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

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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

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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.

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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

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6 INCIDENCE IN RELATION TO THE PREOP HOSPITALIZATION

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7 INCIDENCE IN RELATION TO DIAGNOSIS 64

8 INCIDENCE IN RELATION TO PROPHYLACTIC ANTIBIOTIC

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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

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14 INCIDENCE OF ORGANISM ISOLATED 71

15 ORGANISMS ISOLATED IN WOUND TYPES 72

16 COMPARISON OF ORGANISMS ISOLATED WITH PRE OPERATIVE HOSPITALISATION

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17 ANTIBIOTIC SENSITIVITY SPECTRUM 75

18 ANTIBIOTIC RESISTANCE SPECTRUM 77

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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

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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

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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.

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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.

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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.

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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:

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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

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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

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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.

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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

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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

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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

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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 %

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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

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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

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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.

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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.

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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

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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.

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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

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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.

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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

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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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