Skin & Soft Tissue

Introduction

• 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.
      •  
    • 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.
      • 
  • 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: WBC, ESR, CRP, Serum 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

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