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Surgical
Infections
Department of General
Surgery, RMCH
By: Dr. Shruti Devendra (JR1)
Date: 15.10.19
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
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
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
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
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.
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.
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
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.
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
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.
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.
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
Staph aureus is the causative agent for abscess in 75% of the cases
Copyrights apply
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
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.
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
Empiric oral antibiotic therapy
Combination that covers MRSA + Gram-positive + Gram-negative bacilli +
anaerobes
TMP-SMX + Amoxicillin-Clavulanate
Doxycycline + Amoxicillin-Clavulanate
Doxycycline + Levofloxacin + Metronidazole
Minocycline + Amoxicillin-Clavulanate
Minocycline + Levofloxacin + Metronidazole
Clindamycin + Amoxicillin-Clavulanate
Clindamycin + ciprofloxacin
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
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.
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)
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
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
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).
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.
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.
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
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.
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.
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.
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.
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).
Thank you

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Surgical infections

  • 1. Surgical Infections Department of General Surgery, RMCH By: Dr. Shruti Devendra (JR1) Date: 15.10.19
  • 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
  • 23. Empiric oral antibiotic therapy Combination that covers MRSA + Gram-positive + Gram-negative bacilli + anaerobes TMP-SMX + Amoxicillin-Clavulanate Doxycycline + Amoxicillin-Clavulanate Doxycycline + Levofloxacin + Metronidazole Minocycline + Amoxicillin-Clavulanate Minocycline + Levofloxacin + Metronidazole Clindamycin + Amoxicillin-Clavulanate Clindamycin + ciprofloxacin
  • 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).

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