Contact Me

Topics:
Abdominal Trauma, Abdominal Tuberculosis, Ascitis,
Burns,

Ca Colon,

Chemotherapy for Colorectal Ca,
Colonoscopy,
Constipation,
Esophageal varices,
Evidence based surgery, Gall Bladder,
GERD,

GI Bleed,

GI Endoscopy,
GI Malignancy,
Hernia,
Inflammatory Bowel Disease(1),

Inflammatory Bowel Disease (2),

Intestinal Obstruction,
Laparoscopy Diagnostic,
Laparoscoy FAQs
Laparoscopy Operative,
Liver function,
Obstructive Jaundice, Pancreatitis,
Peptic Ulcer, Piles/Fissure/Fistula,
Portal Hypertension,

PR (per rectal examination)
, Serum tumor markers,
Shock
Lectures:
Ano-rectal abscess
Anti-biotics in coloproctology
Applied anatomy of the Ischio-Rectal Fossa
Bowel Preparation
Diverticulosis
Fissure in Ano
GERD
Hiatal Herniae(1)
Hiatal Herniae(2)
Irritable Bowel Syndrome
Laparoscopy History
Laparoscopy Anaesthesia
Onco Surgery
Pilonidal sinus
PR - Per-rectal examination
Pre-Operative Preparation

The Thyroid Gland
Tuberculous Adenitis

Antibiotics in Coloproctology

 

Compiled and edited by :.

Dr.Barin Bose MS
Consultant Surgeon and Coloproctologist
Jabalpur Hospital and Research Centre.
Jabalpur (M.P.)

GLIMPSES FROM HISTORY – ANTISEPSIS & ANTIBIOTICS

Antisepsis

  • Earlier days- surgery followed by infection & pus –’laudable’.
  • Egyptian embalmers - able to prevent putrefaction – skills of mummification.
  • Hippocrates (460-377 B.C.) recognized the antiseptic properties of wine, oil, and vinegar & used in dressing of wounds.
  • Microscopy - 17th century- confirmed the presence of microbes.
  • Theory of spontaneous generation
  • 1860-Sir Louis Pasteur -Germ theory of disease.
  • Heinrich Koch (1843-1910) proved that germs cause disease. And laid down Koch’s postulates
  • 1843- Ignaz Semmelweiss introduced washing of hands in an antiseptic chloride solution before examining patients.
  • 1867 Sir Joseph Lister, introduced, technique and principles of antisepsis for surgery - LANCET, 1867
  • 1890 - William Halsted, use of Rubber gloves in surgery .

Antibiotics.

  • First systemic antiseptic - Ehrlich – arsenical named Salvarsan- effective against spirochetes-‘ Magic Bullet’
  • 1929 – Sir Alexander Fleming discovered Penicillin- accidentally from a mould Pencillium notatum.
  • 1935- Domagk discovered Prontosil – active ingredient – Sulfanilamide- first of Sulphonamides- effective against Gonorrhea.
  • 1940s, A. Schatz and S. Waksman - Streptomycin, effective against both G -ve bacteria and Mycobacterium tuberculosis.
  • 1947- Chloramphenicol was discovered.

Surgical infections.

Defn: Surgical Infections are those that

    • Present as a result of a surgical procedure – Surgical Site Infections ( SSI)
    • Require surgical intervention as part of the treatment. ( E.g. Intra abdominal abscess, acute appendicitis etc)

Characteristics of a surgical infection:

    • Result of a damaged host defense system- esp. injury to the epithelial barrier.
    • Pathogens causing infection are usually mixed – aerobic & anaerobic.
    • Pathogens are from patients own endogenous flora( Opportunistic).
    • Usually accompanies tissue necrosis.

* Primary principle when treating surgical infection is source control. (E.g. abscess drainage, closure of perforation etc,.)

* Antibiotic treatment and systemic support - only adjunctive therapies , and wont resolve surgical infection without operative Rx

Pathogens in surgical infections.

Bacteria of surgical infections are broadly divided into aerobic & facultative bacteria in one gr and anerobic bacteria in another / into Gram + ve & Gram _ve bacteria / into Bacilli & Cocci.

  • Source of pathogens can be:
  • endogenous or exogenous.

    But most surgical infections are caused by endogenous bacteria.

    Mostly mixed flora- aerobic & anaerobic.

    Specific bacteria found in specific parts of the body , exposed anatomic areas during procedures – source of pathogens.

Endogenous source:

    • acquired from individuals own commensals.
    • Common after trauma , surgery and instrumentation, and in lowered local or general resistance.
    • Commensal flora, not of consistent composition, is constantly changing , altered by antibiotics- broad spectrum .
    • Many commensals are potential pathogens.
  • Skin & mucus membranes: skin is rich in staph epidermidis, micrococci, coryneforms and anaerobic cocci. On mucus membranes flora is predominantly anaerobic. 30% of people are carriers of Staph aureus a potential pathogen particularly in axilla, toe webs, nose.
  • Gastro intestinal tract: few organisms in stomach and small intestine. Large intestine – vast microbial flora, predominantly anaerobic. Such as Bacteroides spp, Bifidobacteria and Clostridia. Also aerobes like E.coli & Enterococcus.

Exogenous source:

  • Acquired from a source outside the patient. Can be from :
    1. Human source.
    2. Animal source

3. Environmental source: community acquired or hospital acquired

Why need to know:

    • for suspecting the possible pathogen causing infection .
    • to suspect the origin of an unknown source of infection in pts with +ve blood culture.
    • for selection of appropriate antibiotics
      • to start intelligent empiric therapy.
      • To direct antimicrobial prophylaxis.

Antibiotics in colorectal surgery

Why & When.

  • To treat established Surgical infections-Antibiotic Therapy.
  • For Antibiotic Prophylaxis prior to surgery.

Antibiotic therapy

Therapy aimed at established surgical infections.

Goal of antibiotic therapy:

  • To achieve a concentration of antibiotic in the infected tissue that exceeds the MIC by 3 or 4 times for at least s of the time between successive doses.

Principles of antibiotic therapy:

 

        • Choice of Antibiotics.
        • Route of administration.
        • Duration & Dose of administration.

Choice of antibiotic:

  • Most surgical infections are caused by mixed bacterial flora, it is difficult to culture all these organisms and bacterial identification takes a minimum of 48 -72 hrs.
  • Hence antibiotics must be started empirically and directed at the most likely pathogens.
  • Gram staining & biochemical tests can help in providing earlier guidances regarding which group of causative bacteria.
  • Bacteria on gram stain
  • Source
  • Initial calculated antibiotic therapy
  • G +ve cocci (chains)
  • Soft tissue
  • Pencillin G (10 mu tds)
  • G +ve cocci (clusters)
  • Soft tissue
  • -do-
  • G –ve rods
  • Abdomen
  • Cefotaxime
  • G +ve rods
  • Soft tissue
  • Pencillin G (10 mu tds)
  • Mixed G +ve & -ve
  • Intra abdominal abscess
  • Cefotaxime + metronidazole / ampicillin+ sulbactum.
  • Facts to be considered when choosing an antibiotic for empiric treatment.
    1. Coverage of the presumed organisms involved should be ensured. Starting with broad spectrum drugs and narrowed down to specific organism isolated.
    2. Concentration of the antibiotic that can be achieved at the site of infection.
    3. Toxicity should be considered , particularly in critically ill patients in which bioavailability & therapeutic & toxic level range are harder to predict.
    4. When a new antibiotic regimen is started , set a time limit for the period for which the antibiotic will be given.
    5. The pathogenicity , synergism, and the antagonism exhibited by the bacteria in various mixed infections.
    6. The negative effects of antibiotics with host defense mechanisms
    7. The results of well controlled clinical studies of unselected patients.
  • If obvious improvement is not seen within 2 or 3 days, one often hears the ques – ‘ which antibiotic should we switch to?’

    This Ques is appropriate only after the following questions have been answered.

        • was the initial operative procedure adequate?
        • the initial procedure was adequate but has a complication occurred?
        • has a super infection developed at a new site?
        • The drug choice is correct, but is enough is being given?
    • The choice of antibiotics is not the most common cause of failure unless the original choice was clearly inappropriate.
  • Route:
    • Because of systemic response to infection & impaired GI function in severe surgical infections – Intravenous route is the preferred route in initial antibiotic therapy.
    • After initial parenteral therapy, patient can be switched to oral antibiotics to complete the course.
  • Duration:
    • Antibiotics are usually given for too long duration & in insufficient dosages, because surgeons have problems distinguishing between contamination, infection and continuing inflammation.
    • Longer duration of therapy indicated in immunocompromised Pt or when focus control is difficult.
  • When to stop ?
    • A reliable guideline is to continue antibiotics until Pt has shown obvious clinical improvement and has had a normal Temp for 48 hrs or more.
    • Signs of improvement include improved mental status, return of bowel function, resolution of tachycardia, and spontaneous diuresis
  • Recommendations - Duration of antibiotic therapy in abdominal infections following source control ..
  • Contamination: NO Postoperative Antibiotics.
    1. Gastroduodenal peptic perforation ( op within 12h )
    2. Traumatic enteric perforations operated within 12h
    3. Peritoneal contamination with bowel contents .
    4. Appendectomy ( early/phlegmonous appendicitis )
    5. Cholecystectomy (early/phlegmonous cholecystitis)
  • Resectable infection : 24 hr post operative antibiotics
    1. Appendectomy for gangrenous appendicitis.
    2. Cholecystectomy for gangrenous cholecystitis.
    3. Bowel resection for ischemic or strangulated bowel without perf.
  •  
  • Cont…..
  • MILD infection: 48 hrs of postoperative antibiotics
    1. Intra abdominal infection from diverse sources with localized pus formation.
  • Late ( more than 12 hr) traumatic bowel perf and Gastro duodenal perf, with no established intra abdominal inf.
  • MODERATE infection : upto 5 days of post op antibiotics.
  • 1. Diffuse established intra abdominal infection from all sources.
  • SEVERE infection: more than 5 days of post op antibiotics.l
    1. Severe intra abdominal infection with the source not easily controllable ( i.e., infected pancreatic necrosis.)
    2. Severe intra abdominal inf, treated with planned re laparotomies.
    3. Post operative intra- abdominal inf. Source: EJS 1997;576

    Surgical site infections.

    • Defined by: Surgical Wound Infection Task Force – 1992.

     

    • Defn. Postoperative infections that present in any location along the surgical tract within 0 to 30 days after a surgical procedure or within 1 yr in procedures involving implants.
    • SSI Classification:
      • Incisional – superficial ( skin, subcutaneous tissue)
      • Incisional – deep ( fascial planes, muscles)
      • Organ/ space related ( anatomic location of procedure) eg : intra abd abscess

    • Incidence of SSI: 38%
    • Most common: incisional infections : 60 -80% of SSIs.
    • Organ related SSIs – 93% of SSI related mortality.

    CRITERIA FOR DEFINING A SURGICAL SITE INFECTION

    Superficial incisional SSI

    Criterias as per Defn. + at least one of the following:

    • 1. purulent drainage, with or without laboratory confirmation, from the superficial incision.
    • 2. organisms isolated from an aseptically obtained culture of fluid or tissue from the superficial incision.
    • 3. at least one of the following signs or symptoms of infection:

    _ pain or tenderness

    _ localised swelling

    _ redness

    _ heat

    • 4.diagnosis of superficial incisional SSI by the surgeon or attending physician

    Deep incisional SSI

    Criterias as per defn + at least one of the following:

    • 1. purulent drainage from deep incision .
    • 2. a deep incision spontaneously dehisces or is deliberately opened by a surgeon when the patient has either

    _ fever (>38C)

    _ localised pain or

    _ tenderness

    • 3. an abscess or other evidence of infection involving the deep incision is found on direct examination, during reoperation, or radiologic examination
    • 4. diagnosis of deep incisional SSI by a surgeon or attending physician.
    • Note: Report infection that involves both superficial and deep incision sites or an organ/space SSI that drains through the incision as deep incisional SSI.

    Organ/space SSI

    Criterias as per definition + at least one of the following:

    • 1.purulent discharge from a drain that is placed through a stab wound into the organ/space
    • 2.organisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space
    • 3.an abscess or other evidence of infection involving the organ/space that is found on direct examination, during reoperation, or by histopathologic or radiologic examination.
    • 4.diagnosis of an organ/space SSI by a surgeon or attending physician.

    Causes and Risk factors:

          • Bacterial factors.
          • Local wound factors.
          • Patient factors.

    Bacterial factors:

      • Bacterial no., Virulence, antimicrobial resistance.
      • Wound classification:
      • Length of preoperative hospital stay.
      • Remote site infection at the time of surgery.
      • Duration of the procedure.
      • Pre operative shaving.
      • Intensive care unit patient.
      • Prior antibiotic therapy.
    • Bacterial no., Virulence, antimicrobial resistance.
      • Toxins, resistance to phagocytosis, intracellular destruction.
      • Surface components ( capsules, lipopolysaccharides)
      • Bacterial load more than 105.
    • Duration of the procedure:

    Prolonged surgeries : > 75th percentile for that procedure.

    • Preoperative shaving:
      • Increases risk by 100%.
      • Extensive shaving not needed. Removal by clippers before procedure preferred.
      • Prior antibiotic therapy : Increases chances of antibiotic resistance.
    • Wound classification:
    Clean uninfected operative wound/ not entered visceral tracts/ primarily closed. 1 to 5%
    Clean

    Contaminated

    Visceral tracts opened under control without much contamination. 3 to 11%
    Contaminated open fresh accidental wounds / operations with breaks in sterile technique/ gross spillage from visceral tracts. 10 to 17%
    Dirty. traumatic wounds with dead tissue/ with clinical inf / perforated viscera > 27%

    Antibiotic Prophylaxis applies to all Elective operations ( first 3 categories) and Emergency operations of the clean type. Other categories – Antibiotic Therapy.

    Local wound factors.

      • Hematoma / seroma.
      • necrosis.
      • Sutures.
      • Drains.
      • Foreign bodies.

     

    • All these factors, increase the risk of SSIs.
    • Good surgical technique – best way to avoid SSIs.

    Patient factors.

          • Comorbidities
          • Age
          • Immunosuppression
          • Malignancy
          • Obesity
          • Diabetes
          • Malnutrition.
          • Perioperative transfusions
          • Cigarette smoking
          • inspired oxygen fraction
          • Body temperature.
          • Glucose control
    • Comorbidities:

    American society of anaesthesiologists - Preoperative risk score ( ASA score) based on Co-morbidities.

    ASA score Physical state
    1 Normal healthy patient
    2 patient with mild systemic disease
    3 Pt with severe systemic disease- limits activity but not incapacitating.
    4 Pt With incapacitating systemic disease- constant threat to life.
    5 Moribund patient- not expected to survive beyond 24hrs.

    An ASA score of > 2 , increases risk of SSI.

    • inspired oxygen fraction: > 80% - ^ oxygen tension & white cell function & decreases SSIs.
    • Body temperature: Normothermia reduces SSIs.
    • Glucose Control: control of glucose levels in perioperative period and later upto 48 hrs reduces SSIs.

    Prevention of SSIs:

    Preventive measures can be:

      • Micro organism related
      • Local wound related
      • Patient related

    Microorganism related.

    Primary measures that have proven effective.

      • Aseptic & antiseptic technique.
      • Proper antimicrobial prophylaxis.
      • Implementation of surveillance programmes.

    Aseptic and antiseptic techniques.

    Environmental & architectural char. of OT.

    • Size
    • Air management
    • Equipment handling
    • Traffic rules
    • Operating Room personnel asepsis and clothing.

    Surgical site preparation.

    • Antiseptic preoperative showers
    • Skin preparation of the surgical site ( germicidal antiseptic, incise drapes)
    • Scrubbing ( 1st time – 5 mins, consecutively 3 mins)
    • Alcoholic hand scrub soln.
    • Sterile drapes & gowns.
    • Double gloving.

    Preventive measures can also be classified as:

    Timing of action Microorganism Local Patient
    Preoperative Shorten preoperative stay

    Preoperative antiseptic shower

    Proper hair removal

    Rx-remote site Inf

    Antimicrobial prophylaxis.

    Proper hair removal Optimize nutrition.

    Pre op warming.

    Glucose control.

    Stop smoking

    Intraoperative Asepsis & antisepsis.

    Avoid spill in GI cases

    Surgical technique:
    • Hemotoma/seroma
    • Good perfusion
    • Complete debridement
    • Dead spaces
    • Monofil sutures
    • Justified drain use( closed)

    Delayed primary closure when indicated.

    Supplemental oxygen

    Intra op warming

    Adequate fluid resusc.

    Glucose control

    Postoperative Protect incision for 48-72 hrs

    Remove drains ASAP

    Avoid post op Bacteremia.

    Post op dressing for 48-72 hrs Early enteral nutrition

    Supplemental oxygen

    Tight glucose control

    Surveillance programs

     

     

     

    Anti microbial prophylaxis

    Prophylaxis: Why?

    • Hospital acquired infection , of which SSI is the commonest, costs about 170 million $ in UK
    • SSI increase morbidity & mortality, Prolong hospital stay, and increase medical care cost.
    • Colorectal surgery -high risk of SSI due to contamination by contents of large bowel
    • Use of antimicrobial prophylaxis - reduces risk of wound infection from 40% to 11%.
    • Reduces need for long term antibiotic Rx- reduces development of resistance.
    • In trials of antibiotics vs No antibiotics use in colorectal surgery , the SSI rate was 12.9% vs 40.2%.

    Reality check:

    • UK audits :25 – 50% of all antibiotics prescribed - for prophylaxis.
    • Prophylactic use is often inappropriate than therapeutic use.
    • Prophylactic antibiotic use is suboptimal in 40-50% of operations.
      • lack of reliable process in the hospital.
      • Lack of understanding.

    Goals of Antibiotic prophylaxis

    • Reduce incidence of SSI.
    • Antibiotic Use supported by evidence of effectiveness.
    • Minimal effect on Pts normal bacterial flora.
    • Minimal adverse effects.
    • Minimal change to Pt’s host defences.

    *Antibiotic prophylaxis is an adjunct to , not a substitute for good surgical technique.

    Principles of antimicrobial prophylaxis

    • Choice of antimicrobial agent and regimen.
    • Timing and duration
    • Route of administration.

    Choice of antimicrobial agent

    • Regimens designed should cover the entire spectrum of suspected microbes. In colorectal surgery – both aerobes & anaerobes..
    • No antibiotic reliably superior than other, when each possessed similar & appropriate antibacterial spectrum.
    • >70 different antibiotic regimens exist- effectiveness similar.
      • Past history of adverse event- preclude use of particular gr of antibiotics.
      • Prophylactic Antibiotics ,chosen as per local prevalence of antibiotic resistance.
      • Search for ideal prophylactic regimen – continuous process. Avoid ,Universal acceptance and use of any particular regimen

     

    Timing and duration

    • Concentration of antibiotics in the surgical wound should exceed MIC of the bacteria at the time of bacterial contamination, to prevent infection.
    • Most effective when begun preoperative & continued per operative.
    • First dose – within 30 mins of anesthesia induction.
    • Antibiotics started as late as 3 hrs after contamination are markedly less effective.
    • Single dose regimen vs multiple dose regimen- no significant difference.
    • For prolonged surgeries – repeated doses at intervals of 1 or 2 half lives for the drug.
    • Decision regarding multiple dose regimen should be based on other factors which increase the risk of infection, such as:

    - Duration of surgery.

    - Peri operative blood transfusion.

    - Presence of drains.

    - Immunocompromised state, etc,,.

     

    Route of administration

    • Prophylactic antibiotics for surgical procedures should be administerd intravenously.
    • Oral + parenteral antibiotic prophylaxis is advocated for colorectal surgery. In RCT of Parenteral alone Vs parenteral + oral antibiotics, significant reduction in infection rate in latter group.

    Antimicrobial therapy of SSI

    • Difficult- resistant bacteria due to pre operative antibiotic therapy.
    • Should cover specific bacteria isolated and facultative & obligate anerobic flora.
    • D O C : 1. 3rd generation Cephalosporin or Quinolone + metronidazole.

    2. Imipenem or expanded spectrum pencillins + b lactamase inhibitor.

    3. In resistant enterobacteria or serratia – aminoglycoside & b lactam inhibitor.

    • Superficial incisional: drainage only , no antibiotics.
    • Deep incisional: Drainage, Control of source, Antibiotic Therapy.
    • Organ/ Space SSI:

    Operative , as any other sec peritonitis.

    or

    Non operative drainage – CT or US guided ( if abscess not associated with anastomosis.) with antibiotic therapy.

    Antimicrobial drugs & their Spectrum

    Pencillins.

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Pencillin G B- lactam mech.- inhibits bact. Cell wall synthesis. short Strep sp. ( expt entrococcus and pneumococcus.), Neisseria sp.
    Antistaph.

    Methicillin, Oxacillin, Nafcillin.

    B- lact mech + pencillinase resistant + acid stable short Staph sp ( meth sensitive)
    Anti G -ve.

    Ampicillin, Amoxicillin

    B- lact mech short Strp sp.( including enterococci), Neisseria sp.. H. influenze, E.coli, proteus.
    Expanded spect.

    Carbenicillin, Ticarcillin

    B- lactam mech short Expanded G –ve act. Mod anaerobic act,
    Very adv spect

    Mezlocillin,piperacillin

    b-lactam mech short Same as expanded spectrum + more act against pseudomonas, acinetobacter, serratia.

    Pencillins + B-lactamase inhibitors

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Clavulinic acid +

    Ticarcillin/amoxicillin

    Inhibits b-lactamase Increases antibacterial act. Of b-lactam antibiotics. Short/

    medium

    + staph, H. influenzae, anaerobes
    Sulbactum +

    Ampicillin

    - do - short + enterococcus
    Tazobactum +

    Piperacillin

    - do - short + staph, some G –ve rods &anaerobes.

    Cephalosporins.

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    First Generation

    Short h/l:Cephalothin, cephapirin.

    Long h/l:Cefazolin.

    b-lactam mech. short Strep sp ( expt enterococci),Staph (meth. Sens.), few G –ve rods.
    Second gen.

    Poor anaerobic act .

    Short h/l: Cefamandole, cefuroxime

    Long h/l: Ceforanide.

    Good anaerobic act.

    Short h/l: cefoxitin.

    Long h/l: cefmetazole, Cefotetan.

    - do - Medium

    Short

    Long

    Short

    long

    Same as I gen cephalosporins +exp G –ve act ( expt pseudomonas, acinetobacter, serratia.

    Same as above + many anerobes.

    Cephalosporins…cont

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Third Gen:

    Poor pseudomonas actShort h/l: cefotaxime, cetizoxime.

    Long h/l:

    Ceftriaxone

    Good pseudomonas act.Cefoperazone, Ceftazidime, Cefepime

    B- lactam mech. Short

    Long

    medium

    Most G –ve rods expt pseudomonas, acinetobacter, serratia. Poor anerobic act. Less act against strep & staph sp.

    Same as above + act against pseudomonas, acinetobacter, serratia.

    same as above + more G +ve act

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Monobactams

    Aztreonam

    B lactam mech. Preference to pbp3 of G –ve bacteria , b lactamase resistant. short Most G –ve , including pseudomonas & serratia. Inactive against G =ve cocci, anaerobes.
    Carbapenems

    Imepenem/ cilastatin

    Meropenem

    Ertapenem

    B lactam Mech + Cilastatin Mech ( inactivates dihydropeptidases.) Short

    Short

    long

    Extremely broad – G +ve & G –ve aerobic & anerobic. Mod active against e-cocci.

    - do -

    More active against enterobacteriae . less against G +ve cocci.

    Quinolones

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Poor anaerobic act.

    Norfloxacin

    Ciprofloxacin

    Ofloxacin

    levofloxacin

    Inhibits DNA-gyrase, inhibits DNA replication Long

    Long

    Long

    Long

    Very broad G –ve act , including Pseudomonas, serratia & acinetobacter.

    G +ve act, Poor anerobic act.

    Better anerobic act.

    Gatifloxacin

    Moxifloxacin

      Very long

    Very long

    As above + better G +ve , G –ve & anerobic coverage.

    Aminoglycosides.

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Gentamycin

    Tobramycin

    Amikacin

    netilimycin

    Binds to 30s ribosome subunit, inhibits protein synthesis medium Broad G –ve coverage. Poor act against strepto sp. No anerobic act.

    Anti anerobes.

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Chloramphenicol Binds to 50s su, inhibits protein syn. long G + ve & few G –ve rods, most anerobes.
    Clindamycin - do - long Strep sp. Expt enterococci, staph sp, anaerobes. Inactive against G –ve rods
    Metronidazole Not fully known , probably cytotoxic. Very long Very act against most anerobes, protozoa. Inactive against facultative & aerobes.

    Miscellaneous.

    Drug class & name Mechanism of action Half life Antibacterial spectrum
    Glycopeptides

    Vancomycin

    Inhibit cell wall synthesis & RNA syn. / affects membrane permeability Very long Strep sp. Including e–cocci, staph ( including MRSA), clostridium Sp. No activity against G –ve rods.
    Streptogram

    ins

    Quinupristin/ dalfopristin

    Binds to 50s su medium Most G +ve bact,( including VRE,MRSA, pencillin resist S- pneu.)
    Macrolides

    Erythromycin

    - do - medium Most G +ve Neisseria, campylobacter, mycoplasma, Chlamydia, rickettsia, legionella
    Tetracyclines

    Tetracycline

    Doxycycline

    Binds to 30s su. inhibits protein syn Long

    Very long

    Many G +ve, easy G + ve rods, some anerobes, rickettsia, Chlamydia, mycopasma.

    Antibiotic prophylaxis in Colorectal surgery.

    • Antibiotic prophylaxis is Highly recommended.
    • The risk of SSI following Colorectal surgery is 40 to 60 % without prophylaxis.

    Preperation for elective colorectal surgery :

    Condon Nichols Preperation.

    Preoperative day: Oral sodium phosphate solution with or without Bisacodyl in a 1 to 2 dose regimen before administration of oral antibiotics .

    + Clear liquid diet.

    + 1 gm each of oral Neomycin & Erythromycin taken at 19, 18 and 9 hours prior to surgery.

    Operative day: Completely evacuate the bowel prior to surgery.

    + Parenteral antibiotics 30 mins

    prior to incision ( an Aminoglycoside or Cephalosporin like Cefotetan / Cefoxitin in combination with Clindamycin / Metronidazole.)

    Benefits of Antibiotic Prophylaxis

    • The benefit of antibiotic prophylaxis in terms of the incidence of SSI after elective surgery is related to the severiy of the Consequences of the SSI. ( for eg. In colon anastomosis , prophylaxis reduces mortality)
    • Shortens the hospital stay.
    • Faster return to normal activity.

    Risks Of Prophylaxis.

    • Inappropriate use of antibiotics for prophylaxis.
    • Increased risk of C.difficile colitis (even single dose increases risk , however more common after prophylaxis of > 24hrs.

    Final decision regarding ,benefits & risks of Prophylaxis for an individual pt will depend on:

      • Patients risk of SSI.
      • The potential severity of the consequences of SSI.
      • The effectiveness of prophylaxis in that operation.
      • The consequences of prophylaxis for that patient

    ( e.g. increased risk of colitis)

    Antibiotic Prophylaxis : Conclusions.

    • Antibiotics or antibiotics combinations should be active against both aerobic & Anaerobic bacteria .
    • Administration should be timed, so that the tissue concentration of antibiotics around the wound area is sufficiently high when bacterial contamination occurs.
    • Single dose regimens are as effective as multiple dose regimens and are associated with less toxicity, fewer adverse effects , lower bacterial resistance rates and lower costs.
    • Universal acceptance and use of one particular regimen should be avoided.
    • Guidelines for prophylaxis should be developed and regularly reviewed, locally by surgeons , microbiologists and pharmacists, taking into account local resistance profiles.
    • Antibiotic prophylaxis is an adjunct to , not a substitute for good surgical technique.