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INFECTION 1

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									Wound Infection

Brig Shabbir Rana
WOUND INFECTION


     Historical Background
Historical Background

 1.  Egyptians were able to prevent putrefaction in
     their skills of mummification
 2. In the nineteenth century Koch laid down the
     first definition of infective disease
    Particular microbe could be considered
     responsible for an infection when it was found
     in adequate numbers in a septic focus
Could be cultured
Could cause similar lesions when injected
into another host.
Louis Pasteur and Joseph Lister applied
this knowledge
 Concept of a ‘magic bullet
    (Antimicrobial)
Which could kill microbes but not their
host led to early sulphonamide
chemotherapy
Antibiotic penicillin was first time used
in police Constable Alexander for
severe staphylococcal illness
Physiology of wound infection
    Barrier to infection

Most extensive physical barrier is the skin
Skin harbors its own resident microflora
that may block the attachment and invasion
of noncommensal microbes
Microbes also are held in check by
chemicals that sebaceous glands secrete
 Constant shedding of epithelial cells
The respiratory tract host defense

 In the upper respiratory tract, respiratory mucus
 traps larger particles including microbes
 Mucus is then passed into the upper airways and
 oropharynx by ciliated epithelial cells
 Smaller particles arriving in the lower respiratory
 tract are cleared via phagocytosis by pulmonary
 alveolar macrophages
  Process that diminishes these host defenses can
 lead to development of bronchitis or pneumonia.
Gastrointestinal Tract

 Significant numbers of microbes are
 encountered in many portions of the
 gastrointestinal tract
 Vast numbers being found within the
 oropharynx and distal colorectum
 Microbes that are not destroyed within
 the stomach enter the small intestine
Approximately 105 to 108 CFU/mL
are present in the terminal ileum
Relatively low-oxygen, static
environment of the colon is
accompanied by the growth of
microbes
Anaerobic microbes outnumber
aerobic species approximately 100:1
in the distal colorectum,
Introduction of infection
 Once microbes enter a sterile body
 compartment (e.g., pleural or
 peritoneal cavity) or tissue host
 defenses act to contain the nidus of
 infection
 Microbes also immediately encounter
 a series of host defense mechanisms
 that reside within the vast majority of
 tissues of the body
Polyporph
Resident macrophages
Complement, proteins and immunoglobulins
(Ig, antibodies)
 Secretion of tumor necrosis factor- (TNF- ), of
interleukins (IL)-1 , 6, and 8; and of interferon-
(INF- ) occurs within the tissue milieu
Interaction of microbes with these first-line host
defenses leads to microbial opsonization
The classical and alternate
complement pathways are activated
both via direct contact with and via
IgM>IgG binding to microbes, leading
to the release of a number of different
complement protein fragments (C3a,
C4a, C5a) that are biologically active,
acting to markedly enhance vascular
permeability
Host response is weakened

 Malnutrition, obesity, rapid weight loss
 Metabolic diseases, diabetes mellitus,
 uraemia and jaundice
 Disseminated cancer,
 immunosuppression caused by
 radiotherapy, chemotherapy, steroids
 and acquired immunodeficiency
 syndrome (AIDS)
When enteral feeding is suspended in
the perioperative period the gut
rapidly becomes colonised and
bacteria, particularly Gram-negative
bacilli, translocate to mesenteric
nodes
Release of endotoxin may follow,
which further increases susceptibility
to infection
Infection or not

 The pathogenicity and size of
 bacterial inoculum
 Poor surgical technique that leaves
 devitalised tissue
 Excessive dead space or haematoma
 may increase this risk of infection
   Foreign materials of any kind,
 including sutures and drains, promote
 infection
Subsequent to microbial invasion
and the interaction of microbes
with host defenses


           (1) eradication,
          (2) containment
  Risk of Infection



Bacterial dose         Virulence




             Impaired
           host resistance
„Decisive period
 There is a delay before host defences
 can become mobilised through acute
 inflammatory, humoral and cellular
 processes
 During these first 4 hours after
 incision that bacterial colonisation and
 established infection can begin
 Prophylactic antibiotics will be most
 effective during this time
Definition
 Infection(SSI)
   Presence of microorganisms in a normally
   sterile site.
 Bacteremia
   Cultivatable bacteria in the blood stream


 Sepsis
   The systemic response to infection.
   If associated with proven or clinically suspected
   infection, SIRS is called “sepsis”.
SIRS
(Systemic Inflammatory Response Syndrome)

  The systemic response to a wide range of
  stresses.
     Temperature >38°C (100.4°) or <36°C (96.8°F).
     Heart rate >90 beats/min.
     Respiratory rate >20 breaths/min or
     PaCO2 <32 mmHg.
     White blood cells > 12,000 cells/ml or < 4,000
     cells/ml or >10% immature (band) forms.
  Note
    Two or more of the following must be present.
    These changes should be represent acute alterations from
    baseline in the absence of other known cause for the
    abnormalities.
Severe Sepsis
 Sepsis with organ hypoperfusion
                      one of the followings :
   SBP < 90 mmHg
   Acute mental status change
   PaO2 < 60 mmHg
   Increased lactic acid/acidosis
   Oliguria
   DIC or Platelet < 80,000 /mm3
   Liver enzymes > 2 x normal
MODS
(Multiple Organ Dysfunction Syndrome)
  Sepsis with multiorgan hypoperfusion
  Two or more of the followings:
    SBP < 90 mmHg
    Acute mental status change
    PaO2 < 60 mmHg on RA (PaO2 /FiO2 <
    250)
    Increased lactic acid/acidosis
    Oliguria
    DIC or Platelet < 80,000 /mm3
    Liver enzymes > 2 x normal
Relationship between SIRS and
Sepsis
Microbiology of Infectious Agents

 Table 5-3 Common Pathogens in Surgical Patients
    Gram-positive aerobic cocci Staphylococcus aureus Staphylococcus
    epidermidis Streptococcus pyogenes Streptococcus
    pneumoniae Enterococcus faecium, E. faecalis Gram-negative aerobic
    bacilli Escherichia coli Haemophilus influenzae Klebsiella
    pneumoniae Proteus mirabilis Enterobacter cloacae, E.
    aerogenes Serratia marcescens Acinetobacter calcoaceticus Citrobacter
    freundii Pseudomonas aeruginosa Xanthomonas maltophilia Anaerobes Gram-
    positive     Clostridium perfringens, C. tetani, C. septicum     Clostridium
    difficile   Peptostreptococcus spp. Gram-negative           Bacteroides
    fragilis    Fusobacterium spp. Other bacteria Mycobacterium avium-
    intracellulare Mycobacterium tuberculosis Nocardia asteroides Legionella
    pneumophila Listeria monocytogenes Fungi Aspergillus fumigatus, A. niger, A.
    terreus, A. flavus Blastomyces dermatitidis Candida albicans Candida glabrata,
    C. paropsilosis, C. krusei Coccidiodes immitis Cryptococcus
    neoformans Histoplasma
    capsulatum Mucor/Rhizopus Viruses Cytomegalovirus Epstein-Barr virus Hepatitis
    B, C viruses Herpes simplex virus Human immunodeficiency virus Varicella zoster
    virus
Classification of Surgical
wounds
Wound Class              Examples of Cases                                Expected Infection
  Rates

Clean (class I)          Hernia repair, breast biopsy                                 1.0 –5.4%




Clean/contaminated (class II)   Cholecystectomy, elective GI surgery                  2.1 –9.5%




Contaminated (class III) Penetrating abdominal trauma, large tissue
                          injury, enterotomy during bowel obstruction                  3.4–13.2%



Dirty (class IV)      Perforated diverticulitis, necrotizing soft tissue infections     3.1 –12.8%
DIAGNOSIS OF INFECTION IN
THE SURGICAL PATIENT
Classic local symptoms and
signs
 Pain
 Swelling
 Redness at the infected site
 Loss of function
  Systemic Response

fever
Systemic leukocytosis with a
preponderance of PMNs
Severe systemic infections may
produce confusion, ileus, hypotension,
and profound shock
Blood, urine, sputum & pus culture
    INVESTIGATIONS

 Examination of the wound
 Chest and sinus radiographs
 Catheter sepsis, urinary tract
infections
U/S SCAN
CT SCAN
MRI SCAN
Prevention and Treatment of
Surgical Infections


         prophylaxis
Prophylaxis

 Maneuvers to diminish the presence
 of exogenous microbes
 Surgeon
 Operating room environment
 Patient
Hair Removal

 Appropriate:
   No hair removal at all
   Clipping


 Inappropriate:
   Razors
Razor Use vs. Clipper Use

 NumberInfected (%)
Shaved      990 13 (1.3%)
Clipped     990   4 (0.4%)
 p < 0.03
Hyperglycemia and Risk of SSI

 Increased risk:
 Diagnosed diabetes
 Undiagnosed diabetes
 Post-op glucose > 200 mg% within
 48h
Perioperative Normothermia

  •   Hypothermia reduces tissue oxygen
      tension by vasoconstriction.

  •   Hypothermia reduces leukocyte
      superoxide production..

  •   Hypothermia increases duration of
      hospital stay even in uninfected patients
Appropriate use of antibiotics

Appropriate use of prophylactic
 antibiotics
    Selection
    Timely administration
    Timely discontinuation of prophylaxis
Appropriate Antibiotic Selection

 Choose prophylactic antibiotics
 consistent with national guidelines
   Special cases:
     Allergy (anaphylactoid) to -lactam
     antibiotics
     High rate of MRSA wound infections locally
     Recent prolonged course of antibiotics or
     ICU stay
Timing of Antibiotics
 Most studies indicate that optimum
 timing for prophylactic antibiotic is
 within one hour of incision time.
 When tourniquet cuff is used, make
 sure all antibiotic is infused prior to
 inflation of cuff.
Dose of Antibiotic for
Prophylaxis
 Always give at least a full therapeutic
 dose of antibiotic.
 Consider the upper range of doses for
 large patients and/or long operations.
 Repeat doses for long operations
 (generally those exceeding four hours
Thank You

								
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