Etiopathogenesis and risk factors

of SSI
Meor Muhammad Muslih bin Meor
Hamdan
012016090880
 Content
Etiopathogenesis of SSI
Common organisms responsible for SSI
pathogenesis
Risk factors associated with SSI
 Important definitions
The existence of bacteria in the wound bed can
be divided into 3 categories
Colonization of bacteria
Bacteria is present in wound, replicating and adhere to
wound surface
No signs or symptoms of systemic inflammation
Less than 10^5 CFU/mL
Contamination
Transient exposure of a wound to bacteria
Microorganism enters but cannot replicate.
Rapidly cleared by immune system
Infection
 More definitions
Infection
Local signs of inflammation which may eventually
become systemic
Unusually, without inflammation
Replicating bacteria presence + host response >
delay in healing
Bacterial counts >10^5 CFU/mL
 Common Organisms
Streptococci
Staphylococci
Clostridium
Aerobic G- Bacilli
 Common Organisms
Streptococci
Species involved
S. Pyogenes
E. Faecalis
S. Epidermidis
Most of them are sensitive to penicillin and
erythromycin.
Cephalosporin is an alternative in the case of allergy
Staphylococci
Clostridium
Aerobic G- Bacilli
 S. Pyogenes
Group A beta hemolytic
Colonizes the pharynx in 5-10%
Respiratory droplet transmission
Virulence caused by streptolysin O and S, streptokinase and
streptodornase
In the context of SSI it can cause:
Erysipelas
Cellulitis
Necrotizing fasciitis
Sepsis
Complications
Glomerulonephritis
Rheumatic fever
 E. Faecalis
Normal intestinal flora, most frequent species isolated from
human intestine samples (80-90%)
Transmission: nosocomial and person to person
Most strain is susceptible to penicillin but resistance are
increasing.
Enterococci have both an intrinsic and acquired resistance
to antibiotics making them a good nosocomial pathogens.
Combination of: Ampicillin + aminoglycoside
Other than wound infection, it can cause:
UTI (urinary catheterisation)
Bacteremia (wound, intraabdominal foci)
Endocarditis
 Common Organisms
Streptococci
Staphylococci
S. Aureus is the most important in this group
Clostridium
Aerobic G- Bacilli
 S. Aureus
Found in nasopharynx in 15% of the population
S. Aureus infections are usually localized and suppurative
(cutaneous abscess). Other presentation includes:
Cellulitis
Osteomyelitis
Septic arthritis
Toxic shock syndrome (TSST-1 Toxin)
Scalded skin syndrome (exfoliatin)
Food poisoning (enterotoxin)
Antibiotic resistance is a problem. MRSA
Handling MRSA outbreak carrier identification, search and destroy,
denial of entry
Most S. Aureus are beta lactamase producer.
However, most strains are still sensitive to flucloxacilin, vancomycin
 Abscess
Features of inflammation
Usually follow a puncture or surgical incision or
bacteremia (so called metastatic)
Content : pus (dead and dying white blood cells, cell
debris, toxins)
Abscess is surrounded by acute inflammatory response
= edema and fibrinous exudate
Granulation tissue later forms around it, if it is not
drained, the abscess may become chronic.
If it is partly sterilized by antibiotic, becomes antibioma
 Clostridium
G+ obligate anaerob, spore producing
C. Perfringens causes gas gangrene (clostridial myonecrosis)
combat injuries of soldiers in the 20th century, because of
nonsterile field surgery
C. Tetani causes tetanus
Tetanus toxoid especially in burns, rusty nails
C. Dificile causes pseudomembranous colitis
Hospital Acquired Infection (HAI)
Especially in excessive usage of antibiotics
Bloody diarrhea
Colitis maybe so severe that it perforates > emergency
colectomy
Photograph before right leg amputation(hemipelvectomy) of a
patient with gas gangrene. The right thigh is edematous and
discoloured with necrotic bullae. Crepitation is detected on
deep palpation. At this juncture, the patient is in shock.
 Aerobic Gram-ve Bacilli
E. Coli, Klebsiella spp.,
Normal inhabitants of large bowel > SSI after bowel
operation (appendicitis, diverticulitis, peritonitis)
Pseudomonas spp.
A hospital acquired infection
Tends to colonize burns, wounds and tracheostomy wound
Opportunistic infection, causes infection in susceptible
people
Treatment usually needed only in cases where there is
progressive infection or systemic signs
Antibiotic resistance (ESBL enzyme) is a problem but most
strain is susceptible to carbapenems and aminoglycoside
 Pathogenesis

Bacterial
dose

Impaired
host Virulence
resistance
 Personal Risk Factors for SSI
Diabetes = poor circulation, neuropathy, immune system deficiency
Patient with hyperglycemia 48 hours within surgery = 3x more likely to
have SSI
Obesity = immune deficiency, more likely to develop ulcers
Malnutrition low preoperative serum albumin
Nicotine use delays wound healing
Steroid use (controversial) immunosuppresion
Colonization of skin or nose with S. Aureus mupirocin studies
Poor vasculature and blood supply (PVD)
Ascites
Extremes of age
Postoperative anemia
 Technical Risk Factors for SSI
Prolonged hospital stay : 1 day=6% > 21 days 15%
Preoperative shave : Depilatory=0.6% > Shaving within
24hours =5.6%
Length of operation : more contamination, more tissue
damage, more suture
Inadequate prophylaxis
Usage of foreign material
Open vs laparoscopy
Hypothermia
Poor surgical asepsis technique
Inadequate skin antisepsis
Inadequate ventilation
 Surgical site infections: reanalysis of
risk factors
Analysis documented that diabetes (insulin- and
non-insulin-dependent), low postoperative
hematocrit, weight loss (within 6 months), and
ascites were significantly associated with
increased SSI.
Tobacco use, steroid use, and chronic obstructive
pulmonary disease (COPD) were not predictors
for SSI.
J Surg Res. 2002 Mar;103(1):89-95. Surgical site
infections: reanalysis of risk factors. Malone DL,
Genuit T, Tracy JK, Gannon C, Napolitano LM.
 References
Williams, N.S., Bulstrode, C.J.K. and OConnell, R.P.
(2013) Bailey and Loves Short Practice of Surgery.
26th edn. Boca Raton: Hodder Education.
Wound Bed Preparation: The Science Behind the Removal
of Barriers to Healing
http://www.medscape.com/viewarticle/459733_8
Wounds. 2003;15(7)
Surgical site infections: reanalysis of risk factors.
Malone DL1, Genuit T, Tracy JK, Gannon C,
Napolitano LM. J Surg Res. 2002 Mar;103(1):89-95.
https://www.ncbi.nlm.nih.gov/pubmed/11855922
 Thank you!

Think outside the wound to stop surgical site

infections