2. Surgical site infection
Infection related to operative procedure that occurs at or near the surgical
incision within 30 days of the procedure or within 90 days if prosthetic
material is implanted at surgery.
Types of Surgical site infections (SSIs):
Superficial incisional
Deep incisional
Organ or body space
SSIs constitute 38% of all the nosocomial infections
Ref: CDC’s NNIS
3. Time to event Extent of tissue
involvement
Clinical features Criteria for diagnosis
Superficial incisional
SSI
Within 30 days of
procedure
Skin and subcutaneous
tissue
Peri-incisional 1. pain
or tenderness
2. Swelling
3. Erythema or heat
At least one clinical
feature AND at least
one of the following
1. Purulent drainage
from the superficial
incision
2. Organisms are
identified by culture
performed for clinical
diagnosis or treatment
3. Incision opened by
the surgeon because of
concern of superficial
SSI
4. Time to event Extent of tissue
involvement
Clinical features Criteria for diagnosis
Deep incisional SSI Within 30 or 90 days
of procedure
Deep soft tissue of the
incision such as the
fascia and muscle
layers
1. Fever (>38℃)
2. Localized pain or
tenderness
At least one clinical
feature AND at least
one of the following
1. Purulent drainage
2. Deep incision that
spontaneously dehisces
or is opened by the
surgeon because of the
concern of deep SSI
3. Organisms identified
by culture
5. Time to event Extent of tissue
involvement
Clinical features Criteria for diagnosis
Organ/space SSI Within 30 or 90 days of
procedure
Any part of the body
deeper than the
fascia/muscle layer that
was opened or
manipulated during the
procedure
Clinical features for
specific organ/space
can be found at CDC
website
example,
At least 2 of the
following:
1. Fever (>38℃)
2. Hypotension
3. Nausea, vomiting
4. Abdominal pain or
tenderness
5. Elevated
transaminases
6. Jaundice
At least one clinical
feature AND at least
one of the following
1. Purulent drainage
from the drain placed
into the organ/space
2. Organisms are
identified by culture of
the fluid or tissue
3. Evidence of abscess
4. Radiologic imaging
suggestive of infection
6.
7. Correlation between wound
classification and SSI rate
Clean – 1.3 to 2.9
Clean-contaminated – 2.4 to 7.7
Contaminated – 6.4 to 15.2
Dirty – 7.1 to 40
Cruse PJ, Foord R. The epidemiology of wound infection: a
10-year prospective study of 62,939 wounds. Surgical Clinics
of North America. 1980 Feb 1;60(1):27-40.
8. Wound classification
Clean wounds are uninfected operative wounds in which no inflammation is
encountered and the wound is closed primarily. By definition, a viscus
(respiratory, alimentary, genital, or urinary tract) is not entered during a clean
procedure.
Clean-contaminated wounds are operative wounds in which a viscus is entered
under controlled conditions and without unusual contamination.
Contaminated wounds are open, fresh accidental wounds, operations with
major breaks in sterile technique, or gross spillage from a viscus. Wounds in
which acute, non-purulent inflammation was encountered also were included
in this category.
Dirty wounds are old traumatic wounds with retained devitalized tissue,
foreign bodies, or fecal contamination or wounds that involve existing clinical
infection or perforated viscus.
9. Source of infection
Endogenous: present in or on the
host e.g. superficial SSI following
contamination of wound from a
perforated viscus.
Human body harbours 1014
organisms that can be released
before, during or after surgery
Exogenous: acquired from the
source outside the body such as
operating theatre (inadequate air
filtration, poor antisepsis) or the
ward (e.g. poor handwashing
compliance). The cause of hospital
acquired infection (HAI).
Devitalized tissue, excessive dead
space or haematoma, all are the
result of poor surgical technique
10. Decisive period
There is up to 4 hour interval before bacterial
growth becomes established enough to cause
infection after a breach in the tissue , whether
caused by trauma or surgery. This interval is called
decisive period and strategies aimed at preventing
infection to take a hold.
Prophylactic antibiotic should be given to cover this
period.
11. Factors for increased risk of
wound infections– Malnutrition (obesity, weight loss)
– Timing of surgery elective/emergency
– Type of surgery minimally invasive/open
– Metabolic disease (diabetes, uraemia, jaundice)
– Immunosuppression (cancer, AIDS, steroids, chemotherapy and
radiotherapy)
– Colonization and translocation in the gastrointestinal tract
– Poor perfusion (systemic shock or local ischaemia)
– Foreign body material
– Poor surgical technique (dead space, haematoma)
– Hand hygiene
– Smoking cessation
12. Colonization and translocation of
GIT
When the enteral feeding is
suspended during perioperative
period, particularly with underlying
disease. The aerobic gram negative
bacilli tend to colonise the normally
sterile upper GI tract. They may
then translocate to mesenteric nodes
and cause release of endotoxins
which can be one cause of harmful
systemic inflammatory response by
release of proinflammatory
cytokines and activation of
macrophages.
13.
14.
15.
16. Abscess
– Abscesses need drainage.
– When the cavity is left open for drainage there is no need of
antibiotic therapy in otherwise healthy individual.
– Antibiotics are indicated if the abscess cavity is not left open to drain
freely.
– An open abscess cavity heals with secondary intention.
– Imaging techniques allow guided needle aspiration.
17. Role of antibiotic therapy — For patients undergoing incision
and drainage of an abscess
● Single abscess ≥2 cm
● Multiple lesions
● Extensive surrounding cellulitis
● Associated immunosuppression or other comorbidities
● Systemic signs of toxicity (eg, fever >100.5°F/38°C,
hypotension, or sustained tachycardia)
● Inadequate clinical response to incision and drainage alone
● Presence of an indwelling medical device (such as prosthetic
joint, vascular graft, or pacemaker)
● High risk for adverse outcomes with endocarditis (these include
a history of infective endocarditis, presence of prosthetic valve,
unrepaired congenital heart defect)
● High risk for transmission of S. aureus to others (such as in
18. Staph aureus is the causative agent for abscess in 75% of the cases
20. Cellulitis and erysipelas
Cellulitis and erysipelas manifest as areas of skin erythema, edema, and
warmth; they develop as a result of bacterial entry via breaches in the
skin barrier.
Cellulitis involves the deeper dermis and subcutaneous fat; erysipelas
involves the upper dermis and superficial lymphatics. Cellulitis may
present with or without purulence; erysipelas is non-purulent.
Cellulitis and erysipelas — The most common cause of cellulitis is
beta-hemolytic streptococci (groups A, B, C, G, and F), most
commonly group A Streptococcus or Streptococcus pyogenes; S. aureus
(including methicillin-resistant strains) is a notable but less common
cause
21. Treatment
Five days of antibiotic therapy is generally sufficient, extension
up to 14 days maybe warranted for slow progress to therapy.
Intravenous antibiotics are recommended for the patients with
systemic signs, comorbidities and in immunocompromised state.
When the systemic signs subside IV antibiotics can be switched to
oral.
In case of non-purulent cellulitis and erysipelas antimicrobial
management is sufficient. With purulent cellulitis with abscess
pockets if drainable then incision and drainage can be done.
22. Oral antibiotic IV antibiotic
Amoxicillin 875 mg 1 BD Ampicillin-sublactum 3 g IV 6 hrly
Amoxicillin-clavulanate 875 mg 1 BD Ceftriaxone 1-2 g IV 24 hrly
Clindamycin 300 mg 1 QID Ciprofloxacin 400 mg IV 12 hrly
Doxycycline 100 mg 1 BD Daptomycin 4-6 mg/kg IV 24 hrly
Levofloxacin 750 mg 1 OD Levofloxacin 750 mg IV OD
Ciprofloxacin 5oo mg 1 QID Piperacillin-tazobactam 4.5 g IV 6 hrly
Metronidazole 500 mg 1 TDS Metronidazole 500 mg IV 8 hrly
Minocycline 200 mg 1 OD 100 mg 1 BD Ticarcillin-clavulanate 3.1 g IV 4 hrly
TMP-SMX 1 to 2 double strength BD Vancomycin 15020 mg /kg/dose IV 8-12
hrly
24. Empiric IV antibiotic therapy
Antibiotic
Antibiotic of choice
Vancomycin
Daptomycin (alternative)
Plus one of the following
Ampicillin-sublactam
Piperacillin-tazobactam
Ticarcillin-clavalunate
Ceftriaxone + Metronidazole
Ciprofloxacin + Metronidazole
Levofloxacin + Metronidazole
25. Necrotizing fasciitis
Necrotizing fasciitis is an infection of the deep soft tissues that
results in progressive destruction of the muscle fascia and
overlying subcutaneous fat. Infection typically spreads along
the muscle fascia due to its relatively poor blood supply;
muscle tissue is frequently spared because of its generous
blood supply.
26. Necrotizing fasciitis type I (polymicrobial)
Necrotizing cellulitis: Non-clostridial anaerobic (crepitant)
cellulitis
Gram-positive rods
Acute clinical presentation
Clostridial myonecrosis (gas gangrene)
C. perfringens – Traumatic (most common)
C. septicum – Spontaneous
C. sordellii – Gynecologic (least common)
27. Necrotizing fasciitis type II (monomicrobial)
Group A Streptococcus or other beta-hemolytic streptococci
Staphylococcus aureus (methicillin-sensitive [MSSA] or
methicillin-resistant [MRSA])
Necrotizing myositis due to group A Streptococcus or other beta-
hemolytic streptococci
28. Treatment
– Obtain blood culture then begin antimicrobial treatment.
– Urgent surgical exploration to evaluate fascia and obtain material for
gram stain, culture and pathologic examination
– Aggressive surgical debridement of all the necrotic tissue until
healthy, viable (bleeding) tissue is reached. Inspection and
debridement should be continued in the operating room every 1 to 2
days.
– In severe cases involving extremities amputation may be needed to
control infections
– Empiric antibiotic therapy
Carbapenem or Beta-lactam beta-lactamase inhibitor +
MRSA cover vancomycin or daptomycin +
Clindamycin
29. Systemic inflammatory response
syndrome (SIRS)
SIRS is a systemic manifestation of sepsis, although the
syndrome may also be caused by multiple trauma, burns or
pancreatitis without infection.
Septic manifestations and multiple organ dysfunction syndrome
(MODS) in SIRS are mediated by the release of proinflammatory
cytokines such as interleukin-1 (IL-1) and tumour necrosis factor
alpha (TNFa).
30.
31. Viral Infections relevant to
surgery
Both hepatitis B and hepatitis C carry risks in surgery as
they are blood-borne pathogens that can be transmitted
both from the surgeon to the patient and vice versa. The
usual mode of transmission is blood to blood contact
through a needle-stick injury or a cut.
The type I human immunodeficiency virus (HIV) is one
of the viruses of surgical importance because it can be
transmitted by body fluids, particularly blood.
32. Involvement of surgeons with HIV
or hepatitis patients (universal
precautions)
Universal precautions have been drawn up by the CDC in the United States and largely adopted
by the National Health Service (NHS) in the UK (in summary):
● use of a full face mask ideally, or protective spectacles;
● use of fully waterproof, disposable gowns and drapes, particularly
during seroconversion;
● boots to be worn, not clogs, to avoid injury from dropped sharps;
● double gloving needed (a larger size on the inside is more
comfortable);
● allow only essential personnel in theatre;
● avoid unnecessary movement in theatre;
● respect is required for sharps, with passage in a kidney dish;
● a slow meticulous operative technique is needed with minimised
bleeding.
33.
34. Streptococci
Gram positive, form chains
Group A, Streptococcus pyogenes is most
Pathogenic. It causes cellulitis, pharyngitis
and cause tissue destruction by enzyme
Streptolysin, streptokinase, and
Streptodornase.
Group D, Streptococcus Faecalis is involved in wound
infection after large bowel surgery
35. Staphylococci
Gram positive, forms clumps
Staphylococcus Aureus found in the
Nasopharynx of up to 15% of the
Population. Causes skin infections,
Organ abscesses. Produces yellow
Pigmentation. Most of the hospital strains are
B-lactamase producers and not sensitive to
penicillin group. Many strains are flucloxacillin, aminoglycosides, vancomycin and
some cephalosporins.
Staphylococcus epidermidis forms biofilms and causes infections with indwelling
cannula/catheters and vascular or orthopaedic prosthesis.
36. Clostridia
Gram-positive, spore forming, obligate anaerobes
Cl. Perfringens produces alpha toxins
(lecithinase) causes myonecrosis (gas
gangrene), hyaluronidase, and
hemolysis.
Cl. Tetani causes tetanus.
Cl. Difficile produces a exotoxin which causes pseudomembranous colitis
secondary to antibiotics such as ciprofloxacin. It may lead to perforation in severe
cases.
37. Ref: Expert Group of the Association of Physicians of India on Adult Immunization in India. The
Association of Physicians of India evidence-based clinical practice guidelines on adult immunization. The
Journal of the Association of Physicians of India. 2009;57:345.
38.
39. Aerobic gram-negative bacilli
Most of these organisms in this group work in synergy with Bacteroides
to cause SSIs after bowel operation (in particular, appendicitis,
diverticulitis, and peritonitis.
E. Coli is a major cause of UTI in patients with indwelling urinary
catheter.
Pseudomonas spp. Produce blue-green pigment. Tend to colonise burns,
tracheostomy wounds, and urinary tract. Hospital strains difficult to
eradicate. They spread resistance by plasmids. The aminoglycosides and
the quinolones are effective. Carbapenems are useful in severe infections.
40. Bacteroides
Non spore forming, strict anaerobes that colonize large
bowel, vagina and oropharynx.
Bacteroides fragilis is the principle organism that acts in
synergy with aerobic gram-negative bacilli to cause SSI,
including intra-abdominal abscesses after colorectal or
gynaecological surgery.
They are sensitive to imidazolines (e.g. metronidazole)
and some cephalosporins (e.g. cefotaxime).