Health

1. ANTIBIOTICSIN
SURGERY
Prof. Dr. Senthil Kumar

2. OUTLINE
• Introduction
• Antibiotics Classification
• Usesof Antibiotics in Surgery
• Prophylaxis
• Therapeutic

3. ANTIBIOTICS: a natural substance produced by a micro-organism to
kill another.
• They include the culture extracts and filtrates of fungi such as
penicillium and cephalosporium and bacteria such as streptomyces
and bacillus species.

4. ANTIMICROBIAL: any natural or synthetic agent that kills
pathogens
• They include the sulfonamides, trimethoprim, cotrimoxazole,
nitrofurantoin, nalidixic acid, metroniadazole, P.aminosalicylic
acid, isoniazid and ethambutol.
• Antifungal agents include nystatin, and flucytosine.

5. NORMALFLORA

6. Mechanism of Action
• Inhibition of Cell Wall Synthesis
• Disruption of Cell Membrane
• Inhibition of Protein Synthesis
• Inhibition of Nucleic acid synthesis
• Interference with Metabolic Processes

7. ANTIBIOTICSCLASSIFICATION

8. Cell wall synthesis inhibitors
• Beta-lactams
• Poly-peptides
Protein synthesis inhibitors
• Aminoglycosides
• Tetracyclins
• Macrolides
• Chloramphenicol
• Clindamycin
Folate antagonists
• Sulfonamides
• Trimethoprim
• Quinolones

9. Beta-lactams Poly-peptides
Classification
Cell wall synthesis inhibitors
Penicillins
Cephalosporin
Monobactam (Aztreonam)
Carabpenems
(Meropenem/Imipenem)
Bacitracin
Vancomycin

10. Cell wall synthesis inhibitors
Penicillins Cephalosporins
Beta lactams
Narrow spectrum – penicillinase sensitive
Benzylpenicillin, Phenoxymethylpenicillin
Narrow spectrum – penicillinase resistant
Methicillin, Oxacillin, Cloxacillin, Dicloxacillin
Broad spectrum penicillins
Ampicillin, Amoxicillin
Extended spectrum penicillins
Carbenicillin, Ticarcillin, Mezlocillin, Pipercillin
First generation –
β-lactamase sensitive
Cephazolin, Cephalexin
Third generation – mostly
β-lactamase resistant
Cefotaxime, Ceftriaxone
Second generation – β-
lactamase sensitive
Cefaclor, Cefamanodole
Cefoxitin
Fourth generation – mostly
β-lactamase restistant
Cefepime, Cefpirome

11. Mechanism of action :
1. The β-lactam binds to Penicillin Binding
Protein (PBP)
2. PBP is unable to crosslink peptidoglycan
chains
3. The bacteria is unable to synthesize a stable
cell wall
4. The bacteria is lysed

12. Classification
Protein synthesis inhibitors
Aminoglycosides
Tetracyclines
Macrolides
Chloramphenicol
Clindamycin

13. Classification
Aminoglycosides
Protein synthesis inhibitors
• Gentamicin
• Tobramycin
• Streptomycin
• Neomycin
• Kanamycin
• Amikacin
Tetracyclines Macrolides
• Tetracycline
• Doxytetracycline
• Minocycline
• Doxycycline
• Erythromycin
• Azithromycin
• Clarithromycin

14. Classification
Sulfonamide
Folate antagonist
• Sulfadiazine
• Sulfadimidine
• Sulfamethoxazole
Quinolones Trimethoprim
• Nalidixic acid
• Ciprofloxacin
• Levofloxacin
• Ofloxacin
• Norfloxacin
• Travofloxacin

16. PrinciplesofAntibiotics in
Surgery
• Indication (prophylaxis vs.therapeutic)
• Susceptibility vs.empirical
• Pharmacokinetic
• Pharmacodynamics
• Combination ?
• Cost
• Availability
• Monitoring
• Compliance

17. Antibiotics Prophylaxis inSurgery
• Use of antibiotic where there is no evidence of infection
but expected to be exposed to pathogens that constitutes
a major risk of infection.
• Single dose regime, based on the most common organism,
which is given at the time of induction to ensure the minimum
inhibitory concentration during skin incision –reduces risk of
surgical site infection (SSI)and post op infection.

18. • Usually a single dose is sufficient. A second dose
may be required in the following situations:
a. in prolonged operations
b. when there is contamination during operation
• Giving more than 1 or 2 doses postoperatively is
generally not advised. The practice of continuing
prophylactic antibiotics until surgical drains have
been removed is not recommended.

19. General Principles ofSurgical
Prophylaxis
• A single preoperative dose of antibiotic is as effective as
full five days course of therapy assuming uncomplicated
procedure.
• Prophylactic antibiotics should be administered within 1
hour prior to incision, preferably with induction of
anesthesia.
• Prophylactic antibiotics should targetanticipated
organisms.

20. • Prophylaxis is generally recommended for clean-
contaminated (risk of infection is 6%) and
contaminated (risk of infection is 15%)
operations.
• In clean operation prophylaxis is also indicated under
certain conditions i.e. where there is prosthesis
implanted, high risk perforation where infection is
catastrophic e.g. neurosurgery or cardiac surgery.

21. Classificationof SurgicalWound

22. GoalsofAntibiotic Prophylaxis
• Reducethe incidence of surgical site infection (SSI)
• Minimize the effect on the patient’s normal bacterial
flora.
• Minimize adverse side effects of antibiotics.
• Minimize the emergence of antibiotics resistant strains of
bacteria.
• Costeffectiveness.

23. PROCEDURE SUGGESTED ANTIBIOTIC
1. GI surgery
2. HBS surgery
IV Cefoperazone 1g PLUS IV
Metronidazole 500mg
1.Hernia repair with mesh
(includes laparoscopic repair)
2. Breast
(not recommended for minor
excision
3.Burns
IV Cloxacillin 1G
Vascular Operation IV Ampicillin/Sulbactam 1.5g
Neurosurgery IV Ceftriaxone 1gm AND
IV Metronidazole 500mg
Urology IV Amoxicillin / clavulanate 1.2g
GUIDELINES FOR SURGICAL
PROPHYLACTICANTIBIOTICS

26. THERAPEUTIC ANTIBIOTICS

27. Therapeutic
Antibiotics:
PRINCIPLES
C&S
Pharmaco-
dynamics&
TDM
Hoststatus
Site of
infection
Combination
Prevent
resistance
Synergism/
Additive
therapy
Multiple
pathogens

28. THERAPEUTIC
ANTIBIOTICS
Empirical
Initiation of treatment
prior to determination of a
firm diagnosis
Definitive
Specific toorganism isolated
inC&S

29. EMPIRIC THERAPY
• When to start?
• Riskof surgicalinfection is high - basedon the underlying disease
process(e.g.perforated appendicitis)[prophylaxis  empiric]
• Significant contamination during surgeryhasoccurred(e.g.
considerablespillageof colon contents)
• In critically ill patients –potential site of infection hasbeenidentified
• Severe sepsisor septicshock
• Short course (3-5days)
• Stop if the presence of alocal site or systemic infection is not
revealed.

30. MONOMICROBIALVS
POLYMICROBIAL
• Monomicrobial infections:
• Nosocomialwhich occurredin postoperative patients, e.g.UTI,
pneumonia, catheter-relatedinfection
• Polymicrobial infections:
culture results lesshelpful
• Thus,antibiotic regimen should not be modified solely on
culture information. Clinical course is moreimportant.

31. Systemic InflammatoryResponse
Syndrome(SIRS)
• Empiric antibiotics are not indicated for all patients with
SIRS
• Indications for antibiotic therapy include the following:
• Suspected or diagnosedinfectious etiology (e.g.UTI,
pneumonia,cellulitis)
• Neutropenia or other immunocompromised states
• Asplenia- Dueto the potential for overwhelming
postsplenectomyinfection

32. • Abdominal trauma –3rd generationCephalosporins,
Cefuroxime, Augmentin,Unasyn
• Perforatedviscus,Peritonitis - 3rd generationCephalosporins
& Flagyl
• Breast abscess(S.aureus) –Cloxacillin
• Mycotic pseudoaneurysm –Cloxacillin
• Prostethic graft infection - 3rd generationCephalosporins
• MRSA-Vancomycin

33. DURATION OF THERAPY
• Duration should be long enough to prevent relapse
yet not excessive, asit canincrease side effects and
resistance.
• Factors suchasdecreasing trend ofWBCsand lack of
fever guide the length of therapy.
• The search for extra abdominal source of infection
or aresidual /ongoing source of intra abdominal
infectionshould be sought.

34. DURATION OFTHERAPY
• Penetrating GItrauma withoutextensive
contamination
• 12-24hours
• Perforated/gangrenous appendicitis
• 3-5days
• Peritoneal soilage due to perforated viscuswith
moderate degrees ofcontamination
• 5-7days
• Extensive peritoneal soilage/immunocompromised
host
• 7-14days

35. SIDE EFFECTS
Antibiotic Side Effects
Penicillins • Allergy (seriousanaphylaxis)
Cephalosporins • Allergy
Aminoglycosides • Hearing loss
• Vertigo
• Renaldysfunction
Carbapenems • Seizures(Imipenem)
• Rashes
Macrolides • Prolonged QTinterval
(Erythromycin)
• Hearing loss
• Jaundice

36. ANTIBIOTICRESISTANCE
• Resistance of amicroorganism to an
antimicrobial agent to which it was previously
sensitive.
• Resistant organisms are able to withstand attack
by antimicrobial medicines so that standard
treatments become ineffective and infections
persist and may spread to others

37. ANTIBIOTICRESISTANCE
Intrinsic
• Drug target is not present in the bacteria’s metabolic
pathways
Acquired
• Mutation
• Transferof genetic material from resistant to susceptible
organisms (plasmids, transposons,bacteriophages)

38. Main factors contributing to resistance are:
• Excessantibiotic usage
• Incorrect useof broad spectrum agents
• Incorrect dosing
• Noncompliance

39. Resistance to Antibiotics
• By genetic mutation — changes to the proteins and other
components of bacterial cells which Antimicrobial use as
binding sites (DRUG INACTIVATION OR
MODIFICATION).
• Gene transfer: plasmids (via conjugation and
transduction);
• By bacteria producing enzymes (β-lactamase) that destroy or
inactivate Antimicrobial.
• Microbes may cease active uptake of certain

40. Resistance to Antibiotics
• Changes in receptors which decrease antibiotic binding and
action : ALTERATION OF TARGET OR BINDING SITE
OF ANTIBIOTICS)
• Microbes may synthesize compounds that antagonize drug
actions.
• By bacteria altering the permeability of their cell membrane
making it difficult for Antimicrobial to enter (ACTIVE
EFFLUX).
• Antibiotic use promotes the emergence of drug-resistant
microbes.

41. THANKYOU