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A PROSPECTIVE CLINICO-BACTERIOLOGICAL STUDY OF SURGICAL
SITE INFECTION AT K.R HOSPITAL
by
Dr. RAJESH B.M.,M.B.B.S.
A Dissertation Submitted to
The Rajiv Gandhi University of Health Sciences Karnataka, Bangalore in partial fulfillment of the requirements for the degree of
MASTER OF SURGERY IN
GENERAL SURGERY
Under the guidance of
Dr. M. RAMACHANDRA., B.Sc, MBBS, MS
Professor of Surgery
DEPARTMENT OF GENERAL SURGERY
MYSORE MEDICAL COLLEGE AND RESEARCH INSTITUTE MYSORE-570 001
APRIL 2012
ii
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ACKNOWLEDGEMENT
It is with great honour that I express my sincere gratitude to
Dr.M.RAMACHANDRA, Professor, Department of General Surgery, Mysore Medical
College and Research Institute, Mysore, for his constant support, inspiration, patience,
invaluable guidance during the course of this study.
I acknowledge my sincere and heartfelt thanks with gratitude to Dr.Avadhani
Geetha K., Dean and Director, MMC&RI and Dr.M.A.SHARIFF, Professor and Head,
Department of General Surgery, Mysore Medical College and Research Institute,
Mysore, for their constant help, support and guidance.
I express my sincere thanks to the Professors, Dr. M.A. Balakrishna,
Dr. Shivananda, Dr. Jagadish, Dr. Chandrashekhar N, Dr. Chandrakanath
Madiwal, Dr. G.M. Kudri and Dr. Mohan, for their valuable advice and support.
I express my heartfelt gratitude to my teachers Dr. Ravikumar G.V.,
Dr. Manjunath R.D., Dr. H.N. Dinesh, Dr. Madhu B.S., Dr. H.S. Prakash,
Dr. Chandrashekar, Dr. Dharmendra, Dr. Prasad H.L., Dr. Balasubrahmanya,
Dr. Narendra, Dr. Anandaravi B.N., Dr. Ramachandra M.L., Dr. Prakash S.S, for
their encouragement.
I express my heartfelt thanks to my colleagues.
I express my heartfelt thanks to OT Staff and Ward Staff, K.R. Hospital.
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LIST OF ABBREVIATIONS
ASA American society of anesthesiologists
BMI Body mass index
CDC Centre for disease control and prevention
DM Diabetes mellitus
ECM Extra-cellular matrix
GOO Gastric outlet obstruction
MRSA Methicillin resistant staphylococcus aureus
NICE National Institute for Health and Clinical Excellence
NNIS National nosocomial infection surveillance
NRC National research council
PDGF Platelet Derived Growth Factor
RTI Respiratory tract infection
SENIC Study on the efficacy of nosocomial infection control
SSI Surgical site infection
TAO Thrombo angiitis obliterans
TGF Transforming growth factor
UTI Urinary tract infection
VRE Vancomycin resistant enterococci
ix
ABSTRACT
Introduction: Surgical Site Infections (SSI) still remain a significant problem following
an operation and the third most frequently reported nosocomial infections. SSI contribute
significantly to increased health care costs in terms of prolonged hospital stay and lost
work days.
Objective: The current study was undertaken to identify incidence of SSI and the risk
factors associated with it, and the common organism isolated and its antibiotic sensitivity
and resistance.
Material and Methods: The prospective study was carried out on 400 surgeries. Infected
samples from patients were collected by following all aseptic precautions and were
processed without delay by the standard microbiological techniques.
Results and Conclusions: The overall infection rate was 9.75%. The SSI rate was 4.68%
in clean surgeries, 10.95% in clean contaminated ones, and 22.58% in contaminated
surgeries. The SSI rate increased with increasing age and it also increased significantly
with the increasing duration of pre-operative hospitalization. The SSI rate was less in
patients who received pre-operative antibiotic prophylaxis and was significantly higher in
emergency surgeries as compared to the elective surgeries. The infection rate was
significantly higher as the duration of the surgery increased. The most commonly isolated
organism from surgical site infections was E-coli (38.46%), followed by staphylococci
and pseudomonas (12.8%). Most of the organisms which were isolated were multidrug
resistant. The high rate of resistance to many antibiotics underscored the need for a policy
that could promote a more rational use of antibiotics.
Keywords: Surgical site infection, National Nosocomial Infections Surveillance (NNIS)
risk index, Antibiotic prophylaxis.
x
TABLE OF CONTENTS
Sl.No. Contents Page no. 1. INTRODUCTION 1 2. OBJECTIVES 3 3. DEFINITIONS 4 4. REVIEW OF LITERATURE 8
o PATHOLOGY OF WOUND HEALING 15
o ETIOLOGY OF WOUND INFECTION 22
o FACTORS AFFECTING INCIDENCE OF SSI 24
o MANAGEMENT OF WOUND INFECTION 41
5. METHODOLOGY 53 6. RESULTS 57 7. DISCUSSION 79 8. CONCLUSION 89 9. SUMMARY 91 10. BIBLIOGRAPHY 92 11. ANNEXURES
(i) PROFORMA 104
(ii) MASTER CHART 107 (iii) KEY TO MASTER CHART 108
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LIST OF TABLES
Table No.
Title Page No.
1 INCIDENCE OF SURGICAL SITE INFECTION 57
2 INCIDENCE IN RELATION TO SEX 58
3 INCIDENCE IN RELATION TO AGE GROUP 59
4 INCIDENCE IN RELATION TO TYPE OF OPERATION 60
5 INCIDENCE IN RELATION TO ANEMIA, HYPOPROTEINEMIA, DIABETES, REMOTE INFECTIONS AND MALIGNANCIES
61
6 INCIDENCE IN RELATION TO THE PREOP HOSPITALIZATION
63
7 INCIDENCE IN RELATION TO DIAGNOSIS 64
8 INCIDENCE IN RELATION TO PROPHYLACTIC ANTIBIOTIC
65
9 INCIDENCE IN RELATION TO TYPE OF SSI 66
10 INCIDENCE IN RELATION TO WOUND CLASS 67
11 INCIDENCE IN RELATION TO DURATION OF SURGERY 68
12 INCIDENCE IN USE OF DRAIN AND MESH 69
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13 INCIDENCE OF INFECTION NOTED ON POST OPERATIVE DAY
70
14 INCIDENCE OF ORGANISM ISOLATED 71
15 ORGANISMS ISOLATED IN WOUND TYPES 72
16 COMPARISON OF ORGANISMS ISOLATED WITH PRE OPERATIVE HOSPITALISATION
73
17 ANTIBIOTIC SENSITIVITY SPECTRUM 75
18 ANTIBIOTIC RESISTANCE SPECTRUM 77
xiii
LIST OF FIGURES
Figure No.
Title Page No.
1 TYPES OF SSI 6
2 HEALING RESPONSE 16
3 INFLAMMATORY RESPONSE DAY 3 17
4 GRAPH OF HEALING 17
5 PHASES OF WOUND HEALING 19
6 SUPERFICIAL SSI OF APPENDICECTOMY WOUND 51
7 DEEP SSI FOLLOWING APPENDICECTOMY (FOR
GANGRENOUS APPENDICITIS) 51
8 INFECTED LAPAROTOMY WOUND WITH PUS DISCHARGE 52
9 WOUND IN HEALING PHASE FOLLOWING SSI 52
10 DISC SHOWING GROWTH OF STAPH AUREUS 56
11 DISC SHOWING ANTIBIOTIC SENSITIVITY 56
1
INTRODUCTION
Surgical infections are those that occur as a result of a surgical procedure or
those that require surgical intervention as part of their treatment. They are
characterized by a breach of mechanical/anatomic defense mechanisms (barriers) and
are associated with greater morbidity, significant mortality, and increased cost of
care.1
The 16th century French surgeon Ambroise Pare is famous for saying, “I
dressed the wound, God healed it”. The implication was that wounds heal by a
mysterious incomprehensible force as long as local care is adequate. This attitude,
unfortunately, has endured. In truth, it is only a quaint remainder of the ignorance
that has lasted well into the present century.
Despite the advances in surgical sciences post operative wound infection
remains one of the common complication which surgeons encounter. This problem if
not evaluated and treated in a timely manner can have significant sequel.
Infection is encountered by all surgeons by nature of their crafts, they
invariably impaired the first line of host defence. The cutaneous or mucosal barrier,
the entrance of microbes into the host tissue is the initial requirement for infection.²
During the years there has been considerable progress in both the prevention
and treatment of infection. Since Pasteur, Cohn, Lister, Koch and Klebs, man has
constantly strove to combat infection. The discovery and confirmation of the link
between microbes and diseases led ultimately to the use of arsenic, mercury and of
2
sulphonamides and following the discovery of penicillin to the steady development of
antibiotics.
Remarkable life saving discoveries have been made but infection causing
organisms have also been successful in combating antibiotics and the search
continues. The cost of an infected operation to the patient and the community cannot
be simply measured in rupees and dollars. Surgeon should understand the real cost by
analysing it in terms of morbidity and monetary. Everything that is done to reduce the
infection rate costs money, so that it is important that the effectiveness of any new
procedures introduced must be evaluated.
SSI can double the length of time a patient stays in hospital and thereby
increase the costs of health care. The main additional costs are related to re-operation,
extra nursing care and interventions, and drug treatment costs. The indirect costs, due
to loss of productivity, patient dissatisfaction and litigation, and reduced quality of
life, have been studied less extensively.
3
AIMS AND OBJECTIVES
Surgical site infections are among the most common complications of
inpatient admissions and have serious consequences for outcomes and costs. Different
risk factors may be involved, including age, sex, nutrition and immunity, prophylactic
antibiotics, operation type and duration, type of shaving, and secondary infections.
This study aimed to determine the risk factors affecting surgical site infections and
their incidence at KRH, Mysore.
OBJECTIVES:
1. To study the incidence of surgical site infections in KRH, Mysore.
2. Risk factors associated with the surgical site infections.
3. Most common organism encountered and its antibiotic sensitivity and
resistance in surgical site infection.
4
DEFINITIONS:
CRITERIA FOR DEFINING A SURGICAL SITE INFECTION (SSI)
The surgical wound infection task force, including representatives from the
Society for Hospital Epidemiology of America, the Association for Practitioners in
infection Control and the Surgical Infection Society, published in 1992, definitions of
surgical site infection. The term surgical wound was intentionally replaced with
surgical site to include infections arising after surgery that were in organ spaces, deep
to skin and soft tissue, such as peritoneum and bone.³
Superficial incisional SSI:
Infection occurs within 30 days after the operation and infection involves only
skin or subcutaneous tissue of the incision and 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,
localized swelling, redness, or heat and superficial incision are deliberately opened by
surgeon, unless incision is culture-negative.
4. Diagnosis of superficial incisional SSI by the surgeon or attending physician.
5
Deep incisional SSI:
Infection occurs within 30 days after the operation if no implant is left in
place or within 1 year if implant is in place and the infection appears to be related to
the operation and infection involves deep soft tissues (e.g., facial and muscle layers)
of the incision and at least one of the following:
1. Purulent drainage from the deep incision but not from the organ/space component
of the surgical site.
2. A deep incision spontaneously dehisces or is deliberately opened by a surgeon
when the patient has at least one of the following signs or symptoms: fever (>38ºC),
localized pain, or tenderness, unless site is culture-negative.
3. An abscess or other evidence of infection involving the deep incision is found on
direct examination, during reoperation, or by histopathologic or radiologic
examination.
4. Diagnosis of a deep incisional SSI by a surgeon or attending physician.
Organ/Space SSI:
Infection occurs within 30 days after the operation if no implant is left in place
or within 1 year if implant is in place and the infection appears to be related to the
operation and infection involves any part of the anatomy (e.g., organs or spaces),
other than the incision, which was opened or manipulated during an operation and at
least one of the following:
6
1. Purulent drainage 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.
FIGURE1: Types of SSI
SURGICAL WOUND CLASSIFICATION:
Class 1: Clean:
An uninfected operative wound in which no inflammation is encountered and
the respiratory, alimentary, genital, or uninfected urinary tract is not entered. In
7
addition, clean wounds are primarily closed and, if necessary, drained with closed
drainage. Operative incisional wounds that follow nonpenetrating (blunt) trauma
should be included in this category if they meet the criteria.
Class 2/Clean-Contaminated:
An operative wound in which the respiratory, alimentary, genital, or urinary
tracts are entered under controlled conditions and without unusual contamination.
Specifically, operations involving the biliary tract, appendix, vagina, and oropharynx
are included in this category, provided no evidence of infection or major break in
technique is encountered.
Class 3/Contaminated:
Open, fresh and accidental wounds. In addition, operations with major breaks
in sterile technique (e.g., open cardiac massage) or gross spillage from the
gastrointestinal tract, and incisions in which acute, nonpurulent inflammation is
encountered are included in this category.
Class 4/Dirty-Infected:
Old traumatic wounds with retained devitalized tissue and those that involve
existing clinical infection or perforated viscera. This definition suggests that the
organisms causing postoperative infection were present in the operative field before
the operation.4
8
REVIEW OF LITERATURE
HISTORICAL ASPECT:
A number of observations by nineteenth-century physicians and investigators
were critical to our current understanding of the pathogenesis, prevention, and
treatment of surgical infections. In 1846, Ignaz Semmelweis, a Magyar physician,
took a post at the Allgemein Krankenhaus in Vienna. He noticed that the mortality
from puerperal ("childbed") fever was much higher in the teaching ward (1:11) than
in the ward where patients were delivered by midwives (1:29). He also made the
interesting observation that woman who delivered before arrival on the teaching ward
had a negligible mortality rate.
He then hypothesized that puerperal fever was caused by putrid material
transmitted from patients dying of this disease by carriage on the examining fingers of
the medical students and physicians who frequently went from the autopsy room to
the wards. The low mortality noted in the midwives' ward, Semmelweis realized, was
due to the fact that midwives did not participate in autopsies. Fired with the zeal of his
revelation, he posted a notice on the door to the ward requiring all caregivers to rinse
their hands thoroughly in chlorine water before entering the area. This simple
intervention reduced mortality from puerperal fever to 1.5%, surpassing the record of
the midwives. In 1861, he published his classic work on childbed fever based on
records from his practice. Unfortunately, Semmelweis' ideas were not well accepted
by the authorities of the time.
9
Louis Pasteur performed a body of work during the latter part of the
nineteenth century that provided the underpinnings of modern microbiology, at the
time known as germ theory. His work in humans followed experiments identifying
infectious agents in silkworms. He was able to elucidate the principle that contagious
diseases are caused by specific microbes and that these microbes are foreign to the
infected organism. Using this principle, he developed techniques of sterilization
critical to oenology (the science and study of all aspects of wine and winemaking)
and identified several bacteria responsible for human illnesses, including
Staphylococcus, Streptococcus, and pneumococcus.
Joseph Lister, the son of a wine merchant, was appointed professor of surgery
at the Glasgow Royal Infirmary in 1859. In his early practice, he noted that more than
50% of his patients undergoing amputation died due to postoperative infection. After
hearing of Pasteur's theory, Lister experimented with the use of a solution of carbolic
acid, which he knew was being used to treat sewage. He first reported his findings to
the British Medical Association in 1867 using dressings saturated with carbolic acid
on 12 patients with compound fractures; 10 recovered without amputation, one
survived with amputation, and one died of causes unrelated to the wound. In spite of
initial resistance, his methods were quickly adopted throughout Europe.
From 1878 until 1880, Robert Koch was the District Medical Officer for
Wollstein (then Prussia, now a part of Poland), which was an area in which anthrax
was endemic. Performing experiments in his home, without the benefit of scientific
equipment and academic contact, Koch developed techniques for culture of Bacillus
anthraces and proved the ability of this organism to cause anthrax in healthy animals.
He developed the following four postulates to identify the association of organisms
10
with specific diseases: (a) the suspected pathogenic organism should be present in all
cases of the disease and absent from healthy animals, (b) the suspected pathogen
should be isolated from a diseased host and grown in a pure culture in vitro, (c) cells
from a pure culture of the suspected organism should cause disease in a healthy
animal, and (d) the organism should be reisolated from the newly diseased animal and
shown to be the same as the original. He used these same techniques to identify the
organisms responsible for cholera and tuberculosis. During the next century, Koch's
postulates, as they came to be called, became critical to our understanding of surgical
infections and remain so today.
The first intra-abdominal operation to treat infection via "source control" (i.e.,
surgical intervention to eliminate the source of infection) was appendectomy. This
operation was pioneered by Charles McBurney at the New York College of
Physicians and Surgeons, among others. McBurney's classic report on early operative
intervention for appendicitis was presented before the New York Surgical Society in
1889.
During the twentieth century, the discovery of effective antimicrobials added
another tool to the armamentarium of modern surgeons. Sir Alexander Fleming, after
serving in the British Army Medical Corps during World War I, continued work on
the natural antibacterial action of the blood and antiseptics. In 1928, while studying
influenza virus, he noted a zone of inhibition around a mold colony (Penicillium
notatum) that serendipitously grew on a plate of Staphylococcus, and he named the
active substance penicillin. This first effective antibacterial agent subsequently led to
the development of hundreds of potent antimicrobials, set the stage for their use as
11
prophylaxis against postoperative infection, and became a critical component of the
armamentarium to treat aggressive, lethal surgical infections.
Subsequently, the initial clinical observations of surgeons such as Frank
Meleney, William Altemeier, and others provided the key, when they observed that
aerobes and anaerobes could synergize to cause serious soft tissue and severe intra-
abdominal infection. Thus, the concepts those resident microbes were nonpathogenic
until they entered a sterile body cavity at the time of surgery, and that many, if not
most, surgical infections were polymicrobial in nature became critical ideas and were
promulgated by a number of clinician-scientists over the last several decades. These
tenets became firmly established after microbiology laboratories demonstrated the
invariable presence of aerobes and anaerobes in peritoneal cultures obtained at the
time of surgery for intra-abdominal infection due to a perforated viscus or gangrenous
appendicitis. Clinical trials provided evidence that optimal therapy for these infections
required effective source control, plus the administration of antimicrobial agents
directed against both types of pathogens.
William Osler, a prolific writer and one of the fathers of American medicine,
made an observation in 1904 in his treatise The Evolution of Modern Medicine that
was to have profound implications for the future of treatment of infection: "Except on
few occasions, the patient appears to die from the body's response to infection rather
than from it”. The discovery of the first cytokines began to allow insight into the
organism's response to infection, and led to an explosion in our understanding of the
host inflammatory response. Expanding knowledge of the multiple pathways activated
during the response to invasion by infectious organisms has permitted the design of
new therapies targeted at modifying the inflammatory response to infection, which
12
seems to cause much of the end-organ dysfunction and failure. Preventing and
treating this process of multiple organ failure during infection is one of the major
challenges of modern critical care and surgical infectious disease.2
INCIDENCE OF SURGICAL WOUND INFECTION:
The earliest record of incidence of sepsis during post Listerian period was by
Theodor Kocher (1889), who reported a sepsis rate of 2.3% out of 325 operations.
In the pre-antibiotic era, scientists like Meleny (1935) and Hund (1939) noted
sepsis rates of 4.8 to 5.0% respectively. Devinish and Miles (1945) reported an
infection rate of 8.4%. There was a fall in the incidence of sepsis after the
introduction of antibiotics. However Howe (1962) reported that in spite of widespread
use of prophylactic antibiotics, infection rate had gone up from 1.09% in 1949 to
3.9% in 1953 and 5.3% in 1955. In 1956 he reported a fall in the rate of penicillin
resistant Staphylococci, after the institution of a simple judicious program of
prevention of contamination and judicious use of antibiotics.4
Blowers et al, (1955) reported a rise of post-operative wound infection from
2% in 1949 to 10.9% in 1952.
In Britain, Clarke (1957) reported a Sepsis rate of 13.6% causing a mean extra
stay in hospital for 8.1 days.
The National Research Council (1964) during a 2 ½ year collaborative study
of 15,613 consecutive operative procedures done in five American university centers
with the support of United States Public Health Service, designated the operative
wounds as Clean, Clean contaminated, Contaminated and Dirty wounds. In the 11,690
clean elective operations in this series, the average wound infection rate was 5.1 %
13
and the overall incidence rate in all types of wounds was 7.4%. The incidence of
infection following 12 Hernioplasty was 19% whereas it was 6.1% for Hysterectomy,
6.9% for Cholecystectomy, 10% for partial Colectomy.5
Cruse and Foord (1980) reported an incidence rate of 4.7% in a study of
62,939 operations and an incidence of 1.5% 7.7%, 15.2% and 40% in clean, clean
contaminated, contaminated and dirty operations. It became apparent that the
incidence of infection varied with the type of operation. They also compared the
incidence of infection with risk factors such as, age, sex, type of operation,
preoperative stay, wound drainage and special factors such as Diabetes.6
Evidence, that careful Surveillance can play a role in reducing wound
infection have been gradually accumulated throughout many years.7 During the 10
year study of 62,939 wounds by Cruse and Foord, a reduction in the clean wound
infection rate from 2.6% to 0.6% was realized.6
In Mary Olson et al, study (1990), the overall wound infection rate for a total
of 1032 surgical wound infections in 40,915 wounds, at the Minneapolis VA Medical
Center in the study period (1977-1986) was 4.2% for the first year and was
significantly lower than this value for every subsequent year, being 2.5% in 1986.7
In India Anvikar et al, from Government Medical College, Agra reported a
sepsis rate of 6.09% in 1999.8
Hernandez K et al, from Lima, Peru, conducted a cohort study from January to
June 1998. Four hundred sixty-eight patients were enrolled. One hundred twenty-five
patients developed SSIs, 18% of which were identified after discharge. The overall
14
incidence rate (IR) was 26.7%. The IR was 13.9% for clean, 15.9% for clean-
contaminated, 13.5% for contaminated and 47.2% for dirty interventions.9
Inigo JJ et al studied surgical site infection in general surgery: 5-year analysis
and assessment of the National Nosocomial Infection Surveillance (NNIS) index,
there were 6,218 patients and 513 SSI (8.25%). The infection rate was 2.27% for
clean surgery, 9.17% for clean-contaminated surgery, 11.40% for contaminated
surgery, and 19.14% for dirty surgery.10
Konishi T, et al studied in Department of Surgery, Kanto Medical Center,
NTT-EC, Tokyo, Japan. In October 2003, total 20,948 cases from 36 institutions have
been studied. SSIs occurred in 1,394 cases, this corresponds to an incidence of 6.7%.
When we look at the numbers of SSIs by the organs operated on, the incidence figures
in the field of gastrointestinal surgery were by far the highest ones.11
Reilly J et al conducted a procedure-specific surgical site infection rates and
post discharge surveillance in Scotland in 2006 Dec, from study information, PDS
data were available for 12,885 operations (59%). A total of 2,793 procedures (13%)
were associated with passive PDS and 10,092 (46%) with active PDS. The SSI rate
among the 8,825 operations with no PDS was 2.61% (95% confidence interval [CI],
2.3%-3.0%), which was significantly lower than the SSI rate found among the 12,885
operations for which PDS was performed (6.34% [95% CI, 5.9%-6.8%].12
Nicola Petrosillo et al. studied, surgical site infections in Italian Hospitals: a
prospective multicenter study in 2008, SSI occurred in 241 (5.2%) of 4,665 patients,
of which 148 (61.4%) during in-hospital and 93 (38.6%) during post discharge
period.13
15
PATHOLOGY OF WOUND HEALING:
Wound repair is the effort of injured tissues to restore their normal function and
structural integrity after injury.
WOUND-HEALING PHASES:
The three phases of wound healing are inflammation, proliferation, and maturation.
The immediate response to injury is the inflammatory (also called reactive) phase.
The body's defenses are aimed at limiting the amount of damage and preventing
further injury.
The proliferative (also called regenerative or reparative) phase is the reparative
process and consists of re-epithelialization, matrix synthesis, and neovascularization
to relieve the ischemia of the trauma itself.
The final maturational (or remodeling) phase is the period of scar contraction with
collagen cross-linking, shrinking, and loss of edema.
16
Figure 2- HEALING RESPONSE
INFLAMMATORY PHASE:
The inflammatory phase is characterized by
• Increased vascular permeability,
• Migration of cells into the wound by chemotaxis,
• Secretion of cytokines and growth factors into the wound, and activation of
the migrating cells.
17
Figure 3 - INFLAMMATORY RESPONSE DAY 3
During an acute tissue injury, blood vessel damage results in exposure of
subendothelial collagen to platelets, which leads to platelet aggregation and activation
of the coagulation pathway. Initial intense local vasoconstriction of arterioles and
capillaries is followed by vasodilatation and increased vascular permeability.
Cessation of hemorrhage is aided by plugging of capillaries with erythrocytes and
platelets, which adhere to the capillary endothelium.
.
Figure 4 - GRAPH OF HEALING
18
PROLIFERATIVE PHASE
As the acute responses of hemostasis and inflammation begin to resolve, the
scaffolding is laid for repair of the wound through angiogenesis, fibroplasia, and
epithelialization. This stage is characterized by the formation of granulation tissue,
which consists of a capillary bed, fibroblasts, macrophages, and a loose arrangement
of collagen, fibronectin, and hyaluronic acid.
ANGIOGENESIS
Angiogenesis is the process of new blood vessel formation and is necessary to
support a healing wound environment. After injury, activated endothelial cells
degrade the basement membrane of postcapillary venules, thereby allowing the
migration of cells through this gap. Division of these migrating endothelial cells
results in tubule or lumen formation. Eventually, deposition of the basement
membrane occurs and results in capillary maturation.
FIBROPLASIA
Fibroblasts are specialized cells that differentiate from resting mesenchymal
cells in connective tissue; they do not arrive in the wound cleft by diapedesis from
circulating cells. After injury, the normally quiescent and sparse fibroblasts are
chemoattracted to the inflammatory site, where they divide and produce the
components of the ECM.
19
EPITHELIALIZATION
Re-epithelialization of wounds begins within hours after injury. Initially, the
wound is rapidly sealed by clot formation and then by epithelial (epidermal) cell
migration across the defect. Keratinocytes located at the basal layer of the residual
epidermis or in the depths of epithelium-lined dermal appendages migrate to resurface
the wound. Epithelialization involves a sequence of changes in wound keratinocytes:
detachment, migration, proliferation, differentiation, and stratification.
Figure 5: PHASES OF WOUND HEALING
20
MATURATIONAL PHASE
Wound contraction occurs by centripetal movement of the whole thickness of
the surrounding skin and reduces the amount of disorganized scar. Wound
contracture, in contrast, is a physical constriction or limitation of function and is a
result of the process of wound contraction. Contractures occur when excessive scar
exceeds normal wound contraction, and it results in a functional disability.
REMODELING
The fibroblast population decreases and the dense capillary network regress.
Wound strength increases rapidly within 1 to 6 weeks and then appears to plateau up
to 1 year after the injury
When compared with unwounded skin, tensile strength is only 30% in the
scar. An increase in breaking strength occurs after approximately 21 days, mostly as a
result of cross-linking. Although collagen cross-linking causes further wound
contraction and an increase in strength, it also results in a scar that is more brittle and
less elastic than normal skin. Unlike normal skin, the epidermodermal interface in a
healed wound is devoid of rete pegs, the undulating projections of epidermis that
penetrate into the papillary dermis. Loss of this anchorage results in increased
fragility and predisposes the neoepidermis to avulsion after minor trauma.
Wound closure types are divided into primary, secondary, and tertiary repair.
21
Primary: or first-intention- The wounds are sealed immediately with simple suturing,
skin graft placement, or flap closure, such as closure of the wound at the end of a
surgical procedure.
Secondary: or spontaneous Intention- Involves no active intent to seal the wound.
Generally, this type of repair is associated with a highly contaminated wound and will
close by re-epithelialization, which results in contraction of the wound.
Tertiary: delayed primary closure. - A contaminated wound is initially treated by
repeated debridement, systemic or topical antibiotics, or negative pressure wound
therapy for several days to control infection. Once the wound is assessed as being
ready for closure, surgical intervention, such as suturing, skin graft placement, or flap
design, is performed.14
22
ETIOLOGY OF WOUND INFECTION:
Bacteria important in surgical infections are broadly divided into aerobic and
facultative bacteria in one group and anaerobic bacteria in the other, into gram-
positive and gram-negative bacteria, and into bacilli (rods) and cocci.
It is important to recognize that the vast majority of infections occurring in
surgical patients are caused by endogenous bacteria. Specific bacteria are found in
specific parts of the body, and the exposed anatomic areas during a surgical procedure
are usually the source of microorganisms that cause infection. It is helpful to know the
normal microbial flora of the body because such knowledge helps direct prophylactic
antibiotics, start intelligent empirical therapy, and suspect the origin of an unknown
source of infection in patients with positive blood cultures.
It is also helpful to be familiar with the different classifications of bacteria
because it can take up to 72 hours for a final culture to give the result as to specific
bacteria; however, Gram stain and biochemical tests can help in providing earlier
guidance regarding which group of bacteria may be responsible for an infection.
23
BIOCHEMICAL TESTS USED TO IDENTIFY SPECIFIC PATHOGENS
WITHIN GRAM-POSITIVE COCCI
BIOCHEMICAL TESTS USED TO IDENTIFY SPECIFIC PATHOGENS
WITHIN GRAM-NEGATIVE RODS.
24
FACTORS AFFECTING THE INCIDENCE OF SSI
PATIENT FACTORS
• Wound classification
• Age
• Nutritional status
• Altered immune response
• Obesity
• Diabetes
• Smoking
• Coexistent infections at a remote body site
• Colonization with microorganisms
• Length of preoperative stay
OPERATION
• Duration of surgical scrub
• Preoperative shaving
• Preoperative skin prep
• Duration of operation
• Hypothermia
• Antimicrobial prophylaxis
• Operating room ventilation
• Foreign material in the surgical site
• Surgical technique
• Use of cautery
25
AGE:
Increasing age is correlated with greater likelihood of certain chronic
conditions, malnutrition and a fall in the body immunological efficiency, causing
more extensive SSI.2
In general the postoperative mortality rate in geriatric surgical patients (over
70 years) is low. Despite the increased prevalence of preoperative chronic medical
conditions, most patients do well postoperatively. However, the ASA classification
(III + IV), emergency surgery, a history of hypertension, pulmonary, neurologic and
coronary artery diseases increases the odds of developing any postoperative adverse
events in elderly patients.15
SEX:
Male gender is associated with increased anastomotic leakage rates after low
rectal anastomoses.16
MALNUTRITION:
With the availability of improved nutritional supplements and reliable data
from well designed meta-analysis on malnourished patients this topic has become
more important for every surgeon. Malnutrition has been recognized as an
independent risk factor of perioperative morbidity for many decades, but there is
currently no standardized definition of malnutrition.17,18 Depending upon the criteria
used for defining malnutrition, its prevalence in gastrointestinal (GI) surgery patients
ranges from 30% to 50%.19 Some scores consist of a questionnaire and others include
also blood values (e.g. Albumin).20, 21
26
A simple score to assess nutritional status based on age, recent weight loss,
BMI, severity of disease and planned surgical intervention is the Nutrition Risk
Screening 2002 (NRS) or Kondrup Score. A score ≥ 3 is considered as an independent
risk factor for complications and perioperative nutritional support should be
considered.22
Various well designed studies have shown beneficial effects of
immunonutrition in reducing infectious complications, length of hospital stay, and
mortality.23 It is imperative that the data be interpreted in the context of individual
patient’s risk since special formulas appear most beneficial in patients at risk of
subsequent complications or those with significant pre-existing malnutrition.
Preoperative immunonutrition in malnourished patients was more beneficial than
perioperative conventional nutrition support.
ALTERED IMMUNE RESPONSE:
Immunosuppression is suppression of the body's immune system and its
ability to fight infections or disease.
Immunosuppression has a variety of causes. One may inherit a condition that
leads to Immunosuppression. The most common inherited cause in adults is called
Common Variable Immunodeficiency, a condition where the body can’t produce
antibodies to combat infection. Immunosuppression can also occur with some
infections like HIV (the virus that produces AIDS) and with some cancers. Finally,
there are several medications that suppress the immune system. These medications
27
include corticosteroids (prednisone, medrol), imuran, methotrexate, cellcept, cytoxan,
remicade, rituximab, chemotherapy, irradiation and several others.
Patients who are receiving steroids or other immune-suppressive drugs
preoperatively may be predisposed to developing SSI 24,25 but the data supporting this
relationship are contradictory. In a study of long-term steroid use in patients with
Crohn’s disease, SSI developed significantly more often in patients receiving
preoperative steroids (12.5%) than in patients without steroid use (6.7%).26 In
contrast, Other investigations have not found a relationship between steroid use and
SSI risk.27,28
OBESITY:
Patients with a BMI over 25 kg/m2 have a higher risk for incisional hernias
and have an increased rate of surgical site infection.29, 30
The literature shows that SSI increases with obesity, one reason being a
decrease in blood circulation in fat tissues.31
Initially, it was thought that obese patients have a higher complication rate
especially in the case of a laparoscopic approach. However, a few well designed
studies have demonstrated that laparoscopic colorectal surgery in obese patients is
feasible and safe, and that all known benefits of a minimally invasive approach were
preserved.32
28
DIABETES:
The contribution of diabetes to SSI risk is controversial33,34 because the
independent contribution of diabetes to SSI risk has not typically been assessed after
controlling for potential confounding factors. Recent preliminary findings from a
study of patients who underwent coronary artery bypass graft showed a significant
relationship between increasing levels of HbA1c and SSI rates.35 Also, increased
glucose levels (>200 mg/dL) in the immediate postoperative period (<48 hours) were
associated with increased SSI risk.36 More studies are needed to assess the efficacy
of perioperative blood glucose control as a prevention measure.
SMOKING:
Not unexpectedly, malnutrition and cigarette smoking have shown evidence of
interaction. Cigarette smoking has been associated with inhibited wound healing and
decreased circulation to the skin due to microvascular obstruction from platelet
aggregation and increased nonfunctioning haemoglobin.37 In addition, smoking has
been found to compromise the immune system and respiratory system. Cigarette
smoking as a host risk factor has had conflicting reports, and that may be partly due to
the fact that some studies that evaluate this factor consider only current smoking to
increase risk of SSI.38
A percentage of patients quit smoking immediately before the surgery, and
then may signify themselves as nonsmokers at the time of surgery, which may be
performed within days or weeks of smoking cessation. The conflicting results may be
dependent on how distant prior smoking must be before there is a significant
29
difference between the groups in terms of outcome. Cigarette smoking may also be
one of the pre-existing patient factors amenable to intervention, especially with the
relatively new smoking cessation supports now available, such as the nicotine patch
or bupropion hydrochloride. At least one month prior to surgery, patients should be
encouraged to cease tobacco use. Patients should also adhere to nutrition and physical
status guidelines including the intake of vitamins such as A, B, C, D, E and K and
supplements of zinc, manganese, magnesium, copper and iron.39
COEXISTENT INFECTIONS AT A REMOTE BODY SITE
Not infrequently, patients harbor indolent dental, urinary or skin soft tissue
infections at the time of surgery. The major concerns about the presence of a pre-
existing infection are that it may: 1) be the source for hematogenous spread, causing
late infections to joint prostheses or cardiac valves, or 2) be a contiguous site for
bacterial transfer.40 These infections at a site remote from the wound have been linked
to increasing SSI rates three- to five-fold.41 Any remote infections should be
identified and treated prior to the operation. It is not uncommon for multiple dental
extractions to be required in order for oral infections to be eliminated preoperatively.
Certain surgical cases, especially those requiring implanted devices, may demand that
the operation be postponed until the infection is resolved.42
COLONIZATION WITH MICROORGANISMS:
The primary source of infection for most surgical sites is the patient’s
endogenous microorganisms.43,44 All patients are colonized with bacteria, fungi and
30
viruses-up to 3 million germs per square centimeter of skin.45 However, not all
patients, bacteria, fungi and viruses are created equal. Patients with a history of
diabetes mellitus (DM), chronic obstructive pulmonary disease (COPD) necessitating
long-term steroid use, or other chronic illness who have had repeated hospitalizations
and/or courses of antibiotics tend to be more heavily colonized with bacteria,
especially with antibiotic-resistant bacteria such as methicillin-resistant
Staphylococcus aureus (MRSA). All surgical wounds will be contaminated with
bacteria during surgery, but only a small percentage becomes infected.46 This is
because most patient’s host defenses are capable of controlling and eliminating the
offending organisms when the wound inoculum is small, the bacterial contaminants
are not overwhelmingly virulent, the wound microenvironment is healthy, and the
host defenses are intact. Staphylococcus aureus nasal carriage, noted in 30% of most
healthy populations, and especially methicillin-resistant staph aureus (MRSA),
predisposes patients to have higher risk of SSI.46 Having an endogenous source for the
bacterium that may be responsible for as many as one out of three wounds can
increase the likelihood of infection ten-fold.47 However, most surgical settings have
not yet instituted routine active surveillance for this common carrier state, so
decolonization strategies are infrequently implemented.
LENGTH OF PREOPERATIVE STAY:
Prolonged preoperative hospital stay is frequently suggested as a patient
characteristic associated with increased SSI risk. However, length of preoperative stay
is likely a surrogate for severity of illness and co-morbid conditions requiring
inpatient work-up and/or therapy before the operation.38,48,49,50
31
OPERATION
DURATION OF SURGICAL SCRUB:
Scrubbing technique, the duration of the scrub, the condition of the hands, or
the techniques used for drying and gloving are examples of such factors. Recent
studies suggest that scrubbing for at least 2 minutes is as effective as the traditional
10-minute scrub in reducing hand bacterial colony counts.51,52,53,54
PREOPERATIVE SHAVING:
Preoperative shaving of the surgical site the night before an operation is
associated with a significantly higher SSI risk than the use of depilatory agents or no
hair removal.38,55,56 In one study, SSI rates were 5.6% in patients who had hair
removed by razor shave compared to a 0.6% rate among those who had hair removed
by depilatory or who had no hair removed.56 The increased SSI risk associated with
shaving has been attributed to microscopic cuts in the skin that later serve as foci for
bacterial multiplication. Shaving immediately before the operation compared to
shaving within 24 hours preoperatively was associated with decreased SSI rates (3.1%
vs. 7.1%); if shaving was performed >24 hours prior to operation, the SSI rate
exceeded 20%.56 Clipping hair immediately before an operation also has been
associated with a lower risk of SSI than shaving or clipping the night before an
operation (SSI rates immediately before = 1.8% vs. Night before = 4.0%). Although
the use of depilatories has been associated with a lower SSI risk than shaving or
clipping,56,57 depilatories sometimes produce hypersensitivity reactions.56 Other
studies showed that preoperative hair removal by any means was associated with
increased SSI rates and suggested that no hair be removed.55, 58
32
PREOPERATIVE SKIN PREP:
Several antiseptic agents are available for preoperative preparation of skin at
the incision site. The iodophors (e.g., povidone-iodine), alcohol-containing products,
and chlorhexidine gluconate are the most commonly used agents. No studies have
adequately assessed the comparative effects of these preoperative skin antiseptics on
SSI risk in well-controlled, operation-specific studies.
Alcohol is readily available, inexpensive, and remains the most effective and
rapid-acting skin antiseptic.59 Aqueous 70% to 92% alcohol solutions have germicidal
activity against bacteria, fungi, and viruses, but spores can be resistant.59,60 One
potential disadvantage of the use of alcohol in the operating room is its
flammability.59,60,61
Both chlorhexidine gluconate and iodophors have broad spectra of
antimicrobial activity.62,63,64 In some comparisons of the two antiseptics when used as
preoperative hand scrubs, chlorhexidine gluconate achieved greater reductions in skin
microflora than did povidone-iodine and also had greater residual activity after a
single application.65,66,67 Further, chlorhexidine gluconate is not inactivated by blood
or serum proteins.59, 62, 68 Iodophors may be inactivated by blood or serum proteins,
but exert a bacteriostatic effect as long as they are present on the skin.61,62
DURATION OF OPERATION:
The risk of wound infection has repeatedly been shown to be proportional to
the duration of the operative procedure. Cruse and Foord6,27 found that the rate of
wound infection increased for longer procedures, roughly doubling with every hour of
33
the procedure. Operations lasting 1 hour or less had a wound infection rate of 1.3%,
whereas those lasting 3 hours or more had a rate close to 4.0%.27 Haley et al69 showed
by using multivariate analysis that an operative time of more than 2 hours is the
second greatest independent predictor of risk (wound contamination being the first).
And by using a different index, Culver et al70 found operative time to be one of three
variables-along with wound class and ASA class-that independently predict infection.
HYPOTHERMIA
In 1996, Kurz et al. published the results of a randomized controlled trial
examining the effects of hypothermia on the incidence of SSI. Patients in the
hypothermia group had a mean intraoperative core temperature of 34.7°C whereas
patients in the normothermia group had a mean intraoperative core temperature of
36.6°C. This small ~2°C difference in core temperature resulted in a 3-fold higher
incidence of SSI in the hypothermia group (19% vs. 6%, p = 0.009). In addition,
sutures were removed one day later in the patients assigned to hypothermia than in
those assigned to normothermia and the duration of hospitalization was prolonged by
a mean of 2.6 days in the hypothermia group. Perioperative hypothermia has also
been established as a risk factor for SSI in several retrospective studies.
The mechanisms by which hypothermia increases the incidence of SSI have
been also defined. Hypothermia suppresses phagocytic activity by decreasing
migration of PMN’s, reducing superoxide anion production, and reducing oxidative
bacterial killing by neutrophils.
34
ANTIMICROBIAL PROPHYLAXIS:
The prophylactic use of antibiotics for surgical procedure has become a
standard practice. Surgeons throughout the world recognize the advantages in
virtually all type of procedures; of having a microbiologically active drug during the
critical interval in which bacterial contamination can occur. To achieve this aim, a
great variety of antibiotics are currently administered before or during the operation
and, if necessary, for some days after the closure of the wound.71,72
Antibiotic prophylaxis designed to reduce the incidence of post operative
infection, may reduce overall costs by avoiding the expenses attributable to infections
and by shortening hospital stay.71
Prophylactic antibiotics are recommended when the risk of post operative
wound infection is high or when the consequence of infection is extreme morbidity or
mortality. The benefit of the antibiotic prophylaxis should outweigh its risks. The
antibiotic selected should be based on site-specific flora responsible for post-operative
wound infection; on the antimicrobial spectrum toxicity and kinetic properties of the
drug; and on the results of prospective clinical trials.72
Choice of Antibiotics
Ideally the prophylactic antibiotic(s) selected should have been proved
effective in randomized, prospective and clinical trials. The regimen chosen should be
compatible with the findings from the hospital infection control wound surveillance
report. The choice of a prophylactic antibiotic should avoid a drug valuable for
definitive therapy. If a number of drugs appear equally acceptable for prophylaxis,
one should pick the agent least likely to be used for definitive therapy. This strategy
35
should minimize selecting organisms resistant to valuable therapeutic agent.72
Peterson et al, (1990) observed the common errors in antibiotic prophylaxis include
choosing the wrong agent, omitting critical intra-operative doses in long operations,
and extending the course for longer than necessary. Indiscriminate antibiotic use is
costly, exposes the patients to adverse effects, and promotes resistance to drugs.71
Doprzanski et al (1991) and Scher et al, have substantiated the reports on these
common errors. They suggest that involvement of clinical pharmacists in the overall
programme of antibiotic prophylaxis, the use of computerized reminders, Satellite
pharmacies and strong positions by the professional staff are effective in combating
these errors.71
The findings supported the literature by showing that administration of
prophylactic antibiotic half an hour before the operation would bring about the best
results and the lowest SSI.73 This was proved for all antibiotics (p = 0.001) with the
exception of cephalothin with (p = 1), which requires a lot more research.
OPERATING ROOM VENTILATION:
Operating room air may contain microbial-laden dust, lint, skin squames, or
respiratory droplets. The microbial level in operating room air is directly proportional
to the number of people moving about in the room.74 Outbreaks of SSIs caused by
group A beta-hemolytic streptococci have been traced to airborne transmission of the
organism from colonized operating room personnel to patients.75,76,77
In these outbreaks, the strain causing the outbreak was recovered from the air
in the operating room.76 It has been demonstrated that exercising and changing of
36
clothing can lead to airborne dissemination of group A streptococci from vaginal or
rectal carriage.75, 77,78
FOREIGN MATERIAL IN THE SURGICAL SITE:
Any foreign body, including suture material, a prosthesis, or drain, may
promote inflammation at the surgical site and may increase the probability of SSI
after otherwise benign levels of tissue contamination. Extensive research compares
different types of suture material and their presumed relationships to SSI
risk.79,80,81,82,83 In general, monofilament sutures appear to have the lowest infection
promoting effects.84
SURGICAL TECHNIQUE:
Excellent surgical technique is widely believed to reduce the risk of
SSI.62,63,85,86,87 Such techniques include maintaining effective hemostasis while
preserving adequate blood supply, preventing hypothermia, gently handling tissues,
avoiding inadvertent entries into a hollow viscus, removing devitalized (e.g., necrotic
or charred) tissues, using drains and suture material appropriately, eradicating dead
space, and appropriately managing the postoperative incision.
Drains placed through an operative incision increase incisional SSI Risk.88
Many authorities suggest placing drains through a separate incision distant from the
operative incision.89 It appears that SSI risk also decreases when closed suction
drains are used rather than open drains.58 Closed suction drains can effectively
evacuate postoperative hematomas or seromas, but timing of drain removal is
37
important. Bacterial colonization of initially sterile drain tracts increases with the
duration of time the drain is left in place.90
USE OF ELECTRIC CAUTERY:
Interplay between wound resistance factors and bacterial innoculum
determines the risk of surgical infection. Since cautery causes more damage than the
scalpel, lower numbers of bacteria are required to infect wounds made by electric
cautery than to infect wounds made with a scalpel.91
The CDC guidelines recommend that surgeons minimize devitalized tissue
and foreign bodies such as sutures, charred tissue, necrotic debris, and dead space at
the surgical site. Using a surgical knife during subcutaneous incisions can reduce
tissue burn and necrosis, which might explain the lower incidence of SSI associated
with the use of a surgical knife than with electric cautery. To reduce necrosis and
charred tissue in the incisional wound, surgeons should avoid making slow incisions
when using electric cautery.92
WOUND CLASSIFICATION
The wound class has been shown to be independently predictive of wound
infection in several large studies using multivariate analysis. In 1980, the Foothills
Hospital study of 62,939 wounds generated a set of wound infection rates for the four
wound classes: clean, 1.5%; clean contaminated, 7.7%; contaminated, 15.2%; and
dirty 40.8%. Culver et al modified the SENIC risk index in 1991, but wound
classification was the only risk factor that was unchanged from the original index.
38
Garibaldi et al also found surgical wound class (by stepwise logistic regression
analysis) to be predictive of wound infection.
In addition, a prospective study of 190 colorectal surgery patients has shown
that a concentration of 5 Colony forming unit per milliliter or higher of bacteria in the
peritoneal fluid are predictive of wound infection; infection rates without and with
contamination were 6.4% and 1.2%, respectively.93
ANTIBIOTIC RESISTANCE
Antibiotic resistance is an escalating problem, particularly in patients in ICUs.
Its implications include longer length of stay, higher cost of care, and more
importantly, increased morbidity and mortality derived from infections treated
unsuccessfully.
Resistance has been broadly divided into two forms, intrinsic resistance, in
which a specific species is inherently resistant to a specific antibiotic (e.g., gram-
negative bacteria resistant to vancomycin), and acquired resistance, in which a change
in the genetic composition of the bacteria occurs. This acquired resistance can be the
result of intrinsic changes within the native genetic material of the pathogen or can be
transferred from another species.
The molecular mechanisms by which bacteria acquire resistance to antibiotics
can be broadly classified into four categories:94
1. Decreased intracellular concentration of antibiotic, either by decreased influx or
increased efflux. Most antibiotics are susceptible to this mechanism
39
(Pseudomonas/Enterobacteriaceae to β-lactam).
2. Neutralization by inactivating enzymes. This is the most common mechanism of
antibiotic resistance and affects all β-lactam antibiotics (e.g. β-lactamases from
gram-positive and gram-negative bacteria).
3. Alteration of the target at which the antibiotic will act. This category affects all
antibiotics and is the main resistance mechanism for some specific bacteria
(Pneumococcus to penicillin or MRSA to all β-lactam antibiotics).
4. Complete elimination of the target at which the antibiotic will act. Some specific
bacteria develop the ability to create new metabolic pathways and completely
eliminate a specific target (e.g., VRE).
Antibiotic resistance is usually achieved by a combination of these different
mechanisms. However, the presence of one of them may confer resistance to one or
more different group of antibiotics.
The bacterial genome is divided into chromosomal DNA, which gives specific
characteristics and metabolic pathways to the bacteria, and smaller, circular and
independent DNA elements (plasmids) that encode information for supplemental
bacterial activities such as virulence factors and resistance mechanisms. Most
resistance mechanisms are plasmid mediated, although they can interchange with
chromosomal information (with the aid of transposons, or mobile DNA elements)
conferring more fixed mechanisms, which will be transmitted vertically. However,
plasmids can also be transmitted horizontally through conjugation, transduction, and
transformation processes in which different bacteria are exposed to a specific plasmid.
40
Risk factors for antibiotic resistance in a specific patient include the use of
antibiotics, prolonged hospital stay, administration of broad-spectrum antibiotics, use
of invasive devices (endotracheal tubes, central lines, Foley catheters, etc.), and the
presence of outbreaks, which may reflect ineffective infection control policies. The
populations at highest risk are ICU patients, in whom the potential absence of
effective antibiotic treatment correlates with higher mortality rates.
Prevention strategies have been studied, and although it is difficult to establish
a clear relationship between their practice and decreased resistance, such strategies
need to be part of a discipline that not only reduces the incidence of antibiotic
resistance but also follows a logical practice for infection control and use of
antibiotics. Some of these strategies include guidelines for the use of antibiotics
(hospital formulary restriction, use of narrow-spectrum antibiotics, antibiotic cycling,
use of new antibiotics), assessment of infection risk and quantitative cultures,
consultation with infectious disease specialists, and area-specific use of antibiotics
(outpatients versus nosocomial, hospital-to-hospital difference, etc.). Nonantibiotic
strategies include prevention of nosocomial infections (general and specific measures)
and prevention of hospital transmission (hand washing, contact precautions). The
battle against antibiotic resistance is definitely multidisciplinary and involves the
development of new antibiotics, as well as strategies in the everyday care of patients
from all health care personnel.14
41
MANAGEMENT OF WOUND INFECTION
Wound infection can be predicted to a certain extent. Because wound defenses
and wound repair are vulnerable to many of the same defects, predictive of infection
are usually also predictors of dehiscence or other wound failure.
Haley and colleagues were the first to publish on the importance of identifying
individual patients who are at high risk of surgical site infection in each category of
operative procedure with the hope that the approach would result in an increase in the
efficiency of routine surgical site infection surveillance and control.
Analyzing 10 possible risk factors by step-wise multiple logistic regression
techniques, a model was developed containing four risk factors
1. Abdominal operations,
2. Operations lasting longer than 2 hours,
3. Contaminated or dirty-infected operation by the traditional wound classification
system, and
4. Patients having three or more different diagnoses, and utilized the resultant formula
to predict an individual patient's probability of developing a postoperative surgical
site infection. This approach was then tested on another group of 59,352 surgical
patients admitted from 1975 to 1976 and was found to be a valid predictor of surgical
site infection.
Haley and colleagues concluded that their simplified index predicted surgical
site infection risk approximately twice as well as the traditional classification of
wound contamination. Utilizing this model, low-, medium-, and high-risk levels of
42
developing surgical site infection were identified in each of the categories of the
traditional wound classification system. The overall surgical site infection rate in this
study did progressively increase from clean (2.9%), to clean-contaminated (3.9%), to
contaminated (8.5%), to dirty-infected (12.6%). However, a wide range of infection
risk in patients in each category was noted in clean operations, 1.1% (low risk) to
15.8% (high risk); in clean-contaminated operations, 0.6% (low risk) to 17.7% (high
risk); in contaminated operations, 4.5% (medium risk) to 23.9% (high risk); and in
dirty-infected operations, 6.7% (medium risk) to 27.4% (high risk). It should be noted
that no low-risk category patients were identified in contaminated and dirty-infected
operations.
Following the work of Haley and colleagues, investigators at the Centers for
Disease Control and Prevention (CDC) reported on a composite risk index used in the
National Nosocomial Infections Surveillance (NNIS) System. This risk index was
based on a modification of the one developed in the Study on the Efficacy of
Nosocomial Infection Control (SENIC) project. The NNIS risk index uses the
traditional wound classification system but attempts to improve on the SENIC index
in several ways. First, instead of utilizing three discharge diagnoses to identify host
factors as a risk of infection, the NNIS risk index uses a dichotomization of the
American Society of Anesthesiology score. Its ease for collecting data and its
objectivity seem advantageous. Second, the NNIS risk index uses a procedure-related
cut point to indicate a long duration of surgery for an individual procedure, rather than
a 2-hour cut point for all procedures.
43
Information for patients and carers
1. Offer patients and carers clear, consistent information and advice throughout
all stages of their care. This should include the risks of surgical site infections,
what is being done to reduce them and how they are managed.
2. Offer patients and carers information and advice on how to care for their
wound after discharge.
3. Offer patients and carers information and advice about how to recognise a
surgical site infection and who to contact if they are concerned. Use an
integrated care pathway for healthcare-associated infections to help
communicate this information to both patients and all those involved in their
care after discharge.
4. Always inform patients after their operation if they have been given
antibiotics.
PREOPERATIVE PHASE
Preoperative showering
Advise patients to shower or have a bath (or help patients to shower, bath or bed
bath) using soap, either the day before, or on the day of, surgery.
Hair removal
1. Do not use hair removal routinely to reduce the risk of surgical site infection.
44
2. If hair has to be removed, use electric clippers with a single-use head on the
day of surgery. Do not use razors for hair removal, because they increase the
risk of surgical site infection.
Patient theatre wear
Give patients specific theatre wear that is appropriate for the procedure and
clinical setting, and that provides easy access to the operative site and areas for
placing devices, such as intravenous annuals. Consider also the patient’s comfort and
dignity.
Staff theatre wear
All staff should wear specific non-sterile theatre wear in all areas where
operations are undertaken.
Staff leaving the operating area
Staff wearing non-sterile theatre wear should keep their movements in and out
of the operating area to a minimum.
Nasal decontamination
Do not use nasal decontamination with topical antimicrobial agents aimed at
eliminating Staphylococcus aureus routinely to reduce the risk of surgical site
infection.
Mechanical bowel preparation
Do not use mechanical bowel preparation routinely to reduce the risk of
surgical site infection.
45
Hand jewellery, artificial nails and nail polish
The operating team should remove hand jewellery before operations. The
operating team should remove artificial nails and nail polish before operations.
Antibiotic prophylaxis
1. Give antibiotic prophylaxis to patients before:
• Clean surgery involving the placement of a prosthesis or implant
• Clean-contaminated surgery
• Contaminated surgery.
2. Do not use antibiotic prophylaxis routinely for clean non-prosthetic uncomplicated
surgery.
3. Use the local antibiotic formulary and always consider potential adverse effects
when choosing specific antibiotics for prophylaxis.
4. Consider giving a single dose of antibiotic prophylaxis intravenously on starting
anaesthesia.
5. Before giving antibiotic prophylaxis, consider the timing and pharmacokinetics (for
example, the serum half-life) and necessary infusion time of the antibiotic. Give a
repeat dose of antibiotic prophylaxis when the operation is longer than the half-life of
the antibiotic given.
6. Give antibiotic treatment (in addition to prophylaxis) to patients having surgery on
a dirty or infected wound.
46
7. Inform patients before the operation, whenever possible, if they will need antibiotic
prophylaxis, and afterwards if they have been given antibiotics during their operation.
INTRAOPERATIVE PHASE
Hand decontamination
The operating team should wash their hands prior to the first operation on the
list using an aqueous antiseptic surgical solution, with a single-use brush or pick for
the nails, and ensure that hands and nails are visibly clean.
Before subsequent operations, hands should be washed using either an alcoholic
hand rub or an antiseptic surgical solution. If hands are soiled then they should be
washed again with an antiseptic surgical solution.
Incise drapes
If an incise drape is required, use an iodophor-impregnated drape unless the
patient has an iodine allergy as non-iodophor impregnated incise drape increases the
risk of SSI.
Sterile gowns
The operating team should wear sterile gowns in the operating theatre during
the operation.
Gloves
Consider wearing two pairs of sterile gloves when there is a high risk of glove
perforation and the consequences of contamination may be serious.
47
Antiseptic skin preparation
Prepare the skin at the surgical site immediately before incision using an
antiseptic (aqueous or alcohol-based) preparation: povidone-iodine or chlorhexidine
are most suitable.
If diathermy is to be used, ensure that antiseptic skin preparations are dried by
evaporation and pooling of alcohol-based preparations is avoided.
Diathermy
Do not use diathermy for surgical incision to reduce the risk of surgical site
infection.
Surgical technique
Use gentle and clean surgical technique. Plan incision keeping in mind the
blood supply. Release mechanical retractors from time to time to allow perfusion.
Keep wound moist, especially during long operation.
Suture material
Modern monofilament absorbable suture materials are preferred for deep
closure and skin closure. Use the finest gauge compatible with the strength needed.
Closure should never be excessively tight and should allow for the inevitable
swelling.
Maintaining patient homeostasis
1. Maintain patient temperature in line with 'Inadvertent perioperative
hypothermia' (NICE clinical guideline 65).
48
2. Maintain optimal oxygenation during surgery. In particular, give patients
sufficient oxygen during major surgery and in the recovery period to ensure
that a haemoglobin saturation of more than 95% is maintained.
3. Maintain adequate perfusion during surgery.
4. Do not give insulin routinely to patients who do not have diabetes to
optimise blood glucose postoperatively as a means of reducing the risk of
surgical site infection.
Wound irrigation and intracavity lavage
Does not use wound irrigation to reduce the risk of surgical site infection. Do
not use intracavity lavage to reduce the risk of surgical site infection.
Antiseptic and antimicrobial agents before wound closure
Do not use intraoperative skin re-disinfection or topical cefotaxime in
abdominal surgery to reduce the risk of surgical site infection.
Wound dressings
Cover surgical incisions with an appropriate interactive dressing at the end of
the operation.
POSTOPERATIVE PHASE
Changing dressings
Use an aseptic non-touch technique for changing or removing surgical wound
dressings.
49
Postoperative cleansing
Use sterile saline for wound cleansing up to 48 hours after surgery. Advise
patients that they may shower safely 48 hours after surgery. Use tap water for wound
cleansing after 48 hours if the surgical wound has separated or has been surgically
opened to drain pus.
Topical antimicrobial agents for wound healing by primary intention
Do not use topical antimicrobial agents for surgical wounds that are healing by
primary intention to reduce the risk of surgical site infection.
Dressings for wound healing by secondary intention
Do not use Eusol and gauze, or moist cotton gauze or mercuric antiseptic
solutions to manage surgical wounds that are healing by secondary intention.
Use an appropriate interactive dressing to manage surgical wounds that are
healing by secondary intention.
Refer to a tissue viability nurse (or another healthcare professional with tissue
viability expertise) for advice on appropriate dressings for the management of surgical
wounds that are healing by secondary intention.
Identification of surgical site infections
1. Rise in temperature of the patient
2. Swelling of the sutured wound
3. Pus coming out of the suture line
4. Open one stitch and drain the pus completely.
50
Antibiotic treatment of surgical site infection and treatment failure
When surgical site infection is suspected (i.e. cellulitis), either de novo or
because of treatment failure, give the patient an antibiotic that covers the likely
causative organisms. Consider local resistance patterns and the results of
microbiological tests in choosing an antibiotic.
Debridement
Do not use Eusol and gauze, or dextranomer or enzymatic treatments for
debridement in the management of surgical site infection.95
51
Figure 6: SHOWING SUPERFICIAL SSI OF APPENDICECTOMY WOUND
Figure 7: SHOWING DEEP SSI FOLLOWING APPENDICECTOMY (FOR
GANGRENOUS APPENDICITIS)
52
Figure 8:SHOWING INFECTED LAPAROTOMY WOUND WITH PUS
DISCHARGE
Figure 9: SHOWING WOUND IN HEALING PHASE FOLLOWING SSI
53
METHODOLOGY
SOURCE OF DATA
The material for the present study was obtained from patient’s undergone
surgery in Department of General Surgery, KRH, Mysore, from 1st Jan 2010 to 30th
June 2011. Surgical site were considered to be infected according to the definition by
NNIS. The wounds were classified according to the wound contamination class
system proposed by U.S. National Research Council.
INCLUSION CRITERIA
All patients above 12 years undergoing surgery in Department of General
Surgery.
EXCLUSION CRITERIA:
1. Patients with known preoperative infection including dirty wounds.
2. Those undergoing revision surgery
3. Stitch abscess cases
Method of collection of data:
An elaborate study of these cases with regard to date of admission, history,
clinical features date of surgery, type of surgery, emergency or elective, preoperative
preparation and postoperative management is done till patient is discharged from
hospital, and then followed up the patient on OPD basis for any signs of wound
infection.
54
The wounds were examined for suggestive Signs/Symptoms of infection in the post
operative period, during wound dressing or when the dressings were soaked.
In history, presenting complaints, duration, associated diseases, coexistent
infections at a remote body site, personal history including diet, smoking, and
alcoholism were noted.
Operative findings which include, type of incision, wound contamination,
drain used and its type, and duration of operation were studied.
Postoperative findings which included, day of wound infection, day of 1st
dressing and frequency of change of dressing.
Findings on the day of diagnosis of wound infection were noted which
included fever, erythema, discharge, type and colour and the exudates was collected
from the depth of the wound using sterile cotton swab and was sent to microbiology
department for culture and sensitivity.
Procedure in laboratory:
In the microbiology department, the swabs were inoculated onto blood agar
plate, McConkey’s agar plates and nutrient broth. Inoculated media were incubated
aerobically at 37°C for 24-48 hrs. Nutrient broth was sub cultured if the original
plates did not yield organisms. The bacteria isolated were identified by their
morphological and cultural characteristics.
The samples collected were processed as follows:
a) Direct microscopic examination of gram stained smear.
55
b) Inoculation of the samples onto different culture media for aerobic and anaerobic
organisms.
c) Preliminary identification
d) Bio-chemical tests
e) Antibiotic sensitivity
56
Figure 10: DISC SHOWING GROWTH OF STAPH AUREUS
Figure 11: DISC SHOWING ANTIBIOTIC SENSITIVITY
57
RESULTS
A study of 400 operated cases was carried out of which 39 were diagnosed to
be having surgical site infection as per the CDC criteria. Thus the incidence of SSI in
this study is 9.75%.
TABLE 1: INCIDENCE OF SURGICAL SITE INFECTION
TOTAL NO
CASES
NO OF CASES
INFECTED
PERCENTAGE
400 39 9.75%
GRAPH 1: INCIDENCE OF SURGICAL SITE INFECTION
58
TABLE 2: INCIDENCE IN RELATION TO SEX
SEX NO.OF CASES INFECTED PERCENTAGE
MALE 282 26 9.21%
FEMALE 118 13 11.01%
GRAPH 2: INCIDENCE IN RELATION TO SEX
Incidence of infection among males is 9.21.%; whereas incidence of infection
among females is 11.01%.
59
TABLE 3: INCIDENCE IN RELATION TO AGE GROUP
AGE NO. OF CASES INFECTED PERCENTAGE
12-20 51 2 3.92%
21-30 114 7 6.14%
31-40 77 7 9.09%
41-50 68 9 13.2%
51-60 49 11 22.4%
61-70 7 3 9.37%
71-80 9 0 0%
TOTAL 400 39
Infection is more commonly seen among 51 to 60y old patients with an
incidence of 22.4% followed by among 41 to 50 and 61 to 70y old patients. Youngest
patient being 19yr old and oldest being 70y old.
60
GRAPH 3: INCIDENCE IN RELATION TO AGE GROUP
TABLE 4: INCIDENCE IN RELATION TO TYPE OF OPERATION
TYPE NO. OF CASES INFECTED PERCENTAGE
ELECTIVE 300 15 5%
EMERGENCY 100 24 24%
TOTAL 400 39 9.75%
Incidence of infection among Emergency surgery is 24% where as among
Elective is 5%.
61
GRAPH 4: INCIDENCE IN RELATION TO TYPE OF OPERATION
TABLE 5: INCIDENCE IN RELATION TO ANEMIA, HYPOPROTEINEMIA,
DIABETES, REMOTE INFECTIONS AND MALIGNANCIES
RISK FACTORS NO. OF CASES INFECTED PERCENTAGE
ANEMIA 61 15 24.59%
HYPOPROTEINEMIA 40 8 20%
DIABETIS MELLITUS 28 5 17.8%
UTI 30 5 16.6%
RTI 36 8 22.2%
MALIGNANCY 21 4 19.04%
62
Most of the patients were anemic (15.5%) with infection rate of 24.59%.
Hypoproteinemic (10%) patients had infection rate of 20%, diabetes mellitus (7%)
had infection rate of 17.8%, UTI (7.5%) had 16.6%, RTI (9%) had infection rate of
22.2% and malignancies (5.25%) had infection rate of 19.04%.
GRAPH 5: INCIDENCE IN RELATION TO ANEMIA, HYPOPROTENIMIA,
DIABETES, REMOTE INFECTIONS AND MALIGNANCIES
63
TABLE 6: INCIDENCE IN RELATION TO THE PREOP
HOSPITALIZATION
NO. OF DAYS NO. OF CASES INFECTED PERCENTAGE
1 to 5 278 25 8.99%
6 to 10 90 9 10%
11 to 15 32 5 15.62%
Total 400 39 -
278 patients had a pre-op hospitalization of 1 to 5 days with infection rate of
8.99%. 90 patients with hospitalization for 6 to 10 days had 10% infection. But
infection was more among patients who had pre op stay of 11 to 15 days with
incidence of 15.62%.
GRAPH 6: INCIDENCE IN RELATION TO THE PREOP
HOSPITALIZATION
0
50
100
150
200
250
300
1-5 6-10 11-15
No. of cases
64
TABLE 7: INCIDENCE IN RELATION TO DIAGNOSIS
DIAGNOSIS NO. OF CASES INCIDENCE PERCENTAGE
Duodenal perforation 32 8 25%
Ileal perforation 8 4 50%
Intestinal obstruction 11 2 18.18%
Acute/ recurrent appendicitis
110 6 5.45%
Inguinal hernia 78 4 5.12%
Gastric outlet obstruction 6 1 16.6%
Cholelithiasis 24 6 25%
Malignancy 15 3 20%
TAO (Lumbar sympathectomy)
5 0 0
Thyroid 23 0 0
Ventral hernias 16 1 6.25%
Varicose vein 10 0 0
Others 62 4 6.45%
Acute/recurrent appendicitis and inguinal hernia were the most common
operations performed. Surgical site infection was more among ileal perforation (50%),
duodenal perforation (25%), cholecystectomy (25%), malignancies (20%) and
intestinal obstruction (18.18%) patients. Surgeries for thyroid lesions, varicose veins
and lumbar sympathectomy had no SSI.
65
GRAPH 7: INCIDENCE IN RELATION TO DIAGNOSIS
TABLE 8: INCIDENCE IN RELATION TO PROPHYLACTIC ANTIBIOTIC
PRE OP
ANTIBIOTIC
NO. OF CASES INCIDENCE PERCENTAGE
GIVEN 156 8 5.12%
NOT GIVEN 244 31 12.7%
TOTAL 400 39
156 of 400 cases received pre op antibiotics, 8 cases were infected with
incidence of 5.12% where as patients who did not receive pre op antibiotics (244) had
an infection rate of 12.7%.
66
GRAPH 8: INCIDENCE IN RELATION TO PROPHYLACTIC ANTIBIOTIC
TABLE 9: INCIDENCE IN RELATION TO TYPE OF SSI
TYPE OF SSI NO. OF CASES PERCENTAGE
Superficial 27 69.23%
Deep 10 25.64%
Organ space 2 5.12%
Total 39
27 Cases of total infected cases (69.23%) had superficial SSI. 10 CASES
(25.64%) deep SSI and 2 cases (5.12%) had organ space infection.
67
GRAPH 9: INCIDENCE IN RELATION TO TYPE OF SSI
TABLE 10: INCIDENCE IN RELATION TO WOUND CLASS
TYPE NO. OF
CASES
INCIDENCE PERCENTAGE
Clean 192 9 4.68%
Clean contaminated 146 16 10.95%
Contaminated 62 14 22.58%
Total 400 39
Out of 400 cases 48% were clean cases, 36.5% were clean contaminated, and
15.5% were contaminated. Out of which clean cases had 4.68% of infection rate,
clean contaminated had incidence of 10.95% and contaminated cases had 22.58% of
infection rate. Infection rate increased with increasing contamination.
68
GRAPH 10: INCIDENCE IN RELATION TO WOUND CLASS
TABLE 11: INCIDENCE IN RELATION TO DURATION OF SURGERY
DURATION IN
HRS
NO. OF CASES INCIDENCE PERCENTAGE
<1 214 11 5.14%
1 to 2 156 22 14.10%
> 2 30 6 20%
53.5% cases had operation in less than 1hrs with incidence of infection of
5.14%, 39% of cases had operation in 1 to 2 hrs with an incidence of infection of
14.10% and 7.5% of cases had duration of operation >2 hrs. Thus incidence of
infection was more with longer duration of surgery.
69
GRAPH 11: INCIDENCE IN RELATION TO DURATION OF SURGERY
TABLE 12: INCIDENCE IN USE OF DRAIN AND MESH
NO. OF CASES INFECTED PERCENTAGE
Drain 138 25 18.11%
Mesh 90 2 2.22%
Drain was used in 138(34.5%) of cases out of which 25 cases were infected
with an incidence of 18.11%. Mesh was used in 90 cases and 2 patients had infection
(2.22%). Drain use is associated with increased rate of wound infection.
70
GRAPH 12: INCIDENCE IN USE OF DRAIN AND MESH
TABLE 13: INCIDENCE OF INFECTION NOTED ON POST OPERATIVE
DAY
DAY NO. OF INFECTED CASES PERCENTAGE
2nd 3 7.69%
3rd 11 28.2%
4th 5 12.8%
5th 8 20.51%
6th 4 10.25%
>6 Days 8 20.51%
Total 39
11 cases (28.2%) had infection detected on 3rd postoperative day, followed by
8 cases (20.5%) detected on 5th postoperative day and > 6 days.
71
GRAPH 13: INCIDENCE OF INFECTION NOTED ON POST OPERATIVE DAY
TABLE 14: INCIDENCE OF ORGANISM ISOLATED
ORGANISM NO. OF CASES PERCENTAGE
Pseudomonas 5 12.8%
Staphylococci 5 12.8%
Mrsa 4 10.25%
Ecoli 15 38.46%
Klebsiella 4 10.25%
Citrobacter 3 7.69%
Others 3 7.69%
TOTAL 39
Out of 39 infected cases 15 cases had E-coli infection, 5 had pseudomonas and
staphylococci, 4 had MRSA and Klebsiella each, 3 had infection with citrobacter and
other organisms. E-coli was the most common isolated organism accounting for
38.46% of cases followed by pseudomonas and staphylococci.
72
GRAPH 14: INCIDENCE OF ORGANISM ISOLATED
TABLE 15: ORGANISMS ISOLATED IN WOUND TYPES
Type Clean Percentage Clean contaminated
Percentage Contaminated Percentage
E-coli 0 0 4 26.6% 11 73.3%
Staphylococci 5 100% 0 0 0 0
Pseudomonas 0 0 4 80% 1 20%
MRSA 1 25% 2 50% 1 25%
Klebsiella 0 0 4 100% 0 0
Citrobacter 3 100% 0 0 0 0
Staphylococcus is commonly isolated in clean (100%) cases. Pseudomonas is
commonly isolated among clean contaminated (80%) cases. E.coli is most commonly
isolated with contaminated (76.6%) cases. Klebsiella was associated with clean
contaminated (100%) cases.
73
GRAPH 15: ORGANISMS ISOLATED IN WOUND TYPES
TABLE 16: COMPARISON OF ORGANISMS ISOLATED WITH PRE
OPERATIVE HOSPITALISATION
DURATION OF HOSPITALISATION
UPTO 5 DAYS 5-10 DAYS >10 DAYS
NO. % NO. % NO. %
E-coli 13 86.6 2 13.3 0 0
Staphylococci 2 40 0 0 3 60
Pseudomonas 3 60 2 40 0 0
MRSA 2 50 0 0 2 50
Klebsiella 1 25 3 75 0 0
Citrobacter 2 66.6 1 33.3 0 0
E- coli causes 86.6% of infection upto 5 days pre op hospitalisation and
pseudomonas causes 60% infection in the same period. Klebsiella causes 75% of
infection in 6 – 10 days pre op period. During >10 days period staphylococcus.
74
GRAPH 16: COMPARISON OF ORGANISMS ISOLATED WITH PRE OPERATIVE HOSPITALISATION
0
2
4
6
8
10
12
14
E-coli
Staphy
lococ
ci
Pseud
omon
as
MRSA
Klebsie
lla
Citrob
acter
Upto 5 days 5-10 days > 10 days
75
TABLE 17: ANTIBIOTIC SENSITIVITY SPECTRUM
No.
Ak % Cf
s
% C
a
% Nt % Cfx
% Pt % C % Do % I % A
t
% C
e
% C
f
% G Ctr
L in % V % Cl %
Ecoli
15 12 80 9 60 3 20 12 80 2 13.3
11 73.3
10 66.6
3 20 14 93.3
10 66.6
5 33.3
2 13.3
1 6.66
2 13.3
9 60 - -
Staph
5 2 40 - 4 80 3 60 0 0 3 60 1 20 2 40 4 80 3 60 4 80 3 60 2 40 4 80 5 100
- -
Pseud
5 4 80 2 40 1 10 3 60 1 20 4 80 1 20 0 0 5 100
3 6o 4 80 2 40 2 40 4 80 - - -
MRSA
4 0 0 0 0 0 0 0 0 0 0 2 50 0 0 0 0 1 25 0 0 0 o 0 0 0 0 0 0 3 75 4 100
3 75
Klebs
4 3 75 2 50 4 100
3 60 0 0 1 25 1 25 0 0 4 100
3 75 1 25 3 75 2 50 0 0 0 0 0 0 0 0
Citro
3 3 100
0 0 1 33 3 100
2 66.6
2 66.6
2 66.6
1 33.3
3 100
2 6.6 0 0% 2 6.66
1 33.3
1 33.3
Ak- Amikacin, CFS – Cefaperazone-Sulbactum, Ca- Ceftazidime, Nt – Netilmycin, Cfx – Cefixime, Pt- Piperacillin, Tazobactum, C-
Chloramphenicol, Do-Doxycycline, I- Imipenum, At – Azithromycin, Ce-Cefotaxim, Cf-Ciprofloxacin, G-gentamycin, Ctr-Ceftriaxone, Lm-
linezolid, V-Vancomycin, C-Clindamycin.
76
GRAPH 17: ANTIBIOTIC SENSITIVITY SPECTRUM
Ecoli is most sensitive for Imepenem (93.3%), amikacin and netilmycin (80%)
followed by piperacillin-tazobactum (73%), azithromycin (66%) and linezolid (60%)
sensitive.
Staphylococci is most sensitive for linezolid (100%) followed by imipenem,
ceftazidime and cefotaxim and ceftriaxone (80%).
Pseudomonas is most sensitive for imipenem (100%), followed by
piperacillin, amikacin and cefotaxim (80%).
MRSA is most sensitive to vancomycin (100%) followed by clindamycin and
linezolid (75% each).
Klebsiella is most sensitive for imipenem and ceftazidime(100%) followed
by amikacin, netilmycin,azithromycin and ciprofloxacin (75%).
Citrobacter is most sensitive to amikacin, netilmycin and imipenem
(100% each).
Overall imipenem and amikacin are the most sensitive antibiotics.
77
TABLE 18: ANTIBIOTIC RESISTANCE SPECTRUM
No.
Ak
% Cf s
% C a
% Nt % Cfx
% Pt % C % Do % I % A t
% C e
% C f
% G Ctr
L in
% V % Cl %
Ecoli
15 3 20 6 40 12 80 3 20 13 86.6
4 26.6
5 33.3
12 80 1 6.66
5 33.3
10 66.6
13 86.6
14 93.3
13
86.6
6 40
- -
Staph
5 3 60 - - 1 20 2 40 5 100
2 40 4 80 3 60 1 20 2 40 1 20 2 40 3 60
1 20 0 0 - -
Pseud
5 1 20 3 60 4 80 2 40 4 80 1 20 4 80 5 100
0 0 2 4o 1 20 3 60 3 60
1 20 - - -
MRSA
4 4 100
4 100
4 100
4 100
4 100
2 50 4 100
4 100
3 75 4 100
4 10o
4 100
4 100
4 100 1 25
0 0 1 25
Klebs
4 1 25 2 50 0 0 1 25 3 75 3 75 3 75 4 100
0 0 1 25 3 75 1 25 2 50
4 100 4 100
0 0 0 0
Citro
3 0 0 3 100
2 66.6
0 0 1 33.3
1 33.3
1 33.3
2 66.6
0 0 1 33.3
3 100
1 33.3
2 66.6
2 66.6
Ak- Amikacin, CFS – Cefaperazone-Sulbactum, Ca- Ceftazidime, Nt – Netilmycin, Cfx – Cefixime, Pt- Piperacillin, Tazobactum, C-
Chloramphenicol, Do-Doxycycline, I- Imipenum, At – Azithromycin, Ce-Cefotaxim, Cf-Ciprofloxacin, G-gentamycin, Ctr-Ceftriaxone, Lm-
linezolid, V-Vancomycin, C-Clindamycin.
78
GRAPH 18: ANTIBIOTIC RESISTANCE SPECTRUM
E-coli is most resistant to gentamycin (6%) followed by cefixime, ceftriaxone,
cefotaxim (13% each) and doxycycline (20%). Staphylococci is most resistant to
cefixime (100%) followed by other antibiotics, pseudomonas is most resistant to
doxycycline (100%), chloramphenicol, cefixime (20% each) followed by other
antibiotics, MRSA is resistant to most of the commonly used antibiotics especially
gentamycin, doxycycline, ceftrixone. Klebsiella is most resistant to dox, ceftriaxone
and linezolid (0%) followed by other antibiotics and citrobacter is most resistant for
cefotaxime.
Over all gentamycin, cefixime and doxycyclin are the most resistant
antibiotics noted.
79
DISCUSSION
The present study was conducted at department of general surgery, KR
Hospital Mysore.
This is a prospective study of 400 cases who underwent surgery and were
followed up from the day of operation to 30 days after discharge to look for the
development of SSI.
INCIDENCE OF SSI The overall infection rate for a total of 400 cases was 9.75%.
The incidence rate in this study is well within the infection rates of 2.8% to 17% seen
in other studies. Different studies from India at different places have shown the SSI
rate to vary from 6.09% to 38.7%.96 The infection rate in Indian hospitals is much
higher than that in other countries; for instance in the USA, it is 2.8% and it is 2-5%
in European countries. The higher infection rate in Indian hospitals may be due to the
poor set up of our hospitals and also due to the lack of attention towards the basic
infection control measures. The following table shows incidence in various other
studies.
80
AUTHOR YEAR COUNTRY NO. OF
OPERATIONS
INFECTION
Cruse and Foord 1980 Canada 62939 4.7%
Edwards 1984 U.S 20,193 2.8%
Anvikar et al 1999 India 3280 6.09%
Umesh s et al 2008 India 114 30.7%
Mahesh c b et al 2010 India 418 20.9%
Present study 2011 India 400 9.75%
The rates of SSIs in male patients were 9.21% and in female patients, they
were 11.01%. The significance of this observation is not well understood.
AGE
The present study shows that the incidence of SSI is more among 51-60 yrs
age group followed by 41- 50 yr group probably because of more number of surgeries
performed in these age groups. The younger age groups had lesser incidence of SSI.
This confirms the understanding that there is a gradual rise in incidence of wound
infection as age advances although in this study the 61-70 age group had lesser
incidence owing to lesser number of surgeries in this group. Likewise Cruse and
Foord observed in their study that older patients are more likely to develop infection
in clean wounds than younger patient.28
Similar findings were demonstrated by Mead, et al, who observed an increased
wound infection in patients less than 1 year old (2.7%) or greater than 50 years old
(2.8%) versus those 1 to 50 years old (0.7%).
81
The high incidence of 22.4% in patients aged 51- 60 years in our study is
perhaps due to decreased immunocompetence and increased chances of co-morbid
factors like Diabetes Mellitus, Hypertension, Chronic ailments like Asthma,
conditions requiring Steroid therapy and personal habits like Smoking and
Alcoholism. Age, obviously is an immutable patient characteristic and even, if it is a
risk factor for wound infection, it appears to be at most a modest one.
EMERGENCY/ ELECTIVE
The SSI rate in elective surgeries was found to be 5%, which was found to
increase to 24% in emergency cases. Our results are comparable well with the results
obtained by other workers. Similar results were obtained in Mahesh C B et al, 2010
for elective 7.61% and for emergency 21.05%.
The high rates of infection in emergency surgeries can be attributed to
inadequate pre operative preparation, the underlying conditions which predisposed to
the emergency surgery and the more frequency of contaminated wounds in emergency
surgeries.
RISK FACTORS LIKE ANEMIA, HYPOPROTENEMIA, DIABETES
MELLITUS, REMOTE INFECTIONS AND MALIGNANCY :
Incidence among the risk factors like anemia 24.59%, hypoprotenimia 20%,
diabetes mellitus 17.8%, UTI 16.6%, RTI 22.2%.and malignancies 19.04%. Similar
results were also obtained in other studies.28
82
Cause being the reduced immunocompetence, wound healing factors, hyperglycemia,
and pre-existing infections.
PRE-OP HOSPITALISATION
Preoperative hospitalization of more than 10 days had an incidence of
15.62%.The rates of SSIs increased with the increasing duration of pre operative
hospitalization. The higher incidence of infections due to a longer stay in the hospital
could be attributed to the increased colonization of patients with nosocomial strains in
the hospital with staphylococcus aureus (60%) and MRSA (50%) and also, a longer
pre-operative stay in the hospital reflected the severity of the illness and the co-
morbid conditions which required patient work- up and or therapy before the
operation. Similar results were obtained in other studies like in the study by Syed
Mansour Razavi et al which showed 1- 15 days of pre op admission had SSI of 18.6%
where as more than 15 days had infection rate of 25.9%. Nongyao Kasatqibal et al
2006 also had increased risk of SSI with increasing duration pre operative hospital
stay.
ANTIBIOTIC PROPHYLAXIS
The pre operative antibiotic prophylaxis reduced the rate of SSIs from 12.7%
to 5.12%. Antibiotic prophylaxis reduced the microbial burden of the intra operative
contamination to a level that could not overwhelm the host defenses. The pre
operative antibiotic prophylaxis could decrease post operative morbidity, shorten the
83
hospital stay and it could also reduce the overall costs which were attributable to the
infection.
Seyd Mansour Razavi in 2005, showed that administration of prophylactic
antibiotic half an hour before the operation would bring about the best results and the
lowest SSI. In 2010 Philipp Kirchhoff showed that antibiotic prophylaxis in
preventing postoperative complications in colorectal surgery is well established
through many studies. However, there is still a debate about the duration of the
antibiotic treatment and the kind of antibiotic which should be used. In summary,
most studies favour one to three intravenous doses of a second generation
cephalosporin with or without metronidazole with the first dose being administered
before skin incision. In 2001 Reiping tang, MD97 et al in contrast to other reports,
there was three times more predominant in surgical procedures preceded by antibiotic
prophylaxis in colonic surgeries. This might be explained by the fact that these were
contaminated wounds with increased risk of infection.
PREPARATION
Pre operative preparation was done with shaving in all the cases. All elective
cases undergone shaving within 24 hours prior to surgery and all emergency cases a
few hours before surgery. Still SSI rate was more among emergency cases. But most
of the studies compared the shaving and non shaving or other types of hair removal.
Court Brown 1981 and Rojanapirom 1992 compared shaving with no hair removal.
Both trials were conducted in abdominal surgery and used observations and swabs to
determine infection. 9.6 %( 17/177) of people who were shaved developed an SSI
84
compared with 6% (11/181) who were not shaved (pooling these two trials using a
random effects model gave an RR 1.59.
INCIDENCE IN RELATION TO TYPE OF SSI
Most of the SSI s were superficial type constituting 69.23% of infected cases
TYPE OF WOUND
In this study incidence in relation to the type of surgery, clean cases had
infection rate of 4.68%, clean contaminated had incidence of 10.95% and
contaminated cases had 22.58%.
Lul Raka et al in 2006 at Kosovo Teaching Hospital had the incidence rate of
SSI differed by wound classification: 3.1% for clean (n=64), 9.8% for clean-
contaminated (n=143), 46.1% for
Contaminated (n=13), and 100% for dirty infected wounds (n=5). The relative
risk of development SSI for contaminated wounds was 5.4-fold higher than for clean
wounds.
Seyd Mansour Razavi 2005 at an Iranian teaching hospital found clean wounds
in 109 cases (13.6%); clean-contaminated wounds in 214 cases (26.7%);
contaminated wounds in 307 cases (45.8%); and dirty infected wounds in 112 cases
(14%).
85
Mahesh C B et al.96 in 2010 at Bagalkot had SSI rate of 11.53% in clean
surgeries, 23.33% in clean contaminated ones, 38.10% in contaminated ones and
57.14% in dirty surgeries.
Our study correlates with most series, incidence among contaminated cases
are more due to the fact most of the cases were bowel perforation cases.
The difference in the rates of SSIs between the clean and the clean
contaminated wounds showed the effect of endogenous contamination and the
difference in the rates of SSIs between the clean contaminated and the contaminated
wounds showed the effect of exogenous contamination. The endogenous or the
exogenous contamination of the wounds by the organisms had a profound influence
on the SSIs.
INCIDENCE IN RELATION TO DURATION OF SURGERY
53.5% cases had operation in less than 1hr with incidence of infection of
5.149%, 39% of cases had operation in 1 to 2 hrs with an incidence of infection of
14.1% and 7.5% cases had operation >2 hrs with incidence of 20%. Incidence was
more in longer duration of surgery. Similar results were present in many studies, Seyd
Mansour Razavi 2005; Lul Raka et al in 2006, Mahesh C B et al in 2010 all had similar
results.
DRAIN
Use of drain had infection rate of 18.11% in our study.
Umesh S. Kamat et al in 2007 studied that patients with post-operative drain
were 5.8 (2.33–14.66) times more likely to develop SSI compared to those without the
drain. While the proportion of those with postoperative drain acquiring SSI was
86
62.5% (15/24), it was 22.2% (20/90) among those without the drain (c2 = 14.448, p =
0.000). Further, the infection rate increases with the increasing duration of the drain.
Similar observations were made in other studies on SSI, and could be attributed to the
nature of operation necessitating the drainage, the drain acting as the portal of entry,
or the effect of the drain itself.
INCIDENCE OF INFECTION NOTED ON POST OPERATIVE DAY
Abdominal surgical site infection was noted most commonly on 3rd post op
day in our study.
Similar results were obtained in other studies at Irani Hospital 2005.
ORGANISM
Most common organism isolated in our study is E-coli 38.46%, followed by
staphylococci 12.8%, and pseudomonas 12.8%.
Similar finding are obtained in some studies like Umesh S. Kamat121 2008
Seventy-nine per cent (79.33%) of the isolates were gram-negative bacteria;
pseudomonas being the commonest one, followed by Staphylococcus pyogenes in the
prospective study of surgical site infections in a teaching hospital in Goa.
Pseudomonas was most common isolate in other studies like Mofikoya Bo et
all Bacterial Agents of Abdominal Surgical Site Infections in Lagos Nigeria in 2009.
25(17.4%) of the 144 patients studied developed surgical site infections.
Pseudomonas was the most frequently cultured aerobic organism in 28% (n=7) of the
cultures, while Bacteroides species was the most common anaerobe isolated.
87
Our findings of a predominance of gram–ve bacilli are similar to that of other
workers. In most cases of SSI the organism is usually patient’s endogenous flora. In
abdominal surgeries the opening of the gastrointestinal tract increases the likelihood
of coliforms, gram negative bacilli which was our finding in this study. This group of
organisms tends to be endemic in hospital environment by being easily transferred
from object to object, they also tend to be resistant to common antiseptics and are
difficult to eradicate in the long term. This group of organisms is increasingly playing
a greater role in the many hospital acquired infections.
ANTIBIOTIC SENSITVITY AND RESISTENCE
In our study Ecoli is most sensitive for Imepenem (93.3%), Amikacin and
Netilmycin (80%) followed by Piperacillin-Tazobactum (73%). Azithromycin (66%)
and Linezolid (60%)
Staphylococci is most sensitive for Linezolid (100%) followed by Imipenem,
Ceftazidime and Cefotaxim and Ceftriaxone (80%).
Pseudomonas is most sensitive for Imipenem (100%), followed by
Piperacillin, Amikacin and Cefotaxim (80%)
MRSA is most sensitive to Vancomycin (100%) followed by Clindamycin and
Linezolid (75% each)
Overall Imipenem and Amikacin are the most sensitive antibiotics.
E-coli is most resistant to Gentamycin (6%) followed by Cefixime,
Ceftriaxone, Cefotaxim (13% each) and Doxycycline (20%). Staphylococci is most
resistant to Cefixime (100%) followed by other antibiotics, pseudomonas is most
resistant to Doxycycline (100%), Chloramphenicol, Cefixime (20% each)followed by
88
other antibiotics, MRSA is resistant to most of the commonly used antibiotics
especially Gentamycin, Doxycycline, Ceftriaxone.
Mofikoya Bo et al had Pseudomonas species 37.5% sensitive for Ceftaxidine followed
by 12.5% Ceftriaxone, and it was most resistant for Cefotaxime.
Umesh S. Kamat 2008 had pseudomonas species 21.4% sensitive for Cephoperazone-
sulbactum combination. The proportion of bacteria resistant to all antibiotics for
which tested was as high as 63.93% (39/61).
Most of the study showed that virtually all of the pathogens were resistant to the
commonly prescribed antibiotics such as Ampicillin and Doxycyclin. The cultured
aerobes also demonstrated less than 50% sensitivity to the cephalosporin’s tested
(Ceftaxidine, Cefuroxime and Ceftriaxone) in over 80% of the infected patients. This
finding further supports the well known high prevalence of multiple antibiotic
resistant nosocomial pathogens in our environment and may reflect the widespread
abuse of antibiotics in the general population.
The relative frequency of different isolates also varied between different studies.
Thus, it can be concluded that the organisms that cause SSIs change from place to
place and from time to time in the same place. The antibiotic sensitivity testing of
different isolates showed multidrug resistance by most of the isolates. The review of
literature indicates that there is gradual increase in drug resistance to many antibiotics
in most of the organisms which are isolated from surgical patients. Our study reveals
that though SSIs have been widely studied since a long time, they still remain as one
of the most important causes of morbidity and mortality in surgically treated patients.
The steps taken to reduce SSIs are still not adequate. Proper infection control
measures and a sound antibiotic policy should reduce SSIs in the future.
89
CONCLUSION
• Incidence of surgical site infection in this study is 9.75%.
• Majority of patients in the study belong to age group of 21-30 years which
account for 28.5%.
• Elective had an incidence of 5% and emergency cases had more incidences of
24%.
• Most of the cases had SSI detected on 3rd post-operative day.
• Anemia was found to be the main risk factor with more number of SSI’s.
• Infection rate was found to be increasing as the number of pre- op
hospitalisation increased.
• Prophylactic antibiotic therapy was found to decrease the rate of SSI’s.
• Longer duration of surgery and use of drain was associated with increased rate
of SSI.
• As expected the rate of infection increased from clean wounds to
contaminated wounds.
• E- coli was the commonest organism isolated.
• Most of the organisms were isolated from the clean contaminated and
contaminated cases.
• Overall imepenem and amikacin were the most sensitive antibiotics.
90
RECOMMENDATIONS
The following methods are recommended for further reducing infection.
1. Setting up of hospital infection control committee with its members.
2. Antibiotic policy and strict adherence to it.
3. Regular surveillance and feedback of results to surgeons and following strict
surgical auditing.
4. Reducing the pre-operative stay to minimum.
5. Ensuring that the patient is as fit medically as possible especially in elective
cases.
6. Minimizing the duration of surgery.
7. Using a good surgical technique.
8. Avoiding wound drains. If this is not possible, using a closed drainage system
and removal of drains as soon as possible.
9. Proper collection and transport of samples from the surgical site, immediately
on suspicion of infection.
10. Awaiting antibiotic sensitivity test results for appropriate antibiotic therapy.
91
SUMMARY
A pre-existing medical illness, prolonged operating time, the wound class,
emergency surgeries and wound contamination strongly predispose to surgical site
infection. Antimicrobial prophylaxis is effective in reducing the incidence of post-
operative wound infections for a number of different operative procedures but, timing
of administration is critical.
Reduction of length of procedures through adequate training of the staff on
proper surgical techniques, proper intra-operative infection control measures and
feedback of appropriate data to surgeons regarding SSIs would be desirable to reduce
the surgical site infection rate.
A surveillance programme for SSI need to be applied by the hospital followed
by auditing the infection rate on a regular basis.
Each and every hospital should adopt an antibiotic policy and strict adherence
to the same is necessary. Apart from this regular review and monitoring of the
implementation of guidelines is equally important.
92
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104
PROFORMA
1. CASE No. 5. IP/ No.
2. NAME 6. UNIT /WARD
3.AGE/SEX 7. DATE OF ADMISSION
4. ADDRESS 8. DATE OF SURGERY
9. DATE OF DISCHARGE
10. CHIEF COMPLAINT
11. CLINICAL DIAGNOSIS:
12. GENERAL PHYSICAL EXAMINATION:
PALLOR: ICTERUS:
EDEMA:
PULSE: BP:
13. INVESTIGATIONS:
CBC, RBS, UREA, CREATININE, LFT, URINE ROUTINE.
CHEST XRAY, XRAY ERECT ABDOMEN
105
14. PRE OP ANTIBIOTIC
15. PRE OP PREPARATION BY SHAVING
TIME BEFORE SURGERY
16. OPERATION DETAILS
1. PROCEDURE
2. TYPE OF SURGERY
- CLEAN SURGERY
- CLEAN CONTAMINATED SURGERY
- CONTAMINATED SURGERY
3. NATURE OF SURGERY:
- ELECTIVE
- EMERGENCY
4. DURATION OF SURGERY (IN HRS):
106
5. PER-OPERATIVE FINDINGS:
6. OPERATIVE DIAGNOSIS:
7. DRAIN / MESH USE:
8. PER OP ANTIBIOTICS
17. POST OPERATIVE
1. ANTIBIOTICS:
2. SIGNS OF SSI
3. DAY OF SSI DETECTED
4. TYPE OF SSI
5.MANAGEMENT
- SUTURE REMOVAL AND DRESSING
-DEBRIDEMENT
-SECONDARY SUTURING
6. WOUND CLUTURE SWAB GROWTH
7. ANTIBIOTIC SENSITIVITY/ RESISTANCE
22. FOLLOW UP
107
108
KEY TO MASTER CHART
M Male Emer Emergency
F Female Elect Elective
DOA Date of admission S Superficial
DOS Date of surgery D Deep
PO Post operative Or Organ space
Sen Sensitive Ca Carcinoma
Res Resistant AK Above knee
BD Block dissection AE Above elbow
DUP Duodenal ulcer perforation Ileos Ileostomy
Lap+PC Laparotomy + perforation closure Ile Cl Ileostomy closure
ILP Ileal perforation APR Abdomino perineal resection
Chole Cholecystectomy Chol Cholelithiasis
Appen Appendicectomy APP Appendicitis
Obst Her Obstructed hernia Lapar Laparotomy
Goo Gastric outlet obstruction TV+GJ Truncal vagotomy+gastrojejunostomy
Ing.her Inguinal hernia Hernio Herniorraphy
Amp Amputation PVD Peripheral vascular disease
Ac.Int.Obs Acute intestinal obstruction Res.Anst Resection anastomosis
MRM Modified radical mastectomy CC Clean contaminated
Cont Contaminated
TY
PE
P.O
.DA
Y
1 CHIKKAPPA 40/M 14540 09.06.11 02.06.11. DUP Emer Cont Lap+PC S 2 Pseud A,pt,Ctr Do,ctr,c2 MANJUNATH 24/M 9865 21.04.11 21.04.11 ILP Emer Cont Ileos D 3 E.coli A, I, Az ce,cf,do3 NAGAMMA 55/F 7321 24.03.11 12.04.11 Ca rectum Elect CC APR D 3 E.coli I,Pi,Az G, cfx,of4 SHRUTHI 21/F 9838 21.04.11 23.04.11 ILP Emer Cont Ileost S 4 E.coli A, Pi, I ce,G,ca5 CHELUVARAJ 37/M 11208 05.05.11 14.05.11 Chol Elect CC Chole S 4 Klebsiella I,A,Ca cfx,do,ctr6 PANCHETHRA 19/F 33299 23.12.10 23.12.10 APP Emer CC Appen S 3 E.coli N,A,Pi Az,cfs,G7 RAJAMMA 42/F 31425 02.12.10 07.12.10 Chol Elect CC Chole D 6 E.coli A,N,I cfs,A,ce8 NARASIMHA 35/M 31437 02.12.10 02.12.10 APP Emer CC Appen S 3 E.coli Pi,L,I6 Do,ctr,c9 DODDAMMA 60/F 29824 13.10.10 13.11.10 DUP Emer Cont Lap+PC S 5 MRSA V,Cl,Pt ce,G,ca10 GANGAMMA 50/F 29559 11.11.10 20.11.10 Ileostomy Elect Clean Ile Cl S 2 Staph. Ca,L,Nt ctr,of,do11 THAMMEGOWDA 50/M 33894 30.12.10 30.12.10 ILP Emer CC Prim Clo S 3 E.coli L,I,C cf,cfx,G12 MOHAN SINGH 35/M 13867 02.06.11 02.06.11 APP Emer CC Appen S 6 E.coli I,A,Az C,Nt,of13 JAYAMMA 60/F 13868 02.06.10 07.06.11 Chol Elect CC Chole S 5 E.coli Cfs,I,pi ce,do,cf14 MOHD.IQBAL 56/M 17431 10.06.11 10.06.11 Obst Her Emer Clean Lapar D 4 Pseudo I,A,Ce cfx,of,Az15 MAHADEVA 45/M 21775 25.05.11 03.06.11 GOO Elect CC TV+GJ S 3 Klebsiella A,Cf,Nt G, cfx,of16 GOPINATH 55/M 15842 26.06.11 28.06.11 Ing Her Elect Clean Mesh rep S >6 Staph I,L,A Do,ctr,c17 SHIVALINGAIAH 55/M 9241 04.04.10 11.04.10 PVD lt ul Elect Clean AE Amp D >6 Cons I,Pt,L Az,cfs,G18 SYED FAIROZ 31/M 3597 11.02.11 13.02.11 Ing Her Elect Clean Mesh rep S 6 Proteus V G, I, Cfx C,Nt,of19 RAJU 27/M 8710 08.04.10 17.04.10 Chol Elect CC Chole S 3 E.coli I,N,L Do,of,ce20 NANJANNA 45/M 21952 19.08.10 19.08.10 DUP Emer Cont Lap+PC S 4 E.coli Pt,C,N cf,I,G21 KAPPANNA 38/M 5405 04.03.10 06.03.10 Ing Her Elect Clean Mesh rep S >6 Pseud I, Ctr,C ce,G,ca22 MAHADEV 27/M 25864 30.09.10 30.09.10 DUP Emer Cont Lap+PC D 3 Citrobacter A,I,Nt Cfs, Ctr, C23 KAMALAMMA 40/F 10532 28.04.11 28.04.11 APP Emer CC Appen S 2 CONS L,Pt,I Cfx, do, Az24 RANGAIAH 60/M 32727 19.12.10 19.12.10 Ac.Int obst Emer Cont Res. Anst D 5 E.coli Az,A,L Do, Cfx, Of25 SUJATHA 20/F 1179 15.01.10 16.01.10 App Emer CC Appen S 5 E.coli I,C,Pi Cf, Do, Cfs26 DODDARAJU 45/M 4892 25.02.10 01.03.10 DUP Emer Cont Lap+PC OR 3 E.coli I,Cfs,N Cf, Do, G27 NANJUNDA NAYAKA 55/M 5469 04.03.10 04.03.10 DUP Emer Cont Lap+PC S >5 E.coli A,I,Pi Ca, Of, G28 LAKSHMAMMA 40/F 17104 01.07.10 03.07.10 Chole Elect Cont Chole S >6 Klebsiella I,Ca,A Ce, G, Az29 VENKATESH 60/M 9333 15.04.10 17.04.10 PVD Lt LL Emer Clean AK Amp S >6 Staph Au L,I,C Ctr, Cf, Of30 NAGEGOWDA 36/M 16435 25.06.10 25.06.10 Ac.Int obst Emer Cont Res. Anst S 3 Klebsiella Ca,I,A Do, Ctr, A31 MANCHAIAH 27/M 568 06.01.11 06.01.11 DUP Emer Cont Lap+PC S 5 Pseudomonas A,Pt,I Do, Cf, G32 PRAKASH ACHAR 43/M 7971 01.04.10 01.04.10 PVD Rt.LL Emer Clean BK Amp S >6 Staph Au L,C,Nt Do, Ct, C33 RECHA 28/M 24374 22.09.10 22.09.10 ILP Emer Cont Ileostomy S 4 Citrobacter I,Nt,A Of, G, Do34 BETTEGOWDA 70/M 1125 14.01.10 16.01.10 CA penis+ILP Elect Clean Lt ing BD D 5 MRSA CI,V,L Co, Ca, Az35 SAVITHRAMMA 60/F 2980 04.02.10 02.03.10 Chole Elect CC Chole D 5 MRSA V,L,pt Ce, C, A36 CHANDRASHEKAR 50/M 31801 01.01.11 01.01.11 DUP Emer Cont Chole D >6 MRSA V,L,Cl Cfs, G, PI37 RAJESHWARI 24/F 33858 31.12.10 31.12.10 APP Emer CC P.Cho S 3 Citrobacter A,Nt,I C, Nt, Cfx38 RAMU 45/M 23856 09.09.10 09.09.10 Obst ing hernia Emer CC Herniorr S 6 Pseudomonas I,Ctr,A3 Cfx, G, C39 LATHAMANI 34/F 3046 10.02.11 19.02.11 Ca breast Elect Clean MRM S >6 Staph Au I,L,C Cfx, Do, Cf
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