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

2. 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

3. classification Complicated ( gram + & gram -)
Simple uncomplicated (mostly Gram +)
cellulitis
Folliculitis
impetigo
erysipelas
simple abscess
furuncles (boils)
carbuncles
Complicated ( gram + & gram -)
decubitus ulcers
necrotizing fasciitis
pyomyositis
gas gangrene

4. Causative pathogens Staphylococcus 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)

5. 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

6. Predisposing factors Breach in the epidermis Dry and irritated skin
Immunocompromised status - Malnutrition, hypoproteinemia, burns, diabetes mellitus, AIDS
Chronic venous insufficiency
Chronic lymphatic insufficiency
Chronic neuropathy

7. 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

8. Cont. Bicarbonate level Creatine phosphokinase level
C-reactive protein level
Additional investigations may be indicated, depending on the severity of systemic toxicity.

9. 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.

10. 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

11. Post-Surgical Risk Factors
Saphenous venectomy
Axillary node dissection for breast cancer
Pelvic lymphadenectomy for malignancy in conjunction with radiotherapy.
Liposuction

12. Fate;
Resolution
Localization abscess formation
Sloughing of overlying skin
Spread
Recurrent attacks lymphatic destruction

13. 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

14. 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

16. 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.

17. Fate;
Resolution
Rupture
Spread
Chronic abscess formation

18. Treatment Rest Pre-suppurative stage Suppurative stage
Elevation
Warm packs
NSAIDs
Antibiotics
Suppurative stage
Incision & Drainage under G.A using Hilton’s method

19. What are the abscess that we do not wait for fluctuation?
Hand infection
Pulp space
Palm space
Tenosynovitis
Parotid abscess
Breast abscess
Buttock abscess
Peri-anal abscess
Peri-nephric abscess

20. Furunculosis (Boils) Etiology
Infection of hair follicle that results in pustule formation
Generally the result of a staph. Aureus infection

21. Signs and Symptoms Management
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

22. 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

24. Folliculitis Etiology Inflammation of hair follicle
Caused by non-infectious or infectious agents
Moist warm environment and mechanical occlusion contribute to condition
Psuedofolliculitis (PFB)

26. Signs and Symptoms Management
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

27. 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

29. 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

31. 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

33. 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

34. Thank you