Surgical infection Flashcards

1
Q

What does the severity of infectious disease depend on

A

Microbial virulence x numbers / host defences

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2
Q

What 3 factors is microbial virulence associated with

A
  • Does not stimulate host defence
  • Withstands host defence
  • Causes host tissue damage (e.g toxin)
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3
Q

What 3 body surfaces act as defence

A

Mucocutaneous surface
Humoural (blood and tissue)
Celluluar (WBC)

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4
Q

What are 3 major proven factors increasing risk of surgical site infection

A
  1. degree of contamination, i.e. surgical wound class
  2. length of operation
  3. Pre-existing illness malignancy, DM, immunosuppression
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5
Q

Another proven factor increasing surgical infection risk

A
  1. patient related - age, obesity
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6
Q

What are 7 suggested but unproven factors that increase risk of surgical site infection

A
  1. length of pre-op hospital stay
  2. reoperation
  3. glove punctures, powder
  4. time of day
  5. month of year
  6. use of adhesive drapes
  7. use of wound irrigation
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7
Q

List 3 ways surgeons reduce surgical infections

A
  1. Where possible, wounds should be left alone for at least 48hrs post-operatively ! wetting, changing dressing too early can lead to contamination of tissues
  2. Patients get better from infection is probably only 40% antibiotics related ! the most important factor is host defence
  3. that’s why surgeons drain abscesses, remove necrotic tissues, and attempt to resurrect normal WBC function and numbers in
    transplant or immunocompromised patients
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8
Q

When do infections generally become apparent in surgical patients

A

> 70% become apparent after patient has left the hospital

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9
Q

Have masks and gowns been shown to reduce post op surgical site infection

A

No

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10
Q

List 4 important infection control measures in peri-op care

A
  1. restriction in numbers and movement of theatre staff ! ?movement of air
  2. cleansing of skin in the operation field by antiseptics
  3. the administration of prophylactic antibiotics prior to skin incision
  4. hair clipping immediately prior to incision NOT razor shaving
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11
Q

When is it best to give prophylactic abx in surgery

A

is at time of induction of anaesthesia, i.e. around 20 minutes prior to incision

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12
Q

For elective procedures lasting 2 hours or less how many abx doses is warranted and why

A

a single dose of prophylactic Abx is enough; continuing therapy after wound
closure should be restricted because of unproven benefit and risk of selection of resistant bacteria

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13
Q

Should you cover all possible encountered microbes

A

no

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14
Q

How many abx for procedures > 2 hours or if there is blood loss

A

one or 2 further doses at intervals 2 times the plasma half
life (i.e. around 2hrly for most Abs) may be required. In such cases, a good time for the final dose is just before wound closure.

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15
Q

3 important principles for selecting abx peri-operatively

A
  • should have minimal interaction with other drug likely to be used at the time of surgery,
  • must be active against the microbes most likely to result in surgical site infection
  • should always have staph aureus cover
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16
Q

In what circumstances may the antibiotic regimen be prolonged (6)

A
  • during an emergency,
  • likelihood of an active infection,
  • an obstruction,
  • unusual blood loss,
  • trauma
  • a high risk patient
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17
Q

Generally speaking what group of abx are suitable for surgical patients

A

First and second generation cephalosporins, in combination with metronidazole where appropriate, seem ideally suited for surgical prophylaxis

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18
Q

Is selective decontamination of the GI tract in critically ill patients of benefit

A

Highly debatable and largely unproven

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19
Q

What bugs need to be covered with abx in large bowel surgery

A
  • Enteric coliforms, e.g. E. coli
  • Obligate anaerobe, bacteroides fragilis
  • staph aureus, important skin wound pathogen in all invasive surgical settings
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20
Q

Why isnt amoxicillin alone suitable for large bowel surgery prophylaxis

A
  • amoxycillin is not enough to cover E. coli (>50% of E.coli are resistant to amoxicillin by B-lactamase)
  • amoxycillin is not enough to cover staph aureus >80% produce penicillinases which inactivate amoxicillin
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21
Q

why isnt flucloxacillin alone suitable for large bowel surgery prophylaxis

A

flucloxacillin is not enough to cover against E. coli

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22
Q

Can aminoglycosides be used as large bowel surgery prophylaxis

A
  • Tobramycin doen’t work against obligate anaerobe
  • In addition, anaesthetic agents may potentiate the neuromuscular blocking effects of aminoglycosides ! so best avoid it
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23
Q

Most significant post op CABG bugs

A
  1. staph, both coagulase negative (e.g. epidermidis) and coagulase positive (e.g. aureus)
  2. E.coli, minor but still significant risk, if untreated, may adhere to any foreign material/implants, more relevant in valve replacement than CABG
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24
Q

Abx prophylaxis in CABG and what bug must be covered

A
  1. cefamandole is an acceptable choice
  2. cover against coagulase negative staph. Must be included in the antibiotic(s) chosen
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25
Pathogens to cover for hip replacement surgery and what type of abx to use
* Staph both aureus and epidermidis * Thus first or second generation cephalosporins are good, first generation better bone penetration and longer half life; second generation better anti-staph effects
26
ABx to use in hip surgery
- Vancomycin should not be used unless MRSA are a major consideration - cephazolin alone
27
Are gram negative coliforms implicated in hip operations
Can be, can result in significant post op infections
28
Incidence of post op hip infections
<1%
29
Where can peritonitis be located
1. diffuse or localized 2. intra or retroperitoneal space 3. on viscera or mesentery
30
Where can intra-abdominal collections travel/ where are abscesses formed
1. form around the involved organs 2. walling off around SB or omentum 3. traveling along paracolic gutters by gravity to pelvis 4. travel up by negative pressure and lymphatic flow to subphrenic space 5. travel to anywhere by operative anipulation
31
What are the 3 types of peritonitis
1. primary (or spontaneous) peritonitis ! don’t know the source of infection, e.g. cirrhosis and ascites 2. secondary peritonitis ! leakage of microbes from an injured or ruptured viscus (e.g. appendix) 3. tertiary peritonitis ! persistent peritonitis in seriously ill patients, e.g. G –ve bacilli or yeasts ! generalized sepsis with shock
32
What is the classical management of peritonitis
1. operative control of contamination/pathology 2. antibiotic therapy 3. intensive care support
33
Describe the biphasic development of secondary peritonitis
- initial phase, diffuse peritonitis, bacteremia with or without specific shock mainly a/w G-ve bacilli, e.g. E.coli, pseudomonas aeruginosa - Second phase, survivors localize infection into abscesses in which bacteroides fragilis often in a/w facultative anaerobes , synergy
34
What bugs leak from terminal ileum and colon
Massive bacterial inoculation; >500 different species ! obligate anaerobes dominate
35
What bugs leak from stomach and upper SB
G-ve enterics, enterococci, and yeasts
36
Do the stomach and SB normally contain lots of microbes?
No Numbers have increased with use of antacids and H2 receptor antagonists, and in presence of malignancy
37
Common anaerobes causing intra abdominal infetions
- bacteriodes fragilis, bacteroides thetaiotamicron and other bacteroirdes group - peptostreptococci - Fusobacteria - clostridia, esp. clostridium perfringens, significant in infections a/w SB ischaemia - Biliphila wadsworthia ! common from abscesses or peritoneal fluid from patients with appendicitis - Prevotella melaninogenica ! peritonitis secondary to acute appendicitis with perforation, and from female genital tract associated infections
38
Aerobes or faculative anaerobes associated with intra abdominal infections
Aerobes - pseudomonas aeruginosa Faculative anaerobes - E.coli - Klebsiella species - Staphylococci - enterobacteriace Streptococci (e.g. streptotoccus anginosus) - Enterococci - yeast Candida albicans
39
Who gets Candidosis
1. patients needing multiple operations for repair of recurrent GIT perforations or anastomotic leak 2. acute pancreatitis
40
Duration of abx for intra-adbominal infection
therapy should be no <4 days if there is associated bacteremia, extending to 7 in those with major peritoneal contamination
41
Most common anaerobe associated with intra-abdominal sepsis
bacteroides fragilis
42
Important virulence factor associated with bacteroides
the presence of the microbes polysaccharide capsule is an important virulence factor
43
Are intra-abdominal abscess polymicrobial
yes
44
Most dominant obligate anaerobe associated with intra-abdominal abscesses
Clostridia
45
Most common location for intra-abdominal abscess
most commonly occur under the diaphragm and in the pelvis of recumbent patients
46
Antibiotics useful for peritonitis in a 78yr old patient following large bowel surgery, who had been hospitalized 6 wks preoperatively are
1. imipenem alone 2. piperacillin/tazobactam (tazocin)
47
Antibiotics acceptable for empiric treatment of intra-abdominal sepsis from rupture of appendix include
imipenem alone
48
With rupture of the large bowel, the most appropriate antibiotics combination include
metronidazole plus ciprofloxacin
49
What bug commonly cause early onsent bacteremia following colon cancer surgery
E coli
50
Risk factors for nectrotising fascitis
1. diabetes and peripheral vascular disease 2. trauma 3. alcoholism, cirrhosis 4. prior infection 5. surgery 6. anti-inflammatory therapy (both corticosteroid and non-steroidal agents)
51
Causative organisms in nec fasc
1. Obligate anaerobic species e.g peptostreptococci, bacteroides species, prevotella species, clostridia and fusobacteria 2. facultative anaerobes G-ve enteric, non-enteric bacilli, staph, strep, enterococci 3. aerobes e.g. pseudomonads
52
Is nec fasc polymicrobial
classically a polymicrobial infection, and not as often quoted predominately a group A strep disease
53
What tissue plane does nec fasc spread along and how does this promote spread of infection
- Superficial fascial plane (not the deep underlying muscle) - poor blood supply of fascia and its inability to clear contaminating microbes
54
What is an essential surgical component of eradication of nesc fasc and why
- Excision with margin is therefore an essential component of therapy - microvascular thrombosis at leading edge of lesion may help promote further spread and development
55
Antibiotic regimen for nec fasc (monomicrobial strep disease)
clindamycin + ceftriaxone
56
Abx regimen for polymicrobial nec fasc
metronidazole, ciprofloxacin and cefuroxime
57
Abx to cover gram positive cocci (nec fasc)
penicillin amoxicillin flucloxacillin clindamycin ceftriaxone cefuroxime
58
Abx to cover gram negative bacilli (nec fasc)
3rd gen cephalosporins (e.g. ceftriaxone) or ciprofloxacin
59
Abx to cover obligate anaerobes (nec fasc)
metronidazole or clindamycin
60
When would it be important to include ciprofloxacin or 3rd gen cephalosporins for nec fasc
- When you need to cover gram negative bacilli - I.e if infection follows trauma, when major environmental contamination or gut source is likely
61
What is the main stay of treatment for Myonecrosis in nec fasc
Aggressive surgical intervention is the primary treatment
62
What other therapies may be used for nec fasc
hyperbaric oxygenation can be used, but must not delay surgical debridement
63
Classically, what is the main stay of abx treatment for nec fasc
Penicillin has been the mainstay of antimicrobial therapy, often in combination with metronidazole or clindamycin
64
Which patients get diabetic foot infections
- in their fifth decade - have had diabetes for around 18yrs - require insulin
65
Average hospital stay for a patient with diabetic foot infection
> 1 month
66
Range of infections associated with diabetes
Superficial Necrotising fasciits Osteomyelitis Gangrenous foot
67
What is the most common presentation of a diabetic foot infection
Neurotrophic ulcer
68
Where do neurotrophic ulcers most commonly occur
1st, 2nd and 5th metatarsal head
69
Cause of neurotrophic ulcer
Occur independently to PVD, result from localised repetitive trauma
70
Treatment of diabetic foot infection
Control of localized infection involves 1. adequate debridement of devitalized tissue 2. provision of a suitable environment for wound healing 3. modification of weight bearing plantar surfaces 4. meticulous nail and skin care
71
Antibiotic considerations for diabetic foot infections
1. consider patient’s environment (e.g. home vs hospital) 2. nature of initial injury (puncture wound, animal bite, or neurotrophic ulcer) 3. whether infection is limb-threatening or not
72
What type of bug is clostridia
- Obligate anaerobic, spore forming bacilli
73
Where is clostridia often found
Soil and GIT of animals
74
Most important type of clostridia
Clostridium perfigrens
75
Classic abx of choice for clostridium
Penicillin often in combination with metronidazole or clindamycin
76
What exacerbates clostridium disease
Presence of foreign bodies
77
Describe the appearance of tissue/ clinical signs of clostridium perfigens
- is a/w marked oedema and necrosis of involved muscle - blood may appear completely haemolysed in the terminal stages - gas bubbles appear early in the gangrenous tissues - lesions DOES NOT reveal marked infiltration of neutrophils
78
What tissue is susceptible to clostridium infection
Tissues with impaired blood supply
79
What is an important microbe to consider when deciding on abx prophylaxis for lower limb amputation
Clostridium perfigens
80
Name an abx clostridium perfigens is susceptible to
Metronidazole
81
Outline the 4 important principles when treating someone for tetanus
1. surgical excision o the wound which is left open 2. administration of penicillin intravenously 3. administration of human hyperimmune globulin intramuscularly, in an attempt to get some passive immune protection 4. sedation of the patient and respiratory support, as most tetanus toxins are hyperexcitability to muscles causing ‘tetanty’,locked jaw and respiratory failure ! thus, need to sedate patient and support respiration
82
What exotoxins do clostridia release and what impact do they have
- lecithinase - hyaluronidase - collagenase Diffuse into tissue, kill cells and damage the local microcirculation, allowing further invasion at an alarming rate - At a later stage, toxins enter the circulation resulting in rapid shock & death
83
Do clostridia lesions elicit PMN infiltrates
No