, and formal identification
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Cat bites: Pasteurella multocida
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50% require surgery—puncture wounds to tendons/joints
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Dog bites: P. multocida, Pasteurella canis
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Marine injuries
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Mycobacterium marinum
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Slow culture at low temperature (30°C)
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Noncaseating granulomas
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Treatment: 3 months of minocycline or clarithromycin
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Erysipelothrix rhusiopathiae
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Erysipeloid—fish handler ’s (also swine handler ’s) disease
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Gram-positive bacillus
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Painful, itchy, spreading, purple ring-shaped lesion
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Treatment: oral penicillin
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Vibrio vulnificus
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Oyster bite
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Bullae and necrotizing fasciitis from gram-negative motile rod
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Gastroenteritis from eating bad oyster
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Treatment: I&D and broad-spectrum antibiotics (ceftazidime)
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Tick bite (Ixodes): Lyme disease
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Borrelia burgdorferi (a spirochete)
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Erythema migrans: bull’s-eye lesion
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Vector: white-footed deer mouse in northeast and Pacific north
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Knee effusions
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Neurologic disease: Bell palsy common
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Treatment: amoxicillin versus doxycycline
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Rabies (neurotropic virus)
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Raccoon/skunk/bat bites
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CNS irritation, “hydrophobia,” paralysis, and death
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Death if not treated before symptoms occur
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Treatment: human rabies immune globulin
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Septic bursitis
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Similar pathology whether in olecranon, prepatellar, or pretibial bursa
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Redness, swelling, pain, and subcutaneous fluctuance
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About 80% caused by S. aureus, others streptococci
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Chronic recurrent cases can be fungal or mycobacterial
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Aspiration with Gram stain and culture if redness is presence
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Treatment
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Tetanus
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Serial aspirations and oral antibiotics
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IV antibiotics for systemic symptoms and in immunocompromised patients
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Bursectomy for persistent or recurrent cases
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Potentially lethal neuroparalytic disease leading to trismus (lockjaw)
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Exotoxin from anaerobe C. tetani
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Tetanospasmin blocks inhibitory nerves.
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Deep wounds and devitalized tissues are at high risk.
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Wounds more than 6 hours old, more than 1 cm deep, ischemic, crush, grade III
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Contaminated with soil or feces, animal bite
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Vaccination
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Tetanus toxoid (Td) 0.5-mL diphtheria-tetanus toxoid booster every 10 years
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Adults with at-risk wounds, give Td booster
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Status unknown or history of fewer than three doses: give both Td and tetanus immune globulin (TIG)
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