1. Introduction to
Surgical Site Infections
Dr.Sujith Mathew Jose
PG in General Surgery
Coimbatore Medical College
Coimbatore
2. History
First concept of infection and methods
to prevent it can be traced back to
Egyptians by there mummification skills
HIPPOCRATES, The Father of
Medicine used Wine and vinegar to
irrigate open infected wound
3. Galen recognised locatisation of
infection (=suppuration ) in
gladiatorial wound
Ambroise Pare observed clean
wounds closed primarily heal
without infection
4. Austrian obstetrician Ignac
Semmelweis showed that
SIMPLE ACT OF HAND
WASHING between cases
decreased puerperal sepsis
Sir Joseph Lister, applied
Louis Pasteur’s idea of
microbiology to promote the
idea of antiseptic surgery
5. Koch’s Postulates
An infective Organism
• Must be found in considerable
number in septic focus
• Must be cultured in pure form
from septic focus
• Must be able to produce similar
lesions when injected into
another host
6. Wound infection depends on
• Host Response
• Virulence of the agent
• Vascularity and health of tissue involved
• Presence of dead or foreign tissue
• Use of antibiotics
7. Intact epithelial surface prevents
the entry of microorganisms
SKIN IS THE BEST BARRIER
TO ENTRY OF PATHOGEN
These are broken down in
Trauma
Surgery
Other protective mechanisms are
Chemical- low gastric pH
Humoral - antibodies, compliments
Cellular - phagocytes and macrophages
8. What is SSI?
Infections that occur
in the wound
created by an
invasive surgical
procedure are
generally referred to
as surgical site
infections
10. SSI is MOST COMMON hospital acquired infection in surgical
patients.
3rd most common hospital acquired infection.
Preventable
Prolong the hospital stay (7.3 days)
Expenditure
Over one-third of postoperative deaths
Poor scar, persistent pain and itching, restriction of movement
and a significant impact on emotional wellbeing
11. • SSIs are associated with considerable
morbidity and it has been reported that
over one-third of postoperative deaths are
related to SSI
12.
13. During perioperative period,
When the enteral feeding is suspended
Bacterial (mainly gram negative bacteria)
colonise normal sterile upper GIT
Then they translocate to mesentric
lymphnodes and release endotoxins
14. These endotoxins are lipopolysaccharides in bacterial cell wall
They activate macrophages to release proinflammatory
cytokines
Cytokines finally leads to MODS and SIRS
15. The wound healing process
• The ‘normal’ wound healing process has
been identified as involving three
overlapping major phases:
– Inflammation, early (first 24 hours) and late
phases (normally up to 72 hours)
– Regeneration
– Maturation.
16. • The key cells that are involved in this
process have been identified as:
– inflammation – platelets, neutrophils,
lymphocytes and macrophages
– regeneration and maturation – macrophages and
fibroblasts, the latter of which are linked with the
deposition and regulation of collagen as well as
wound contraction (myofibroblasts).
17. Microbiology of SSI
• Nature of the
Procedure
• Location of the
incision
• Whether hollow
viscus entered
GRAM POSITIVES
Staph Epidermidis
Staph Aureus
Enterococcus Species
GRAM NEGATIVES
E Coli
Klebsella
PHARYNX
LOWER GIT
FEMALE
GENITAL TRACT
ANAEROBES
18. After a breach in the epithelial surface,
Acute inflammatory response take up to 4
HOURS to get mobilised
DECISIVE PERIOD
Prophylactic antibiotics should cover this
period