Download Skin and Soft Tissue Infections (SSTIs)

Skin and Soft Tissue Infections (SSTIs)
Dr.Hisham Ahmed,M.D,MRCS.Eng
Asst.Professor of General & Pediatric Surgery
Background
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Skin and soft tissue infections (SSTIs), which include
infections of skin, subcutaneous tissue, fascia, and
muscle, encompass a wide spectrum of clinical
presentations, ranging from simple cellulitis to
rapidly progressive necrotizing fasciitis.
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Diagnosing the exact extent of the disease is critical
for successful management of a patient of soft tissue
infection
classification
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Simple uncomplicated (mostly Gram +)
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cellulitis
Folliculitis
impetigo
erysipelas
simple abscess
furuncles (boils)
carbuncles
• Complicated ( gram + & gram -)
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decubitus ulcers
necrotizing fasciitis
pyomyositis
gas gangrene
Causative pathogens
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Staphylococcus aureus (the most common pathogen)
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Streptococcus pyogenes
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Site-specific infections - Indigenous organisms (e.g.,
gram-negative bacilli in perianal abscess)
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Immunocompromised hosts and complicated SSTIs Multiple organisms or uncommon organisms (e.g.,
Pseudomonas aeruginosa, beta-hemolytic streptococci,
Enterococcus)
Cont.
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Polymicrobial necrotizing fasciitis - Mixed infection
with both aerobes (e.g., streptococci, staphylococci, or
aerobic gram-negative bacilli) and anaerobes (e.g.,
Peptostreptococcus, Bacteroides, or Clostridium)
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Monomicrobial necrotizing fasciitis: S pyogenes
Predisposing factors
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Breach in the epidermis
Dry and irritated skin
Immunocompromised status - Malnutrition,
hypoproteinemia, burns, diabetes mellitus, AIDS
Chronic venous insufficiency
Chronic lymphatic insufficiency
Chronic neuropathy
Laboratory tests
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Patients with uncomplicated SSTIs usually do not require any
investigations and need not be hospitalized. However, patients with
symptoms and signs of systemic toxicity, such as tachycardia and
hypotension, should undergo the following tests:
Blood culture and drug susceptibility
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Complete blood count (CBC) with differential
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Creatinine level
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Cont.
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Bicarbonate level
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Creatine phosphokinase level
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C-reactive protein level
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Additional investigations may be indicated,
depending on the severity of systemic toxicity.
Cellulitis
 Acute diffuse non-suppurative inflammation affecting epidermis
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and dermis
Inflammation with little or no necrosis, edema Lymphatic
involvement
tense ill defined area showing criteria of inflammation.
Lymphangitis & lymphadenitis
Complications: Abscess and osteomyelitis
Streptococcus pyogenes
fibrinolysin & hyaluronidase
enzymes
facilitate spread of infection.
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Obesity
Edema
◦ Venous insufficiency
◦ Lymphatic obstruction
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Fissured toe webs
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Inflammatory dermatoses – eczema
Repeated cellulitis
Subcutaneous injection
Previous cutaneous damage
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All lead to breaches in the skin for organism invasion
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◦ Maceration
◦ Fungal infection
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Saphenous venectomy
Axillary node dissection for breast cancer
Pelvic lymphadenectomy for malignancy
in conjunction with radiotherapy.
Liposuction
Fate;
 Resolution
 Localization
abscess formation
 Sloughing of overlying
skin
 Spread
 Recurrent attacks
lymphatic destruction
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Treatment ;
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Medical in the form of
Antibiotics e.g. ampicillin, Vancomycin and
Clindamycin for resistant cases suspecting MRSA
Leg elevation
Elastic stocking GIII
Weight reduction
Care of the skin esp. web space
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Impetigo Contagiosa & Erysipelas
◦ Etiology
 Caused by A-beta-hemolytic streptococci, S aureus or
combination of these bacteria
 Spread through close contact
 Impetigo occurs most in children
 Erysipelas can also occur in the elderly
◦ Signs and Symptoms
 Mild itching and soreness followed by eruption of small
vesicles and pustules that rupture and crust
 Generally develops in body folds that are subject to
friction
◦ Management
 Cleansing and topical antibacterial agents
 Systemic antibiotics e.g. Ampecillin
abscess
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Abscess is a localized collection of pus, Surrounded by a pyogenic
membrane
Staphylococcus aureus is the causative organism…coagulase
enzyme……localization
The route of infection either, direct, blood or lymphatic spread.
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Painful compressible mass that is red, warm to touch, and tender.
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Fate;
Resolution
 Rupture
 Spread
 Chronic abscess formation
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Treatment
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Pre-suppurative stage
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Rest
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Elevation
Warm packs
NSAIDs
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Antibiotics
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Suppurative stage
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 Incision & Drainage under G.A using Hilton’s method
What are the abscess that we do not wait
for fluctuation?
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Hand infection
Pulp space
Palm space
Tenosynovitis
Parotid abscess
 Breast abscess
 Buttock abscess
 Peri-anal abscess
 Peri-nephric abscess
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Furunculosis (Boils)
Etiology
 Infection of hair
follicle that results
in pustule
formation
 Generally the
result of a staph.
Aureus infection
◦ Signs and Symptoms
 Pustule that becomes reddened and enlarged as well as
hard from internal pressure
 Pain and tenderness increase with pressure
 Most will mature and rupture
◦ Management
 Care involves protection from additional irritation
 Referral to physician for antibiotics
 Keep athlete from contact with other team members
while boil is draining
 Carbuncles
◦ Etiology
 Similar in terms of early stage development as
furuncles
◦ Signs and Symptoms
 Larger and deeper than furuncle and has several
openings in the skin
 May produce fever and elevation of WBC count
 Starts hard and red and over a few days emerges into
a lesion that discharges yellowish pus
◦ Management
 Surgical drainage combined with the administration
of antibiotics
 Warm compress is applied to promote circulation
 Folliculitis
◦ Etiology
 Inflammation of hair
follicle
 Caused by noninfectious or infectious
agents
 Moist warm
environment and
mechanical occlusion
contribute to condition
 Psuedofolliculitis (PFB)
◦ Signs and Symptoms
 Redness around follicle that is followed by development of
papule or pustule at the hair follicle
 Followed by development of crust that sloughs off with the
hair
 Deeper infection may cause scarring and alopecia in that
area
◦ Management
 Management is much like impetigo
 Moist heat is used to increase circulation
 Antibiotics can also be used depending on the condition
Necrotizing Fasciitis
“Flesh Eating Strep”
Streptococcus pyogenes (Group A Strep)
 Tissue digesting enzymes
◦ Hyaluronidase
◦ Streptokinase
◦ Streptolysins
 Rapidly spreading cellulitis may lead
to loss of limb
Necrotizing Fasciitis
Disease starts as localized infection
• Pain in area, flu-like symptoms
 Invasive and spreading
 May lead to toxic shock (drop in blood
pressure)
 Incidence 1-20/100,000
 30-70% mortality
 Surgical removal, antibiotics
•
 Gas
Gangrene
◦ Signs and symptoms
 Blackening of infected muscle and skin
 Presence of gas bubbles
◦ Pathogens and virulence factors
 Caused by several Clostridium species
 Bacterial endospores survive harsh conditions
 Vegetative cells secrete endotoxins
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Gas Gangrene
◦ Pathogenesis and epidemiology
 Traumatic event must introduce endospores into
dead tissue
 Mortality rate exceeds 40%
◦ Diagnosis, treatment, and prevention
 Appearance is usually diagnostic
 Rapid treatment is crucial
 Surgical removal of dead tissue
 Administration of antitoxin and penicillin
 Prevent with proper cleaning of wounds
Thank you