Skin and Soft Tissue Infections (SSTIs)Dr.Hisham Ahmed,M.D,MRCS.EngAsst.Professor of General & Pediatric Surgery

Background

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.

Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection

classification Simple uncomplicated (mostly Gram +)

cellulitis Folliculitis impetigo erysipelas simple abscess furuncles (boils) carbuncles

• Complicated ( gram + & gram -) decubitus ulcers necrotizing fasciitis pyomyositis gas gangrene

Causative pathogensStaphylococcus aureus (the most common pathogen)

Streptococcus pyogenes

Site-specific infections - Indigenous organisms (e.g., gram-negative bacilli in perianal abscess)

Immunocompromised hosts and complicated SSTIs - Multiple organisms or uncommon organisms (e.g., Pseudomonas aeruginosa, beta-hemolytic streptococci, Enterococcus)

Cont.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)

Monomicrobial necrotizing fasciitis: S pyogenes

Predisposing factorsBreach in the epidermisDry and irritated skinImmunocompromised status - Malnutrition,

hypoproteinemia, burns, diabetes mellitus, AIDSChronic venous insufficiencyChronic lymphatic insufficiencyChronic neuropathy

Laboratory tests 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

Complete blood count (CBC) with differential

Creatinine level

Cont. Bicarbonate level

Creatine phosphokinase level

C-reactive protein level

Additional investigations may be indicated, depending on the severity of systemic toxicity.

Cellulitis Acute diffuse non-suppurative inflammation affecting epidermis

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.

Risk Factors for Cellulitis

Obesity Edema

◦ Venous insufficiency ◦ Lymphatic obstruction

Fissured toe webs ◦ Maceration◦ Fungal infection

Inflammatory dermatoses – eczema Repeated cellulitis Subcutaneous injection Previous cutaneous damage

All lead to breaches in the skin for organism invasion

Post-Surgical Risk Factors

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

Treatment ; 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

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 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.

Painful compressible mass that is red, warm to touch, and tender.

Fate;Resolution Rupture Spread Chronic abscess formation

Treatment

Pre-suppurative stage Rest Elevation Warm packs NSAIDs

Antibiotics • Suppurative stage Incision & Drainage under G.A using Hilton’s

method

What are the abscess that we do not wait for fluctuation? Hand infection Pulp space Palm space Tenosynovitis

Parotid abscessBreast abscessButtock abscessPeri-anal abscessPeri-nephric abscess

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 non-infectious 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

Streptococcus pyogenes (Group A Strep)

Tissue digesting enzymes◦Hyaluronidase◦Streptokinase◦Streptolysins

Rapidly spreading cellulitis may lead to loss of limb

Necrotizing Fasciitis“Flesh Eating Strep”

Necrotizing Fasciitis• Disease starts as localized

infection• Pain in area, flu-like symptomsInvasive and spreadingMay lead to toxic shock (drop in

blood pressure)Incidence 1-20/100,00030-70% mortalitySurgical 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

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