Draft Guideline for the Prevention of Surgical Site Infection, 1998

SUMMARY: This notice is a request for review of and comment on the

Draft Guideline for the Prevention of Surgical Site Infection, 1998.

The guideline consists of two parts: Part 1. ``Surgical Site Infection,

an Overview'' and Part 2. ``Recommendations for the Prevention of

Surgical Site Infections'', and was prepared by the Hospital Infection

Control Practices Advisory Committee (HICPAC), the Hospital Infection

Program (HIP), the National Center for Infectious Diseases (NCID), CDC.

DATES: Written comments on the draft document must be received on or

before August 17, 1998.

ADDRESSES: Comments on this document should be submitted in writing to

the CDC, Attention: SSI Guideline Information Center, Mailstop E-69,

1600 Clifton Road, N.E., Atlanta, Georgia 30333. To order copies of the

Federal Register containing the document, contact the U.S. Government

Printing Office, Order and Information Desk, Washington, DC 20402-9329,

telephone (202) 512-1800. In addition, the Federal Register containing

this draft document may be viewed and photocopied at most libraries

designated as U.S. Government Depository Libraries and at many other

public and academic libraries that receive the Federal Register

throughout the country. Addresses and telephone numbers of the U.S.

Government Depository Libraries are available by fax by calling U.S.

Fax Watch at (202) 512-1716 and selecting option 5 from the main menu.

The Federal Register is also available online at the Superintendent of

Documents home page at: http://www.access.gpo.gov/su__docs, or the

Hospital Infection Program Home page at: http://www.cdc.gov/ncidod/hip/

hip.htm

FOR FURTHER INFORMATION CONTACT: The CDC Fax Information Center,

telephone (888) 232-3299 and order document number 370160 or telephone

(888) 232-3228, then press 2, 2, 3, 2, 2, 1, 5 to go directly to the

guideline information.

SUPPLEMENTARY INFORMATION: This 2-part document updates and replaces

the previously published CDC Guideline for the Prevention of Surgical

Wound Infection. Part 1, ``Surgical Site Infection, an Overview''

serves as the background for the consensus recommendations of the

Hospital Infection Control Practices Advisory Committee (HICPAC) that

are contained in Part 2, ``Recommendations for Prevention of Surgical

Site Infections''.

HICPAC was established in 1991 to provide advice and guidance to

the Secretary and the Assistant Secretary for Health, DHHS; the

Director, CDC, and the Director, NCID regarding the practice of

hospital infection control and strategies for surveillance, prevention,

and control of nosocomial infections in U.S. hospitals. The committee

also advises CDC on periodic updating of guidelines and other policy

statements regarding prevention of nosocomial infections.

The Guideline for the Prevention of Surgical Site Infection, 1998

is the third in a series of CDC guidelines being revised by HICPAC and

NCID, CDC.

Dated: June 5, 1998.

Joseph R. Carter,

Acting Associate Director for Management and Operations, Centers for

Disease Control and Prevention (CDC).

Executive Summary

This ``Guideline for the Prevention of Surgical Site Infection,

1998'' represents the third revision of the Centers for Disease Control

and Prevention's (CDC) recommendations for the prevention of surgical

site infection (SSI), formerly called surgical wound infections. This

two-part guideline updates and replaces previous guidelines.\1\ \2\

Part I, ``Surgical Site Infection: An Overview,'' describes the

epidemiology, definitions, microbiology, pathogenesis, and surveillance

of SSIs. Part I also discusses SSI prevention measures such as

antimicrobial prophylaxis, barrier precautions, operating room

environment, sterilization practices, and surgical technique.

Recommended strategies for the prevention of SSIs are found in Part

II, ``Recommendations for the Prevention of Surgical Site Infection.''

These recommendations represent the consensus of the Hospital Infection

Control Practices Advisory Committee (HICPAC). This 12-member committee

advises CDC on issues related to surveillance, prevention, and control

of nosocomial infections in United States hospitals.\3\ Whenever

possible, the recommendations in Part II are based on data from well-

designed scientific studies. However, it must be kept in mind that a

limited number of studies establish the validation of SSI risk factors

and SSI prevention measures. By necessity, available studies have often

been conducted in narrowly defined patient populations or for specific

kinds of operations, making generalization of their findings to all

specialties and types of operations potentially problematic. This is

especially true regarding the implementation of SSI prevention

measures. Finally, some of the infection control practices routinely

used by surgical teams cannot be rigorously studied for ethical or

logistical reasons (e.g., wearing vs. not wearing gloves or masks).

Thus, some of the recommendations in Part II are based on a strong

theoretical rationale and suggestive evidence in the absence of

confirmatory scientific knowledge.

This document does not specifically address issues unique to burns,

trauma, transplant procedures, or transmission of bloodborne pathogens

from health-care worker to patient. Neither does it specifically cover

minimally invasive (e.g., laparoscopic) procedures

or procedures performed by surgeons outside of the operating room

(e.g., endoscopic procedures). This document does not cover invasive

procedures not performed by surgeons (e.g., cardiac catheterization, or

interventional radiologic procedures). However, it is likely that many

of the prevention strategies recommended in this document could be

applied or adapted to prevent infections that complicate these

procedures. The document does not recommend specific antiseptic agents

for patient preoperative skin preparations or for health-care worker

hand/forearm antisepsis. Hospitals should choose from the appropriate

products categorized by the Food and Drug Administration (FDA).\4\

Finally, this document is primarily intended for use in acute-care

hospitals by surgeons, operating room nurses, infection control

professionals, anesthesiologists, hospital epidemiologists, and other

hospital personnel responsible for the prevention of nosocomial

infections.

---------------------------------------------------------------------------

\\ Currently, for minimally invasive and laparoscopic

procedures no differences in infection control practices

(preoperative, intraoperative, or postoperative) have been

identified.

---------------------------------------------------------------------------

Part I. Surgical Site Infection (SSI): An Overview

Introduction

Before the mid-19th century, surgical patients commonly developed

postoperative ``irritative fever,'' followed by purulent drainage from

their incisions, overwhelming sepsis, and often death. It was not until

the late 1860s, after Joseph Lister had introduced the principles of

antisepsis, that postoperative infectious morbidity

[[Page 33169]]

decreased substantially. Lister's work radically changed surgery from

an activity associated with infection and death to a discipline that

could eliminate suffering and prolong life.

Currently, in the United States alone, an estimated 27 million

surgical procedures are performed each year, and nearly one-third of

patients undergoing these operations are 65 years of age.\5\

The CDC's National Nosocomial Infections Surveillance (NNIS) system,

established in 1970, monitors reported trends in nosocomial infections

in U.S. acute-care hospitals. Based on NNIS system reports, SSIs are

the second most frequently reported nosocomial infection, accounting

for 15% to 18% of all nosocomial infections among hospitalized

patients.\6\ During 1986-1996, hospitals conducting SSI surveillance in

the NNIS system reported 15,523 SSIs following 593,344 operations.

Among surgical patients, SSIs were the most common nosocomial

infection, accounting for 38% of all nosocomial infections. Of these

SSIs, 67% were incisional and 33% organ/space SSIs. Of the deaths among

surgical patients with an SSI, 77% were related to the infection

itself; the majority (93%) were organ/space SSIs. In 1980, Cruse showed

that an SSI increased a patient's hospital stay by about 10 days, and

cost an additional $2,000.\7\ \8\ 1992 estimates suggested that each

SSI resulted in 7.3 additional postoperative hospital days, adding

$3,152 in extra charges.\9\ Other studies corroborate that increased

length of hospital stay and cost are associated with SSIs.\10\ \11\

Deep (organ/space) SSIs, as compared to superficial (incisional) SSIs,

are associated with an even greater increase in hospital cost.\12\ \13\

In this document, SSIs refer to infections of incisions that are

closed primarily (i.e., skin edges are re-approximated at the end of

the operation). SSIs are classified as incisional SSIs or organ/space

SSIs. Incisional SSIs are further divided into those involving only

skin and subcutaneous tissue (superficial incisional SSI) and those

involving deeper soft tissues of the incision (deep incisional SSI).

Organ/space SSIs involve any part of the anatomy (e.g., organs or

spaces) other than incised body wall layers opened or manipulated

during operations (Figure 1). Standardized criteria have been developed

for defining superficial incisional, deep incisional, and organ/space

SSIs are shown in Table 1. Table 2 lists specific sites used to

differentiate organ/space SSIs. For example, in a patient who had an

appendectomy and subsequently developed a subdiaphragmatic abscess, the

infection would be reported as an organ/space SSI at the intra-

abdominal specific site. Failure to use objective criteria to define

SSIs has been shown to substantially impact SSI rates.\14\ \15\ The CDC

NNIS definitions of SSIs have been applied consistently by surveillance

and surgical personnel in many settings and currently are a de facto

national standard.\16\ \17\

Advances in infection control practices include improved operating

room ventilation, sterilization, barriers, surgical technique, and

availability of antimicrobial prophylaxis. Despite these activities,

SSIs remain a substantial cause of morbidity and mortality among

hospitalized patients. In part, this may be explained by the fact that

many surgical patients today are of advanced age and/or have a wide

variety of chronic, debilitating or immunocompromising underlying

diseases. An increase in survival of low-birth-weight infants (e.g.,

1000 g) may pose unique surgical challenges. There also are

increased numbers of implants used and more organ transplants

performed. Other factors include emergence of resistant pathogens,

increased numbers of contaminated and dirty procedures (e.g., trauma-

associated gunshot wounds and motor vehicle accidents). Thus, to reduce

the risk of an SSI, a systematic but realistic approach must be applied

with the awareness that this risk is influenced by characteristics of

the hospital, surgical team, patient, and operation.

Microbiology of SSIs

According to the NNIS system the distribution of pathogens isolated

from SSIs has not changed markedly during the last decade (Table

3).6 18 \19\ Staphylococcus aureus, coagulase-

negative staphylococci, Enterococcus spp., and Escherichia coli remain

the most frequently isolated pathogens. However, SSIs are increasingly

caused by antimicrobial-resistant pathogens, such as methicillin-

resistant S. aureus (MRSA), vancomycin-resistant enterococcus, and gram

negative rods.20 \21\ In one 4-year study of 245 consecutive

SSIs, 50% of all staphylococcal isolates were MRSA, 11% were

gentamicin-resistant E. coli, and Klebsiella spp. demonstrated an

increased resistance to aminoglycosides.\22\

The isolation of fungi from SSI, particularly Candida albicans,

also has increased.\23\ From 1991-1995, among patients at NNIS

hospitals, the incidence of fungal SSIs increased from 0.1 to 0.3 per

1000 discharges.\23\ The increased proportion of SSIs caused by

resistant pathogens and Candida spp. may reflect an increased severity

of illness of surgical patients, an increased number of surgical

patients who are immunocompromised, and/or more widespread use of

prophylactic and therapeutic antimicrobial agents.

Outbreaks or clusters of SSIs have also been caused by unusual

pathogens, such as Rhizopus oryzae, Clostridium perfringens,

Rhodococcus bronchialis, Legionella pneumophila and dumoffii, and

Pseudomonas multivorans. These rare outbreaks have been traced to

contaminated adhesive dressings,\24\ elastic bandages,\25\ colonized

health care personnel,\26\ tap water,\27\ or contaminated disinfection

solution.\28\ When a cluster of SSIs is caused by an unusual pathogen,

a formal epidemiologic investigation should be conducted to determine

the source of infection.

Pathogenesis of SSI

Microbial contamination of the surgical site is a necessary

precursor of SSI. The risk of SSI can be conceptualized according to

the following relationship \29\:

[GRAPHIC] [TIFF OMITTED] TN17JN98.000

Quantitatively, it has been shown that if a surgical site is

contaminated with >10 \5\ microorganisms per gram of tissue, the risk

of SSI is markedly increased, whereas contamination with 30-32 The risk of SSI is increased when foreign

material, such as sutures,\33\ indwelling devices, or prostheses are

placed. For example, researchers have shown that the insertion of

foreign material can decrease the infecting dose of staphylococci from

>10 \6\ to 34-36

Organisms may contain or produce substances or toxins that increase

their ability to invade a host, produce damage

[[Page 33170]]

within the host, or survive on or in colonized or infected host tissue;

promoting the development of an SSI.37-40 For example,

endotoxin has numerous effects as a component of the outer membrane of

gram negative bacteria, such as a stimulator of cytokine production,

and as an initiator of endogenous mediator pathways with significant

systemic effects (e.g., hypotension, fever).41 \42\ Some

bacterial surface components (notably polysaccharide extracellular

capsules) inhibit phagocytosis.\43\ Some bacteria, such as Clostridium

spp., produce powerful cytolytic exotoxins that disrupt cell membranes

or alter cellular metabolism.32 \44\ Glycocalyx and the more

loosely associated component, ``slime'', are produced by a variety of

microorganisms, of particular significance gram-positive bacteria, and

most notably coagulase negative staphylococci.45-47 The

glycocalyx material slime develops into a biofilm and can shield

infecting bacteria from phagocytosis, as well as inhibit the action of

antimicrobial agents.\47\ Glycocalyx biofilms have been implicated as a

significant contributor to infection of surgically implanted

prostheses.47-52 Despite knowledge of these and other

virulence factors, in most cases the mechanistic relationship between

their presence and SSI development has not yet been fully defined.

The primary reservoir for organisms causing SSI is the patient's

endogenous flora. Exogenous sources of SSI pathogens include the

operating room environment, hospital personnel (especially those in the

operating room),53-55 or seeding of the operative site from

a distant focus of infection.56-60 Seeding from distant foci

is particularly important in patients who have prostheses or other

implants placed during the operation since the device provides a nidus

for attachment of the organism.61-66 The endogenous flora

causing SSIs vary according to the specific body

site.19 67-71 For example, an SSI arising from the skin is

predominant due to gram-positive organisms (e.g., staphylococci). SSIs

arising from the gastrointestinal system are composed of a more mixed

group of organisms, including enteric, gram-negative bacilli (e.g., E.

coli), anaerobes (e.g., B. fragilis), and gram-positive organisms

(staphylococci and enterococci). SSIs arising from the genitourinary

system are predominantly due to gram-negative organisms (e.g., E. coli,

Klebsiella spp., and Pseudomonas), and enterococci. The organisms

causing SSIs in the female reproductive system include enteric, gram-

negative bacilli; enterococci; group B streptococci; and anaerobes.

Exogenous flora are primarily gram-positive organisms (e.g.,

staphylococci and streptococci) and other aerobes.\19\

Fungal pathogens rarely cause SSIs, and their pathogenesis is not

well understood. Factors that increase the risk of fungal infections in

surgical patients include (1) fungal colonization of the upper

gastrointestinal tract following exposure to broad-spectrum

antimicrobials, (2) use of proton pump inhibitors or histamine-2

blockers that decrease stomach acidity and promote growth of

microorganisms, including yeast, (3) disruption of the gastrointestinal

mucosal barrier, (4) impaired host defenses,\53\ (5) implantation of

foreign bodies (e.g., prosthetic heart valves), and (6) colonized

operating room personnel (e.g., fungal colonization of artificial

nails).\72\

Risk and Prevention of SSIs

The term ``risk factor'' has a particular meaning in epidemiology

and, in the context of SSI pathophysiology and prevention, strictly

refers to a variable that has a significant, independent association

with the development of SSIs. Risk factors are identified by

multivariable analyses in epidemiologic studies. Unfortunately, the

term risk factor often is used in the literature in a broad sense to

include patient or operation features which, although associated with

SSI development, are not themselves independent.\73\ The literature

cited in the sections that follow includes both the strict and broad

definition of risk factor. Recommendations given a category ranking of

IA are generally based on studies using the strict definition.

SSI risk factors (Table 4) are valuable in two ways: (1) they allow

useful stratification of operations, making surveillance data more

comprehensible, and (2) preoperative knowledge of risk factors may

allow for targeted prevention interventions. For example, it is known

that remote site infection is an independent SSI risk factor in some

operations. If a patient has such an infection, the surgical team may

choose to delay an elective operation until the infection resolves.

An SSI prevention measure can be defined as an action or set of

actions intentionally taken by caregivers to reduce the risk of an SSI.

Many such techniques, to be described subsequently, involve reducing

the opportunities for microbial contamination of the patient's tissues

or sterile surgical instruments. Other techniques are adjunctive, such

as using antimicrobial prophylaxis or avoiding unnecessary traumatic

tissue dissection. In general, SSI prevention measures have been based

on direct scientific evidence, theoretical rationale, or tradition. In

the discussion that follows, the foundation for each given prevention

measure will be described. Optimum application of SSI prevention

measures requires that a variety of patient and operation

characteristics be carefully considered.

In certain kinds of operations, patient characteristics that may be

associated with an increased risk of an SSI include coincident remote

site infections (e.g., urinary tract, skin, or respiratory

tract),1 31 74-76 diabetes,77-80 cigarette

smoking,78 81-85 systemic steroid use,77 80 86

obesity (> 20% ideal body weight),78-80 87-90 extremes of

age,85 91-95 and poor nutritional

status.78 87 91 96-98

The contribution of diabetes to SSI risk is controversial

77-79 91 99 because the independent contribution of diabetes

to SSI risk has not typically been assessed after controlling for

potential confounding factors. In one prospective study of 130 pregnant

women, no correlation was found between SSI risk and perioperative

glycemic control, as measured by glycosylated hemoglobin (HgA1c)

levels. However, the sample size in the study was small and the use of

prophylactic antimicrobial agents was not assessed. More recently, the

relationship between HgA1c levels and SSI risk in coronary artery

bypass graft patients was assessed; a significant relationship was

found between increasing levels of HbA1c and SSI rates.100

Also, increased glucose levels (>200 mg/dl) in the immediate

postoperative period (48 hours) were associated with

increased SSI risk.101 102 More studies are needed to assess

the efficacy of perioperative blood glucose control as an adjunctive

measure.

Nicotine use delays primary wound healing and may increase the risk

of SSI.78 In a large prospective study, current cigarette

smoking was an independent risk factor for sternal and/or mediastinal

SSI following cardiac surgery.78 Other studies have

corroborated cigarette smoking as an important SSI risk

factor.81-85 The limitation of these studies, however, is

that terms like ``current cigarette smoking'' and ``active smokers''

are not always accurately defined. To appropriately determine the

contribution of tobacco use to SSI risk, standardized definitions of

smoking history must be adopted and used in studies designed to control

for confounding variables.

[[Page 33171]]

Patients who are receiving steroids or other immunosuppressive

drugs preoperatively also may be predisposed to developing

SSI.77 80 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%).86 In contrast, other

investigators have not found a relationship between steroid use and SSI

risk.103-105

There may be an increased risk of SSI in patients who are

malnourished, but the exact relationship between nutritional status and

risk of SSI is unclear. Low serum albumin (78 96-98 More

precise definitions of malnutrition are needed, along with prospective

observational studies, to resolve this issue.

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.8 18 19 75 93 104 106 107

Preoperative Issues

Preoperative Antiseptic Showers

A preoperative antiseptic shower or bath will decrease the

patient's skin microbial colony count. In a study of >700 patients who

received preoperative antiseptic showers, chlorhexidine reduced

bacterial colony counts nine-fold (2.8 x 102 to 0.3),

while povidone-iodine or triclocarban-medicated soap reduced colony

counts by 1.3 and 1.9-fold, respectively.108 A smaller

uncontrolled study corroborated these findings.109 Despite

the fact that preoperative showers reduce the skin's microbial colony

counts, it has not definitively been shown to reduce SSI

rates.110-112

Preoperative Shaving/Hair Removal

Preoperative shaving of the surgical site the night before an

operation is associated with a significantly higher SSI risk. This risk

is greater than that accompanying the use of depilatory agents or no

hair removal.8 113-115 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 had no hair

removal.113 The increased SSI risk associated with shaving

has been attributed to microscopic cuts in the skin that later serve as

foci for infection. Shaving immediately before the operation compared

to shaving within 24 hours or > 24 hours preoperatively is associated

with decreased SSI rates (3.1% vs. 7.1% and 20%

respectively).113 Clipping hair immediately before an

operation is also 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%).116-119 Although the use of

depilatories is associated with a lower SSI risk than shaving or

clipping,113 114 depilatories sometimes produce

hypersensitivity reactions.113 Other studies show that

preoperative hair removal is associated with increased SSI rates and

suggest that no hair be removed.93 120 121

Patient Skin Preparation in the Operating Room

Several antiseptic agents are available for preoperative

preparation of skin at the incision site (Table 5). The iodophors

(e.g., povidone-iodine), alcohol-containing products, and chlorhexidine

gluconate are the most commonly used agents.18 31 122 No

studies have adequately assessed the comparative effects of these

preoperative skin antiseptics on SSI risk in well-controlled procedure-

specific studies.

Alcohol is defined by the Food and Drug Administration as having

one of the following active ingredients: ethyl alcohol 60-95% by volume

in an aqueous solution, or isopropyl alcohol 503-91.3% by volume in an

aqueous solution.\4\ In this document, -propyl alcohol is included in

the definition of alcohol. Alcohol is readily available, inexpensive,

and remains the most effective and rapid acting skin

antiseptic.123 Aqueous 70%-92% alcohol solutions have

germicidal activity against bacteria, fungi, and viruses, but spores

can be resistant.123 124 One potential disadvantage of the

use of alcohol in the operating room is its

flammability.123-125

Both chlorhexidine gluconate and iodophors have broad spectra of

antimicrobial activity.18 31 124 126 In some comparisons of

the two antiseptics, chlorhexidine gluconate achieved greater reduction

in skin microflora than did povidone-iodine and also had greater

residual activity after a single application.127-129

Further, chlorhexidine gluconate is not inactivated by blood or serum

proteins.18 123 130 131 Iodophors may be inactivated by

blood or serum proteins, but exert a bacteriostatic effect as long as

they are present on the skin.18 125

Before the skin preparation of a patient is initiated, the skin

should be free of gross contamination (i.e., dirt, soil, or any other

debris).132 The patients skin is prepped by applying an

antiseptic preparation in concentric circles, beginning in the area of

the proposed incision. The prepped area should be large enough to

extend the incision or create new incisions or drain sites, if

necessary.1 124 133 The application of the skin preparation

may need to be modified, depending on the condition of the skin (e.g.,

burns) or location of the incision site (e.g., face).

Some modifications of the preoperative skin preparation process

include: (1) removing, drying, or wiping off the skin prep antiseptic

agent after application, (2) using an antiseptic-impregnated adhesive

drape, (3) painting the skin with an antiseptic in lieu of the

traditional scrub, or (4) using a ``clean'' versus a ``sterile''

surgical skin prep kit. None of these modifications adds to further

reductions in bacterial colony counts at the surgical site or reduces

SSI risk.134 -137

Preoperative Hand/Forearm Antisepsis

Members of the surgical team universally wash their hands and

forearms by performing a traditional procedure known as scrubbing (or

the surgical scrub) immediately before donning sterile gowns and

gloves. Ideally, the optimum antiseptic agent should have a broad

spectrum of activity, be fast-acting, and have a persistent

effect.1 138 139 Antiseptic agents commercially available in

the United States contain alcohol, chlorhexidine, iodine/iodophors,

para-chloro-meta-xylenol, or triclosan (Table

5).18 123 124 140 141 Alcohol is considered the ``gold

standard'' for surgical hand preparation in several European

countries.142-145 Alcohol-containing preps have been used

less frequently in the United States than in Europe, possibly because

of concerns about flammability and skin irritation. Povidone-iodine and

chlorhexidine gluconate are the current agents of choice for most U.S.

surgical team members.124 However, when 7.5% povidone-iodine

or 4% chlorhexidine gluconate was compared to alcoholic chlorhexidine

(60% isopropanol and 0.5% chlorhexidine gluconate in 70% isopropanol),

alcoholic chlorhexidine was found to have greater residual

antimicrobial activity.138 146 No agent is ideal for every

situation, and a major factor aside from the efficacy of any product is

its acceptability by operating room personnel after repeated usage.

Unfortunately, most studies evaluating surgical scrub antiseptics have

focused on measuring hand bacterial colony counts. No clinical trials

have evaluated

[[Page 33172]]

the impact of scrub agent choice on SSI risk.141 147-151

Factors other than the choice of antiseptic agent influence the

effectiveness of the 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. The ideal duration of

scrubbing is unknown. Recent studies suggest that scrub times of 3-5

minutes are as effective as the traditional 10-minute scrub in reducing

hand bacterial colony counts.152 153

A surgical team member who wears artificial nails may have

increased hand bacterial and fungal colonization even after performing

an adequate hand scrub.154 155 Hand carriage of gram-

negative organisms has been shown to be greater among wearers of

artificial nails than among non-wearers.155 An outbreak of

Serratia marcescens SSIs in cardiovascular surgery patients was found

to be associated with a surgical nurse who wore artificial

nails.72 Long nails, artificial or natural, may be

associated with tears in gloves.31 124 154 The influence on

SSI risk of operating room team members wearing nail polish or jewelry

has not been adequately studied.140 154 156-158

Antimicrobial Prophylaxis

Well-designed, randomized clinical trials have demonstrated the

benefit of antimicrobial prophylaxis in certain kinds of

operations.12 70 159-195 Prophylaxis should not be confused

with therapy. Prophylaxis is the administration of an antimicrobial

agent for operations where minimal microbial contamination of the

surgical site is expected (i.e., clean or clean-contaminated

operations, Table 6).47 Therapy is the administration of an

antimicrobial agent in operations where substantial microbial

contamination already has occurred (i.e., contaminated or dirty

operations).47 196 197 For prophylaxis to be maximally

effective, an appropriate agent must be administered at the correct

time to ensure microbiocidal tissue levels before the incision is made,

be maintained at adequate levels for the duration of the operation, and

not be continued postoperatively.69-71 198-200 There is no

evidence that antimicrobial agents given after incision closure have

prophylactic effect on bacterial contamination acquired before incision

closure.47 Also, use of antimicrobial prophylaxis beyond the

intraoperative period may increase the risk of toxicity and the

development of antimicrobial-resistant organisms.47 71 201

Antimicrobial prophylaxis is reserved for clean and clean-

contaminated operations. The purpose of antimicrobial prophylaxis in

clean operations in which prostheses, grafts, or implants are placed in

the patient is to prevent the attachment of organisms to the device

since the device can serve as a nidus for infection.\47\ \69\ \197\

\202\ \203\ In clean operations in which no implant or device is

placed, there is controversy regarding the use of antimicrobial

prophylaxis. Because the risk of developing an SSI following clean

operations is generally low,\87\ the risk of infection versus the risk

of prophylaxis must be considered. The purpose of using antimicrobial

prophylaxis in clean-contaminated operations is primarily to reduce the

number of mucosal-associated organisms.\71\ \202\

A prophylactic antimicrobial agent should be chosen based on its

efficacy against the SSI pathogens expected as contaminants for a

particular operation. Table 6 lists clean and clean-contaminated

operations and the most frequently isolated SSI pathogens. The most

commonly used agents are cephalosporins, particularly first and second

generation cephalosporins.\202\ Vancomycin should not be used routinely

as a prophylactic agent \69\ \70\ \197\ \204\ However, at institutions

with high numbers of infections due to (MRSA) or methicillin-resistant

Staphylococcus epidermidis, vancomycin has been recommended as a

prophylactic agent in major operations involving implantation of

prosthetic materials or devices (e.g., cardiac, vascular and orthopedic

operations).\69\ \204\ \205\

Intravenous administration of the prophylactic antimicrobial agent

is the most commonly used route. The intravenous route produces

adequate serum and tissue concentrations in a relatively short period

of time.\202\ A major exception to using the intravenous route is with

operations involving the gastrointestinal tract, mainly colorectal

operations.71 181 182 184 202 206-213 In these operations,

the antimicrobial agent is administered orally to reduce endogenous

flora in the gastrointestinal tract .

Timing and duration of prophylaxis are very important issues. The

objective is to administer the antimicrobial agent before the operation

starts to assure adequate microbiocidal tissue levels before the skin

incision is made. A large, prospective study of antimicrobial

prophylaxis in surgical patients undergoing elective clean and clean-

contaminated operations showed that when prophylaxis was given 0-2

hours before incision, the SSI rate was 0.59% (10/1708). If given

earlier or later, the SSI rate increased (3.8 % [14/369] and 3.3% [16/

488], respectively).\214\ For a cesarean section, the prophylactic

agent is given immediately after umbilical cord clamping to prevent the

infant from being exposed to the agent.\69\ \70\

In modern surgical practice, the optimum strategy for most commonly

used agents (first and second generation cephalosporins) entails

infusion of the preoperative dose approximately 30 minutes before skin

incision and administration of additional doses approximately every 2

hours intraoperatively.\18\ \69\ \71\ \197\ \202\ \203\ Because an

elective operation can be unexpectedly delayed, the practice of

administering prophylactic agents ``on call'' to the operating room is

not recommended.\70\ \215\ Appropriate timing of prophylaxis may be

enhanced by administering the agent as close as possible to the time of

anesthetic induction. In general, the duration of an operation will

dictate the necessity infusing one or more additional doses of the

prophylactic agent to maintain appropriate tissue levels (i.e., for

operations whose duration exceeds the estimated serum half-life). Other

reasons for additional intraoperative dosing include operations with

major intraoperative blood loss or operations on morbidly obese

patients.47 69 71 201 203 216-218

Intraoperative Issues

Operating Room Environment

Air/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.\219\ Therefore, efforts should be made to minimize personnel

traffic during operations. 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.220-223 In these outbreaks, the strain causing the

outbreak was recovered from the air in the operating room,\220\ \221\

\224\ or on settle plates in a room in which the human carrier

exercised.221-223

Operating rooms should be maintained at positive pressure with

respect to corridors and adjacent areas.\225\ Positive pressure

prevents air flow from less clean areas into clean areas. All

ventilation or air conditioning systems in hospitals, including those

in operating rooms, should have two filter beds in series with the

efficiency of filter bed one ``30% and filter bed two

[[Page 33173]]

2'' 90%.\226\ Conventional operating room ventilation systems produce a

minimum of about 15 air changes of filtered air per hour. Three (20%)

of these air changes/hour must be fresh air.\226\ \227\ Air should be

introduced at the ceiling and exhausted near the floor.\227\ \228\

Recommended ventilation parameters for operating rooms have been

published by the American Institute of Architects, and the U.S.

Department of Health and Human Service (Table 7).\226\

Laminar air flow is designed to move particle-free air (called

``ultraclean air'') over the aseptic operating field at a uniform

velocity (0.3 to 0.5 m/sec), sweeping away particles in its

path. This air flow can be directed vertically or horizontally, and

recirculated air is usually passed through a high efficiency

particulate air (HEPA) filter.\229\ \230\ HEPA filters, commonly used

in hospitals, remove particles 0.3m in diameter with an

efficiency of 99.97%.\74\ \227\ \229\ \231\ Ultraviolet (UV) light has

been used as an infection control measure to reduce SSI risk. However,

neither laminar flow nor UV light has been conclusively shown to

decrease overall SSI risk.87 225 232-237

Environmental Surfaces

Environmental surfaces in U.S. operating rooms (e.g., tables,

floors, walls, ceilings, lights, and the like) are rarely implicated as

the sources of pathogens important in the development of SSIs.

Nevertheless, it is important to perform routine cleaning of

environmental surfaces to reestablish a clean environment after each

operation.\31\ \154\ \227\ \229\ There are no data to support routine

disinfecting of environmental surfaces or equipment between operations

in the absence of contamination or visible soiling. When visible

soiling of surfaces or equipment occurs during an operation, an

Environmental Protection Agency (EPA)-approved hospital disinfectant

should be used to decontaminate the affected areas before the next

operation.31 154 227 229 238-240 This is in keeping with the

Occupational Safety and Health Administration (OSHA) requirement that

all equipment and environmental surfaces be cleaned and decontaminated

after contact with blood or other potentially infectious

materials.\240\ Wet-vacuuming with an EPA-approved hospital

disinfectant is performed routinely after the last operation of the day

or night. Care should be taken to insure that medical equipment is

covered and that solutions used for cleaning and disinfecting do not

contact sterile devices or equipment. There are no data to support

special cleaning procedures or closing an operating room after a

contaminated or dirty operation has been performed.\227\ \228\

Tacky mats placed outside the entrance to an operating room/suite

have not been shown to reduce the number of organisms on shoes or

stretcher wheels, nor do they reduce the risk of SSI.\1\ \18\ \219\

\228\

Microbiologic Sampling

Because there are no standards or acceptable parameters for

comparison of microbial levels for ambient air or environmental

surfaces in the operating room, routine microbiologic sampling cannot

be justified. Such environmental sampling should only be performed as

part of an epidemiologic investigation.

Conventional Sterilization of Surgical Instruments

Inadequate sterilization of surgical instruments has resulted in

SSI outbreaks.\229\ \241\ \242\ Surgical instruments can be sterilized

by steam under pressure, by dry heat, by ethylene oxide, or other

approved methods. The importance of monitoring the quality of

sterilization procedures has been established.\1\ \31\ \154\ \226\

Microbial monitoring of steam autoclaves performance is necessary and

can be accomplished by use of a biological indicator.\154\ \239\ \243\

Detailed recommendations for sterilization of surgical instruments have

been published.\154\ \239\ \244\ \245\

Flash Sterilization of Surgical Instruments

The Association for the Advancement of Medical Instruments (AAMI)

defines flash sterilization as ``the process designated for the steam

sterilization of patient care items for immediate use''.\245\ During

any operation, the need for emergency sterilization of equipment may

arise (e.g., to reprocess an inadvertently dropped instrument). Flash

sterilization is intended to be used for emergent sterilization of

surgical instruments and other items and is never used for reasons of

convenience such as an alternative to purchasing additional instrument

sets and as a general time-saver. Some of the reasons that flash

sterilization has not been recommended as a routine sterilization

method include lack of timely biologic indicators to monitor

performance, absence of protective packaging following sterilization,

possible contamination during transportation to the operating rooms,

and use of minimal cycle parameters (i.e., time, temperature,

pressure).\243\ The AAMI has published sterilization cycle parameters

for flash sterilization (Table 8).

Until studies are performed to demonstrate that routine flashing

for purposes other than emergencies does not increase SSI risk, flash

sterilization should be restricted to its intended purpose. Also, flash

sterilization is not recommended for implantable

devices because of the potential for serious

infections.\239\ \244\-\246\

---------------------------------------------------------------------------

According to the FDA, an implantable device is

a ``device that is placed into a surgically or naturally formed

cavity of the human body if it is intended to remain there for a

period of 30 days or more''.\245\

---------------------------------------------------------------------------

Surgical Attire and Drapes

In this section the term ``surgical attire'' refers to scrub suits,

caps/hoods, shoe covers, masks, gloves, and gowns. Although

experimental data show that live microorganisms are shed from hair,

exposed skin, and mucous membranes of operating room personnel,\126\

\247\-\252\ few controlled clinical studies have evaluated

the relationship between the use of surgical attire and the risk of

SSI. Nevertheless, the use of barriers seems prudent to minimize

exposure of a patient to the skin, mucous membranes, or hair of

surgical team members and operating room personnel, and to protect

operating room personnel from bloodborne pathogens (e.g., human

immunodeficiency virus and hepatitis virus).

Scrub Suits

Hospital personnel, especially operating room nurses, surgeons, and

anesthesiologists, often wear a uniform throughout the day that

consists of pants and top/shirt and is called a ``scrub suit.''

Procedures for laundering, wearing, covering, and changing scrub suits

vary greatly. In some facilities, scrub suits are laundered only by the

hospital, while in others, scrub suits also may be laundered at the

health-care worker's home. Although, there are no well-controlled

studies evaluating SSIs risk among hospital-versus home-laundered scrub

suits,\253\ the Association of Operating Room Nurses (AORN) recommend

scrub suits only be laundered in an approved and monitored laundry

facility.\154\ Some facilities require that scrub suits be worn only in

operating room suites, while others allow the wearing of cover gowns

over scrub suits when personnel leave the operating room suites. AORN

recommends changing scrub suits when they are visibly soiled.\154\ OSHA

requires that ``if a garment(s) is penetrated by blood or other

potentially infectious materials, the garment(s) shall

[[Page 33174]]

be removed immediately or as soon as feasible.'' \240\

Masks

Data regarding the possible effect of using surgical masks on SSI

risk are limited. However, there is a strong theoretical rationale for

wearing surgical masks during all operations. Some studies have

evaluated the efficacy of surgical masks in reducing SSI risk and have

raised issues regarding cost vs benefit.\254\-\258\ Although surgical

masks are effective at filtering out some bacteria, they may not

completely prevent passage of organisms around the sides and edges of

the mask.\250\, \259\, \260\ Nevertheless, masks protect the surgical

team from inadvertent exposures to blood (i.e., splashes) and other

body fluids. OSHA requires that masks in combination with eye

protection devices, such as goggles or glasses with solid shields, or

chin-length face shields be worn whenever splashes, spray, spatter, or

droplets of blood or other potentially infectious material may be

generated and eye, nose, or mouth contamination can be reasonably

anticipated.\240\

Surgical Caps/Hoods and Shoe Covers

Surgical caps/hoods are inexpensive and reduce the shedding of hair

and scalp organisms. Rarely, SSI outbreaks have been traced to

organisms isolated from the hair or scalp (S. aureus and Group A

Streptococcus),\248\ \261\ even when caps were worn by personnel during

the operation and in the operating suites.

The use of shoe covers has never been shown to decrease SSI risk or

decrease floor bacterial counts.\262\ \263\ Shoe covers may protect a

health care worker from exposures to blood and other body fluids during

an operation. OSHA stipulates that surgical caps or hoods and/or shoe

covers or boots shall be worn in instances when gross contamination can

reasonably be anticipated (e.g., autopsies, orthopaedic surgery).\240\

Sterile Gloves

There is a strong theoretical rationale for the use of sterile

gloves by all members of the surgical team. Sterile gloves are worn to

minimize transmission of microorganisms from the hands of operating

room personnel to patient's and to prevent contamination of personnel

hands with blood and body fluids. If the integrity of a glove is

compromised (e.g., punctured) it should be changed as promptly as

safety permits.240 264-266 Double gloving (i.e., wearing two

pairs of gloves) has been shown to reduce bloodborne pathogen

contamination of surgical team members' hands.267-270

Sterile gloves are put on after donning sterile gowns.

Gowns and Drapes

Both sterile surgical gowns and drapes are used to create an

aseptic barrier between the surgical site incision and possible sources

of bacteria. Gowns are worn by operating room personnel and drapes are

laid over the patient. There are limited data to substantiate the

impact of surgical gowns and drapes on reducing SSI risk. The wide

variation in the products studied and the study designs make available

data difficult to evaluate.251 271-275

Gowns and drapes are classified as disposable (single use) or

reusable (multiple use). Regardless of the material used to manufacture

gowns and drapes, these items should be impermeable to liquids and

viruses 276 277 and effective when wet.1 In

general, only gowns reinforced with films, coatings, or membranes

appear to meet standards developed by the American Society for Testing

and Material (ASTM).276-278 However, the gowns that do meet

these standards ``liquid proof'' gowns may be uncomfortable because

they also inhibit the evaporation of sweat and heat loss from the

wearer's body. These factors should be considered when selecting

gowns.278

Practice of Anesthesiology

Anesthesiologists and nurse anesthetists perform invasive

procedures (e.g., placement of intravascular devices, endotracheal

intubation, administering intravenous solutions) and work in close

proximity to sterile surgical fields, thus it is imperative that they

strictly adhere to recommended infection control

practices.154 279-281 Breaks in aseptic technique,282

including use of common syringes,283 284 contaminated

infusion pumps,282 285-287 and the assembly of equipment in

advance of procedures,283 288 have been associated with SSI

outbreaks. Although a barrier (i.e., sterile drape) is placed between

the anesthesiologist's work area and the surgical field, SSIs have

occurred in which the source of the pathogen was the anesthesiologist

or a member of the anesthesia team (e.g., anesthesia

technician).289-293 Continued efforts must be undertaken to

educate and reinforce the importance of good infection control

practices in preventing SSIs, not only to surgeons and operating room

nurses but to all members of the surgical team.282 294

Hypothermia in surgical patients, defined as a core body

temperature below 36 deg.C, may result from general anesthesia,

exposure to cold, or intentional cooling such as, in cardiac procedures

to protect the myocardium or central nervous systems.295-297

In one study of patients undergoing colorectal operations hypothermia

was associated with an increased risk of SSI.298 However,

since any alteration in normal homeostasis alters normal host

responses, more studies are needed to establish a relationship between

hypothermia and SSI risk.

Surgical Technique

Excellent surgical technique can reduce SSI risk. Maintaining

effective hemostasis while preserving adequate blood supply, gently

handling tissues, avoiding inadvertent entries into a viscus, removing

devitalized (e.g., necrotic or charred) tissues, using drains and

suture material appropriately, eradicating dead space, and appropriate

post-operative incision management are widely believed to reduce the

risk of SSI.18 19 31 32 299 300

Any foreign body, including suture material or drains, may promote

inflammation at the surgical site 87 and may increase the

probability of infection for some levels of tissue contamination. There

are two types of suture material: absorbable and non-absorbable. There

is extensive literature comparing different types of suture material

and their presumed relationships to SSI risk.301-310 In

general, monofilament sutures appear to have the lowest infection-

promoting effects.3 18 31 87

While appropriate decisions regarding drain placement are beyond

the scope of this document, general points should be briefly noted.

Drains placed through an operative incision increase SSI

risk.67 Many researchers suggest placing drains through a

separate incision distant from the operating

incision.67 197 311 It appears that SSI risk decreases when

closed suction drains are used in comparison to open drains.

312 313 Closed suction drains are useful in evacuating

postoperative hematomas, seromas, and purulent material. Also, the

timing of drain removal is important; bacterial colonization of drains

tracts may increase as the duration of drainage

increases.314

Postoperative Issues

Postoperative Incision Care

Whether the incision is closed primarily (i.e., the skin edges are

re-approximated at the end of the operation), left open to be closed

later, or left open to heal by secondary

[[Page 33175]]

intention determines the details of postoperative incision care.

When a surgical incision is closed primarily, as most are, the

surgeon has determined that it is relatively free of microbial

contamination (i.e., clean or clean-contaminated). The primarily closed

incision is covered with a sterile dressing for 24-48 hours until the

incision edges are sealed.315 316 Beyond 48 hours, it is

unclear whether an incision must be covered by a dressing or whether

showering or bathing is detrimental.

When a surgical incision is left open for a few days before it is

closed (delayed primary closure), a surgeon has determined that it is

likely to be contaminated, or that the patient's condition prevents

primary closure (e.g., edema at the site). At the end of the operation,

such an incision is packed with a sterile dressing (usually moist) and

is inspected daily during dressing changes until the decision is made

to close it. When a surgical incision is left open to heal by secondary

intention, it is also packed with sterile moist gauze and covered with

a sterile dressing. For wounds healing by secondary intention, there is

no consensus on the benefit of using sterile technique (i.e., using

sterile gloves and dressings) vs clean technique during dressing

changes. The American College of Surgeons, CDC, and others have

described changing dressings with sterile gloves and

equipment.31 317-320 However, a pilot study of 30 patients

examined the difference between sterile vs clean technique for dressing

changes of surgical incisions left open. No difference was found in SSI

rates and the clean technique was less expensive. However, larger

studies are needed to confirm these preliminary findings.321

Discharge Planning: Care of the Surgical Site

Today, many patients are discharged soon after their operation,

with surgical incisions in the early process of healing.322

There are no set, specific protocols for home incision care, and much

of what is done at home by the patient, family, or home care agency has

to be individualized for each patient. The intent of discharge planning

is to maintain integrity of the healing incision, educate the patient

about the signs and symptoms of infection, and inform the patient about

whom to contact to report any problems. Written instructions and

repeated demonstrations may help reinforce consistency in following

verbal directions. It is the responsibility of the surgeon, nurse,

discharge planners, and home health agencies to educate the patient and

family in a uniform, concise, and coordinated fashion.

SSI Surveillance

Surveillance of SSI with feedback of appropriate data to surgeons

has been shown to be an important component of strategies to reduce SSI

risk.8, 323, 324 A successful surveillance program includes

epidemiologically sound infection definitions (Tables 1 and 2),

effective surveillance methods, and stratification of SSI rates

according to risk factors associated with SSI development.17

SSI Risk Stratification

Concepts

From the factors found to be associated with SSI, three categories

of variables have emerged as good predictors: (1) those that estimate

the intrinsic degree of microbial contamination of the surgical site,

(2) those that measure the duration of an operation, and (3) those that

serve as markers for host susceptibility.17 The probability

of developing an SSI depends upon the interaction of these variables in

a given patient.

A widely accepted scheme for classifying the degree of intrinsic

microbial contamination of a surgical site was developed by the 1964

National Academy of Sciences/National Research Council cooperative

research study and modified in 1982 by CDC for use in SSI surveillance

(Table 9).2, 87 In this scheme, a member of the surgical

team classifies the patient's wound at the completion of the operation.

Because of its ease and wide availability, the surgical wound

classification has been used to predict the risk of

SSI.8, 87, 325-330 Some researchers have suggested that

surgeons compare clean wound SSI rates with those of other

surgeons.8, 323 However, two CDC efforts--the Study on the

Efficacy of Nosocomial Infection Control (SENIC) Project and the NNIS

system--incorporated other predictor variables into SSI risk indices.

These showed that even within the category of clean wounds, the risk of

SSI varied from 1.1% to 15.8% and from 1.0% to 5.4%,

respectively.328,331 In addition, sometimes the incision is

neither classified at the time of surgery nor assigned by a member of

the surgical team, calling into question the reliability of the

classification. Therefore, reporting SSI rates stratified by wound

class alone is not recommended.

Data on 10 variables collected in the SENIC Project were analyzed

by using logistic regression modeling to develop a simple additive SSI

risk index.331 Four of these were found to be independently

associated with the risk of SSI: (1) an abdominal operation, (2) an

operation lasting >2 hours, (3) a surgical site with a wound

classification of either contaminated or dirty/infected, and (4) an

operation performed on a patient having 3 discharge

diagnoses. Each of these equally weighted factors contributes a point

when present, such that the risk index values range from 0 to 4. By

using these factors, the SENIC index was able to predict the risk of

SSI twice as well as the traditional wound classification scheme alone.

The NNIS risk index is operation specific and applied to

prospectively collected surveillance data. The index can range from 0

to 3 points and is defined by three independent and equally weighted

variables. A surgical patient scores one point when any of the

following are present: (1) American Society of Anesthesiologists (ASA)

class is 3 (Table 10), (2) wound classification is either

contaminated or dirty/infected, and (3) operation lasts >T hours, where

T is the approximate 75th percentile of the duration of the specific

operation being performed.328 The ASA class replaced

discharge diagnoses of the SENIC risk index as a proxy for the

patient's underlying severity of illness (host susceptibility) \332\

\333\ and is readily available in the chart during the patient's

hospital stay (Table 10). Unlike SENIC's constant 2 hour cut-point for

duration of operation, the operation-specific cut-points used in the

NNIS risk index have been shown to increase discriminatory

power.328

Issues

Adjustment for variables known to confound rate estimates is

critical if valid comparisons of SSI rates are to be made between

surgeons or hospitals.334 Risk stratification, as described

above, has proven useful for this purpose, but relies on the ability of

surveillance personnel to consistently and correctly find and record

the data. For the three variables used in the NNIS risk index, only one

study has focused on how accurately any of them are recorded. Cardo et

al. found that surgical team members' accuracy in assessing wound

classification for general and trauma surgery was 88% (95% CI: 82%-

94%).335 However, there are sufficient ambiguities in the

wound class definitions themselves to warrant concern about the

reproducibility of Cardo's results. The accuracy of recording the

duration of operation (i.e., time from skin incision to skin closure)

and the ASA class has not been studied. In an unpublished report from

the NNIS system, there was some evidence that

[[Page 33176]]

over-reporting of high ASA class existed in some hospitals (Emori TG,

personal communication). Further validation of how well the risk index

variables are recorded is needed.

Additionally, NNIS data show that the NNIS risk index does not

adequately discriminate the risk of SSI for all types of

operations.\336\ \337\ It seems likely that a combination of risk

factors specific to patients undergoing an operation will be more

predictive. A few studies have been performed to develop procedure-

specific risk indices 338-342 and the NNIS system continues

research in this area.

SSI Surveillance Methods

SSI surveillance methods used in both the SENIC Project and the

NNIS system were designed for monitoring inpatients at acute-care

hospitals. Over the past decade, the shift from inpatient to outpatient

surgical care (also called ambulatory or day surgery) has been

dramatic. It has been estimated that 75% of all operations in the

United States will be performed in outpatient settings by the year

2000.\343\ While it may be appropriate to use common definitions of SSI

for inpatients and outpatients, 344 the types of operations

monitored, the risk factors assessed, and the case-finding methods used

may differ. New predictor variables may emerge from analyses of SSIs

among outpatient surgery patients, which may lead to different ways of

estimating SSI risk in this population.

Deciding upon which operations to monitor should be done jointly by

surgeons and infection control personnel. Rarely do hospitals have the

resources to monitor all surgical patients all the time, nor is that

level of surveillance intensity probably necessary for certain low-risk

procedures. Instead, hospitals should target surveillance efforts

towards high-risk procedures.345

Inpatient SSI Surveillance

Two methods, alone or together, have been used to identify

inpatients with SSIs: (1) direct observation of the surgical site by

the surgeon, trained nurse surveyor, or infection control personnel

8 90 323 326 346-350 and (2) indirect detection by infection

control personnel through review of laboratory reports, patient

records, and discussions with primary care

providers.7 77 323 326 329 346 348 351-357 The surgical

literature suggests that direct observation of surgical sites is the

most accurate method to detect SSIs, although sensitivity data are

lacking.8 323 326 347 348 Much of the SSI data reported in

the infection control literature have relied on indirect case-finding

methods,328 331 352 355 356 358-360 but some studies of

direct methods also have been conducted.90, 346 Some studies

use both methods of detection.77 325 346 354 357 361 A study

that focused solely on the sensitivity and specificity of SSIs detected

by indirect methods found a sensitivity of 83.8% (95% CI: 75.7%-91.9%)

and a specificity of 99.8% (95% CI: 99%-100%).346 Another

study showed that chart review triggered by a computer-generated report

of antibiotic orders for post-cesarean section patients had a

sensitivity of 89% for detecting endometritis.362 It is

recommended that hospitals use direct, indirect, or a combination of

both methods for detecting SSI in postoperative inpatients.

Indirect SSI detection can readily be performed by infection

control personnel during surveillance rounds. The work includes

gathering demographic, infection, surgical, and laboratory data on

patients who have undergone operations of interest to the

investigator.224 These data can be obtained from patients'

medical records, including microbiology and histopathology laboratory

data and radiology reports, and records from the operating room.

Pharmacy records may be useful if data on prophylactic antimicrobial

use are to be collected. Additionally, hospital admissions, emergency

room, and clinic visit records are sources of data for those

postdischarge surgical patients who re-admitted or seek follow-up care.

The optimum frequency of case-finding by either method is unknown

and varies from daily to 3 times per week, continuing until

the patient is discharged from the hospital. Because duration of

hospitalization is now so short, postdischarge SSI surveillance has

become increasingly important to obtain accurate SSI rates (see

``Postdischarge SSI Surveillance'' section).

To calculate meaningful SSI rates, data must be collected on all

patients undergoing the operations of interest (i.e., the population at

risk). In the NNIS system, because one of its purposes is to develop

strategies for risk stratification, the following data are collected on

all surgical patients surveyed: operation date; NNIS operative

procedure category; 363 surgeon identifier; patient

identifier, age, and sex; duration of operation; wound class; general

anesthesia; ASA class; emergency; trauma; multiple procedures;

endoscopic approach; and discharge date.224 With the

exception of discharge date, these data can be obtained manually from

operating room logs or be electronically downloaded into surveillance

software, thereby substantially reducing manual transcription and data

entry errors.224 Depending on the needs for risk-stratified

SSI rates by infection control, surgery, and quality assurance, not all

data elements may be pertinent for every type of operation. At minimum,

however, variables found to be predictive of increased SSI risk should

be collected (see ``SSI Risk Stratification'' section).

Postdischarge SSI Surveillance

Between 12% and 84% of SSIs are detected after patients are

discharged from the hospital. 91 259 326 358 364-383 At

least two investigators have shown that most SSIs become evident within

21 days after operation.360 376 Since the length of

postoperative hospitalization continues to decrease, true estimates of

SSI risk will only be possible by performing a combination of inpatient

and postdischarge surveillance.

Postdischarge surveillance methods have been used with varying

degrees of success for different procedures and among hospitals and

include (1) direct examination of patients' wounds during follow-up

visits to either surgery clinics or physicians'

offices,323 326 329 360 365 369 370 376 381 384 385

(2) review of medical records of surgery clinic

patients,329, 360, 368 (3) questionnaire administration to

patients by mail or telephone,364 366 367 370

371 374 375 377 378 384 386 388 or

(4) questionnaire administration to surgeons by mail or

telephone.91 358 360

366 368 372 373 375 377 379 380 384 One study found that

patients have difficulty assessing their own wounds for infection (52%

specificity, 26% positive predictive value),389 suggesting

that data obtained by patient questionnaire may inaccurately represent

actual SSI rates.

Recently, Sands et al. performed a computerized search of three

data bases--ambulatory encounter records for diagnostic, testing, and

treatment codes; pharmacy records for specific antimicrobial

prescriptions; and administrative records for rehospitalizations and

emergency room visits. The purpose of the search was to determine which

best identified SSIs.375 These researchers found that

pharmacy records indicating a patient had received antimicrobial agents

commonly used to treat soft tissue infections had the highest

sensitivity (50%) and positive predictive value (19%).

As integrated health information systems expand, tracking surgical

patients through the course of their care may become more feasible,

practical, and effective. Until then, there is no

[[Page 33177]]

consensus on which postdischarge surveillance methods are the most

sensitive, specific, and practical. Infection control and surgery

personnel must choose from a variety of methods to find those that work

for their unique mix of operations, personnel resources, and data

needs.

Outpatient SSI Surveillance

Both direct and indirect methods have been used to detect SSIs that

complicate outpatient operations. One study used home visits by

district health nurses combined with a questionnaire completed by the

surgeon at the patient's 2-week postoperative clinic visit to identify

SSIs in an 8-year study of operations for hernia and varicose

veins.390 While ascertainment was very high, essentially

100%, this method is impractical for widespread implementation. High

response rates have been obtained from questionnaires mailed to

surgeons (72%->90%).372 373 375 384 391 393 Response rates

from telephone questionnaires administered to patients were more

variable (38%,386 81%,388 and 85%

384), and response rates from questionnaires mailed to

patients were quite low (15% 384 and 33% 375). At

this time, no single detection method can be recommended. Available

resources and data needs determine which method(s) should be used and

which operations should be monitored. It is recommended that the CDC

NNIS definitions of SSI (Tables 1 and 2) be used without modification

in the outpatient setting.

Guideline Evaluation Process

Users of the HICPAC guidelines determine their value. To help

assess that value, HICPAC is developing an evaluation tool to learn how

guidelines meet user expectations, and how and when these guidelines

are disseminated and implemented.

Part II--Recommendations for the Prevention of Surgical Site

Infections (SSIs)

Introduction

As in previous CDC guidelines, each recommendation is categorized

on the basis of existing scientific data, theoretical rationale,

applicability, and possible economic impact. However, the previous CDC

system for categorizing recommendations has been modified to include a

designation of those recommendations that are required by federal

regulations. The document does not recommend specific antiseptic agents

for patient preoperative skin preparations or for health-care worker

hand/forearm antisepsis. Hospitals should choose from the appropriate

products categorized by the Food and Drug Administration (FDA).\4\

Category IA. Strongly recommended for all hospitals and strongly

supported by well-designed experimental or epidemiological studies.

Category IB. Strongly recommended for all hospitals and viewed as

effective by experts in the field and a consensus of Hospital Infection

Control Practices Advisory Committee (HICPAC), based on strong

rationale and suggestive evidence, even though definitive scientific

studies may not have been done.

Category II. Suggested for implementation in many hospitals.

Recommendations may be supported by suggestive clinical or

epidemiological studies, a strong theoretical rationale, or definitive

studies applicable to some, but not all hospitals.

No recommendation; unresolved issue. Practices for which

insufficient evidence or no consensus regarding efficacy exists.

Recommendations

1. Preoperative preparation of the patient

a. Adequately control serum blood glucose level in all diabetic

patients before elective operation and maintain blood glucose level

77-79 100-102 Category IB

b. Always encourage tobacco cessation. At minimum, instruct

patients to abstain for at least 30 days before elective operation from

smoking cigarettes, cigars, pipes or any other form of tobacco

consumption (e.g., chewing/dipping).78 81 83-85 Category IB

c. No recommendation to taper or discontinue steroid use (when

medically permissible) before elective

operation.77 80 86 103-105 Unresolved issue

d. Consider delaying an elective operation in a severely

malnourished patient. A good predictor of nutritional status is serum

albumin.78 96-98 Category II

e. Attempt weight reduction in obese patients before elective

operation.78 79 89 90 Category II

f. Identify and treat all infections remote to the surgical site

before elective operation.31 74-76 Do not perform elective

operations in patients with remote site infections. Category IA

g. Keep preoperative hospital stay as short as

possible.18 75 93 104 106 Category IA

h. Prescribe preoperative showers/baths with an antiseptic agent

the night before and the morning of the operation.108 109

Category IB

i. Do not remove hair preoperatively unless the hair at or around

the incision site will interfere with the

operation.8 93 113 114 120 121 Category IA

j. If hair is removed, it should be removed immediately before the

operation using electric clippers rather than razors or

depilatories.\115\ \117\ \119\ Category IA

k. Thoroughly wash and clean at and around the incision site to

remove gross contamination before performing antiseptic skin

preparation.\154\ Category IB

l. Use an acceptable antiseptic agent for skin preparation, such as

alcohol (usually 70%-92%), chlorhexidine (4%, 2%, or 0.5% in alcohol

base), or iodine/iodophors (usually 10% aqueous with 1% iodine or

formulation with 7.5%) (Table 5).\123\ \124\ Category IB

m. Apply preoperative antiseptic skin preparation in concentric

circles moving out toward the periphery. The prepped area must be large

enough to extend the incision or create new incisions or drain sites,

if necessary.\31\ \124\ \154\ Category IB

2. Preoperative Hand/Forearm Antisepsis

All members of the surgical team:

a. Keep nails short and do not wear artificial nails.\31\ \72\

\124\ \154\ \155\ Category IB

b. No recommendation on wearing nail polish. Unresolved Issue

c. Do not wear hand/arm jewelry. Category II

d. Perform a preoperative surgical scrub that includes hands and

forearms up to the elbows before the sterile field, sterile

instruments, or the patient's prepped skin is touched. Category IB

e. Clean underneath each fingernail prior to performing the

surgical scrub.\31\ \140\ \154\ Category IB

f. Perform the surgical scrub for a duration of 3-5 minutes \124\

\152\ \153\ with an appropriate antiseptic (see Table 5).\123\

\124\-\140\ Category IB

g. After performing the surgical scrub, keep hands up and away from

the body (elbows in flexed position) so that water runs from the tips

of the fingers toward the elbows. Dry hands with a sterile towel and

don a sterile gown and gloves.\154\ Category IB

3. Antimicrobial Prophylaxis

a. Select a prophylactic antimicrobial agent based on its efficacy

against the most common pathogens causing SSI for a specific operation

(Table 6). Category IA

b. Administer the antimicrobial prophylactic agent by the

intravenous route except for colorectal operations.\202\ In colorectal

operations the antimicrobial agent is administered orally, or a

combination of oral and intravenous route is used. Category IA

[[Page 33178]]

c. Administer the antimicrobial agent before the operation starts

to assure adequate microbiocidal tissue levels before the skin incision

is made, ideally antimicrobial prophylaxis should be administered

within 30 minutes before, but not longer than 2 hours before, the

initial incision.\69\ \71\ \202\ \203\ \214\ Category IA

d. For cesarean section, administer prophylaxis immediately after

the umbilical cord is clamped.\69\ \70\ Category IA

e. Administer prophylactic antimicrobial agent as close as possible

to the time of induction of anesthesia. Category II

f. Do not extend prophylaxis

postoperatively.47 71 199 -201 Category IB

g. Consider additional intraoperative doses under the following

circumstances: (1) operations whose duration exceeds the estimated

serum half-life of the agent, (2) operations with major intraoperative

blood loss, and (3) operations on morbidly obese

patients.47 69 71 201 203 216 -218 Category IB

h. Do not routinely use vancomycin for prophylaxis.\204\ \205\

Category IB

4. Intraoperative Issues

4-1. Operating Room Environment

A. Ventilation

a. Maintain positive-pressure ventilation in the operating room

with respect to the corridors and adjacent areas.\226\ Category IB

b. Maintain a minimum of 15 air changes per hour, of which at least

3 should be fresh air.\226\ Category IB

c. Filter all air, recirculated and fresh, through the appropriate

filters per the American Institute of Architects recommendations.\226\

Category IB

d. Introduce all air at the ceiling and exhaust near the

floor.\227\ \228\ Category IB

e. No recommendation for the use of laminar flow ventilation or

ultraviolet lights in the operating room to prevent

SSI.87 225 232 -237 Unresolved issue

f. Keep operating room doors closed except as needed for passage of

equipment, personnel, and the patient.\219\ Category IB

g. Limit the number of personnel entering the operating room to

necessary personnel.\219\ Category IB

B. Cleaning and Disinfection of Environmental Surfaces

a. No recommendation on disinfecting operating rooms between

operations in the absence of visible soiling of surfaces or equipment.

Unresolved issue

b. When visible soiling or contamination, with blood or other body

fluids, of surfaces or equipment occurs during an operation, use an

EPA-approved hospital disinfectant to clean the affected areas before

the next operation.31 154 227 -229 238 -240 Category IB*

c. Wet vacuum the operating room floor after the last operation of

the day or night with an EPA-approved hospital disinfectant.\154\

Category IB

d. Do not perform special cleaning or disinfection of operating

rooms after contaminated or dirty operations.\227\ \228\ Category IA

e. Do not use tacky mats at the entrance to the operating room

suite for infection control; this is not proven to decrease SSI

risk.1 18 219 228 Category 1A

C. Microbiologic Sampling

Do not perform routine environmental sampling of the operating

room. Perform microbiologic sampling of operating room environmental

surfaces or air only as part of an epidemiologic investigation.

Category IB

D. Sterilization of Surgical Instruments

a. Sterilize all surgical instruments according to published

guidelines.\154\ \226\ \239\ \245\ Category IB

b. Perform flash sterilization only in emergency

situations.239 244 -246 Category IB

c. Do not use flash sterilization for routine reprocessing of

surgical instruments. Category IB

4-2. Surgical Attire and Drapes

a. No recommendations on how or where to launder scrub suits, on

restricting use of scrub suits to the operating suite or for covering

scrub suits when out of the operating suite.\154\ \277\ Unresolved

issue

b. Change scrub suits when visibly soiled, contaminated and/or

penetrated by blood or other potentially infectious materials.\154\

\240\ Category IB *

c. Wear a surgical mask that fully covers the mouth and nose when

entering the operating room if sterile instruments are exposed, or if

an operation is about to begin or already under way. Wear the mask

throughout the entire operation.\154\ \240\ Category IB *

d. Wear a cap or hood to fully cover hair on the head and face when

entering the operating room suite.\154\ \240\ \248\ \261\ Category IB *

e. Do not wear shoe covers for the prevention of SSI.\262\ \263\

Category IA

f. Wear shoe covers when gross contamination can reasonable be

anticipated.\240\ Category II *

g. The surgical team must wear sterile gloves, which are put on

after donning a sterile gown.\240\ \264\-\266\ Category IB *

h. Use materials for surgical gowns and drapes that are effective

barriers when wet.\1\ \154\ \169\ \277\ Category IB

4-3. Practice of Anesthesiology

Anesthesia team members must adhere to recommended infection

control practices during operations.\154\ \279\-\281\

Category IA

4-4. Surgical Technique

a. Handle tissue gently, maintain effective hemostasis, minimize

devitalized tissue and foreign bodies (i.e., sutures, charred tissues,

necrotic debris), and eradicate dead space at the surgical site.\18\

\19\ \31\ \32\ Category IB

b. Use delayed primary closure or leave incision open to close by

secondary intention, if the surgical site is heavily contaminated

(e.g., Class III and Class IV). Category IB

c. If drainage is deemed necessary, use a closed suction drain.

Place the drain through a separate incision, rather than the main

surgical incision. Remove the drain as soon as possible.\312\ \313\

Category IB

5. Postoperative Surgical Incision Care

a. Protect an incision closed primarily with a sterile dressing for

24-48 hours postoperatively. Also ensure that the dressing remains dry

and that it is not removed bathing.\315\ \316\ Category IA

b. No recommendation on whether or not to cover an incision closed

primarily beyond 48 hours, nor on the appropriate time to shower/bathe

with an uncovered incision. Unresolved Issue

c. Wash hands with an antiseptic agent before and after dressing

changes, or any contact with the surgical site. Category IA

d. For incisions left open postoperatively, no recommendation for

dressing changes using a sterile technique vs. clean technique.

Unresolved Issue

e. Educate the patient and family using a coordinated team approach

on how to perform proper incision care, identify signs and symptoms of

infection, and where to report any signs and symptoms of infection.

Category II

6. Surveillance

a. Use CDC definitions of SSI \16\ without modification for

identifying SSI among surgical inpatients and outpatients. Category IB

---------------------------------------------------------------------------

*Federal regulation--Occupational Safety and Health

Administration

---------------------------------------------------------------------------

b. For inpatient case-finding, use direct prospective observation,

indirect prospective detection, or a combination of both direct and

indirect methods for the duration of the patient's hospitalization, and

include a method of postdischarge surveillance that accommodates

available resources and data needs. Category IB

[[Page 33179]]

c. For outpatient case-finding, use a method that accommodates

available resources and data needs. Category IB

d. For each patient undergoing an operation chosen for

surveillance, record those variables shown to be associated with

increased SSI risk (e.g., surgical wound class, ASA class, and duration

of operation). Category IB

e. Upon completion of the operation, a surgical team member assigns

the surgical wound classification. Category IB

f. Periodically calculate operation-specific SSI rates stratified

by variables shown to be predictive of SSI risk. Category IB

g. Report appropriately stratified, operation-specific SSI rates to

surgical team members. The optimum frequency and format for such rate

computations will be determined by stratified case-load sizes and the

objectives of local, continuous, quality improvement initiatives.

Category IB

h. No recommendation to make available to the infection control

committee coded surgeon-specific data. Unresolved issue

Bibliography

1. Garner JS. Guideline for prevention of surgical wound

infections, 1985. Infect Control 1986; 7:193-200.

2. Simmons BP. Guideline for prevention of surgical wound

infections. Infect Control 1982; 3:188-196.

3. Garner JS. The CDC Hospital Infection Control Practice

Advisory Committee. Am J Infect Control 1993; 21:160-162.

4. Food and Drug Administration. Alcohol drug products for

topical antimicrobial over-the-counter human use; establishment of a

monograph; and reopening of administrative record. (No. 99) Vol. 47

ed. 1982; Federal Register.

5. U.S. Department of Health and Human Services, Centers for

Disease Control and Prevention, National Center for Health

Statistics. Vital and Health Statistics, Detailed Diagnoses and

Procedures, National Hospital Discharge Survey, 1994. Series 13.

Hyattsville, Maryland: DHHS Pub No. 127, 1997.

6. Emori TG, Gaynes RP. An overview of nosocomial infections,

including the role of the microbiology laboratory. Clin Microbiol

Rev 1993; 6:428-442.

7. Cruse P. Wound infection surveillance. Rev Infect Dis 1981;

4:734-737.

8. Cruse PJE, Foord R. The epidemiology of wound infection: a

10-year prospective study of 62,939 wounds. Surg Clin North Am 1980;

60:27-40.

9. Martone WJ, Jarvis WR, Culver DH, Haley RW. Incidence and

nature of endemic and epidemic nosocomial infections. In: Bennett

JV, Brachman PS, eds. Hospital infections. Third ed. Boston: Little,

Brown and Co., 1992:577-596.

10. Boyce JM, Potter-Bynoe G, Dziobek L. Hospital reimbursement

patterns among patients with surgical wound infections following

open heart surgery. Infect Control Hosp Epidemiol 1990; 11:89-93.

11. Poulsen KB, Bremmelgaard A, Sorensen AI, Raahave D, Petersen

JV. Estimated costs of postoperative wound infections. A case-

control study of marginal hospital and social security costs.

Epidemiol Infect 1994; 113:283-295.

12. Vegas AA, Jodra VM, Garcia ML. Nosocomial infection in

surgery wards: a controlled study of increased duration of hospital

stays and direct cost of hospitalization. Eur J Epidemiol 1993;

9:504-510.

13. Albers BA, Patka P, Haarman HJ, Kostense PJ. Cost

effectiveness of preventive antibiotic administration for lowering

risk infection by 0.25%. [German]. Unfallchirurg 1994; 97:625-628.

14. Ehrenkranz NJ, Richter EI, Phillips PM, Shultz JM. An

apparent excess of operative site infections: analyses to evaluate

false-positive diagnoses. Infect Control Hosp Epidemiol 1995;

16:712-716.

15. Taylor G, McKenzie M, Kirkland T, Wiens R. Effect of

surgeon's diagnosis on surgical wound infection rates. Am J Infect

Control 1990; 18:295-299.

16. Horan TC, Gaynes RP, Martone WJ, Jarvis WR, Emori TG. CDC

definitions of nosocomial surgical site infections, 1992: a

modification of CDC definitions of surgical wound infections. Infect

Control Hosp Epidemiol 1992; 13:606-608.

17. SHEA, APIC, CDC, SIS. Consensus paper on the surveillance of

surgical wound infections. Infect Control Hosp Epidemiol 1992;

13:599-605.

18. Mayhall CG. Surgical infections including burns. In: Wenzel

RP, ed. Prevention and control of nosocomial infections. 2nd ed.

Baltimore: Williams and Wilkins, 1993:614-664.

19. Wong ES. Surgical site infections. In: Mayhall CG, ed.

Hospital epidemiology and infection control. 1st ed. Baltimore:

Williams and Wilkins, 1996:154-174.

20. Schaberg DR., Resistant gram-positive organisms. Ann Emerg

Med 1994; 24:462-464.

21. Schaberg DR, Culver DH, Gaynes RP. Major trends in the

microbial etiology of nosocomial infection. Am J Med 1991; 91:72S-

75S.

22. Esuvaranathan K, Kuan YF, Kumarasinghe G, Bassett DCJ, Rauff

A. A study of 245 infected surgical wounds in Singapore. J Hosp

Infect 1992; 21:231-240.

23. Jarvis WR. Epidemiology of nosocomial fungal infections,

with emphasis on Candida species. Clin Infect Dis 1995; 20:1526-

1530.

24. Centers for Disease Control and Prevention. Nosocomial

outbreak of Rhizopus infections associated with elastoplast wound

dressings--Minnesota. MMWR 1978; 27:33-34.

25. Pearson RD, Valenti WM, Steigbigel RT. Clostridium

perfringens wound infections associated with elastic bandages. JAMA

1980; 244:1128-1130.

26. Richet HM, Craven PC, Brown JM, Lasker BA, Cox CD, McNeil

MM, et al. A cluster of Rhodococcus (Gordona) bronchialis sternal-

wound infections after coronary-artery bypass surgery. N Engl J Med

1991; 324:104-109.

27. Lowery PW, Blakenship RJ, Gridley W, Troup NJ, Tompkins LS.

A cluster of Legionella sternal-wound infections due to

postoperative topical exposure to contaminated tap water. N Engl J

Med 1989; 324:109-113.

28. Bassett DCJ, Stokes KJ, Thomas WRG. Wound infection with

Pseudomonas multivorans: water-borne contaminant of disinfectant

solutions. Lancet 1970; 1:1188-1191.

29. Cruse PJ. Surgical wound infection. In: Wonsiewicz MJ, ed.

Infectious diseases. Philadelphia: W.B.Saunders Company, 1992:758-

764.

30. Krizek TJ, Robson MC. Evolution of quantitative bacteriology

in wound management. Am J Surg 1975; 130:579-584.

31. Altemeier WA, Burke JF, Pruitt BA, Sandusky WR. Manual on

control of infection in surgical patients. 2nd ed. Philadelphia:

J.B.Lippincott Company, 1984.

32. Dellinger EP. Surgical infections and choice of antibiotics.

In: Sabiston DC, Lyerly HK, eds. Sabiston textbook of surgery. The

Biological basis of modern surgical practice. 15th ed. Philadelphia:

W.B.Saunders Co, 1997:264-280.

33. Elek SD, Conen PE. The virulence of Staphylococcus pyogenes

for man: a study of problems with wound infection. British Journal

of Experimental Pathology 1957; 38:573-586.

34. Waldvogel FA, Vaudaux PE, Pittet D, Lew PD. Perioperative

antibiotic prophylaxis of wound and foreign body infections:

microbial factors affecting efficacy. Rev Infect Dis 1991; 13 (Suppl

10):S782-S789.

35. Noble WC. The production of subcutaneous staphylococcal skin

lesions in mice. British Journal of Experimental Pathology 1965;

46:254-262.

36. James RC, MacLeod CJ. Induction of staphylococcal infections

in mice with small inocula introduced on sutures. British Journal of

Experimental Pathology 1961; 42:266-277.

37. Brubaker RR. Mechanisms of bacterial virulence. Annu Rev

Microbiol 1985; 39:21-50.

38. Falkow S, Small P, Isberg R, Hayes SF, Corwin D. A molecular

strategy for the study of bacterial invasion. Rev Infect Dis 1987;

9(Suppl 5):S450-S455.

39. Henderson B, Poole S, Wilson M. Microbial/host interactions

in health and disease: who controls the cytokine network?

Immunopharmacology 1996; 35:1-21.

40. Printzen G. Relevance, pathogenicity and virulence of

microorganisms in implant related infections. Injury 1996; 27:SC9-

SC15.

41. Morison DC, Ryan JL. Endotoxins and disease mechanisms. Annu

Rev Med 1987; 38:417-432.

42. Viriyakosol S, Kirkland T. Knowledge of cellular receptors

for bacterial endotoxin--1995. Clin Infect Dis 1995; 21(Suppl

2):S190-S195.

43. Kasper DL. Bacterial capsule--old dogma and new tricks. J

Infect Dis 1986; 153:407-415.

44. Joiner KA. Other Virulence Factors. In: Wonsiewicz MJ, ed.

Infectious Diseases. Philadelphia: W.B.Saunders Company, 1992:23-30.

[[Page 33180]]

45. Smith H. Microbial surfaces in relation to pathogenicity.

Bacteriological Reviews 1977; 41:475-500.

46. Goldmann DA, Pier GB. Pathogenesis of infections related to

intravascular catheterization. Clin Microbiol Rev 1993; 6:176-192.

47. Ehrenkranz NJ. Antimicrobial prophylaxis in surgery:

mechanisms, misconceptions, and mischief. Infect Control Hosp

Epidemiol 1993; 14:99-106.

48. Dougherty SH, Simmons RL. Endogenous factors contributing to

prosthetic device infections. Infect Dis Clin North Am 1989; 3:199-

209.

49. Santini C, Baiocchi P, Venditti M, Brandimarte C, Tarasi A,

Rizzo L, et al. Aorto-femoral graft infections: a clinical and

microbiological analysis. J Infect 1993; 27:17-26.

50. Patrick CC, Plaunt MR, Hetherington SV, May SM. Role of the

Staphylococcus epidermidis slime layer in experimental tunnel tract

infections. Infect Immun 1992; 60:1363-1367.

51. Bergamini TM, Peyton JC, Cheadle WG. Prophylactic

antibiotics prevent bacterial biofilm graft infection. J Surg Res

1992; 52:101-105.

52. Bergamini TM, Corpus RA, Jr., Brittian KR, Peyton JC,

Cheadle WG. The natural history of bacterial biofilm graft

infection. J Surg Res 1994; 56:393-396.

53. Giamarellou H, Antoniadou A. Epidemiology, diagnosis, and

therapy of fungal infections in surgery. Infect Control Hosp

Epidemiol 1996; 17:558-564.

54. Calia FM, Wolinsky E, Mortimer EA, Jr., Abrams JS,

Rammellcamp CH, Jr. Importance of the carrier state as a source of

Staphylococcus aureus in wound sepsis. J Hyg 1969; 67:49-57.

55. Weinstein WM, Onderdonk AB, Bartlett JG, Gorbach SL.

Experimental intra-abdominal abscesses in rats: development of an

experimental model. Infect Immun 1974; 10:1250-1255.

56. Slaughter L, Morris JE, Starr A. Prosthetic valvular

endocarditis: a 12-year review. Circulation 1973; XLVII:1319-1326.

57. Carlsson AS, Lidgren L, Lindberg L. Prophylactic antibiotics

against early and late deep infections after total hip replacements.

Acta Orthop Scand 1977; 48:405-410.

58. Hunter JG, Padilla M, Cooper-Vastola S. Late Clostridium

perfringens breast implant infection after dental treatment. Ann

Plast Surg 1996; 36:309-312.

59. Stuesse DC, Robinson JH, Durzinsky DS. A late sternal wound

infection caused by hematogenous spread of bacteria. Chest 1995;

108:1742-1743.

60. Howe CW. Experimental wound sepsis form transit E. coli

bacteremia. Surgery 1966; 3:570-574.

61. Cioffi GA, Terezhalmy GT, Taybos GM. Total joint

replacement: a consideration for antimicrobial prophylaxis. Oral

Surg Oral Med Oral Pathol 1988; 66:124-129.

62. Heggeness MH, Esses SI, Errico T, Yuan HA. Late infection of

spinal instrumentation by hematogenous seeding. Spine 1993; 18:492-

496.

63. Mont MA, Waldman B, Banerjee C, Pacheco IH, Hungerford DS.

Multiple irrigation, debridement, and retention of components in

infected total knee arthroplasty. J Arthroplasty 1997; 12:426-433.

64. Ozuna RM, Delamarter RB. Pyogenic vertebral osteomyelitis

and postsurgical disc space infections. Orthop Clin North Am 1996;

27:87-94.

65. Schmalzried TP, Amstutz HC, Au MK, Dorey FJ. Etiology of

deep sepsis in total hip arthroplasty: the significance of

hematogenous and recurrent infections. Clin Orthop 1992; 280:200-

207.

66. Goeau-Brissonniere O, Leport C, Guidoin R, Lebrault C,

Pechere JC, Bacourt F. Experimental colonization of an expanded

polytetrafluoroethylene vascular graft with Staphylococcus aureus: a

quantitative and morphologic study. J Vasc Surg 1987; 5:743-748.

67. Cruse PJE. Wound infections: epidemiology and clinical

characteristics. In: Howard RL, ed. Part VI Wound infections. San

Mater: Appleton & Lange, 1988:319-329.

68. Kaiser AB. Postoperative infections and antimicrobial

prophylaxis. In: Mandell GL, Douglas RG, Bennett JE, eds. Principles

and practice of infectious diseases. 3rd ed. New York: Churchill

Livingstone, 1990:2245-2257.

69. Anonymous. Antimicrobial prophylaxis in surgery. Med Lett

Drugs Ther 1997; 39:97-102.

70. Page CP, Bohnen JMA, Fletcher JR, McManus AT, Solomkin JS,

Wittmann DH. Antimicrobial prophylaxis for surgical wounds:

guidelines for clinical care. Arch Surg 1993; 128:79-88.

71. Nichols RL. Antibiotic prophylaxis in surgery. J Chemother

1989; 1:170-178.

72. Passaro DJ, Waring L, Armstrong R, Bolding F, Bouvier B,

Rosenberg J, et al. Postoperative Serratia marcescens wound

infections traced to an out-of-hospital source. J Infect Dis 1997;

175:992-995.

73. Lee JT. Surgical wound infections: surveillance for quality

improvement. In: Fry DE, ed. Surgical infections. 1st ed. Boston/New

York/Toronto/London: Little, Brown and Company, 1995:145-159.

74. Velasco E, Thuler LCS, Martins CAS, deCastroDias LM,

Conalves VMSC. Risk factors for infectious complications after

abdominal surgery for malignant disease. Am J Infect Control 1996;

24:1-6.

75. Bruun JN. Post-operative wound infection. Predisposing

factors and the effect of a reduction in the dissemination of

staphylococci. Acta Med Scand 1970; 514(Suppl):1-89.

76. Simchen E, Roxin R, Wax Y. The Israeli study of surgical

infection of drains and the risk of wound infection in operations

for hernia. Surgery, Gynecology & Obstetrics 1990; 170:331-337.

77. Gil-Egea MJ, Pi-Sunyer MT, Verdaguer A, Sanz F, Sitges-Serra

A, Eleizegui LT. Surgical wound infections: prospective study of

4,486 clean wounds. Infect Control 1987; 8:277-280.

78. Nagachinta T, Stephens M, Reitz B, Polk BF. Risk factors for

surgical-wound infection following cardiac surgery. J Infect Dis

1987; 156:967-973.

79. Lilienfeld DE, Vlahov D, Tenney JH, Mclaughlin JS. Obesity

and diabetes as risk factors for postoperative wound infections

after cardiac surgery. Am J Infect Control 1988; 16:3-6.

80. Slaughter MS, Olson MM, Lee JT, Jr., Ward HB. A fifteen-year

would surveillance study after coronary artery bypass. Ann Thorac

Surg 1993; 56:1063-1068.

81. Bryan AJ, Lamarra M, Angelini GD, West RR, Breckenridge IM.

Median sternotomy wound dehiscence: a retrospective case control

study of risk factors and outcome. J R Coll Surg Edinb 1992; 37:305-

308.

82. Jones JK, Triplett RG. The relationship of cigarette smoking

to impaired intraoral wound healing: a review of evidence and

implications for patients care. J Oral Maxillofac Surg 1992; 50:237-

239.

83. Vinton AL, Traverso LW, Jolly PC. Wound complications after

modified radical mastectomy compared with tylectomy with axillary

lymph node dissection. Am J Surg 1991; 161:584-588.

84. Holley DT, Toursarkissian B, Vansconez HC, Wells MD, Kenady

DE, Sloan DA. The ramifications of immediate reconstruction in the

management of breast cancer. Am Surg 1995; 61:60-65.

85. Beitsch P, Balch C. Operative morbidity and risk factor

assessment in melanoma patients undergoing inguinal lymph node

dissection. Am J Surg 1992; 164:462-466.

86. Post S, Betzler M, vonDitfurth B, Schurmann G, Kuppers P,

Herfarth C. Risks of intestinal anastomoses in Crohn's disease. Ann

Surg 1991; 213:37-42.

87. National Academy of Sciences, National Research Council,

Division of Medical Sciences, Ad Hoc Committee on Trauma.

Postoperative wound infections: the influence of ultraviolet

irradiation of the operating room and of various other factors. Ann

Surg 1964; 160:1-192.

88. Nystrom P, Jonstam A, Hojer H, Ling L. Incisional infection

after colorectal surgery in obese patients. Acta Orthop Scand 1987;

153:225-227.

89. He GW, Ryan WH, Acuff TE, Bowman RT, Douthit MB, Yang CQ, et

al. Risk factors for operative mortality and sternal wound infection

in bilateral internal mammary artery grafting. J Thorac Cardiovasc

Surg 1994; 107:196-202.

90. Barber GR, Miransky J, Brown AE, Coit DG, Lewis FM, Thaler

HT, et al. Direct observations of surgical wound infections at a

comprehensive cancer center. Arch Surg 1995; 130:1042-1047.

91. Cruse PJE, Foord R. A five-year prospective study of 23,649

surgical wounds. Arch Surg 1973; 107:206-210.

92. Claesson BE, Holmlund DE. Predictors of intraoperative

bacterial contamination and postoperative infection in elective

colorectal surgery. J Hosp Infect 1988; 11:127-135.

93. Mishriki SF, Law DJW, Jeffery PJ. Factors affecting the

incidence of postoperative wound infection. J Hosp Infect 1990;

16:223-230.

94. Doig CM. Wound infection in a children's hospital. Br J Surg

1976; 63:647-650.

95. Sharma LK, Sharma PK. Postoperative wound infection in a

pediatric surgical service. J Pediatr Surg 1986; 21:889-891.

96. Casey J, Flinn WR, Yao JST, Fahey V, Pawlowski J, Bergan JJ.

Correlation of

[[Page 33181]]

immune and nutritional status with wound complications in patients

undergoing vascular operations. Surgery 1983; 93:822-827.

97. Greene KA, Wilde AH, Stulberg BN. Preoperative nutritional

status of total joint patients: relationship to postoperative wound

complications. J Arthoplasty 1991; 6:321-325.

98. Weber TR. A prospective analysis of factors influencing

outcome after fundoplication. J Pediatr Surg 1995; 30:1061-1064.

99. Lidgren L. Postoperative orthopaedic infections in patients

with diabetes mellitus. Acta Orthop Scand 1973; 44:149-151.

100. Gordon SM, Serkey JM, Barr C, Cosgrove D, Potts W. The

relationship between glycosylated hemoglobin (HgA1c) levels and

postoperative infections in patients undergoing primary coronary

artery bypass surgery (CABG). Infect Control Hosp Epidemiol 1997;

18:29.

101. Zerr KJ, Furnary AP, Grunkemeier GL, Bookin S, Kanhere V,

Starr A. Glucose control lowers the risk of wound infection in

diabetics after open heart operations. Ann Thorac Surg 1997; 63:356-

361.

102. Terranova A. The effects of diabetes mellitus on wound

healing. Plastic Surgical Nursing 1991; 11:20-25.

103. Ziv Y, Church J, Fazio V, King T, Lavery I. Effect of

systemic steroids on ileal pouch-anal anastomosis in patients with

ulcerative colitis. Dis Colon Rectum 1996; 39:504-508.

104. Cruse PJE, Foord R. A five-year prospective study of 23,649

surgical wounds. Arch Surg 1973; 107:206-210.

105. Pons VG, Denlinger SL, Guglielmo BJ, Octavio J, Flaherty J,

Derish PA, et al. Ceftizoxime versus vancomycin and gentamicin in

neurosurgical prophylaxis: a randomized, prospective, blinded

clinical study. Neurosurgery 1993; 33:416-422.

106. Lee JT. Operative complications and quality improvement. Am

J Surg 1996; 171:545-547.

107. Altemeier WA, Culbertson WR. Surgical infection. In: Moyer

C, et al. eds. Surgery, principles and practice, 3rd ed. 3rd ed.

Philadelphia: JB Lippincott, 1965.

108. Garibaldi RA. Prevention of intraoperative wound

contamination with chlorhexidine shower and scrub. J Hosp Infect

1988; 11 (Suppl) B:5-9.

109. Paulson DS. Efficacy evaluation of a 4% chlorhexidine

gluconate as a full-body shower wash. Am J Infect Control 1993;

21:205-209.

110. Rotter ML, Larsen SO, Cooke EM, Dankert J, Daschner F,

Greco D, et al. A comparison of the effects of preoperative whole-

body bathing with detergent alone and with detergent containing

chlorhexidine gluconate on the frequency of wound infections after

clean surgery. J Hosp Infect 1988; 11:310-320.

111. Leigh DA, Stronge JL, Marriner J, Sedgwick J. Total body

bathing with `Hibiscrub' (chlorhexidine) in surgical patients: a

controlled trial. J Hosp Infect 1983; 4:229-235.

112. Ayliffe GAJ, Noy MF, Babb JR, Davies JG, Jackson J. A

comparison of pre-operative bathing with chlorhexidine-detergent and

non-medicated soap in the prevention of wound infection. J Hosp

Infect 1983; 4:237-244.

113. Seropian R, Reynolds BM. Wound infections after

preoperative depilatory versus razor preparation. Am J Surg 1971;

121:251-254.

114. Hamilton HW, Hamilton KR, Lone FJ. Preoperative hair

removal. Can J Surg 1977; 20:269-272.

115. Olson MM, MacCallum J, McQuarrie DG. Preoperative hair

removal with clippers does not increase infection rate in clean

surgical wounds. Surgery, Gynecology & Obstetrics 1986; 162:181-182.

116. Alexander JW, Fischer JE, Boyajian M, Palmquist J, Morris

MJ. The influence of hair-removal methods on wound infections. Arch

Surg 1983; 118:347-352.

117. Masterson TM, Rodeheaver GT, Morgan RF, Edlich RF.

Bacteriologic evaluation of electric clippers for surgical hair

removal. Am J Surg 1984; 148:301-302.

118. Sellick JA, Jr., Stelmach M, Mylotte JM. Surveillance of

surgical wound infections following open heart surgery. Infect

Control Hosp Epidemiol 1991; 12:591-596.

119. Ko W, Lazenby D, Zelano JA, Isom W, Krieger KH. Effects of

shaving methods and intraoperative irrigation on suppurative

mediastinitis after bypass operations. Ann Thorac Surg 1992; 53:301-

305.

120. Moro ML, Carrieri MP, Tozzi AE, Lana S, Greco D. Risk

factors for surgical wound infections in clean surgery: a

multicenter study. Italian PRINOS study group. Ann Ital Chir 1996;

67:13-19.

121. Winston KR. Hair and neurosurgery. Neurosurgery 1992;

31:320-329.

122. Osler T. Antiseptics in surgery. In: Fry DE, ed. Surgical

infections. Boston, New York, Toronto, London: Little, Brown and

Company, 1995:119-125.

123. Larson E. Guideline for use of topical antimicrobial

agents. Am J Infect Control 1988; 16:253-266.

124. Hardin WD, Nichols RL. Handwashing and patient skin

preparation. In: Malangoni MA, ed. Critical issues in operating room

management. Philadelphia: Lippincott-Raven Publishers, 1997:133-149.

125. Ritter MA, French MLV, Eitzen HE, Gioe TJ. The

antimicrobial effectiveness of operative-site preparative agents. J

Bone Joint Surg 1980; 62A:826-828.

126. Hardin WD, Nichols RL. Aseptic technique in the operating

room. In: Fry DE, ed. Surgical infections. Boston, New York,

Toronto, London: Little, Brown and Company, 1995:109-118.

127. Lowbury EJL, Lilly HA. Use of 4% chlorhexidine detergent

solution (Hibiscrub) and other methods of skin disinfection. Br Med

J 1973; 1:510-515.

128. Aly R, Maibach HI. Comparitive antibacterial efficacy of a

2-minute surgical scrub with chlorhexidine gluconate, povidone-

iodine, and chloroxylenol sponge-brushes. Am J Infect Control 1988;

16:173-177.

129. Peterson AF, Rosenberg A, Alatary SD. Comparative

evaluation of surgical scrub preparations. Surgery, Gynecology &

Obstetrics 1978; 146:63-65.

130. Brown TR, Ehrlich CE, Stehman FB, Golichowski AM, Madura

JA, Eitzen HE. A clinical evaluation of chlorhexidine gluconate

spray as compared with iodophor scrub for preoperative skin

preparations. Surgery, Gynecology & Obstetrics 1984; 158:363-366.

131. Lowbury EJL, Lilly HA. The effect of blood on disinfection

of surgeons hands. Br J Surg 1974; 61:19-24.

132. Rutala W, Gergen M, Weber D. Evaluation of a rapid readout

biological indicator for flash sterilization with three biological

indicators and three chemical indicators. Infect Control Hosp

Epidemiol 1993; 14:390-394.

133. AORN. Recommended practices for skin preparation of

patients. AORN J 1996; 64:813-816.

134. Kutarski PW, Grundy HC. To dry or not to dry? An assessment

of the possible degradation in efficiency of preoperative skin

preparation caused by wiping skin dry. Ann R Coll Surg Engl 1993;

75:181-185.

135. Gauthier DK, O'Fallon PT, Coppage D. Clean vs sterile

surgical skin preparation kits. Cost, safety, effectiveness. AORN J

1993; 58:486-495.

136. Hagen KS, Treston-Aurand J. A comparison of two skin preps

used in cardiac surgical procedures. AORN J 1995; 62:393-402.

137. Shirahatti RG, Joshi RM, Vishwanath YK, Shinkre N, Rao S,

Sankpal JS, et al. Effect of pre-operative skin preparation on post-

operative wound infection. J Postgrad Med 1993; 39:134-136.

138. Larson EL, Butz AM, Gullette DL, Laughon BA. Alcohol for

surgical scrubbing? Infect Control Hosp Epidemiol 1990; 11:139-143.

139. Faoagali J, Fong J, George N, Mahoney P, O'Rouke V.

Comparison of the immediate residual, and cumulative antibacterial

effects of Novaderm R, Novascrub R, Betadine Surgical Scrub,

Hibiclens, and liquid soap. Am J Infect Control 1995; 23:337-343.

140. Larson EL. APIC guideline for handwashing and hand

antisepsis in health care settings. Am J Infect Control 1995;

23:251-269.

141. Rubio PA. Septisol antiseptic foam: a sensible alternative

to the conventional surgical scrub. Int Surg 1987; 72:243-246.

142. Lowbury EJL, Lilly HA, Ayliffe GAJ. Preoperative

disinfection of surgeons' hands: use of alcoholic solutions and

effects of gloves on skin flora. Br Med J 1974; 4:369-372.

143. Rotter ML. Hygienic hand disinfection. Infect Control 1984;

5:18-22.

144. Ayliffe GAJ. Surgical scrub and skin disinfection. Infect

Control 1984; 5:23-27.

145. Lilly HA, Lowbury EJL, Wilkins MD, Zaggy A. Delayed

antimicrobial effects of skin disinfection by alcohol. J Hyg (Camb)

1979; 82:497-500.

146. Wade JJ, Casewell MW. The evaluation of residual

antimicrobial activity on hands and its clinical relevance. J Hosp

Infect 1991; 18 (Suppl B):23-28.

147. Babb JR, Davies JG, Ayliffe GA. A test procedure for

evaluating surgical hand disinfection. J Hosp Infect 1991; 18(Suppl

B):41-49.

148. Holloway PM, Platt JH, Reybrouck G, Lilly HA, Mehtar S,

Drabu Y. A multi-center evaluation of two chlorhexidine-containing

[[Page 33182]]

formulations for surgical hand disinfection. J Hosp Infect 1990;

16:151-159.

149. Kobayshi H. Evaluation of surgical scrubbing. J Hosp Infect

1991; 18:29-34.

150. Nicoletti G, Boghossian V, Borland R. Hygienic hand

disinfection: a comparative study with chlorhexidine detergents and

soap. J Hosp Infect 1990; 15:323-337.

151. Rotter ML, Koller W. Surgical hand disinfection: effect of

sequential use of two chlorhexidine preparations. J Hosp Infect

1990; 16:161-166.

152. O'Shaughnessy M, O'Malley VP, Corbett G, Given HF. Optimum

duration of surgical scrub-time. Br J Surg 1991; 78:685-686.

153. Hingst V, Juditzki I, Heeg P, Sonntag HG. Evaluation of the

efficacy of surgical hand disinfection following a reduced

application time of 3 instead of 5 min. J Hosp Infect 1992; 20:79-

86.

154. AORN. Standards, recommended practices, guidelines. Denver:

Association of Operating Room Nurses, Inc. 1997.

155. Pottinger J, Burns SJ, Manske C. Bacterial carriage by

artificial versus natural nails. Am J Infect Control 1989; 17:340-

344.

156. Baumgardner CA, Maragos CS, Walz J, Larson E. Effects of

nail polish on microbial growth of fingernails. AORN J 1993; 58:84-

88.

157. Jacoboson G, Thiele JE, McCune JH, Farrell LD. Handwashing:

ring-wearing and number of microorganisms. Nurs Res 1985; 34:186-8.

158. Hoffman PN. Microorganisms isolated from skin under wedding

rings worn by hospital staff. Br Med J (Clin Res) 1985; 290:206-7.

159. Ehrenkranz NJ, Blackwelder WC, Pfaff SJ, Poppe D, Yerg DE,

Kaslow RA. Infections complicating low-risk cesarean sections in

community hospitals: efficacy of antimicrobial prophylaxis. Am J

Obstet Gynecol 1990; 162:337-343.

160. Soper DE. Infections following cesarean section. Curr Opini

in Obstet Gynecol 1993; 5:517-520.

161. Enkin M, Enkin E, Chalmers I, Hemminki E. Prophylactic

antibiotics in association with cesarean section. In: Chalmers I,

Enkin M, Keiser MJNC, eds. Effective care in pregnancy and

childbirth. London: Oxford University, 1989:1246-1269.

162. Allen JL, Rampon JF, Wheeless CR. Use of a prophylactic

antibiotic in elective major gynecologic operations. Obstet Gynecol

1972; 39:218-224.

163. The Multicenter Study Group. Single dose prophylaxis in

patients undergoing vaginal hysterectomy: cefamandole versus

cefotaxime. Am J Obstet Gynecol 1989; 160:1198-1201.

164. Roy S, Wilkins J, Galaif E, Azen C. Comparative efficacy

and safety of cefmetazole or cefoxitin in the prevention of

postoperative infection following vaginal and abdominal

hysterectomy. J Antimicrob Chemother 1989; 23:109-117.

165. Friese S, Willems FTC, Loriaux SM, Meewis J. Prophylaxis in

gynaecological surgery: a prospective randomized comparison between

single dose prophylaxis with amoxycillin/clavulanate and the

combination of cefuroxime and metronidazole. J Antimicrob Chemother

1989; 24:213-216.

166. Senior CC, Steirad SJ. Are preoperative antibiotics helpful

in abdominal hysterectomy? Am J Obstet Gynecol 1986; 154:1004-1008.

167. Hemsell DL, Martin JN, Jr., Pastorek JG, II., Nobles BJ.

Single dose antimicrobial prophylaxis at abdominal hysterectomy.

Cefamandole vs cefotaxime. J Reprod Med 1988; 33:939-944.

168. Hemsell DL, Hemsell PG, Heard ML, Nobles BJ. Preoperative

cefoxitin prophylaxis for elective abdominal hysterectomy: Am J

Obstet Gynecol 1985; 153:225-226.

169. Berkeley AS, Freedman KS, Ledger WJ, Orr JW, Benigno BB,

Gordon SF, et al. Comparison of cefotetan and cefoxitin prophylaxis

for abdominal and vaginal hysterectomy. Am J Obstet Gynecol 1988;

158:706-709.

170. Rimoldi RL, Haye W. The use of antibiotics for wound

prophylaxis in spinal surgery. Orthop Clin North Am 1996; 27:47-52.

171. Bullock R, vanDellen JR, Ketelbey W, Reinach SG. A double-

blind placebo-controlled trial of perioperative prophylactic

antibiotics for elective neurosurgery. Neurosurgery 1988; 69:687-

691.

172. Djindjian M, Lepresle E, Homs JB. Antibiotic prophylaxis

during prolonged clean neurosurgery: results of a randomized double-

blind study using oxacillin. J Neurosurg 1990; 73:383-386.

173. Young RF, Lawner PM. Perioperative antibiotic prophylaxis

for prevention of postoperative neurosurgical infections: A

randomized clinical trial. Neurosurgery 1987; 66:701-705.

174. VanEk B, Dijkmans BAC, VanDulken H, VanFurth R. Antibiotic

prophylaxis in craniotomy: a prospective double-blind placebo-

controlled study. Scand J Infect Dis 1988; 20:633-639.

175. McQeen M, Littlejohn A, Hughes SPF. A comparison of

systemic cefuroxime and cefuroxime loaded bone cement in the

prevention of early infection after total joint replacement.

International Orhtopaedis 1987; 11:241-243.

176. Buckley R, Hughes GNF, Snodgrass T, Huchcroft SA.

Perioperative cefazolin prophylaxis in hip fracture surgery. Can J

Surg 1990; 33:122-127.

177. Henley MB, Jones RE, Wyatt RWB, Hofmann A, Cohen RL.

Prophylaxis with cefamamdole nafate in elective orthopedic surgery.

Clin Orthopaed Rel Res 1986; 209:249-254.

178. Boyd RJ, Burke JF, Colton T. A double-blind clinical trial

of prophylactic antibiotic in hip fractures. J Bone Joint Surg 1973;

55A:1251-1258.

179. Burnett JW, Gustilo RB, Williams DN, Kind AC. Prophylactic

antibiotics in hip fractures: a double-bind, prospective study. J

Bone Joint Surg 1980; 62:457-462.

180. Madsen MS, Neumann L, Andersen JA. Penicillin prophylaxis

in complicated wounds of hands and feet: a randomized , double-bind

trial. Injury 1996; 27:275-278.

181. Nichols RL. Bowel preparation. Sci Am 1995; 1-11.

182. Nichols RL. Prophylaxis in bowel surgery. Current Clin Top

Infect Dis 1995; 15:76-96.

183. Lewis RT, Goodall RG, Marien B, Park M, Lloyd-Smith W,

Wiegand FM. Efficacy and distribution of single-dose preoperative

antibiotic prophylaxis in high-risk gastroduodenal surgery. Can J

Surg 1991; 34:117-122.

184. Nichols RL, Webb WR, Jones JW, Smith JW, LoCicero J, III.

Efficacy of antibiotic prophylaxis in high risk gastroduodenal

operations. Am J Surg 1982; 143:94-98.

185. Browder W, Smith JW, Vivoda LM, Nicholas RL. Nonperforative

appendicitis: a continuing surgical dilemma. J Infect Dis 1989;

159:1088-1094.

186. Krige JEJ, Isaacs S, Stapleton GN, McNally J. Prospective,

randomized study comparing amoxycillin-clavulanic acid and

cefamandole for the prevention of wound infection in high-risk

patients undergoing elective biliary surgery. J Hosp Infect 1992; 22

(Suppl A):33-41.

187. Targarona EM, Garau J, Munoz-Ramos C, Roset F, Lite J,

Matas E, et al. Single-dose antibiotic prophylaxis in patients at

high risk for infection in biliary surgery: a prospective and

randomized study comparing cefonicid with mezlocillin. Surgery 1990;

107:327-334.

188. Bernard A, Pillet M, Goudet P, Viard H. Antibiotic

prophylaxis in pulmonary surgery. J Thorac Cardiovasc Surg 1994;

107:896-900.

189. Bennion RS, Hiatt JR, Williams RA, Wilson SE. A randomized;

prospective study of perioperative antimicrobial prophylaxis for

vascular access surgery. J Cardiovasc Surg 1985; 26:270-274.

190. Doebbeling BN, Pfaller MA, Kuhns KR, Massanari RM, Behrendt

DM, Wenzel RP. Cardiovasular surgery prophylaxis: a randomized,

controlled comparison of cefazolin and cefuroxime. J Thorac

Cardiovasc Surg 1990; 99:981-989.

191. Nichols RL, Smith JW, Muzik AC, Love JW, McSwain NE,

Timberlake G, et al. Preventive antibiotic usage in traumatic

thoracic injuries requiring closed tube thoracostomy. Chest 1994;

106:1493-1498.

192. Kaiser AB, Petracek MR, Lea JWI, Kernodle DS, Roach AC,

Alford WCJ, et al. Efficacy of cefazolin, cefamandole, and

gentamicin as prophylactic agents in cardiac surgery: result of a

prospective, randomized, double-blind trial in 1030 patients. Ann

Surg 1987; 206:791-797.

193. Gentry LO, Zeluff BJ, Cooley DA. Antibiotic prophylaxis in

open-heart surgery: a comparison of cefamandole, cefuroxime, and

cefazolin. Ann Thorac Surg 1988; 46:167-171.

194. Miedzinski LJ, Callaghan JC, Fanning EA, Gelfand ET,

Goldsand G, Modry D, et al. Antimicrobial prophylaxis for open heart

operations. Ann Thorac Surg 1990; 50:800-807.

195. Platt R. Guidelines for perioperative antibiotic

prophylaxis. Saunders Infection Control Reference Service 1997; 229-

234.

196. Wenzel RP. Preoperative antibiotic prophylaxis. N Engl J

Med 1992; 326:337-339.

197. Ehrenkranz NJ, Meakins JL. Surgical infections. In: Bennett

JV, Brachman PS, eds. Hospital Infections. 3rd ed. Boston: Little,

Brown and Company, 1992:685-710.

198. Scher KS. Studies on the Duration of Antibiotic

Administration for Surgical Prophylaxis. Am Surg 1997; 63:59-62.

[[Page 33183]]

199. DiPiro JT, Cheung RPF, Bowden TA, Jr., Mansberger JA.

Single dose systemic antibiotic prophylaxis of surgical wound

infections. Am J Surg 1986; 152:552-559.

200. Nooyen SMH, Overbeek BP, Brutel dl, Storm AJ, Langemeyer

JJM. Prospective randomized comparison of single-dose versus

multiple-dose cefuroxime for prophylaxis in coronary artery bypass

grafting. Eur J Clin Microbiol Infect Dis 1994; 13:1033-1037.

201. Kernodle DS, Kaiser AB. Postoperative infections and

antimicrobial prophylaxis. In: Mandell GL, Bennett JE, Dolin R, eds.

Principles and practice of infectious diseases. 4th ed. New York:

Churchill Livingstone, 1995:2742-2756.

202. Nichols RL. Surgical antibiotic prophylaxis. Med Clin North

Am 1995; 79:509-522.

203. Trilla A, Mensa J. Perioperative Antibiotic Prophylaxis.

In: Wenzel RP, ed. Prevention and control of nosocomial infections.

2nd ed. Baltimore: Williams and Wilkins, 1993:665-682.

204. HICPAC. Recommendation for preventing the spread of

vancomycin resistance. Infect Control Hosp Epidemiol 1995; 16:105-

113.

205. Maki DG, Bohn MJ, Stolz SM, Kroncke GM, Archer CW,

Myerowitz PD. Comparitive study of cefazolin, cefamandole, and

vancomycin for surgical prophylaxis in cardiac and vascular

operations. J Thorac Cardiovasc Surg 1992; 104:1423-1434.

206. Clarke JS, Condon RE, Bartlett JG, Gorbach SL, Nichols RL,

Ochi S. Preoperative oral antibiotics reduce septic complications of

colon operations: results of postoperative, randomized, double-blind

clinical study. Ann Surg 1977; 186:251-259.

207. Wapnick S, Guinto R, Reizis I, LeVeen HH. Reduction of

postoperative infection in elective colon surgery with preoperative

administration of kanamycin and erythromycin. Surgery 1979; 85:317-

321.

208. Washington JAI, Dearing WH, Judd ES. Effect of preoperative

antibiotic regimen on development of infection after intestinal

surgery: prospective, randomized, double-blind study. Ann Surg 1974;

108:567-572.

209. Condon RE, Bartlett JG, Greenlee H, Schulte WJ, Ochi S,

Abbe R, et al. Efficacy of oral and systemic antibiotic prophylaxis

in colorectal operations. Arch Surg 1983; 118:496-502.

210. Bartlett JG, Condon RE, Gorbach SL, Clarke JS, Nichols RL,

Ochi S. Veterans Administration cooperative study on bowel

preparation for elective colorectal operation: impact of oral

antibiotic regimen on colonic flora, wound irrigation cultures and

bacteriology of septic complications. Ann Surg 1978; 188:249-254.

211. Maki DG, Aughey DR. Comparative study of cefazolin,

cefoxitin and ceftizoxime for surgical prophylaxis in colo-rectal

surgery. J Antimicrob Chemother 1982; 10(Suppl C):281-287.

212. Nichols RL. Surgical infections: prevention and treatment

1965-1995. Am J Surg 1996; 172:68-74.

213. Nichols RL, Smith JW, Garcia RY, Waterman RS, Holmes JWC.

Current practices of preoperative bowel preparation among North

American colorectal surgeons. Clin Infect Dis 1997; 24:609-619.

214. Classen DC, Evans RS, Pestotnik SL, Horn SD, Menlove RL,

Burke JP. The timing of prophylactic administration of antibiotics

and the risk of surgical wound infection. N Engl J Med 1992;

326:281-286.

215. Polk HC, Wilson MA. Systemic antibiotic prophylaxis in

surgery. In: Fry DE, ed. Surgical infections. New York: Little,

Brown and Company, 1995:127-133.

216. Martin C. Antimicrobial prophylaxis in surgery: general

concepts and clinical guidelines. Infect Control Hosp Epidemiol

1994; 15:463-471.

217. Dellinger EP, Gross PA, Barrett TL, Krause PJ, Martone WJ,

McGowan JE, Jr., et al. Quality standard for antimicrobial

prophylaxis in surgical procedures. Clin Infect Dis 1994; 18:422-

427.

218. Forse RA, Karam B, MacLean LD, Christou NV. Antibiotic

prophylaxis for surgery in morbidly obese patients. Surgery 1989;

106:750-757.

219. Ayliffe GAJ. Role of the environment of the operating suite

in surgical wound infection. Rev Infect Dis 1991; 13:S800-S804.

220. Gryska PF, O'Dea AE. Postoperative streptococcal wound

infection. The anatomy of an epidemic. JAMA 1970; 213:1189-1191.

221. Stamm WE, Feeley JC, Frachklam RR. Wound infection due to

group A Streptococcus traced to a vaginal carrier. J Infect Dis

1978; 138:287-292.

222. Berkelman RL, Martin D, Graham DR. Streptococcal wound

infection caused by a vaginal carrier. JAMA 1982; 247:2680-2682.

223. McIntyre DM. An epidemic of Streptococcus pyogenes

puerperal and postoperative sepsis with an unusual carrier site-the

anus. Am J Obstet Gynecol 1968; 101:308-314.

224. Gaynes RP, Horan TC. Surveillance of nosocomial infections.

In: Mayhall CG, ed. Hospital epidemiology and infection control.

Baltimore: Williams & Wilkins, 1996:1017-1031.

225. Lidwell OM. Clean air at operation and subsequent sepsis in

the joint. Clin Orthop 1986; 211:91-102.

226. American Institute of Architects Committee. Guideline for

construction and equipment of hospital and medical facilities.

Washington: American Institute of Architects Press, 1996.

227. Nichols RL. The operating room. In: Bennett JV, Brachman

PS, eds. Hospital infections. 3rd ed. Boston: Little, Brown and

Company, 1992:461-473.

228. Laufman H. The operating room. In: Bennett JV, Brachman PS,

eds. Hospital infections. 2nd ed. Boston/Toronto: Little, Brown &

Company, 1986:315-323.

229. Pittet D, Ducel G. Infectious risk factors related to

operating rooms. Infect Control Hosp Epidemiol 1994; 15:456-462.

230. Hambraeus A. Aerobiology in the operating room--a review. J

Hosp Infect 1988; 11(Suppl A):68-76.

231. Babb JR, Lynam P, Ayliffe GA. Risk of airborne transmission

in an operating theater containing four ultraclean air units. J Hosp

Infect 1995; 31:159-168.

232. Charnley J. A clean-air operating enclosure. Br J Surg

1964; 51:202-205.

233. Lidwell OM, Lowbury EJL, Whyte W, Blowers R, Stanley SJ,

Lowe D. Effect of ultraclean air in operating rooms on deep sepsis

in the joint after total hip or knee replacement: a randomized

study. Br Med J 1982; 285:10-14.

234. Hill C, Flamant R, Mazas F, Evrard J. Prophylactic

cefazolin versus placebo in total hip replacement: report of a

multicentre double-blind randomized trial. Lancet 1981; 1:795-796.

235. Ha'eri GB, Wiley AM. Total hip replacement in a laminar

flow environment with special reference to deep infections. Clin

Orthop 1980; 148:163-168.

236. Collis DK, Steinhaus K. Total hip replacement without deep

infection in a standard operating room. J Bone Joint Surg 1976;

58A:446-450.

237. Taylor GD, Bannister GC, Leeming JP. Wound disinfection

with ultraviolet radiation. J Hosp Infect 1995; 30:85-93.

238. Cavanillas AB, Rodriguez-Contreras R, Rodriguez MD, Abril

OM, Gigosos RL, Solvas JG, et al. Preoperative stay as a risk factor

for nosocomial infection. Eur J Epidemiol 1991; 7:670-676.

239. Favero M, Bond W. Sterilization, disinfection, and

antisepsis in the hospital. Washington, DC: American Society of

Microbiology, 1991:183-200.

240. U.S. Department of Labor. Occupational exposure to

bloodborne pathogens final rule. CFR Part 1910.1030. Federal

Register: 1991; 56: 64004 p.

241. Centers for Disease Control and Prevention. Postsurgical

infection associated with nonsterile implantable devices. MMWR 1992;

41:263.

242. Soto LE, Bobadilla M, Villalobos Y, Sifuentes J, Avelar J,

Arrieta M, et al. Post-surgical nasal cellulitis outbreak due to

Mycobacterium chelonae. J Hosp Infect 1991; 19:99-106.

243. Favero M, Manian F. Is eliminating flash sterilization

practical? Infect Control Hosp Epidemiol 1993; 14:479-480.

244. Anonymous. Recommended practices for central service,

continuous quality improvement. American Society of Healthcare

Central Service Professionals of the American Hospital Association,

1993: 7-10.

245. Anonymous. Flash sterilization: steam sterilization of

patient care items for immediate use. Arlington, VA: Association for

the Advancement of Medical Instrumentation, 1996.

246. Lind N. Flash Sterilization techniques. Infection Control &

Sterilization Technology 1997; 40-43.

247. Wiley AM, Ha'eri GB. Routes of infection: a study of using

``tracer particles'' in the orthopedic operating room. Clin Orthop

1979; 139:150-155.

248. Dineen P, Drusin L. Epidemics of postoperative wound

infections associated with hair carriers. Lancet 1973; 2:1157-1159.

249. Dineen P. The role of impervious drapes and gowns

preventing surgical infection. Clin Orthop Rel Res 1973; 96:210-212.

250. Ha'eri GB, Wiley AM. The efficacy of standard surgical face

masks: an investigation using ``tracer particles.'' Clin Orthop

1980; 148:160-162.

251. Moylan JA, Fitzpatrick KT, Davenport KE. Reducing wound

infections: improved gown and drape barrier performance. Arch Surg

1987; 122:152-157.

[[Page 33184]]

252. Moylan JA, Balish E, Chan J. Intraoperative bacterial

transmission. Surgical Forum 1974; 25:29-30.

253. Copp G, Mailhot CB, Zalar M, Slezak L, Copp AJ. Cover gowns

and the control of operating room contamination. Nurs Res 1986;

35:263-268.

254. Beck WC. The surgical mask: another `sacred cow'? (Guest

editorial) AORN J 1992; 55:955-957.

255. Mitchell NJ, Hunt S. Surgical face masks in modern

operating rooms--a costly and unnecessary ritual? J Hosp Infect

1991; 18:239-242.

256. Tunevall TG, Jorbeck H. Influence of wearing masks on the

density of airborne bacteria in the vicinity of the surgical wound.

Eur J Surg 1992; 158:263-266.

257. Tunevall TG. Postoperative wound infections and surgical

face masks: a controlled study. World J Surg 1991; 15:383-388.

258. Orr NWM. Is a mask necessary in the operating theater? Ann

R Coll Surg Engl 1981; 63:390-392.

259. Lee JT. Making surgical care better: hard work, small

gains. Infect Control Hosp Epidemiol 1997; 18:6-8.

260. Jarvis WR, Bolyard EA, Bozzi CJ, Burwen DR, Dooley SW,

Martin LS, et al. Respirators, recommendations, and regulations: the

controversy surrounding protection of health care workers from

tuberculosis. Ann Intern Med 1995; 122:142-146.

261. Mastro TD, Farley TA, Elliott JA, Facklam RR, Perks JR,

Hadler JL, et al. An outbreak of surgical-wound infections due to

group A streptococcus carried on the scalp. N Engl J Med 1990;

323:968-972.

262. Humphreys H, Marshall RJ, Ricketts VE, Russell AJ, Reeves

DS. Theater over-shoes do not reduce operating theater floor

bacterial counts. J Hosp Infect 1991; 17:117-123.

263. Weightman NC, Banfield KR. Protective over-shoes are

unnecessary in a day surgery unit. J Hosp Infect 1994; 28:1-3.

264. Whyte W, Hambraeus A, Laurell G, Hoborn J. The relative

importance of the routes and sources of wound contamination during

general surgery. II. Airborne. J Hosp Infect 1992; 22:41-54.

265. Whyte W, Hambraeus A, Laurell G, Hoborn J. The relative

importance of routes and sources of wound contamination during

general surgery. I. Non-airborne. J Hosp Infect 1991; 18:93-107.

266. Dodds RDA, Guy PJ, Peacock AM, Duffy SR, Barker SGE, Thomas

MH. Surgical glove perforation. Br J Surg 1988; 75:966-968.

267. Tokars JI, Culver DH, Mendelson MH, Sloan EP, Farber BF,

Fligner DJ, et al. Skin and mucous membrane contacts with blood

during surgical procedures: risk and prevention. Infect Control Hosp

Epidemiol 1995; 16:703-711.

268. Tokars JI, Bell DM, Culver DH, Marcus R, Mendelson MH,

Sloan EP, et al. Percutaneous injuries during surgical procedures.

JAMA 1992; 267:2899-2904.

269. Chang HJ, Luck JV, Jr., Bell DM, Benson DR, Glasser DB,

Chamberland ME. Transmission of Human Immunodeficiency Virus

infection in the surgical setting. J Am Acad Orthop Surg 1996;

4:279-286.

270. Panlilio AL, Shapiro CN, Schable CA, Mendelson MH,

Montecalvo MA, Kunches LM, et al. Serosurvey of human

immunodeficiency virus, hepatitis B virus, and hepatitis C virus

infection among hospital-based surgeons. J Am Coll Surg 1995;

180:16-24.

271. Garibaldi RA, Maglio S, Lerer T, Becker D, Lyons R.

Comparison of nonwoven and woven gown and drape fabric to prevent

intraoperative wound contamination and postoperative infection. Am J

Surg 1986; 152:505-509.

272. Muller W, Jiru P, Mach R, Polaschek F, Fasching W. The use

of disposable draping materials in the operating room and its effect

on the postoperative wound infection rate. Weiner Klinische

Wochenschrift 1989; 101:837-842.

273. Smith JW, Nicholas RL. Barrier efficiency of surgical

gowns. Are we really protected from our patients' pathogens? Arch

Surg 1991; 126:756-763.

274. Artz CP, Conn JH, Howard HS. Protection of the surgical

wound with a new plastic film. JAMA 1960; 174:1865-1868.

275. Chiu KY, Lau SK, Fung B, Ng KH, Chow SP. Plastic adhesive

drapes and wound infection after hip fracture surgery. Aust N Z J

Surg 1993; 63:798-801.

276. American Society for Testing Materials. Emergency standard

test method for resistance of protective clothing materials to

synthetic blood. ASTM 1992;

277. American Society for Testing Materials. Emergency standard

test method for resistance of protective clothing materials to

penetration by bloodborne pathogens using viral penetration as a

test system. ASTM 1992;

278. McCullough EA. Methods for determining the barrier efficacy

of surgical gowns. Am J Infect Control 1993; 21:368-374.

279. American Association of Nurse Anesthetists. Infection

control guide. 2nd ed. Park Ridge, IL: American Association of Nurse

Anesthetists, 1993.

280. American Society of Anesthesiologists. Recommendations for

infection control for the practice of anesthesiology. Park Ridge,

IL: American Society of Anesthesiologist, 1992.

281. Centers for Disease Control. CDC guideline for handwashing

and hospital environmental control, 1985. Section 2: Cleaning,

disinfecting, and sterilizing patient care equipment. Infect Control

1986; 7:236-240.

282. Herwaldt LA, Pottinger J, Coffin SA. Nosocomial infections

associated with anesthesia. In: Mayhall CG, ed. Hosp Epidemiol

Infect Control. Baltimore: Williams & Wilkins, 1996:655-675.

283. Bennett SN, McNeil MM, Bland LA, Arduino MJ, Villarino ME,

Perrotta DM, et al. Postoperative infections traced to contamination

of an intravenous anesthetic, propofol. N Engl J Med 1995; 333:147-

154.

284. Froggatt JW, Dwyer DM, Stephens MA. Hospital outbreak of

hepatitis B in patients undergoing electroconvulsive therapy

[Abstract]. Program and Abstracts of the 31st Interscience

Conference on Antimicrobial Agents and Chemotherapy, Chicago 1991;

157:347.

285. Centers for Disease Control. Postsurgical infections

associated with an extrinsically contaminated intravenous anesthetic

agent--California, Illinois, Maine, and Michigan,1990. MMWR 1990;

39:426-427,433.

286. Daily MJ, Dickey JB, Packo KH. Endogenous Candida

endophthalmitis after intravenous anaesthesia with propofol. Arch

Ophthalmol 1991; 109:1081-1084.

287. Villarino ME, McNeill MM, Hall WN. Postsurgical infections

associated with an extrinsically contaminated intravenous anesthetic

agent [Abstract]. Program and Abstracts of the 31st Interscience

Conference on Antimicrobial Agents and Chemotherapy, Chicago 1991;

156:346.

288. Rudnick JR, Beck-Sague CM, Anderson RL, Schalbe B, Miller

JM, Jarvis WR. Gram-negative bacteremia in open-heart-surgery

patients traced to probable tap water contamination of pressure

monitoring equipment. Infect Control Hosp Epidemiol 1996; 17:281-

285.

289. Walter CW, Kundsin RB, Harding AL, Page LK. The infector on

the surgical team. Clin Neurosurg 1966; 14:361-379.

290. Payne RW. Severe outbreak of surgical sepsis due to

Staphylococcus aureus of unusual type and origin. Br Med J 1967;

4:17-20.

291. Schaffner W, Lefkowitz LB, Jr., Goodman JS, Koenig MG.

Hospital outbreak of infections with group A streptococci traced to

an asymptomatic anal carrier. N Engl J Med 1969; 280:1224-1225.

292. Centers for Disease Control. Hospital outbreak of

streptococcal wound infection--Utah. MMWR 1976; 25:141.

293. Paul SM, Genese C, Spitalny K. Postoperative group A beta-

hemolytic Streptococcus outbreak with the pathogen traced to a

member of a healthcare worker's household. Infect Control Hosp

Epidemiol 1990; 11:643-646.

294. Rosenberg AD, Bernstein RL, Ramanathan S, Albert DB,

Marshall MH. Do anesthesiologists practice proper infection control

precautions? [Abstract]. Anesthesiology 1989; 71:A949.

295. Tollofsrud SG, Gundersen Y, Anderson R. Perioperative

hypothermia. Acta Anaesthesiol Scand 1984; 28:511-515.

296. Sessler DI, McGuire J, Hynson J, Moayeri A, Heier T.

Thermoregulatory vasoconstriction during isoflurane anesthesia

minimally decreases cutaneous heat loss. Anesthesiology 1992;

76:670-675.

297. Sessler DI. Mild perioperative hypothermia. N Engl J Med

1997; 336:1730-1737.

298. Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia

to reduce the incidence of surgical-wound infection and shorten

hospitalization. Study of wound infection and temperature group. N

Engl J Med 1996; 334:1209-1215.

299. Zacharias A, Habib RH. Delayed primary closure of deep

sternal wound infections. Tex Heart Inst J 1996; 23:211-216.

300. Smilanich RP, Bonnet I, Kirkpactrick JR. Contaminated

wounds: the effect of initial management on outcome. Am Surg 1995;

61:427-430.

301. Blomstedt GC. Infections in neurosurgery: a randomized

comparison

[[Page 33185]]

between silk and polyglycolic acid. Acta Neurochir 1985; 76:90-93.

302. Scher KS, Bernstein JM, Jones CW. Infectivity of vascular

sutures. Am Surg 1985; 51:577-579.

303. Durdey P, Bucknall TE. Assessment of sutures for use in

colonic surgery: an experimental study. J R Soc Med 1984; 77:472-

477.

304. Chu CC, Williams DF. Effects of physical configuration and

chemical structure of suture materials on bacterial adhesion: a

possible link to wound infection. Am J Surg 1984; 147:197-204.

305. Askew AR. A comparison of upper abdominal wound closure

with monofilament nylon and polyglycolic acid. Aust N Z J Surg 1983;

53:353-356.

306. Kapadia CR, Mann JB, McGeehan D, Jose Biglin JE, Waxman BP,

Dudley HAF. Behavior of synthetic absorbable sutures with and

without synergistic enteric infection. Eur Surg Res 1983; 15:67-72.

307. Bucknall TE, Teare L, Ellis H. The choice of a suture to

close abdominal incisions. Eur Surg Res 1983; 15:59-66.

308. Bucknall TE. Factors influencing wound complications: a

clinical and experimental study. Ann Royal Coll Surg Engl 1983;

65:71-77.

309. Varma S, Lumb LW, Johnson LW, Ferguson HL. Further studies

with polyglycolic acid (Dexon) and other sutures in infected

experimental wounds. Am J Vet Res 1981; 42:571-574.

310. Bucknall TE, Ellis H. Abdominal wound closure--a comparison

of monofilament nylon and polyglycolic acid. Surgery 1981; 89:672-

677.

311. Cruse PJE. Wound infections: epidemiology and clinical

characteristics in surgical infectious disease. In: Anonymous. Surgical

infectious disease. 2nd ed. Norwalk, CT: Appleton and Lange, 1988:324-

325.

312. Moro ML, Carrieri MP, Tozzi AE, Lana S, Greco D, Italian

PRINOS Study Group. Risk factors for surgical wound infections in

clean surgery: a multicenter study. Ann Ital Chir 1996; 117:13-18.

313. Moro ML, Carrieri MP, Tozzi AE, Lana S, Greco D. [The

effect of hanging some patient care practices on the incidence of

surgical wound infections following ``clean'' interventions. PRINOS

group study]. [Italian]. Minerva Chir 1997; 52:61-67.

314. Drinkwater CJ, Neil MJ. Optimal timing of wound drain

removal following total joint arthroplasty. J Arthroplasty 1995;

10:185-189.

315. DuMortier JJ. The resistance of healing wounds to

infection. Surgery, Gynecology & Obstetrics 1933; 56:762-766.

316. Morain WD, Colen LB. Wound healing in diabetes mellitus.

Clin Plast Surg 1990; 17:493-499.

317. Palmer MB. Infection Control : A Policy and Procedure

Manual. Philadelphia: W.B.Saunders Company, 1984.

318. American Hospital Association. Infection control in the

hospital. 4th ed. Chicago: American Hospital Association, 1979.

319. Castle M, Ajemian E. Hospital infection control: principles

and practice. 2nd ed. Denver: John Wiley and Sons, Inc. 1987.

320. Centers for Disease Control, U.S.Department of Health and

Human Services. Isolation techniques for use in hospitals.

Washington: Public Health Service Publication, 1970.

321. Stotts NA, Barbour S, Griggs K, Bouvier B, Buhlman L.

Sterile versus clean technique in postoperative wound care of

patients with open surgical wounds: a pilot study. Journal of Wound,

Ostomy, and Continence Nursing 1997; 24:10-18.

322. Kravitz M. Outpatient wound care. Critical Care Nursing

Clinics of North America 1996; 8:217-233.

323. Condon RE, Schulte WJ, Malangoni MA, Anderson-Teschendorf

MJ. Effectiveness of a surgical wound surveillance program. Arch

Surg 1983; 118:303-307.

324. Haley RW, Culver DH, White JW, Morgan WM, Emori TG, Munn

VP, et al. The efficacy of infection surveillance and control

programs in preventing nosocomial infections in U.S. hospitals. Am J

Epidemiol 1985; 121:182-205.

325. Lennard ES, Hargiss CO, Schoenknecht FP. Postoperative

wound infection surveillance by use of bacterial contamination

categories. Am J Infect Control 1985; 13:147-153.

326. Olson MM, Lee JT. Continuous, 10 year wound infection

surveillance: results, advantages, and unanswered questions. Arch

Surg 1990; 125:794-803.

327. Olson M, O'Connor MO, Schwartz ML. A 5-year prospective

study of 20,193 wounds at the Minneapolis VA Medical Center. Ann

Surg 1984; 199:253-259.

328. Culver DH, Horan TC, Gaynes RP, Martone WJ, Jarvis WR,

Emori TG, et al. Surgical wound infection rates by wound class,

operative procedure, and patient risk index. Am J Med 1991; 91:152S-

157S.

329. Weigelt JA. Risk of wound infections in trauma patients. Am

J Surg 1985; 150:782-784.

330. Weigelt JA, Haley RW, Seibert B. Factors which influence

the risk of wound infection in trauma patients. J Trauma 1987;

27:774-781.

331. Haley RW, Culver DH, Morgan WM, Emori TG, Munn VP, Hooton

TM. Identifying patients at high risk of surgical wound infection: a

simple multivariate index of patient susceptibility and wound

contamination. Am J Epidemiol 1985; 121:206-215.

332. Anonymous. New classification of physical status.

Anesthesiology 1963; 24:111.

333. Owens WD. ASA physical status classifications: a study on

consistency of ratings. Anestheiology 1978; 49:239-243.

334. Centers for Disease Control. Nosocomial infection rates for

interhospital comparison: limitations and possible solutions. Infect

Control Hosp Epidemiol 1991; 12:609-621.

335. Cardo DM, Falk PS, Mayhall CG. Validation of surgical wound

classification in the operating room. Infect Control Hosp Epidemiol

1993; 14:255-259.

336. Centers for Disease Control and Prevention. National

Nosocomial Infection Surveillance (NNIS) report, data summary from

October 1986-April 1996. Issued May 1996. Am J Infect Control 1996;

24:380-388.

337. Horan TC, Gaynes RP, Culver DH, National Nosocomial

Infections Surveillance (NNIS) System. Development of predictive

risk factors for nosocomial surgical site infections (SSI)

[abstract]. Infect Control Hosp Epidemiol 1994; 15:46(M72).

338. Nichols RL, Smith JW, Klein DB, Trunkey DD, Cooper RH,

Adinolfi MF, et al. Risk of infection after penetrating abdominal

trauma. N Engl J Med 1984; 311:1065-1070.

339. Nichols RL, Smith JW, Robertson GD, Muzik AC, Pearce P,

Ozmen V, et al. Prospective alterations in therapy for penetrating

abdominal trauma. Arch Surg 1993; 128:55-64.

340. Horan TC, Culver DH, Gaynes RP, National Nosocomial

Infections Surveillance (NNIS) System. Results of a multicenter

study on risk factors for surgical site infections (SSI) following

C-Section (CSEC) [abstract]. Am J Infect Control 1996; 24:84.

341. Richet HM, Chidiac C, Prat A, Pol A, David M, Maccario M,

et al. Analysis of risk factors for surgical wound infections

following vascular surgery. Am J Med 1991; 91:170-172.

342. Roy MC, Herwaldt LA, Embrey R, Kuhns K, Wenzel RP, Perl TM.

Does the NNIS risk index (NRI) predict which patients develop wound

infection (SWI) after cardiothoracic (CT) surgery? 34th Interscience

Conference on Antimicrobials Agents and Chemotherapy 1994; Orlando,

FL, p96.

343. Hecht AD. Creating greater efficiency in ambulatory

surgery. J Clin Anesth 1995; 7:581-584.

344. Lee TB. Surveillance in acute care and nonacute care

settings: current issues and concepts. Am J Infect Control 1997;

25:121-124.

345. Lee JT. Wound infection surveillance. Infect Dis Clin North

Am 1992; 6:643-656.

346. Cardo DM, Falk PS, Mayhall CG. Validation of surgical wound

surveillance. Infect Control Hosp Epidemiol 1993; 14:211-215.

347. Mead PB, Pories SE, Hall P. Decreasing the incidence of

surgical wound infections: validation of a surveillance-notification

program. Arch Surg 1986; 121:458-461.

348. Kerstein M, Flower M, Harkavy LM, Gross PA. Surveillance

for postoperative wound infections: practical aspects. Am Surg 1978;

44:210-214.

349. Poulsen KB, Jepsen OB. Failure to detect a general

reduction of surgical wound infections in Danish hospitals: results

from a representative national sentinel database. Dan Med Bull 1995;

42:485-488.

350. Haley RW, Schaberg DR, McClish DK, Quade D, Crossley KB,

Culver DH, et al. The accuracy of retrospective chart review in

measuring nosocomial infection rates. Am J Epidemiol 1980; 111:516-

533.

351. Mulholland SG, Creed J, Dierauf LA, Bruun JN, Blakemore WS.

Analysis and significance of nosocomial infection rates. Ann Surg

1974; 180:827-830.

352. Wenzel RP, Osterman CA, Hunting KJ, et.al. Hospital

acquired infections. I. Surveillance in a university hospital. Am J

Epidemiol 1976; 103:251-260.

353. Simchen E, Shapiro M, Michel J, Sacks T. Multivariate

analysis of

[[Page 33186]]

determinants of postoperative wound infection: a possible basis for

intervention. Rev Infect Dis 1981; 3:678-682.

354. Collier C, Miller DP, Borst M. Community hospital surgeon-

specific infection rates. Infect Control 1987; 8:249-254.

355. Ehrenkranz NJ, Shultz JM, Richter EI. Recorded criteria as

a ``Gold Standard'' for sensitivity and specificity estimates of

surveillance of nosocomial infection: a novel method to measure job

performance. Infect Control Hosp Epidemiol 1995; 16:697-702.

356. Hirshhorn LR, Currier JS, Platt R. Electronic surveillance

of antibiotic exposure and coded discharge diagnoses as indicators

of postoperative infection and other quality assurance measures.

Infect Control Hosp Epidemiol 1993; 14:21-28.

357. Simchen E, Wax Y, Pevsner B, Erdal M, Michel J, Modan M, et

al. The Israeli Study of Surgical Infections (ISSI): I. Methods for

developing a standardized surveillance system for a multicenter

study of surgical infections. Infect Control Hosp Epidemiol 1988;

9:232-240.

358. Burns SJ, Dippe SE. Postoperative wound infections detected

during hospitalization and after discharge in a community hospital.

Am J Infect Control 1982; 10:60-65.

359. Laxon LB, Blaser MJ, Parkhurst SM. Surveillance for the

detection of nosocomial infections and the potential for nosocomial

outbreaks. Am J Infect Control 1984; 12:318-324.

360. Mertens R, Jans B, Kurz X. A computerized nationwide

network for nosocomial infection surveillance in Belgium. Infect

Control Hosp Epidemiol 1994; 15:171-179.

361. Ehrenkranz NJ. Surgical wound infection occurrence in clean

operations: Risk stratification for interhospital comparisons. Am J

Med 1981; 909-914.

362. Baker C, Luce J, Chenoweth C, Friedman C. Comparison of

case-finding methodologies for endometritis after cesarean section.

Am J Infect Control 1995; 23:27-33.

363. Horan TC, Emori TG. Definitions of key terms used in the

NNIS system. Am J Infect Control 1997; 25:112-116.

364. Polk BF, Shapiro M, Goldstein P, Tager IB, Goren-White B,

Schoenbaum SC. Randomized clinical trial of perioperative cefazolin

in preventing infection after hysterectomy. Lancet 1980; 1:437-441.

365. Salem RJ, Johnson J, Devitt P. Short term metronidazole

therapy contrasted with povidone-iodine spray in the prevention of

wound infection after appendectomy. Br J Surg 1979; 66:430-431.

366. Walsh A, Roberts FJ, Bryce EA. Post-discharge surveillance

of surgical wound infections [letter]. Can J Infect Control 1996;

11:29.

367. Brown RB, Bradley S, Opitz E, Cipriani D, Pieczarka R,

Sands M. Surgical wound infections documented after hospital

discharge. Am J Infect Control 1987; 15:54-58.

368. Rosendorf LL, Octavio J, Estes JP. Effect of methods of

postdischarge wound infection surveillance on reported infection

rates. Am J Infect Control 1983; 11:226-229.

369. Ferraz EM, Ferraz AAB, Coelho HSTD, Viana VP, Sobral SML,

Vasconcelos MDMM, et al. Postdischarge surveillance for nosocomial

wound infection: Does judicious monitoring find cases? Am J Infect

Control 1995; 23:290-294.

370. Andenaes K, Amland PF, Lingaas E, Abyholm F, Samdal F,

Giercksky K. A prospective, randomized surveillance study of

postoperative wound infections after plastic surgery: A study of

incidence and surveillance methods. Plast Reconstr Surg 1995;

96:948-956.

371. Keeling NJ, Morgan MWE. Impatient and post-discharge wound

infections in general surgery. Ann R Coll Surg Engl 1995; 77:245-

247.

372. Manian FA, Meyer L. Adjunctive use of monthly physician

questionnaires for surveillance of surgical site infections after

hospital discharge and in ambulatory surgical patients: report of a

seven-year experience. Am J Infect Control 1997; 25:390-394.

373. Manian FA, Meyer L. Comprehensive surveillance of surgical

wound infections in outpatient and inpatient surgery. Infect Control

Hosp Epidemiol 1990; 11:515-520.

374. Reimer K, Gleed C, Nicolle LE. The impact of postdischarge

infection on surgical wound infection rates. Infect Control 1987;

8:237-240.

375. Sands K, Vineyard G, Platt R. Surgical site infections

occurring after hospital discharge. J Infect Dis 1996; 173:963-970.

376. Weigelt JA, Dryer D, Haley RW. Necessity and efficiency of

wound surveillance after discharge. Arch Surg 1992; 127:77-82.

377. Gravel-Tropper D, Oxley C, Memish Z, Garber GE.

Underestimation of surgical site infection rates in obstetrics and

gynecology. Am J Infect Control 1995; 23:22-26.

378. Taylor S, Pearce P, McKenzie M, Taylor GD. Wound infection

in total joint arthroplasty: Effect of extended wound surveillance

on wound infection rates. Canadian J Surg 1994; 37:217-220.

379. Hulton LJ, Olmsted RN, Treston-Aurand J, Craig CP. Effect

of postdischarge surveillance on rates of infectious complications

after cesarean section. Am J Infect Control 1992; 20:198-201.

380. Law DJW, Mishriki SF, Jeffery PJ. The importance of

surveillance after discharge from hospital in the diagnosis of

postoperative wound infection. Ann R Coll Surg Engl 1990; 72:207-

209.

381. Donovan A, Ellis D, Gatehouse D, Little G, Grimley S,

Armistead S, et al. One-dose antibiotic prophylaxis against wound

infection after appendicectomy: a randomized trial of clindamycin,

cefazolin sodium and a placebo. Br J Surg 1979; 66:193-196.

382. Bates T, Down RHL, Houghton MCV. Topical ampicillin in the

prevention of wound infection after appendicectomy. Br J Surg 1974;

61:489-492.

383. Mendelson M, Solomon R, Shekletski E. Evaluation of blunt

suture needles in preventing percutaneous injuries among health-care

workers during gynecologic surgical procedures. MMWR 1997; 46:25-29.

384. Fanning C, Johnston BL, MacDonald S, LeFort-Jost S,

Dockerty E. Postdischarge surgical site infection surveillance. Can

J Infect Control 1995; 10:75-79.

385. Garibaldi RA, Cushing D, Lerer T. Risk factors for

postoperative infection. Am J Med 1991; 91:158S-163S.

386. Manian FA, Meyer L. Comparison of patient telephone survey

with traditional surveillance and monthly physician questionnaires

in monitoring surgical wound infections. Infect Control Hosp

Epidemiol 1993; 14:216-218.

387. Holbrook KF, Nottebart VF, Hameed SR, Platt R. Automated

postdischarge surveillance for postpartum and neonatal nosocomial

infections. Am J Med 1991; 91:125S-130S.

388. Zoutman D, Pearce P, McKenzie M, Taylor G. Surgical wound

infections occuring in day surgery patients. Am J Infect Control

1990; 18:277-282.

389. Seaman M, Lammers R. Inability of patients to self-diagnose

wound infections. J Emerg Med 1991; 9:215-219.

390. Goulbourne IA, Ruckly CV. Operations for hernia and

varicose veins in a day-bed unit. Br Med J 1979; 2:712-714.

391. Craig CP. Infection surveillance for ambulatory surgery

patients: an overview. Quality Review Bulletin 1983; 9:107-111.

392. Garvey JM, Buffenmeyer C, Rycheck RR, Yee R, McVay J,

Harger JH. Surveillance for postoperative infections in outpatient

gynecologic surgery. Infect Control 1986; 7:54-58.

393. Flanders E, Hinnant JR. Ambulatory surgery postoperative

wound surveillance. Am J Infect Control 1990; 18:336-339.

394. Haines SJ, Walters BC. Antibiotic prophylaxis for

cerebrospinal fluid shunts: a metanalysis. Neurosurgery 1994; 34:87-

93.

395. Langley JM, LeBlanc JC, Drake J, Milner R. Efficacy of

antimicrobial prophylaxis in placement of cerebrospinal fluid

shunts: meta-analysis. Clin Infect Dis 1993; 17:98-103.

396. Starr MB. Prophylactic antibiotics for ophthalmic surgery.

Surv Ophthalmol 1983; 27:353-373.

397. Starr MB, Lally JM. Antimicrobial prophylaxis for

ophthalmic surgery. Surv Ophthalmol 1995; 39:485-501.

398. Gatell JM, Riba J, Lozano L, Mana J, Ramon R, Sanmiguel G.

Prophylactic cefamandole in orthopaedic surgery. J Bone Joint Surg

1984; 66A:1219-1222.

399. Kent KC, Bartek S, Kuntz KM, Anninos E, Skillman JJ.

Prospective study of wound complications in continuous infrainguinal

incisions after lower limb arterial reconstruction: incidence, risk

factors, and cost. Surgery 1996; 119:378-383.

400. Wymenga AB, vanHorn JR, Theeuwes A, Muytjens HL, Slooff

TJJH. Perioperative factors associated with septic arthritis after

arthroplasty: prospective multicenter study of 362 knee and 2,651

hip operations. Acta Orthop Scand 1992; 63:665-671.

401. Stambough JL, Beringer D. Postoperative wound infections

complicating adult spinal surgery. J Spinal Disord 1992; 5:277-285.

402. Tripple SB. Antibiotic-impregnated cement in total joint

arthroplasty. J Bone Joint Surg 1986; 68A:1297-1302.

403. Nungu KS, Olerud C, Rehnberg L, Larsson S, Nordell P,

Allvin I, et al. Prophylaxis with oral cefadroxil versus intravenous

cefuroxime in trochanteric

[[Page 33187]]

fracture surgery: A clinical multicentre study. Arch Orthop Trauma

Surg 1995; 114:303-307.

404. Norden CW. Antibiotic prophylaxis in orthopedic surgery.

Rev Infect Dis 1991; 13:S842-S846.

405. Aznar R, Mateu M, Miro JM, Gatell JM, Gimferrer JM, Aznar

E, et al. Antibiotic prophylaxis in non-cardiac thoracic surgery:

cafazolin versus placebo. Eur J Cardiothorac Surg 1991; 5:515-518.

406. Cant PJ, Smyth S, Smart DO. Antibiotic prophylaxis is

indicated for chest stab wounds requiring closed tube thoracostomy.

Br J Surg 1993; 80:464-466.

407. Pitt HA, Postier RG, MacGowan WAL, Frank LW, Surmak AJ,

Sitzman JV, et al. Prophylactic antibiotics in vascular surgery:

topical, systemic, or both? Ann Surg 1980; 192:356-364.

408. Kaiser AB, Clayson KR, Mulherin JL, Jr., Roach AC, Allen

TR, Edwards WH, et al. Antibiotic prophylaxis in vascular surgery.

Ann Surg 1978; 188:283-289.

409. Bauer T, Vennits B, Holm B, Hahn-Pedersen J, Lysen D,

Galatius H, et al. Antibiotic prophylaxis in acute nonperforated

appendicitis. Ann Surg 1989; 209:307-311.

410. Krukowski ZH, Irwin ST, Denholm S, Matheson NA. Preventing

wound infection after appendicectomy: a review. Br J Surg 1988;

75:1023-1033.

411. Skipper D, Corder AP, Karran SJ. A randomized prospective

study to compare ceftizoxime with cephradine as single dose

prophylaxis in elective cholecystectomy. J Hosp Infect 1991; 17:303-

306.

412. Kaufman Z, Engelberg M, Eliashiv A, Reiss R. Systemic

prophylactic antibiotics in elective biliary surgery. Arch Surg

1984; 119:1002-1004.

413. Grant MD, Jones RC, Wilson SE, Bombeck CT, Flint LM,

Jonasson O, et al. Single dose cephalosporin prophylaxis in high-

risk patients undergoing surgical treatment of the biliary tract.

Surgery, Gynecology & Obstetrics 1992; 174:347-354.

414. Lewis RT, Goodall RG, Marien B, Park M, Lloyd-Smith W,

Wiegand FM. Biliary bacteria, antibiotic use, and wound infection in

surgery of the gallbladder and common bile duct. Arch Surg 1987;

122:44-47.

415. Saltzstein EC, Mercer LC, Peacock JB, Dougherty SH.

Oupatient open cholecystectomy. Surgery, Gynecology & Obstetrics

1992; 174:173-175.

416. Meijer WS, Schmitz PIM, Jeekel J. Meta-analysis of

randomized controlled clinical trails of antibiotic prophylaxis in

biliary tract surgery. Br J Surg 1990; 77:283-290.

417. Kaiser AB, Herrington JL, Jr., Jacobs JK, Mulherin JL, Jr.,

Roach AC, Sawyers JL. Cefoxitin versus erythromycin, neomycin, and

cefazolin in colorectal operations. Ann Surg 1983; 198:525-530.

418. Schoetz DJ, Jr., Roberts PL, Murray JJ, Coller JA,

Veidenheimer MC. Addition of parenteral cefoxitin to regimen of oral

antibiotics for elective colorectal operations. Ann Surg 1990;

212:209-212.

419. Edmondson HT, Rissing JP. Prophylactic antibiotics in colon

surgery. Arch Surg 1983; 118:227-231.

420. Rotman N, Hay JM, Lacaine F, Fagniez PL, The Association de

Recherche en Chirurgie Cooperative Group. Prophylactic

antibiotherapy in abdominal surgery: first- vs. third-generation

cephalosporins. Arch Surg 1989; 124:323-327.

421. Lewis RT, Allan CM, Goodall RG, Marien B, Park M, Lloyd-

Smith W, et al. Cefamandole in gastroduodenal surgery: a controlled,

prospective, randomized, double-blind study. Can J Surg 1982;

25:561-563.

422. McArdle CS, Morran CG, Anderson JR, Pettit L, Gemmell CG,

Sleigh JD, et al. Oral ciprofloxacin as prophylaxis in

gastroduodenal surgery. J Hosp Infect 1995; 30:211-216.

423. Grandis JR, Vickers RM, Rihs JD, Yu VL, Johnson JT.

Efficacy of topical amoxicillin plus clavulanate/ticarcillin plus

clavulanate and clindamycin in contaminated head and neck surgery:

effect of antibiotic spectra and duration of therapy. J Infect Dis

1994; 170:729-732.

424. Johnson JT, Yu VL, Myers EN, Wagner RL. An assessment of

the need for gram-negative bacterial coverage in antibiotic

prophylaxis for oncological head and neck surgery. J Infect Dis

1987; 155:331-333.

425. Elledege ES, Whiddon RG, Jr., Fraker JT, Stambaugh KI. The

effects of topical oral clindamycin antibiotic rinses on the

bacterial content of salvia on healthy human subjects. Otolaryngol

Head Neck Surg 1991; 105:836-839.

426. Johnson JT, Yu VL, Myers EN, Wagner RL, Sigler BA.

Cefazolin vs. moxalactam? Arch Otolaryngol Head Neck Surg 1986;

112:151-153.

427. Jones RC, Thal ER, Johnson NA, Gollohar LN. Evaluation of

antibiotic therapy following penetrating abdominal trauma. Ann Surg

1985; 201:576-585.

428. Nichols RL. Empiric antibiotic therapy for intraabdominal

infections. Rev Infect Dis 1983; 5:S90

BILLING CODE 4163-18-P

[[Page 33188]]

[GRAPHIC] [TIFF OMITTED] TN17JN98.001

BILLING CODE 4163-18-C

[[Page 33189]]

Table 1.--Criteria for Defining Surgical Site Infection (SSI).\16\

------------------------------------------------------------------------

-------------------------------------------------------------------------

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 is deliberately opened by surgeon, unless

incision is culture-negative.

4. Diagnosis of superficial incisional SSI by the surgeon or

attending physician.

Do not report the following conditions as SSI:

1. Stitch abscess (minimal inflammation and discharge confined to

the points of suture penetration).

2. Infection of an episiotomy or newborn circumcision site.3

3. Infected burn wound.3

4. Incisional SSI that extends into the fascial and muscle layers

(see deep incisional SSI).

------------------------------------------------------------------------

DEEP INCISIONAL SSI

------------------------------------------------------------------------

Infection occurs within 30 days after the operation if no implant 4 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., fascial 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 (>38 deg.C), 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.

Notes:

1. Report infection that involves both superficial and deep incision

sites as deep incisional SSI.

2. Report an organ/space SSI that drains through the incision as a

deep incisional SSI.

------------------------------------------------------------------------

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, that was opened or manipulated during the

operative procedure and at least one of the following:

1. Purulent drainage from a drain that is placed through a stab

wound 5 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.

------------------------------------------------------------------------

3 Specific criteria are used for infected episiotomy and circumcision

sites and burn wounds.

4 NNIS definition--A nonhuman-derived implantable foreign body (e.g.,

prosthetic heart valve, nonhuman vascular graft, mechanical heart, or

hip prosthesis) that is permanently placed in a patient during

surgery.

5 If the area around a stab wound becomes infected, it is not an SSI1.

It is considered a skin or soft tissue infection, depending on its

depth.

Table 2.--Specific Sites of Organ/Space Surgical Site Infection \16\

------------------------------------------------------------------------

-------------------------------------------------------------------------

Arterial or venous infection

Breast abscess or mastitis

Disc space

Ear, mastoid

Endocarditis

Endometritis

Eye, other than conjunctivitis

Gastrointestinal tract

Intraabdominal, not specified elsewhere

Intracranial, brain abscess or dura

Joint or bursa

Mediastinitis

Meningitis or ventriculitis

Myocarditis or pericarditis

Oral cavity (mouth, tongue, or gums)

Osteomyelitis

Other infections of the lower respiratory tract (e.g., abscess or

empyema)

Other male or female reproductive tract

Sinusitis

Spinal abscess without meningitis

Upper respiratory tract, pharyngitis

Vaginal cuff

------------------------------------------------------------------------

Table 3.--Distribution of Pathogens Isolated * From Surgical Site

Infections, National Nosocomial Infections Surveillance System, 1986-

1996.\6\ \18\ \19\

------------------------------------------------------------------------

Percent of isolates

----------------------------------------

1986-1989 1990-1996

------------------------------------------------------------------------

Pathogen....................... (N=16,727) (N=17,671)

Staphylococcus aureus.......... 17 20

Coagulase-negative 12 14

staphylococci.

Escherichia coli............... 10 8

Enterococcus spp............... 8 12

[[Page 33190]]

Pseudomonas aeruginosa......... 8 8

Enterobacter spp............... 8 7

Proteus mirabilis.............. 4 3

Klebsiella pneumoniae.......... 3 3

Other Streptococcus spp........ 3 3

Candida albicans............... 2 3

Group D streptococci........... ................... 2

Other gram-positive aerobes.... ......

This text is long and has been trimmed here. Open the source document for the complete record.