1. Soft tissue infections Guidlines for manegment of SSTIs
Walid Elshazly
Prof of surgery

2. Disclaimer
This presentation is based on a zero-fees contract with GSK; I did not receive any honoraria.

3. Community-Acquired Infections
SKIN AND SOFT TISSUE INFECTIONS
BREAST ABSCESS
PERIRECTAL ABSCESS
GAS GANGRENE
TETANUS
HAND INFECTIONS
FOOT INFECTIONS
BILIARY TRACT INFECTIONS
ACUTE PERITONITIS
VIRAL INFECTIONS

4. Hospital-Acquired Infections
PULMONARY INFECTIONS
UTI
WOUND INFECTIONS
INTRAABDOMINAL INFECTION
EMPYEMA
FOREIGN BODY-ASSOCIATED INFECTION
FUNGAL INFECTIONS
MULTIPLE ORGAN FAILURE

5. Skin and Soft Tissue Infection
Surgical site infections
Superficial infections
Impetigo
Erysipelas
Folliculitis
Furuncles and carbuncles
Hairadenitis supportiva
Superficial cellulites
Bites (animal or human)
Deep infections
Deep cellulites necrotizing form
Necrotizing fasciitis
Myo-necrosis
Gas gangrene
Streptococcal Toxic-Shock Syndrome

6. History
Soft tissue infections were first defined slightly more than a century ago. In 1883, Fournier described a gangrenous infection of the scrotum that continues to be associated with his name.
In 1924, Meleney documented the pathogenic role of streptococci in soft tissue infection.
Shortly thereafter, Brewer and Meleney described progressive polymicrobial postoperative infection of the muscular fascia with necrosis (the term necrotizing fasciitis was not introduced until the 1950’s).
The association between toxic-shock syndrome and streptococcal soft tissue infection was delineated as this disease reemerged in the 1980s.

7. Pathogenesis

8. Necrotizing Fascitis
Contact Dermatitis
Cellulitis
Erysipelas
Erythema Multiforme
Ecthyma
Deep Vein Thrombosis
Folliculitis
Impetigo

9. Definitions and Etiologies
Group of diseases that involve the skin and underlying subcutaneous tissue, fascia, or muscle. May be localized to a small area or may involve a large portion of the body.
May affect any part of the body, though the lower extremities, the perineum, and the abdominal wall are the most common sites of involvement.
Some are relatively harmless if treated promptly and adequately; others can be life-threatening even when appropriately treated.

10. Definitions and Etiologies
Symptoms and signs of SSIs
Pain (localized tendernes)  loss of sensation
erythema, edema / induration
Blisters, crusted plaques
(Epi)dermal erosion and necrosis
Fluctuation, crepitus
Systemic signs of SIRS/Sepsis:
fever, tachycardia, hypotension, organ dysfuction

11. Definitions and Etiologies
Simple vs. complex
Primary vs. secondary vs. tertiary
Cellulitis vs. abscess
Superficial vs. deep
Necrotizing vs. non-necrotizing
Traumatic vs. non-traumatic
Dermatitis, fasciitis, myositis ( combinations)
Single vs. multiple pathogens
Classic syndromes:
Rapidly progressive infections
toxic shock syndromes
Specific etiologies or pathogens

12. Definitions and Etiologies
Non-traumatic - “Spontaneous”
Glandular infection (folliculitis, furuncle, carbuncle, hidradenitis, perianal-, perineal-, …)
Micro-trauma (cuts, insect bites, …)
Trauma (wounds - including surgical)
Clean Wounds: An uninfected operative wound in which no inflammation is encountered and the respiratory, alimentary, genital, or uninfected urinary tracts are not entered.
Clean-Contaminated Wounds: Operative wounds in which the respiratory, alimentary, genital, or urinary tracts are entered under controlled conditions and without unusual contamination.
Contaminated Wounds: Includes open, fresh, accidental wounds. In addition, operations with major breaks in sterile technique (e.g., open cardiac massage) or gross spillage from the gastrointestinal tract, and incisions in which acute, non-purulent inflammation is encountered are included in this category.
Dirty or Infected Wounds: Includes old traumatic wounds with retained or devitalized tissue and those that involve existing clinical infection or perforated viscera.

13. Classification of Wounds
Clean
Gram- Positive
OR, Team, Pt skin 3%
Hernia, Thyroid, O/H
Clean- Contaminated
Poly- Microbial
Endogen- colonization
5%-15%
Gastrectomy, CBD, ele.colon
Contaminated
Gross colonization
15%-40%
Spill in GI, perf. PUD
Dirty
Established inf.
40%
Abd.Abscess, dead bowel

14. Surgical Site Infections
Factors that Increase Incidence of SSI
LOCAL Wound Hematoma 2.Necrosis Foreign Body Obesity
SYSTEMIC Age Shock
3.DM Malnutrition, Alcoholism 5.Immunotherapy Steroids Chemotherapy
Hb increases virulence coz ferritin up bac virulence. Ischemia,acidosis,low O2

15. Surgical Site Infections
SSI Prevention
Debridement, Irrigation, Bleeding control, Dirt and FB removal.
Preserve Oxygenation and Perfusion
Classification system of Wounds
Surgical Asepsis
Perioperative Antibiotics

16. Surgical Site Infections Surgical Asepsis
Clean wound infection is the Indicator of overall Sterile Technique in OR
Limit preoperative Hospitalization
Cleansing
Hair removal
OR time
Hemostasis, but beware of many sutures
Drains. Closed-suction, separate stab
Personnel, Respiration, Attire, Scrubbing, Gowns

17. Surgical Site Infections Perioperative Antibiotics- Prophylactic
Prophylactic antibiotics should exist at time of contamination. Clean- contaminated and Contaminated showed reduction
In clean only when Foreign Body is inserted
Preoperative, close to cutting time, long half- life, selected against specific pathogens, 4-6 hours later, and for 2 postoperative doses
Colon surgery: Oral antibiotics, poorly absorbed; neomycin- erythromycin along with mechanical preparation, and IV systemic
Dirty: fascial closure, wet-to-dry dressing and delayed primary closure in 4-5 days

18. Impetigo

19. Superficial infections
Impetigo
highly contagious, confined to the epidermis
usually face or extremities.
most common in infants and preschool children
dominant pathogen is S. aureus, less common S. pyogenes
skin lesions usually resolve spontaneously within 2 to 3 weeks.
antibiotic therapy accelerates the resolution

20. Erysipelas

21. Superficial infections
Erysipelas
principally involves the dermis. infection extends through the dermal lymphatic vessels
tender, pruritic, intensely erythematous, hyperthermic, sharply demarcated, and raised plaque
most cases preceded by influenza like symptoms pain (local, myalgia) , often high fever, and leukocytosis.
lymphangitis and -adenopathy sometimes present
lower leg most common site, followed by face, arms, and upper thighs.
almost invariably caused by S. pyogenes

22. Superficial infections
Erysipelas
antibiotic treatment
uncomplicated erysipelas: penicillin, cephs, amoxicillin are effective in at least 80% of cases. Oral and intravenous antibiotic regimens are equally efficacious.
patients with erysipelas of the lower extremity should be placed on bed rest, and the involved leg should be elevated
once the patient is able to resume normal activities, he or she should be fitted with elastic stockings, to help reduce the recurrence of edema and lower the risk of lymphedema.
For patients with tinea pedis, a topical antifungal agent is used to treat the infection and prevent recurrence.

23. Folliculitis

24. Superficial infections
Folliculitis
infection of the hair follicle
painful, tender, erythematous papule with a central pustule single or multiple lesions in the skin of any hair-bearing area
typically caused by S. aureus. most resolve spontaneously within 7 to 10 days.
topical therapy: clindamycin, erythromycin, or mupirocin ointments chlorhexidine or benzoyl peroxide + warm soaks may accelerate resolution
with refractory or disseminated follicular infections: oral antibiotics S. aureus: dicloxacillin, erythromycin, cephalexin, cefadroxil, or clindamycin
Gram neg: oral ciprofloxacin; more aggressive therapy with systemic symptoms of sepsis

25. Carbuncle
Furuncle, or boil

26. Superficial infections
Furuncle, or boil: small abscess
firm, tender, erythematous nodule
occurs in skin areas exposed to friction ( inner thighs and the axilla). also face, neck, upper back, and buttocks.
Initial treatment:
warm compresses to help promote drainage
oral antimicrobial agent effective against S. aureus
incision-and-drainage necessary when lesions do not drain spontaneously. Failure to drain these lesions adequately may result in recurrence, as well as in progression to a more serious infection.

27. Superficial infections
Carbuncle: deep cutaneous infection involving multiple hair follicles
characterized by destruction of fibrous tissue septa and formation of a series of interconnected abscesses. Patients commonly present with relatively large skin lesions (confluence) associated with chronic drainage, sinus tracts, and scarring
typically painful, red, tender, indurated area of skin with multiple sinus tracts.
Systemic manifestations (e.g., fever and malaise) are common.
occurs most frequently on nape of the neck, upper part of the back, or the posterior thigh.
Therapy:
incision-and-drainage w. thorough search for loculated areas should be undertaken
Wide local excision of the involved skin and subcutaneous fat is often necessary to prevent recurrent disease.
oral antistaphylococcal agent

28. Cellulites

29. Superficial infections
Cellulites
acute bacterial infection of the dermis and subcutaneous tissues
primarily lower extremities - can affect all other areas
Non-necrotizing Form = overwhelming majority
typically pain, soft tissue erythema, and constitutional symptoms (e.g., fever, chills, or malaise)
erythema with advancing borders, skin warmth, tenderness, edema. +/-Lymphangitis or -adenitis
usually single aerobic pathogen mostly S. pyogenes and S. aureus

30. Superficial infections
Cellulitis
Therapy: empirical antibiotic regimen attempts to isolate pathogen are usually unsuccessful;
needle aspiration / skin biopsy at advancing margin positive < 15% / 40%
bacteremia is uncommon: blood cultures positive < 2% to 4% unless Sx of sepsis
In an otherwise healthy adult, uncomplicated cellulitis w/o systemic manifestations: oral antibiotic on an outpatient basis
majority of Strep and Staph are PCNase + cefadroxil ,amox/clav, cephalexin, dicloxacillin, erythromycin, or clindamycin
Diabetic or immunocompromised pts. and w. high fever or rapidly spreading cellulitis / cellulitis refractory to oral Abx (>48 h): admission for I.V. Abx.
Nafcillin, Cefazolin or ampicillin-sulbactam
Clindamycin for suspected MRSA and PCN allergies; Vancomycin, other Abx. and combination regimen

31. Superficial infections
Cellulitis
Necrotizing form: superficial vs. deep
“Superficial” necrotizing cellulitis
similar etiology and pathogenesis to nonnecrotizing cellulitis
Predominantly in PVD, diabetes, pressure ulcer, venostasis, lymphedema or neglected primary cellulitis
more serious and often progressive
pathogens similar + anaerobes clostridia, peptostreptococcus, bacteroides, …
Therapy: broad-spectrum Abx. urgent operative debridement is indicated +/- hyperbaric O2 therapy

32. Deep infections Cellulitis Necrotizing form:
Deep necrotizing cellulitis: (Necrotizing dermatitis, fasciitis, myositis)
extension of superficial infection or
primary deep space infection
crush / penetration / neglect / hematogenous
does not have to have skin necrosis
often lack of specific early signs & Sx, delayed diagnosis
most are polymicrobial
early: localized pain, tenderness, mild edema / erythema may be subtle -> cave: systemic illness > local signs
Later: bullae, intense erythema, skin necrosis, crepitus

34. Deep infections Necrotizing form: Deep necrotizing cellulitis:
Necrotizing fasciitis
angiothrombotic microbial invasion and liquefactive necrosis of deep subqutaneous tissues, fascia +/- muscle
Hallmark: dishwater tissue fluid, thrombosis of vessels frank necrosis occurs later initially, tissue invasion proceeds horizontally,
Myo-necrosis
rapidly progressive life-threatening infection
indicates involvement of Clostridium species.
short incubation: severe progressive disease in < 24 h
acute severe pain, often minimal physical findings
systemic signs of toxicity/ sepsis

35. Deep infections Necrotizing form: Deep necrotizing cellulitis:
Therapy:
broad-spectrum Abx to include MRSA, Gr.Neg and Clostridia bacteriocidal agents!
when clostridia suspected or confirmed, penicillin G, 2 to 4 million U every 4 hours immediately; clindamycin, 900 mg every 8 hours, should be added.
hyperbaric O2 therapy
operative debridement.

36. Deep infections
Gas gangrene : is a bacterial infection that produces gas tissues in gangrene. It is a deadly form of gangrene usually caused by anaerobic bacteria. It is a medical emergency.

37. Streptococcal Toxic-Shock Syndrome
hemolytic streptococci of group A (S. Pyogenes)
more than 60% of patients with STSS have bacteremia.
current incidence 1.5 per 100,000 - STSS 10% to 15%, necrotizing fasciitis in 6%.
severe pain is the most common initial symptom sudden onset / generally precedes physical findings –> rapid progression.
hypotension invariably develops within 4 to 8 hours after presentation -> Shock, ,MOF, ARDS
Hemoglobinuria and an elevated serum creatinine, even w. adequate resuscitation

38. Streptococcal Toxic-Shock Syndrome
Clinical treatment failure sometimes w. penicillin alone attributable to the large inoculum size = Eagle effect
Clindamycin
more effective than b-lactam agents it suppresses bacterial toxin synthesis and inhibits M-protein synthesis,
Clindamycin also suppresses synthesis of penicillin-binding proteins, and it can act synergistically with penicillin.

39. Risk of infection 2-Infection agent : -Virulence -Numbers
1-Host :
-Diet – vit.C .
-Extreme age.
-Chronic illness.
-D.M, CLD, CRF
-Medications: Steroid
-Impaired immunity: HIV
3-Battle ground wound :
-Ischemia
-Necrosis
-Gangreneous
-Decrease WBC ,Abs

40. Risk of infection 2-Infection agent : -Virulence -Numbers
1-Host :
-Diet – vit.C .
-Extreme age.
-Chronic illness.
-D.M, CLD, CRF
-Medications: Steroid
-Impaired immunity: HIV
3-Battle ground wound :
-Ischemia
-Necrosis
-Gangreneous
-Decrease WBC ,Abs

41. Risk of infection 2-Infection agent : -Virulence -Numbers
1-Host :
-Diet – vit.C .
-Extreme age.
-Chronic illness.
-D.M, CLD, CRF
-Medications: Steroid
-Impaired immunity: HIV
3-Battle ground wound :
-Ischemia
-Necrosis
-Gangreneous
-Decrease WBC ,Abs

42. Risk of infection 2-Infection agent : -Virulence -Numbers
1-Host :
-Diet – vit.C .
-Extreme age.
-Chronic illness.
-D.M, CLD, CRF
-Medications: Steroid
-Impaired immunity: HIV
3-Battle ground wound :
-Ischemia
-Necrosis
-Gangreneous
-Decrease WBC ,Abs

44. Ceftriaxone (3r generation cephalosporin)
SKIN AND SKIN STRUCTURE INFECTIONS caused by Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogeneus, Viridans group streptococci, Escherichia coli, Enterobacter cloacae, Klebsiella oxytoca, Klebsiella pneumoniae, Proteus mirabilis, Morganella morganii,* Pseudomonas aeruginosa, Serratia marcescens, Acinetobacter calcoaceticus, Bacteroides fragilis* or Peptostreptococcus species.
BACTERIAL SEPTICEMIA caused by Staphylococcus aureus, Streptococcus pneumoniae, Escherichia coli, Haemophilus influenzae or Klebsiella pneumoniae.

45. Ceftriaxone (3r generation cephalosporin)
SURGICAL PROPHYLAXIS: The preoperative administration of a single 1 gm dose of ceftroiaxone may reduce the incidence of postoperative infections in patients undergoing surgical procedures classified as
contaminated or
potentially contaminated

46. Thank you