Soft tissue infections

Introduction

• Must differentiate purulent vs. non-purulent
• Erysipelas – Superficial skin infection involving upper dermis with clear demarcation between involved and uninvolved skin with prominent lymphatic involvement
• Folliculitis – Superficial hair follicle infection without involvement of deeper tissues
• Furuncles – Single, deep nodules involving hair follicles that are often suppurative
• Carbuncles – Multiple interconnecting furuncles that drain through several openings

Cellulitis

• General risk factors
  • Lymphoedema
  • Skin breakdown
  • Venous insufficiency
  • Leg oedema
  • Obesity
  • Neutropaenia
  • Immunocompromise
  • Hypogammaglobulinaemia
  • Chronic renal disease
  • Cirrhosis

Cellulitis

• Erysipelas more common in young and elderly. Cellulitis in between
• 10% hospitalised; majority of these over 65yo
• 80% due to Gram-positive bacteria
• MRSA/MSSA more likely if purulent
• Beta-haemolytic strep more likely if non-purulent
• Erysipelas usually beta-haemolytic strep
• Bullous erysipelas may represent synergistic infection of staph aureus and beta-haemolytic strep
• Chronic changes from recurrent cellulitis lead to impaired lymphatic drainage, permanent swelling, dermal fibrosis and epidermal thickening known as elephantiasis nostra with increased risk of further attacks

Erysipelas

• Also get peau d’orange dimpling
• Classic malar butterfly distribution
• Entire ear involvement = Milian ear sign (ear does not contain deeper tissues)
• Desquamates on resolution

Treatment

• Elevation, I&D of any abscess, antibiotics and management of predisposing conditions
• Treat skin dryness with topical emollients
• Refer for management of lymphoedema and chronic venous insufficiency
• Treat for MRSA if high-risk
  • Purulent soft tissue infection
  • Antibiotic use in past month
  • Failed MSSA therapy
  • Previous MRSA colonisation or infection
  • Preceding spider bite
  • High-prevalence in community
  • Prisoner/high-care nursing facility in past year/soldiers/daycare/boarding schools
  • Contact sports
  • Haemodialysis
  • IVDU
  • MSM

Causative organisms

• MRSA
• Beta-haemolytic strep: Nonpurulent
• Gram-negative: Elderly, diabetic foot infection, fish bone injuries
• Aeromonas: Fresh water, contact with wet soil
• Vibrio: Salt water, fish bone, cirrhosis
• Pseudomonas: Neutropaenia, IVDU, hot tub exposure
• Anaerobes/Clostridia: Bite wounds, DM, necrotising infections, gas in tissues
• Polymicrobial: Diabetic foot, bite wounds
• Pasteurella: Dog, cat bites
• Capnocytophaga: Dog/cat bites
• Mycobacterium marinum: Fish tank exposure
• S. pneumoniae and H. influenzae: Non-immunised

Differential diagnosis

• Necrotising soft tissue infections: Rapid progression, triad of severe pain, swelling and fever, pain out of proportion, severe toxic, haemorrhagic or bluish bullae, gas or crepitus in tissues, skin necrosis, extensive necrosis/ecchymosis
• Bursitis
• Contact dermatitis: Pruritis vs. pain, no fever, non-toxic appearance
• Cutaneous abscess
• DVT: Usually not febrile
• Gouty arthritis
• Herpes zoster
• Insect stings: Pain worse at onset
• Osteomyelitis: Deeper involvement, comorbidities
• Superficial thrombophlebitis: Usually afebrile
• Toxic shock syndrome: Hypotension, MODS, severe toxicity
• Chronic venous insufficiency
• Venous eczema
• Lipodermatosclerosis

Treatment

• Exclusions from cellulitis pathway (PAH)
  • Water-associated, bites, diabetic foot, facial or orbital cellulitis, upper limb, boils, severe obesity and paediatrics
• No systemic signs AND no significant comorbidity (diabetic, immunosuppressed, alcoholic, obesity, chronic venous insufficiency)
  • Dicloxacillin 500mg PO q6h for 7-10 days
  • Clindamycin 450mg PO q8h for 7-10 days (if MRSA risk)
• More severe systemic signs, unstable comorbidities (PVD, DM, immunosuppression), limb-threatening infection or necrotising fasciitis
  • Flucloxacillin 2g q6h (q4h if septic)
  • Lincomycin 600mg q8h IV or vancomycin 25-30mg/kg load then 15mg/kg BD if MRSA risk

Treatment (eTG)

• Treat all below with usual cellulitis agents +
• If fresh or brackish water-related
  • Ciprofloxacin 400mg IV q12h or 500mg PO q12h (expert advice) for 14 days
  • Typically Aeromonas patients have malignancy
• Mycobacterium marinum
  • Excise single lesion and clarithromycin 500mg PO for 1-2 months (expert advice)
• If salt or brackish water-related
  • Doxycycline 200mg then 100mg BD usually at least 14 days
  • Add ceftriaxone if severe infection
  • Seek expert advice
  • High risk of complications if cirrhotic or haemochromatosis

Failed cellulitis therapy

• Risk factors
  • Fever
  • Lymphoedema
  • Chronic oedema
  • Chronic leg ulcers
  • Prior cellulitis of same area
  • Cellulitis at a wound site

IV vs. PO antibiotics

• Aboltins et al. 2015
• Randomised control non-inferiority trial single centre
• <5 days cellulitis which ED physician thought needed IV Ab’s due to severity or failure of PO antibiotics
• Oral cephalexin 1g QID for 10 days vs. Cefazolin 2g BD until no longer progressing and afebrile then switched to oral for total 10 days
• Primary outcome: Time to no further progression
• 47 patients
• Oral non-inferior to IV
• No difference in complications

IV vs. PO antibiotics

• There are 3 other RCT’s, none of which show superiority of IV over PO
• All small
• Cochrane meta-analysis showed PO therapy superior to IV therapy (RR 0.85) Killburn 2010
• Potential harms of IV
  • Increased risk of antibiotic-associated diarrhea
  • Phlebitis
  • Thrombosis
  • Extravasation
  • Bacteraemia
  • Expensive

Cutaneous abscess

• Risk factors
  • Any breach in skin
  • Close contact to persons with skin abscesses
  • Insect bites
  • IVDU
  • DM
  • Immunosuppression

Cutaneous abscesses

• Management
  • Extremely large or deep collections should be drained in OT
  • Palms/soles/nasolabial folds also require specialist drainage
  • Small boils – Warm compresses to promote cutaneous drainage
    • Sitz baths for furuncles on buttock/perineum
  • Needle aspiration is inadequate for abscesses caused by staph
  • I&D is required (consider prophylactic Ab if endocarditis risk)
  • Infiltrate skin over abscess then deeper into abscess itself
  • No.11 or 15 scalpel incise over area of greatest fluctuance
  • Break up loculations with haemostat. Can place gauze if desired
  • Apply warm compresses 3 times daily after this and f/u in 2-3 days
  • Antibiotics if significant surrounding cellulitis, systemic toxicity, immunosuppression or multiple lesions

Recurrent staph skin infections

• Staph eradication successful in 50%
• Collect nasal and/or perineal swabs prior to eradication therapy to ensure susceptible to planned regime
• Routine decolonisation of household contacts is not recommended but should be considered if measures below fail to prevent further infections in index case OR if household contacts also have history of recurrent skin infections
• Once all acute lesions have healed can start eradication therapy
• Mupirocin 2% nasal ointment twice daily for 5 days + Chlorhex 2% or triclosan 1% once daily wash for 5 days
• Wash bed linen in hot water initially and then weekly
• Wash towels after each use

Necrotising soft tissue infections

• Deceptively benign early in course but typically pain out of proportion from early phase
• Risk factors: Alcohol, DM, peripheral vascular disease, advanced age, hIV, cancer, heart disease, renal failure, NSAID use, decubitus ulcers, chronic skin infections, IVDU and immunosuppression
• Bacteraemia seen in 30% and strong predictor of mortality
• Poor prognostic factors
  • Age <1 or >60, IVDU, comorbid renal/CCF/cancer, + BC, trunk or perineal involvement, peripheral vascular disease and delayed diagnosis
• Type I – Polymicrobial
  • 55-75% of all necrotising soft tissue infections
  • Gram pos cocci, gram neg bacilli and anaerobes
  • Clostridia uncommon now due to improved sanitation
• Type II (monomicrobial)
  • Mostly GAS. 20-30% of all necrotising soft tissue infections
  • Typically healthy young person in periphery following wound or surgery or Varicella
  • CA-MRSA common organism in IVDU, athletes and institutionalised individuals
• Type III – Vibrio vulnificus
  • Seen in Asia with significant trauma in seawater
• Type IV – Fungal in immunocompromised

Necrotising soft tissue infections

• Pathophysiology
  • Direct spread from skin defect or perforated viscus
  • Bacteria release exotoxins leading to tissue ischaemia, liquefactive necrosis and systemic toxicity
  • Skin involvement occurs through vasculitis and thrombosis of perforating blood vessels
  • Ischaemic environment promotes bacterial growth with spread of infection 1 inch/hr
  • Early on have minimal skin changes as need extensive capillary thrombosis before skin ischaemia arises
  • In polymicrobial infections, bacteria act synergistically as facultative gram-negatives lower oxygen reduction potential of tissue, facilitating anaerobic growth + anaerobic bacteria impede phagocyte function which stimulates aerobic bacterial growth
  • Clostridial alpha-toxin causes tissue necrosis and cardiovascular collapse
  • Antibiotics cannot penetrate infection due to ischaemia thus immediate surgical intervention remains critical to successful cure

• Clinical features
  • Severe pain, anxiety and diaphoresis
  • Pain out of proportion specifically tenderness beyond margin of erythema
  • 10-40% of cases have preceding trauma to area
  • Brawny oedema and crepitus (10-30%)
  • Later signs include bronze/brown discolouration, bullae and malodourous serosanguinous discharge
  • Low-grade fever with tachycardia out of proportion to fever

• Diagnosis
  • Hard signs present in <50% – Crepitus, skin necrosis, bullae, hypotension, gas on X-ray
  • Consult surgery early for debridement
  • X-ray may miss deep gas collections and is not sensitive
  • CT with contrast has 80-97% sensitivity but has false-positive rate of 19%
    • Non-enhancing deep tissues is most reliable (<36% of cases)
  • MRI sensitivity 90-100% but false positive rates up to 40%
  • Bedside USS cannot rule out necrotising soft tissue infection

• Lab factors (LRINEC >= 6 associated with increased risk of nec fasc but misses many cases)
  • CRP >150 (4 lab risk indicator of nec fasc points)
  • WCC >15 (1)
  • WCC >25 (2)
  • Hb <135 (1)
  • Hb <110 (2)
  • Na <135 (2)
  • Creatinine > 160(2)
  • Glucose > 8 (1)
  • K > 5 (associated with extremity infections)
  • Band count >7% (associated with Vibrio)
  • Albumin <20 (associated with Vibrio)
  • Plt <80 (associated with Vibrio)

• Treatment
  • Aggressive fluid resuscitation, transfusions if anaemic (haemolytic), avoid vasoconstrictors if possible
  • Empirical Meropenem 1g IV q8h + Vancomycin 30mg/kg IV load then 15mg/kg BD + Clindamycin 600mg IV q8h (antitoxin effect)
    • Minimum 5 days and cater to micro results
  • Early surgical consultation: Fasciotomy, debridement +- amputation
  • Mortality skyrockets if debridement delayed >24 hours
  • ADT as indicated
  • IVIG and hyperbaric O2 therapy may play a role

Confirmed organism

• Group A strep (S. pyogenes)
  • BenPen 1.8g IV 14h + Clindamycin 600mg IV q8h + IVIG 1-2g/kg IV up to 2 doses in 72 hours
• Clostridial
  • BenPen 2.4g IV q4h

Folliculitis

• Micro
  • Usually S. aureus and nasal carriage is a risk factor
  • Hot tub folliculitis due to Pseudomonas
  • Whirlpool baths at nail salons risk mycobacterial furunculosis
  • Candida if broad-spec ab’s, steroids or immunosuppressed
• Clinical
  • Pseudomonal lesions often >3cm (vs. <5mm for staph)
  • Pseudofolliculitis – Folliculitis barbae is seen in dark skinned individuals following shaving with curling of beard hair into follicle (initially not infected) but can cause deep facial scarring and infection
• Usually on apocrine regions (buttocks, hips, upper chest, back and axilla)

• Treatment
  • Twice daily cleanse with hand soap
  • Stop hottubs
  • Warm compresses multiple times daily if refractory
  • Bacitracin topical antibiotic can be used
  • Avoid shaving
  • If painful or extensive, oral antibiotics (cephalexin, dicloxacillin)
  • For pseudofolliculitis – allow hairs to grow to 2-3mm then use commercially available razor for this condition

Pilonidal abscess

• Staph is most common
• Contamination with enteric organisms is also possible
• Can develop into chronic draining fistulous tract if not surgically treated
• Needs wide excision with removal of excess hair and debris from abscess cavity and healing by secondary intention
• Primary closure heals more quickly but risks recurrence

Infected epidermoid and pilar cysts

• Epidermoid cysts arise from epidermis
• Pilar cysts arise from hair follicles
• Both contain thick keratin and sebum
• True sebaceous cysts from sebaceous glands are very rare
• Once bacterial invasion of cyst occurs, becomes infected
• Simple I&D in ED +- cyst wall removal is key to therapy
• Capsule excision can be performed at follow-up if unable to be grasped in inflammatory environment in ED

Bartholin gland abscess

• If perimenopausal, needs gynae f/u to rule out carcinoma
• Pea-sized glands at 4 and 8 o’clock in labia minora
• Not palpable if not infected
• Polymicrobial vaginal flora, anaerobes, N. gonorrhoea and C. trachomatis (minority)
• Usually fluctuant 2-4cm mass
• Requires operative marsupialisation

Pressure injuries

• Staging
  • Stage 1 – Intact skin with localised area of nonblanchable erythema
  • Stage 2 – Partial thickness loss of skin with exposed dermis. Wound bed is viable, pink, moist with no granulation tissue/slough or eschar
  • Stage 3 – Full-thickness loss of skin with exposed adipose, granulation tissue and epibole (rolled wound edges) often evident. Slough and eschar may be visible
  • Stage 4 – Full-thickness with visible fascia, muscle, tendon, ligament, cartilage or bone. Slough and eschar may be visible.
  • Unstageable – Extent of tissue loss cannot be confirmed as obscured by eschar or slough. Once this is removed, either Stage 3 or 4
  • Stable eschar (i.e. dry, adherent, intact without erythema or fluctuance) on heel or ischaemic limb should not be removed. Otherwise remove and examine
  • Examination after debridement is more effective than US/CT
• General care
  • Treat contributing factors e.g. malnutrition, bed cares
  • Local wound care including debridement (blunt or sharp)
  • Consider negative pressure therapy
  • Control pain
  • Treat infection if apparent

Last Updated on November 4, 2020 by Andrew Crofton