Surgical Infections 1

Dr. Valentine Mbithi

General Surgeon
AIC Litein Hospital
Introduction
Surgical Infections include infections requiring
surgical management and those as a result of surgery.
Host Defense Mechanisms
A: Barriers
Skin
Mechanical barrier
Acidic pH 5-6
Relative lack of water
Constant epithelial cell turnover
Host Defense Mechanisms: Barriers
Respiratory Tract epithelium
Mucous blanket- traps inhaled particles
IgA produced by lymphoid tissue: Prevents microbe
adherence to respiratory epithelium
Cilliary mechanism: steadily rolls mucous to pharynx,
than expelled and coughed or swallowed
 Barriers
Stomach: Acidic pH: prevents growth of most bacteria.
Antacids, PPI and H2 blockers increase risk of bacterial
and fungal colonisation and thus pneumonia especially in
the case of aspiration or in intubated patients
Urinary tract: IgA, long urethra in males
B)Microbial Flora
Small and Large Intestines: Abundant normal flora that
prevent growth of pathogenic microbes. Peristalsis
keeps population constant.
Normal Small intestine and Colon Flora
Anaerobes: Bacteroided Fragilis, Fusobacterium,
Peptostreptococcus, more that aerobes
Aerobes: Escherichia Coli, Enterococcus fecalis
C: Immunology
 Phagocytic leukocytes ingest pathogens via
phagocytosis and act as Antigen Presenting Cells to T
cells.
Monocytes and granulocytes(neutrophils and eosinophils).
Macrophages are differentiated monocytes residing in all
body tissues but heavily concentrated in lungs, liver and
spleen.
Migrate to areas of inflammation by chemotaxis
Opsonisation by complement and immunoglobulins
facilitate recognition of pathogens.
Opsonisation and phagocytosis are body’s primary
defence mechanism against extracellular pathogens.
Immunology
Cellular Immunity: Deals with intracellular microbes:
viruses
Afferent limb: recognises foreign pathogen. Involves
antigen presentation and T cell activation
Efferent limb: destroys infected cell. Includes cytotoxic
T cells, monocytes, macrophages and granulocytes
Humoral responses
Immunoglobulins: IgA, IgD, IgE, IgG, IgM
 Neutralise viruses and bacterial toxins
 Inhibit microbial attachment to host cells
 Opsonise pathogens
 Activate complement cascade
Complement: a nonspecific defence system that is
activated by antibody and initiates a cascade of reactions
that lead to cell lysis.
Surgical Microbiology and Pathogenicity:
Viruses
 Obligate intracellular pathogens
Viral infections of surgical importance
 TORCH: Congenital Malformations
 HIV: Altered Immune function
 HTLV1, HPV increased cellular proliferation and
oncogenesies
 Enterovirus: Appendicitis
 CMV: Ulcerative Colitis
 Adenovirus: Intussusception
 Hepatitis B and C: End Stage Liver Disease requiring Liver
transplantation
Bacteria
Are pathogenic single cells: either rods, spheres or
spirals. Either gram positive or negative depending on
cell wall structure.
Pathogenicity: bacteria adheres to epithelial surface
and cause disease by
Invading host tissues e.g Streptococcus pneumoniae
Producing toxins : Endotoxins and exotoxins e.g.
Clostridium perfringens, C. difficile, S. Pyogenes, S.
Aureus
Inciting pathologic Immune response
Fungi
 Rarely cause infection in immunocompetent host.
 Risk factors for fungal infection: HIV, transplant
patients, diabetes, prolonged hospitalisation, Central
Lines, prolonged or broad spectrum antibiotic use,
parenteral nutrition, immunosupressive drugs, burns,
trauma and malnutrition.
 Infection occurs by
Inhalation e.g. aspergillosis, histoplasmosis , blastomycosis
Innoculation of subcutaneous tissues: sporotrichosis
Colonisation of mucosal surfaces: oral or esophageal
candidiasis
Antimicrobial Therapy
Proper Selection of antibiotic requires knowledge of
The most common pathogens causing specific infection
The mechanism of action of the selected agent
Potential side effects of selected agent
Sensitivity patterns of most common microbes in the
area.
Inhibitors of Cell Wall Synthesis: B-Lactam
Antibiotics
 The B lactam ring inhibits cell wall peptidoglycan synthesis
causing cell lysis.
 Resistance is caused by bacterial production of B-lactamase.
 Penicillins: Penicillin G, Amoxicillin, ampicillin,
flucloxacillin, Piperacillin: different bacterial coverages.
Allergic reaction is major adverse effect.
 Cephalosporins: 1st to 4 th generation antibiotics. Do not
cover enterococcus. Cross allergic reaction with penicillins
more common in lower generations
 Imipenem and Meropenem: Broadest spectrum
 Vancomycin: Good gram positive coverage, good for MRSA
Inhibitors of ribosomal Protein Synthesis
Aminoglycosides e.g gentamycin, amikacin
Bactericidal. Adverse effect of renal and ototoxicity.
Aerobic gram negative coverage
Macrolides: Erythromycin, clindamycin
Tetracyclines: Tetracycline, minocycline.
Broadspectrum.
Chloramphenicol: Broad spectrum, good BBB
penetration
Inhibitors of folic acid synthesis
Sulfonamides and Trimethoprim: synergistic action
Good for UTI, MRSA, PCP.
Sulfur allergy
Inhibitors of DNA synthesis
Fluoroquinilones: Ciprofloxacin, Norfloxacin,
Ofloxacin: Good for GI and GU infections
Metronidazole: Anaerobes.
Antifungals
Fluconazole: few adverse effects
Amphotericin B: nephrotoxicity, electrolyte
disturbance, leukopenia, anemia, thrombocytopenia
Chlotrimazole
Griseofulvin
Capsofungin
 Surgical Prophylaxis and prevention of
surgical Site infections
 SSIs are most common nosocomial infections and result
in prolonged hospitalisation, increased costs and
significant morbidity.
 Wound infections can be attributed to endogenous
contamination from skin flora and GI contamination or
exogenous contamination from break in sterile technique.
 Operative site should be scrubbed using germicidal
detergent folowed by application of povidone or
chlorhexidine paint.
 Hair clipping and not shaving.
 If GI or GU tracts entered, gloves should be changed after
dirty part of procedure is done
Pre-operative antibiotics reduce infection risk for
clean- contaminated and contaminated wounds
Clean cases do not require antibiotic prophylaxis
except in implant or bioprosthetic material placement.
Cefazolin for most wounds. Vancomycin if allergic to
penicillins and cephalosporins
Second generation antibiotic eg cefotetan or cefoxitin
in bowel surgery plus metronodazole
Other measures to decrease operative wound infections
include: obliteration of dead space, removal of necrotic
tissue, wound closure without tension, hemostasis.
Drains may help evacuate hematoma or seroma but are
foreign bodies and increase infection risk and should
not be used routinely.
Immunotherapy: Tetanus toxoid for dirty wounds
Classification of Operative wounds
Clean: Elective, nontraumatic, primarily closed, no
acute inflammation, no break in sterile technique. No
entry to respiratory, GI, GU, biliary tract
Clean Contaminated: Urgent or emergent cases that are
otherwise clean, elective with opening of GI, GU,
Biliary,respiratory tracts, not encountering infeected
bile or urine, minor break in sterile technique
Contaminated: Nonpurulent inflammantion, gross
spillage from GI tract, entry to infected GU or biliary
tract, major break in sterile technique, penetrating
trauma < 4 hrs old, chronic wounds for grafting
Dirty: Purulent inflammation, preoperative perforation
of GI, GU, biliary, resp tracts, penetrating trauma > 4
hrs
Surgical Infections 2
Intra-abdominal Infections
Cellulitis
Necrotising Soft Tissue Infection
Gram Negative Bacterial Sepsis
Catheter and Prosthetic Device Infection
UTI
HIV in the Surgical Patient
Diabetic Foot
Empyema Thoracis