Skin & Soft Tissue

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    Introduction

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    • Two organisms often responsible:
      • Group A Streptococcus (GAS) [ B-hemolytic Strep]
        • Lymphangitis - "Peau d'orange" appearance of skin 
      • Staphylococcus aureus
        • (including community acquired methicillin-resistant S. aureus) (CA-MRSA)
        • Causes abscess or drainage from wound (i.e. previous trauma)
    • Anatomically
      • Superficial:
        • impetigo
        • Erysipelas
          • superficial in upper dermis (primarily Group A Strep)...
          • Tender warm, intensely erythematous plaques with well demarcated/indurated borders + edema are characteristic findings.
          •  erysipelas.jpg
        • folliculitis
      • Deeper
        • furunculosis (hair follicles)
        • hidradenitis (sweat glands)
        • Cellulitis
          • Distinguish from Erysipelas as cellulitis is deeper and not well demarcated.
          • Can be due to staph or strep.
          • If furuncles, carbuncles or abscesses are present --> usually staph aureus.
          • cellulitis.jpg
      • Fascia plane
        • Necrotizing faciitis  (GAS)
          • Thrombosis of vessels in fascia, requires fasciotomy.
      • Wost case:
        • Necrotizing faciitis --> necrotizing myositis (myonecrosis) --> sepsis --> irreversible septic shock

     

    Notable Cellulitis Pathogens

    • Most Common
      • Staph aureus  (furuncles, carbuncles, abscesses, purulent cellulitis)
        • Includes MSSA
        • Includes MRSA
          • v
      • Group A Strep (erysipelas, cellulitis)
    •  
    • Diagnosis
      • 5% positive blood cultures.
      • Cultures by punch biopsy or needle aspiration are possible, but not routine.

    Cellulitis

    • Infection of skin with some extension into subcutaneous tissues.
    • On exam:
      • need to find portal of entry (tinea pedis, psoriasis, eczema)
      • Comment on whether it is well-demarcated
      • Comment on crepitus (anaerobic component)
    • Causes:
      • B-Hemolytic strep (Groups A, B, C, and G)
      • S. aureus
      • H.infuenzae in kids.
      • Special:
        • Bite wounds - skin and oropharynx of biter
        • Fresh water exposure (Aeromonas hydrophila)
        • Seawater exposure (Vibrio vulnificus)
        • Diabetic foot ulcer (Polymicrobial)
    • Risk factors:
      • Venous or lymphatic compromise. (surgery, trauma, CHF)
      • Diabetes (peripheral neuropathy and vessel occlusion)
      • Chronic Alcoholism (trauma, poor hygenine)
    • SPECIAL types of cellulitis:
      • Erysipelas:
        • Swelling and sharp demarcation
        • Almost always GAS (occasionally Group C, G, or B)
      • Clostridial cellulitis
        • Superficial infeciton of Clostridium perfringens
        • Preceded by local trauma or surgery.
        • Gas found in skin. (crepitus)
        • "Forest fire" progression... most active (red) at the leading edge.
        • Do MRI/CT and CK to see if muscle involved
      • Non-clostridial anaerobic cellulitis
        • Most often in diabetes.
        • Distinguish from nec fac and myonecrosis by surgical exploration.
           
      • Other Causes of Cellulitis:
        • Aeromonas hydrophila - freshwater lakes, streams, rivers, leeches.
        • Vibrio - Salt water, raw seafood.
        • Erysipelothrix rhusiopathiae - saltwater marine life (sometimes even freshwater fish).
        • Pasteurella multocida - Contact with cats.
        • Capnocytophaga canimorsus - Contact with dogs.   (or Asplenic patients)
        • Bacillus anthracis - bioterrorism. (painless lesions)
        • Francisella tularensis - animal (usually cats) or arthropod bites
        • Mycobacterium marinum - fresh water, salt water, fish tanks, swimming pools.

     

    • Treatment:
      • Mild and early cellulitis  (i.e. erysipelas b/c almost always GAS)
        • Penicillin
      • If suspect S. aureus
        • Penicillinase-resistant penicillin (nafcillin, dicloxacillin, cloxacillin?)
      • Most commonly:
        • Cephalexin, cefazolin, cloxacillin, (ceftriaxone also good coverage, but broad).
      • First-gen cephalosporin (cefazolin) covers S. aureus and GAS
      • If pen-allergy:
        • Use Vancomycin (also covers MRSA)
      • For MRSA:
        • For Community Acquired MRSA - oral therapies:
          • Use septra, tetracyclines, clinda, linezolid.  
          • NOTE: However, Septra/tetracyclines aren't reliable against strep, so need second agent)
        • IV: Use vancomycin, linezolid, daptomycin, etc...
        • SEE CA-MRSA SECTION FOR DETAILS
      • Other measures:
        • Elevate, cool, sterile saline dressing to remove exudates. (helps pain too).
        • Need 1-2 weeks of therapy.
      • Local desquamation can be sen and convalescence.

    Necrotizing Fasciitis

    • Infection that extends beyond the epidermis, dermis, and subcutaneous fat tissues.
    • Involvement of the deep fascial plane in abdomen, perineum, and extremities.
    • Hard to distinguish from cellulitis or milder infections.  Worry if:
      • +++ pain!  or FEVER, or other systemc effects (tachy etc..)
    • Classically (initial): erythematous lesions associated with significant pain and edema.
    • Two types: (based on bacteriology and manifestations)
      • Type I  (often in Diabetics!)
        • Polymicrobial w/ G+ and G- aerobic and anerobic.  (4-5 usually isolated)
          • S.aureus, GAS, E.coli, peptostreptococcus, Clostridium, Prevotella, Porphyromonas, Bacteroides, etc..
        • Associated with:
          • Diabetes - usually on feet.  Suspect nec fasc if systemic symptoms (tachy, leukocytosis, hyperglycemia, acidosis).
          • Cervical necrotizing fasciitis - Odontogenic infection after surgery (mucous membranes).  In H&N, bacterial penetration into fascia can give:
            • "Ludwig's angina" (rapidly expanding inflammation in the submandibular and sublingual spaces after dental surgery).
          • Fournier's gangrene - Perineal Fasciitis, penetrates into GI and urethral mucosa, abdominal wall, gluteal muscles (+scrotum and penis in males).
      • Type II 
        • Single organism: classicaly Group A B-hemolytic strep (Streptococcus pyogenes).
          • aka "streptococcal gangrene" and "streptococcal toxic shock syndrome".
          • Streptococcal gangrene associated with toxic shock syndrome. (50%?).
          • Others that can cause similar infections:
            • Vibrio (curved gram- rod in warm salty water - gulf of mexico!)
              • Typically immunodeficient host: Classically iron overload or cirrhosis.
              • Ingestion of raw/uncooked shell fish or broken skin exposed to contaminated sea water.
            • Staph aureus
            • Staph agalactiae.
            • Clostridium perfiringens myonecrosis (aka "Gas Gangrene").
        • MRSA and CA-MRSA are common.
    • NOTE: Do serum CK.
    • Symptoms:
      • Erythematous lesions associated with significant PAIN!!! (typically out of proportion with skin findings), Edema.
        • Typically pre-existing skin infection or trauma (i.e. pressure ulcers), typically portal of entry.
      • Lesions progress rapidly to form violaceous bullous/gangrenous appearance.
         
      • Palpation: woody induration, crepitus (soft tissue gas).
      • Systemic Toxicity:
        • Fever
        • Hypotension
        • Mental status change
        • Tachycardia
        • Leukocytosis
        • Laboratory: multi-organ dysfunction.
    • Labs:
      • Evidence of Systemic Inflammation: WBCESRCRPSerum CK.
      • MRI: Finds extent of fascial plane involvement. 
      • C&S + Stain of wound is helpful.
    • Treatment:
      • Treatment URGENT!!! (30-70% mortality).
      • Surgery if severe pain, sepsis, fever, elevated CK.
        • Usually need surgery for debridement and determine extent of necrosis.
        • Cultures should be obtained.
        • Need surgical re-evaluation 24-48hrs post-op and continued daily.
      • Empiric Broad-Spectrum Abx:
        • Cover Strep, GN's, Anaerobes, CA-MRSA, MSSA,
          • Pip-tazo OR cefepime+metronidazole OR carabapenem (mero/imipenem).
            • + Clindamycin (If suspect B-hemolytic Group A Strep or Clostridium is shown to suppress toxin production and improve outcome)
          • US Guidelines: + Anti-MRSA Agent (Vancomycin, Daptomycin, Linezolid) is indicated, or if community prevalence is high. 
      • Type II Necrotizing Fasciitis
        • 2ndary to Group A Strep or Clostridium:
          • Penicillin G + Clinamycin indicated.
      • Stop Abx when after debridement and clinical improvement evident.
      • IVIG: To neutralize exotoxins.  Studies conflicting.  No definitive recommendations.  Some experts recommend in toxic shock or high risk of death

     

    • FLUIDS! and pressors to maintain perfusion pressure.

    Myonecrosis

    • Uncommon infection of muscle that develops rapidly and is life-threatening.
    • Primarily caused by Clostridium perfringens and C. septicum (latter associated with bowel cancer).
    • Usually following deep penetrating trauma, but source depends on flora:
      • Penetrating trauma --> c. perfringens.
      • Bowel -> C. septicum  (bowel lesion seeds C. speticum... dies depsite abx treatment and debridement)
      • Vagina --> C. sordellii  (D&C)
    • Myositis other conditions:
      • Tropical myositis or pyomyositis
        • (S. aureus and others cause primary muscle abscess, common in tropical areas)
      • Necrotizing infections by Vibrio vulnificus
        • Can involve skin, vascia, muscle.  (esp in cirrhosis, raw seafood, living in coastal regions).
    • Pathophysiology
      • Initial penetrating trauma introduces organisms into deep tissue.  Producing anaerobic acidic environment.
      • Rapid tissue desctruction by Clostridium
      • alpha-toxin secreted has phospholipase C and sphingomyelinase activity --> induces platelet and PMN aggregation --> blood vessel occlusion and rapid tissue necrosis --> enhances anaerobic environment --> more clostridial growth.
      • Alpha-toxin + theta-toxin suppresses cardiac contractility, causes vasodilation --> more tissue hypoperfusion and anaerobic environment.
    • Symptoms:
      • Skin appears brownish/bronze.  --> then purplish red.
      • Presence of crepitus locally.
      • Signs of systemic sepsis quickly develop. (tachy, low-grade fever, hypotension, shock, multi-organ failure).
      • Clostridial bactermia --> extensive hemolysis.
      • Gas in soft tissues _> Xray, CT, MRI.
    • Treatment: URGENT!
      • Removal of necrotic tissue, amputation.
      • IV pencillin and clindamycin.
        • abx:
          • Penicillin, clindamycin, metronidazole, cephalosporins all excellent.
          • Typically penicillin + clindamycin used to kill + suspend alpha+theta toxin production.
      • Hyperbaric O2.
      • Outcome often fatal despite treatment.

     

    Burns

    • Provides fertile environment for bacterial growth
    • Invasive infection can happen:
      • Gram+ aerobies (Staph aureus, S. epidermidis, enterococci
      • Gram - aerobes (Enterobacter, E. coli Klebsiella, Pseudomonas, and Acinetobacter)
    • Burn patients already are febrile, sinus tachycardia, sudden worsening can indicate sepsis.
    • Debridement and topical abx are mainstays.
    • Give Broad-spectrum if sepsis suspected.

    Less Severe but Common

    Impetigo

    • Superficial, vsiculopustular skin infection.
    • Warm, humid conditions (kids), easily spread btwn families.
    • GAS and S. aureus.
      • Post-strep GN is RARE, but can be prevented with abx.
    • Treatment:
      • topical, but if multiple lesions: may need systemic.
      • Penicillin is good, but many S. aureus resistant. (produce B-lactamases)
      • Amox-clav, erythromycin, cephalexin, dicloxacillin and topical mupirocin ointment are effective.
      • Preferred: oral erythromycin (250mg or in kids: 12.5 mg/kg q6h x10d).
      • OR mupirocin ointment in a polyethylene glycol base locally.
      • OR cephalexin (250mg q6h or 500mg BID x10 days).

    Folliculitis

    • S. aureus is common if carrier. (in nasal opening)
    • Pseudomonas if in whirlpools, or pools with inadequate chlorination.  "whirlpool folliculitis".
    • Abx or steroid therapy --> Candida folliculitis.
    • Treatment:
      • Treat S. aureus, but pseudomonas and candida can also cause this.
      • Systemic abx --> NOT helpful.
      • Warm saline compresses, topical antibacterial or antifungal agents.
      • To decolonize from nose:  Monthly mupirocin ointment to anterior nares bilat twice daily x5 days each month prevents nasal S.aureus colonization. 
      • If recurrent, and not immunocompromised --> consider P. aeruginosa.
      • Complications --> Furunculosis and Carbuncles

     

    Furunculosis and Carbuncles

    • Furunculosis --> inflammatory painful nodule surrounds hair follicle.  (after folliculitis).
      • Carbuncle --> Larger subcutaneous abscess that progreses from furuncle.  Often need drainage.
    • Both caused by S. aureus, MRSA is concern (prisons, hospitals, contact sports, etc.)
    • Usually in areas with friction and perspiration (back of neck, face, axillae, buttocks).
    • Systemic sx are uncommon.  Fever is rare.
    • Treatment:
      • warm compresses to promote spontaneous drainage.
      • If fever --> Dicloxacillin (cloxacillin?).
        • If pen-allergic --> cephalexin or clindamycin.
      • If MRSA suspected:
        • TMP-SMX
      • Surgically drain if do not drain spontaneously.
        • Seeds hematogenously.. may need to prophylax against endocarditis.
    • If recurrent:
      • Prophylaxis:
        • Chlorhexidine
        • Personal hygeine.
        • Nasal muprocin to decolonize S. aureus.
        • Prophylatic abx.
    • Dangerous!:
      • On face --> cavernous sinus infection.
      • Bacteremia can occur if manipulated.

    Skin Abscesses

    • S.aureus most common
    • Tx same as Furuncles / Carbuncles.
    • Consider oral clindamycin if anaerobes are involved.
    • If recurrent:
      • R/O D/M
      • Neutrophil dysfunction
      • Immunoglobulin E syndrome.
    • May need to prophylax for endocarditis before I&D.

    Rare, Indolent

    • Often chronic skin infections, non-responsive to abx.
    • Water-pathogens:
      • Erysipelothrix --> fisherman cut fingure on fish spine.  (penicillin, clinda, cipro)
      • Mycobacterium marinum (minocycline or clarithromycin).   (acquariums, fresh/salt water)
    • Plants/soil
      • Sporotrichosis (itraconazole) - gardeners cut finger on bush thorn.
      • Nocardiosis (TMP-SMX, azole).
    • Tetanus
      • human tetanus immunoglobulin.
      • tetanus toxoid vaccine
      • IV metronidazole
      • benzos and pancuronium, or intrathecal baclofen to control spasms.
      • Short acting B-blockers, VI magnesium sulfate, vasopressors for autonomic instability.
      • Intubation and tracheostomy is often required.
      • PREVENT!
        • vaccine tetanus toxoid q10y.
        • Booster q5y or so if contaminated wound.
        • Patients high risk may need tetanus Ig.

    Animal Bites

    • Infection of bites due to oral flora of the animal.
    • Infection after dog + cat bites due to mix of aerobic and anaerobic organisms.
    • DOG bites are less likely to get infected than cat bites.
      • Most commonly with pet animal bites: Pasteurella  (50% of cat bites and 70% of dog bites) - GN coccobacilli.
        • P. canis in dog bites
        • P. multocida in cat bites.
        • Other organisms cultured form bite wounds:
          • S. aureus
          • Streptococci  (staph+strep in 40% of bite wounds)
          • Capnocytophaga canimorsus
            • Gram neg rod can cause overwhelming sepsis (mostly in asplenia).
          • Anaerobes 
    • Result infections are often polymicrobial
    • Must irrigate and debride the wound.
    • DO NOT CLOSE THE WOULD INITIALLY
    • Wound irrigation + cleaning.
    • If animal is unprovoked:
      • Tetanus prophylaxis
      • Rabies prophylaxis (vaccine/IgG)
      • Capture animal and observe for rabies.
    • Prophylaxis is recommended:
      • Recommended for:
        • Immunocompromised
        • Wound on hands or near joint/bone.
        • Moderate-severe wounds.
        • Crush injuries
        • Wounds associated with edema.
      • Oral amox-clav (875 mg bid x3-5 days)
        • If Penicillin allergic:
          • Fluroquinolone (i.e. cipro 400mg IV then 500mg PO BID) or doxycycline or TMP/SMX
            • + ADD clindamycin (900mg IV + 300mg PO Q6h) for anaerobic coverage.
      • In children: clinda + trimethoprim-sulfamethoxazole recommended.
    • Treatment:  (IF infected)
      • All infected dog/cat bite wounds require antimicrobial therapy
      • Same oral regimen as prophyalxis, but longer (10-28days)
      • Do not use 1st gen cephalo, dicloxacillin, erythromycin b/c organisms resistant. (i.e. P. multocida)
      • Hospitalize if:
        • Severe/deep infections
        • Nerve/tendon/crush injuries
        • Infected hand bites.
      • If hospitalized use IV:
        • pip-tazo (other B-lac + inhibitor), cefoxitin, carbapenem.
          • If Pen-allergic, use fluoroquinolone + clindamycin.
          • Consider vancomycin if MRSA suspected.
      • Duration of therapy:
        • <2w treatment
        • 3-4w if joint infection
        • 4-6w if bone infection.

     

    • Cat Scratch Disease

      • Occurs in immunocompetent children and young adult following innoculation with:
        • Bartonella henselae (Gram neg)
      • Pustular papule or erythema at the site days to weeks after scratch/bite.
        • + tender regional lymphadenopathy, takes months to resolve.
      • Diagnosis:
        • Clinically
        • Can do laboratory dx with culture/serology/histoy/PCR.
      • Treatment:
        • Self-limited
        • Some recommend short course of abx (usually azithromycin).

    Human Bites

    • Infections usually polymicrobial
    • Categorized by:
      • Self-inflicted  (thumb sucking, nail biting)
      • Occlusional  (confrontation)
      • Clenched-fist injuries
    • Organisms:
      • S. viridans
      • S. aureus
      • Anaerobes:
        • Eikenella corrodens  (concern b/c resistant to oxacillin, nafcillin, clinda, metronid. and also many cephalosporins)
        • Bacteroides sp.
        • Fusobacterium sp.
        • Peptostreptococci.
    • Prophylaxis
      • All human bite wounds require antimicrobial prophylaxis
      • with amox-clav   (3-5days)
        • Avoid oxacillin, nafcillin, clindamycin, metronid. and many cephalosporins.
      • Clenched-fist injuries (prone to deeper infections of tendons/joints/bones)
        • Xray, consult hand surgeon, and possible hospitalizations. 
      • Often also think about:
        • HIV, Syphilis, HSV, HepB/C
    • Treatment with ampicillin-sulbactam IV, icarcillin-clavulanate, or cefoxitin.
      • Duration based on severity of injury - joints, bones, tendons.

     

    Diabetic Foot Infections

    • Diabetic foot infections common due to neuropathy, impaired vascular supply, immunodeficiency of diabetes.
      • Typically come after trauma.
    • Categorized as:
      • Mild
        • Caused by staph and strep.
        • Symtoms: purulence or inflammation (pain, tenderness, warmth, erythema, induration)
        • Cellulitis ≤2cm around the ulcer (no deep involvement)
        • NO systemic findings
      • Moderate
        • Cellulitis >2cm around the ulcer, gangrene, lymphangitic spread, deep tissue abscess, deep tissue spread (muscle, tendon, bone)
      • Severe
        • Limb threatening
        • Systemic toxicity (fever, tachycardia, hypotension, renal insufficiency, mental status, leukocytosis).
        • Polymicrobial: strep, staph, enteric gram negatives, pseudomonas, anaerobes.
    • Physical Exam:
      • RULE OUT:
        • Arterial insufficiency
        • Osteomyelitis
          • Bone changes related to neuropathy and charcot changes can mimic osteomyelitis.
    • Imaging (R/O Osteomyelitis):
      • Xrays are insensitive for osteomyelitis (sens 0.54), can show underlying gas or foreign bodies.
      • MRI is much better for osteomyelitis and abscesses.
      • IF cannot do MRI, can do bone scan.
    • Labs:
      • Evaluate for systemic toxicity
      • Can get cultures from aspiration or deep tissue cultures from surgery.
        • Do not swab (misleading, AVOID)
    • Treatment:
      • NOT ALL ULCERS ARE INFECTED
        • Some don't have purulence, inflammation.
        • Do not need antibiotics.
      • Mild + Moderate:
        • Abx - aerobic staph and strep coverage. 
      • Severe Limb Threatening
        • Surgical Evaluation
          • + cultures
        • Initial broad spectrum abx. 
      • Rule out Osteomylitis:
        • Challenging: bone changes related to neuropathy and charcot changes (repeated trauma) mimic OM.
        • Typically requires MRI (occult) or bone scan.
        • OM becomes apparent over time as wound drainage recurs after healing or ulcer closure.
        • ESR and CRP  - insufficient evidence.
        • High likelihood if can touch bone through ulcer with hard object.
          • NOTE: Probe to bone test (ADA, Diabetes Care, 2007): PPV 0.57, and NPV 0.98 (low positive predictive valuve, but good for ruling out).
      • Duration of therapy:
        • No Osteomyelitis: 7-10days.
        • If Osteomyelitis: 6 weeks.
      • Wound care (clensing, debridement, offloading foot pressure).. essential!
        • Involve podiatrists and wound care specialists.
      • Rule out arterial insufficiency
        • Ankle-Brachial Index!
        • Revascularization may help.
      • Other therapies lacking evidence:
        • Hyperbaric oxygen, maggots, vacuum assisted dressing.

    Why Cellulitis Not Resolving?

    • Consider:
      • Not right drug for bug.
      • Drug does not get to bug
      • Complication (Abscess etc..)
      • Wrong diagnosis (Stasis dermatitis)
      • Impatient MD
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