INTRODUCTION:
Surgical site infections are one of the most common hospital
acquired infections, which constitute 38% of surgical infections. It creates great burden to the patients by increasing hospital stay by 7-10 days. Also, it increases hospital expenditures creating an economic burden to the patient and country.
AIMS AND OBJECTIVES
The objective of the study was to evaluate the role of
prophylactic antibiotics to prevent surgical site infections in clean and
elective surgeries.
Surgeries included in the study were:
1. Hernia repair:
Open hernioplasty, Laparoscopic hernioplasty.
2. Neck: Thyroid surgeries, Lipoma nape of neck.
3. Breast: Modified radical mastectomy, Excision biopsy.
4. Scrotal surgeries: Hydrocele, Epididymal cyst excision.
PROPHYLACTIC ANTIBIOTIC VS NO ANTIBIOTICS:
To compare the surgical site infection in two groups of
patients,
1. one receiving prophylactic antibiotics (Study group) and
2. the other group without any prophylaxis before surgery.
(Control group).
ANTIBIOTICS:
To compare the surgical site infection in two groups of
patients,
· one receiving prophylactic antibiotics (Study group) and
· the other group without any prophylaxis before surgery.
(Control group)
REVIEW OF LITERATURE
Historical background:
As surgeons, though we deal with infections since the dawn of
time, our understanding to treat wound infection became clear only after
the development of theory of antisepsis and the evolution of germ
theory. Many observations made by nineteenth century physicians were
crucial in our knowledge regarding the pathophysiology, treatment and
prevention of surgical site infections.
Louis Pasteur formulated germ theory and elucidated that
contagious diseases are caused by specific microbes. With the help of
these principles, he pioneered techniques of sterilization. Also, he
identified certain organisms responsible for human infections like
Staphylococcus, Streptococcus, and pneumococcus.
Joseph lister used a solution of carbolic acid, which were used to
treat sewage in his times in Europe, to dress the patients. As this reduced
the post operative infection incredibly, it was quickly adopted
throughout his country.
In 1880, Robert Koch, through his experiments identified
pathogenic organisms associated with specific disease like cholera and
tuberculosis.
Charles Mc Burney pioneered the principle of source control (i.e,
surgical intervention to eliminate the source and thereby treat the
infection) by performing appendicectomy as treatment of appendicitis,
which was previously known to be a fatal disease. This was popularised
after been performed on the King Edward VII of England, by Sir
Frederick Treves.
The discovery of effective antimicrobials helped the modern
surgeons to treat wound infections in a much better way, during the
twentieth century. During world war I, Sir Alexander Fleming, an army
medical officer in British Medical Corps identified the first antibacterial
agent Penicillin through his works on the natural action of blood against
bacteria and sepsis. During his study on influenza virus, in 1928, he
noticed a zone of inhibition around Penicillium notatum colony that
grew profusely on a plate of Staphylococcus. He then named the
substance derived as ‘penicillin’.
This subsequently led to the development of hundreds of potent
antimicrobial agents against infectious organisms, which set an example
for their use as prophylaxis against postoperative wound infection, and
became a very crucial component in the treatment of aggressive and
potentially fatal surgical wound infections.
Prolific advances in the field of clinical microbiology paved way
for the discovery of many new anti microbial agents against those
microbes. Also the discovery of autochthonous microflora of skin,
respiratory tract, alimentary tract helped modern surgeons to enhance
their knowledge about the organisms which will be encountered during
surgery. However, whether these organisms were pathogenic or non
pathogenic remained unclear.
With clinical observations made by veteran surgeons, Frank
Meleny and William Altemier, the fact that aerobes and anaerobes
synergise to cause serious infections (soft tissue infections and
intraabdominal sepsis) came into limelight. So the concept that
inhabitant microorganisms were not pathogenic to human body was
vanished as these organisms have the potential to cause surgical
infections when entered into sterile cavity during the time of surgery.
Over the few last decades, new ideas of polymicrobial nature of surgical
infections were propagated. Aspirates from the peritoneal fluid of
patients with perforated viscus or gangrenous appendicitis also showed
the presence of aerobes and anaerobes. Trials were conducted to know
the effective source control to treat these infections and antimicrobial
agents were administered targetting both pathogens and commensals.
William osler, one of the pioneers of American Medicine, from his
observations noted that patient died due to inflammatory response in the
body to a organism. This allowed our insight into the host inflammatory
response to infection. It is because of activation of multiple pathways in
response to an infection. So many new therapies were formulated
tagetting the modified inflammatory response. Exaggerated
inflammatory response seems to be the cause of end organ failure and
multi organ dysfunction. Thus, treating surgical infections and thereby
preventing multi organ failure is one of the challenges faced by surgeons
like us.
PATHOGENESIS OF INFECTION:
Host defences:
� Barrier
� Microbial flora
� Humoral responses
� Cellular responses
� Cytokine production
Defense barriers:
� Physical barriers
� Chemical barriers
� Immunologic barriers
Mammalian host possesses intrinsic defense mechanisms that help
to prevent invasion of microbes, multiplication of organisms and
thereby cause containment of infection. Our host defences are highly
regulated system and are very effective in coping the invaders. They
include:-
1. Site specific defences (SSD)
2. Systemic defenses
Site specific defenses provide protection at tissue level.
Systemic defences begin immediately after invasion of pathogen
into sterile area of body.
Any micro organism will have to face number of barriers in the
body.
1. Epithelial barrier
2. Mucosal barrier.
Mucosal barriers provided by mucosa of respiratory,
gastrointestinal and urogenital system.
Host barrier cells prevent invasion of microbes and proliferation
by secreting certain substances. Skin commensals adherent to surface
preclude virulent organism invasion, thereby forming colonisation
resistance.
PHYSICAL BARRIERS:
Skin:
Skin, the largest organ in the body provides most extensive
physical barrier. Resident or commensal microflora on the surface of
skin block the attachment of pathogens. Some of the endogenous
microflora include staphylococcus, streptococcus, corynebacterium,
propionibacterium species. Also, Enterococcus faecalis, Enterococcus
faecium, Escherichiae coli, Enterobacteriacae and Candida albicans are
isolated from skin surface below the umbilicus. Skin diseases can be
associated with abnormal proliferation of skin commensals.
Respiratory tract:
Host defences in respiratory tract help to maintain sterile
environment in distal bronchi and alveoli under normal circumstances.
Larger particles are trapped in the mucosa of respiratory tract which are
later cleared through cough. Smaller particles reaching the lower
respiratory tract are cleared by pulmonary macrophages through
phagocytosis. Any breach in this process leads to bronchitis or
pneumonia.
Gastrointestinal tract:
Numerous microbes are encountered in many portions of gastro
intestinal tract. Places where resident microflora are absent include
urogenital, biliary and pancreatic ductal system under normal
circumstances. However, in case of inflammation, malignancy, stone
formation or catheterisation, microorganisms may proliferate.
Vast number of micro organisms are found in oropharynx and
colorectal region. But, organisms found in entire gastro intestinal tract
are not always from oropharynx. It is because of the following reasons:
1. Highly acidic environment in stomach kills the microbes.
2. Low motility in stomach during initial phases of digestion.
Thus, microbial population in stomach accounts to approximately
102 to 103 colony forming units (CFU). But this may be increased during
disease states or drug intake.
In terminal ileum, microbial proliferation occurs, increasing count
to approximately 105 to 108 CFUs. Exponential growth occurs in colon
due to its relatively static and hypoxic environment, where aerobic
species are outnumbered by anaerobic organisms to approximately 10:
1.
FIGURE 1 MICROFLORA IN GASTROINTESTINAL TRACT
Part of GIT Microbial population(CFU/ ML)
Stomach 102 to 103
Small intestine 105 to 108
Distal colorectum 1011 to 1012
Along with facultative and obligate anaerobes like Bacteroides,
Lactobacillus, Clostridium, Fusobacterium and Eubacterium, some
aerobic microbes like Escherichia coli, Enterococcus faecalis,
Enterococcus faecium, Enterobacteriacae and Candida albicans are also
present in the colon. These organisms provide colonisation resistance
and prevent the entry of other organisms like Vibrio cholera, Shigella,
Salmonella. But when pathology like perforation occur, the commensal
organism provide nidus of infection for the pathogens to proliferate.
Surprisingly very little host organisms contribute to the intra abdominal
infection.
When pathogens enter specific body compartments or tissue,
defense mechanisms act to eliminate or remove the nidus of infection.
Apart from providing physical barrier, certain proteins like
1. Lactoferrin and Transferrin sequester microbial growth factor iron.
2. Fibrinogen in inflammatory fluid trap micro organisms and
polymerises to fibrin.
3. Diaphragmatic pumping mechanism on the undersurface of
diaphragm help in expunging micro organisms from peritoneal
fluid.
4. Omentum, ‘the policeman of abdomen’ serves to limit infection.
Immunologic barriers:-
Defense mechanisms in tissues of the body ;-
a) Resident macrophages regulate cellular host defense.
b) Secretion of cytokines is upregulated by substances like TNF –
alpha, IL- 1 beta and INF Gamma.
When microbes interact with defense mechanisms in body,
opsonisation occurs. Extracellular destruction of organisms occur by
formation of membrane attack complex and intracellular destruction by
formation of phagocytic vacuoles.
Complement pathways, both alternate and classical pathways get
activated after microbial invasion. Release of complement fragment
(C3a, C4a, C5a) increases vascular permeability. When microbial insult
occurs, chemotaxis (i.e., attraction of neutrophils to the micro organisms
to the site of insult) occurs. This further leads to the influx of
inflammatory fluid to the area of insult. Diapedesis of neutrophils occur
within minutes and it peaks within a period of hours or days.
Response to an infection depends upon several factors:
1) Number of micro organisms entering the body.
2) Proliferation of organisms
3) Virulence of organisms
4) Potency of defense mechanism
Invasion of microbes can lead to one of the following possible
outcomes.
a) Eradication of infection
b) Limitation of infection ( purulent infection is the hall mark of
chronic infection)
c) Locoregional infection (cellulitis, soft tissue infection)
d) Systemic infection (bacteremia)
Infection is defined as an ‘identification of microorganisms in host
tissue or bloodstream, plus an inflammatory response to their presence’.
The inflammatory signs of ‘rubor, tumor, calor, and dolor’ are common,
at the site of infection. Apart from these local manifestations, certain
systemic manifestations like increased pulse rate and respiratory rate,
elevated temperature and elevated white blood cell (WBC) count.
Above noted systemic manifestations comprise the ‘systemic
inflammatory response syndrome ‘(SIRS).
Fig 2. Causes of SIRS
“Sepsis is not an antibiotic deficiency syndrome”
SIRS when it is caused by microbial infection is termed as sepsis
and it is mediated by production of a cascade of numerous
proinflammatory mediators produced in response to the products of
microbial invasion. These products can be a lipopolysaccharide
(endotoxin) derived from gram-negative bacteria; or a peptidoglycan
and teichoic acid from gram-positive bacteria; multiple fungal cell wall
components such as mannan and numerous others. Patients have sepsis
if they meet the following clinical criteria for SIRS and have an evident
local or systemic infection.
Severe sepsis is defined as sepsis along with the occurence of
new-onset failure of organs. It is the frequent cause of death in surgical
intensive care units, with a very high mortality rate. i.e., when a patient
with sepsis needs ventilatory support and is unresponsive to fluid
resuscitation or one who requires vasopressors to correct hypotension, is
considered to have severe sepsis.
Septic shock is a state in which patient has acute circulatory
failure which is usually identified by the occurence of persistent
hypotension (systolic blood pressure <90 mmHg) inspite of aggressive
fluid resuscitation, with no other identifiable causes. It is the severe
manifestation of infection. It can occur in approximately 40% of patients
with severe sepsis; with a very high mortality rate.
PATHOGENS OF INTEREST FOR SURGEONS:
1. BACTERIA
These are little organisms which are of great importance for the
surgeons, as they form the vast majority of surgical site infections.
Cell wall staining:
� There are a number of species of bacteria which are identified by
a specific staining called Gram’s stain.
� This staining imparts specific colour to bacterial cell wall through
which it is classified as gram positive and gram negative.
a) When they stain blue, they are termed as gram-positive
bacteria.
b) And when a bacteria stains red, it is termed as gramnegative.
Growth characteristics:
• Every bacteria have certain specific growth characteristics
in its specific media.
• Based on a number of some characteristics, bacteria can be
further classified.
It can be depending on
a) Morphological characteristics
b) the pattern of multiplication [e.g., single or multiplication in
groups of organisms, i.e., in pairs (diplococci) or in clusters
(staphylococci), or in chains of organisms. (streptococci).
c) and the presence of spores and its location.
� Terminal spores
� Subterminal spores
Gram +ve
cocci
Gram –ve
bacilli
Gram-positive bacteria
The bacteria that cause surgical site infections are:
a) skin commensals
� Staphylococcus aureus and
� Staphylococcus epidermidis and
� Streptococcus pyogenes and
These organisms cause infections either alone or in combination
with other pathogenic organisms.
b) commensals of GIT such as
Enterococci faecalis and
Enterococci faecium.
They have the capability to cause nosocomial infections like
respiratory infections, catheter associated infections urinary tract
infections (UTIs) and septicaemias in immunologically compromised or
chronically debilitated patients. But in healthy individuals, these are of
little importance.
Gram-negative bacteria:
The organisms which a surgeon specially interested among gram
negative species include:
� E. coli,
� Proteus vulgaris and mirabilis
� Klebsiella pneumoniae
� Serratia marcescens
� Pseudomonas aeruginosa, P. fluorescens.
� Enterobacter
Anaerobic organisms
• These organisms are not able to multiply or divide in the presence
of atmospheric air.
• This is because of the absence of the enzyme catalase, which is
important for the metabolism of reactive oxygen species.
• They are the predominantly available in many areas of the human
body, including oropharynx and colorectum among which flora in
oropharynx is different from the one in colorectum.
� C. Perfringens
� C.difficile
� C. tetani
� C. Septicum or novyi.
� Bacteroides fragilis
� Propionibacterium
� Fusobacterium spp.
Other bacteria of interest to surgeons include:
� Mycobacterium tuberculosis
� M. avium-intracellulare and M. Leprae.
� Nocardia
• These are acid fast and are very slow growing bacilli.
• They are not easily cultivated in laboratory and need specific
culture media to grow which may take several weeks to months.
• They are notorious in causing severe pulmonary and extra
pulmonary infections which is still prevalent in our country.
Viruses:
• Though small in their size, they cause wide variety of infections,
especially in immunocompromised patients.
• Mostly these organisms are intracellular.
• They are extremely difficult to cultivate in artificial culture
media.
• They are usually identified by the presence of DNA and RNA
using specific techniques in polymerase chain reactions.
Viruses of specific importance for surgeons include:
� Hepatitis viruses B and C
� Ebstein barr virus
� Cytomegalovirus
� Herpes simplex virus
� Herpes zoster virus.
Fungi
• Fungi cause a number of nosocomial infections.
• They are identified by special staining methods.
• This can be
� potassium hydroxide
� Giemsa
� India ink
� methenamine silver
• These can be present in yeast form, budding forms or can be
observed with numerous branching along with septations.
• They can cause surgical site infections combined with bacteria.
• They cause severe infections in immunocompromised patients.
• Fungi of interest to surgeons include:
� C. albicans
� Mucor
� Rhizopus
� Absidia spp
� Cryptococcus neoformans
� Aspergillus fumigates and A. niger,
� Coccidioides immitis.
SURGICAL SITE INFECTIONS
NOMENCLATURE
• DEFINITIONS:
Earlier, the term, ‘Surgical Wound Infection Task Force’
(SWITF) was used to ascribe surgical site infections.
The term ‘SURGICAL WOUND’–was replaced by ‘SURGICAL
SITE INFECTION’. This term was formulated by CDC in 1992.
Figure-3 Classification of surgical site
infection
Figure-4 Superficial SSI
CATEGORIES OF SSI
SSI were categorized into two,
1. Incisional SSI
» Superficial
» Deep
2. Organ/space SSI.
Of surgical infections, 60 to 80% are incisional and the
remainder are organ/space infections.
SUPERFICIAL SSI
A superficial SSI can be defined as ‘An Infection occuring within
30 days of surgery and it involves only the skin and subcutaneous tissue
of incision’.
It includes:
• Purulent aspirate from the site of incision associated with or
without positive culture
• Local signs of infection and inflammation – pain, tenderness,
localised swelling, redness, heat and this is usually followed by
FIGURE 5 DEEP INCISIONAL SSI
FIGURE 6 DEEP INCISIONAL SSI
• deliberate opening of the superficial incision by surgeon, unless
the results of culture reports are negative.
• Micro organisms obtained from the culture of fluid or tissue taken
aseptically from a superficial incision
• Diagnosis of superficial infection made by the surgeon
Conditions which should not be considered as SSI include:
1. Stitch abscess
2. Episiotomy wound
3. Infection at the site of circumcision in a new born child.
4. Infected burn wound
DEEP INCISIONAL SSI
Deep incisional SSI can be defined as ‘An Infection that is
occurring within 30 days of surgery ( 1yr if an implant is in place) and
infection involving deep soft tissues.
It usually includes:
• Purulent discharge from the site of deep incision.
• Fever of 38 degree celsius or More.
• Local pain / tenderness at the incision site and incision dehisces
spontaneously or is opened deliberately.
• Abscess or other evidence of infection which involves the deep
incision and found on direct examination / visual / radiological /
histological examination.
• Diagnosis made by the physician / surgeon.
ORGAN / SPACE SSI
An organ or space SSI can be defined as ‘An Infection occuring
within 30 days ( 1yr of implant ) or Infection involving any other part of
the anatomy other than that of the incision site which was opened /
manipulated at the time of surgery.
It may include :
• Purulent aspirate from the organ / space operated which is
identified by a drain
• Micro organisms from the culture obtained aseptically
• Infection identified during reoperation / Histological
examination/ imaging.
• ORGAN SPACE SSI MASQUERADING INCISIONAL SSI
The following organ space surgical site infection pretends to be an
incisional SSI.
• Imaging studies done to rule out subfascial collection / fistula
from hollow organs.
• Presumptive usage of systemic antibiotics.
• Interventional radiology/ re-operation done.
• Trigger the lethal MOF( multi organ failure).
FIGURE 7 DEEP/ORGAN SPACE SSI
CLASSIFICATION OF SURGICAL WOUND INFECTION:
CLASS – I : Clean wound
(Expected wound infection rate is 1-3%)
Definition:-
- Atraumatic wound
- There are no signs of inflammation
- Gastrointestinal, Respiratory, Genito Urinary, Biliary
tracts are not entered.
Organisms :-- Staphylococcus aureus, Staphylococcus
epidermidis
Example:-- Hernia repair, Breast surgeries, Thyroid surgeries.
CLASS – II :–
Clean contaminated
(5-10% expected infection rate)
Definition :-
Elective operation of GIT, Genito Urinary, respiratory tract
have been entered during surgery under controlled conditions
Organism:-- Endogenous micro flora of the organ that has been entered
Example:-- Cholecystectomy, Elective bowel resection
CLASS – III:
CONTAMINATED WOUNDS
( Expected infection rate is 15%)
Definition :--
traumatic wounds(fresh)
any breach in the sterile
technique used
Gross
