Antibacterial Prophylaxis in Dermatologic Surgery

Antibacterial Prophylaxis in Dermatologic SurgeryAn Evidence-Based Review

Helena Rosengren and Anthony Dixon

Skin Cancer Department, Bond University, Belmont, Victoria, Australia

Contents

Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35

1. Characteristics of Surgical Site Infections (SSIs) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

1.1 Incidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

1.2 Wound Classification . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36

1.3 Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

1.4 Pathogens Involved . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

1.5 Medical Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37

1.6 Surgical Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2. Outcome of the Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.1 Aims of the Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.2 SSI Prophylactic Agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.2.1 Dressings and Topical Agents Containing Silver for Treatment and Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.2.2 Honey for Treatment and Prevention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2.2.3 Oral Antibacterial Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

2.2.4 Topical Antibacterial Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39

2.2.5 Use of Prophylactic Mupirocin Ointment in Staphylococcus aureus Nasal Carriers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

2.2.6 Intraincisional Antibacterial Prophylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

2.2.7 Prophylaxis of Bacterial Endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40

2.2.8 Prophylaxis of Prosthesis Infection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

3. Conclusion and Recommendations. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41

Abstract Clean, non-contaminated skin surgery is associated with low rates of surgical site infection (SSI), bacterial

endocarditis, and joint prosthesis infection. Hence, antibacterial prophylaxis, which may be associated with

adverse effects, the emergence ofmultidrug-resistant pathogens, and anaphylaxis, is generally not recommended

in dermatologic surgery. Some body sites and surgical reconstructive procedures are associated with higher

infection rates, and guidelines for SSI antibacterial prophylaxis have been proposed for these cases. Large

prospective, controlled trials are needed to ascertain the role of oral SSI prophylaxis for these surgical sites and

procedures especially in patients with diabetes mellitus who are intrinsically at greater risk of SSI. Topical

antibacterial ointment and sterile paraffin appear to make no difference to healing or the incidence of SSIs in

clean wounds. Although further research is needed, preliminary studies have shown that intraincisional anti-

bacterials, which may be associated with fewer adverse effects and a lower risk of multidrug-resistant bacteria,

could potentially be helpful for SSI prophylaxis. Trials using honey- and silver-impregnated dressings have

found no advantage in the healing of chronic wounds. However, several case studies, which need corroboration

in larger studies, suggest that these dressings may be helpful in preventing and treating SSIs.

Bacterial endocarditis and joint prosthesis infection prophylaxis are not routinely recommended

in cutaneous surgery. The updated 2007 American Heart Association guidelines now advocate bacterial

REVIEWARTICLEAm J Clin Dermatol 2010; 11 (1): 35-44

1175-0561/10/0001-0035/$49.95/0

ª 2010 Adis Data Information BV. All rights reserved.

endocarditis prophylaxis for high-risk cardiac patients having surgery involving the oral mucosa or infected

skin. The latest American Dental Association/American Academy of Orthopaedic Surgery guidelines re-

commend considering antibacterial prophylaxis for oral procedures where bleeding is anticipated and for

surgery involving acute orofacial skin infections if the patient has had a total joint replacement within 2 years

or is in a high-risk group and has had a joint replacement at any time.

The incidence of surgical site infection (SSI), bacterial

endocarditis, and joint prosthesis infection in clean, non-

contaminated dermatologic surgery is very low.[1-4] Indiscrimi-

nate use of antibacterials is causingmultidrug-resistant bacteria

to emerge. Furthermore, antibacterials can cause anaphylactic

reactions and even death in rare cases. There are also known

interactions between several medications taken long term for

underlying health problems and antibacterials.[5] Therefore,

routine use of prophylactic antibacterials in cutaneous surgery

is generally contraindicated.[1-4] Despite this, medical practi-

tioners vary greatly in their use of antibacterial prophylaxis and

frequently overprescribe antibacterials for the prevention of

SSI, bacterial endocarditis, and prosthesis infection.[6-9]

Though the overall risk of SSI in dermatologic surgery is

low, studies have shown that some dermatologic surgical sites

and reconstructive procedures are associated with infection

rates thatmay be unacceptably high. This article discusses those

studies and considers the use of antibacterial prophylaxis for

higher risk dermatologic sites and surgical procedures.

The real risk of bacterial endocarditis and joint prosthesis

infection following dermatologic surgery is unknown as no

large prospective trials have ever been done to measure this.

Bacterial endocarditis or prosthesis infection may occur as a

result of bacteremia (bacteria entering the vascular space)

during surgery or from a distant site of active infection.[1-3]

Bacteremia during surgery on clean intact skin is <2%, even

for complex and prolonged dermatologic surgery.[10] This is

slightly lower than that found in healthy individuals without

infection living normally. The risk of bacterial endocarditis

and prosthesis infection from bacteremia at the time of skin

surgery is therefore thought to be very low. However, the risk

of bacteremia is far greater for surgery breaching the oral

mucosa. This is reflected in the most recent guidelines from

the American Heart Association (AHA)[11] and the American

Dental Association/American Academy of Orthopaedic Sur-

gery (ADA/AAOS).[12]

A surgical site skin infection can serve as a bacterial source

for infective endocarditis or hematogenous total joint infec-

tion.[13-17] Therefore, it is prudent to manage all dermatologic

wound infections aggressively in high-risk patients, not only to

treat the infected site but also to provide prophylaxis against

infective endocarditis or joint prosthesis infection. This is

taken into account in the latest AHA[11] and ADA/AAOS[12]

guidelines.

1. Characteristics of Surgical Site Infections (SSIs)

1.1 Incidence

Overall, rates of wound infection in cutaneous surgery are

generally very low in clean wounds, with 1–3% quoted in most

studies.[18-22] A well designed study in subtropical Australia

found infection rates as high as 8.6%,[23] which calls into

question the role of humidity and ambient temperature in

postoperative dermatologic infection. Even following Mohs

surgery, where wounds are left open for prolonged periods

awaiting histologic confirmation of tumor clearance, the infec-

tion rate is low.[2,20,24] The infection rate in wounds left to heal

by secondary intention is <1% for most body sites,[25,26] though

one study found infection rates as high as 5% for wounds on the

ear that were left to heal by secondary intention.[10]

A study involving 5091 skin surgery cases with an overall

infection rate of 1.47% found SSI rates >5% below the knee

(6.92%), in the groin area (10%), for wedge excisions of the lip

and ear (8.57%), and for grafts (8.7%).[18] Other studies have

confirmed higher infection rates below the knee,[27] in the groin,[22]

and on the thighs, legs, and feet.[28] Additional body sites iden-

tified as at high risk for infection are the nose,[20,29] ear,[20,29]

and axilla.[30] A study of 3491 patients with an overall infection

rate of 1.9% found higher rates of SSI for surgical closure in-

volving a reconstructive procedure (4.3%).[19] Another study

has confirmed higher infection rates for flaps and grafts.[29]

1.2 Wound Classification

Wounds can be classified (class I–IV) according to the site

and status of the wound preoperatively (table I). This classifi-

cation, based on the 1985 Centers for Disease Control (CDC)

guidelines for prevention of surgical wound infections,[32] has

been found to be a strong predictor of subsequent infection

rates.[33,34]

36 Rosengren & Dixon

ª 2010 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2010; 11 (1)

The need for prophylactic antibacterials depends on the

wound classification.[1,3,6,20,33,34] Class I wounds (primary clo-

sure of wounds on clean, non-contaminated skin under sterile

conditions) should generally not receive antibacterial prophy-

laxis. Only immunocompromised patients with class II wounds

(involving oral and nasal mucosa or the axillary and anogenital

areas) should receive antibacterial prophylaxis. All class III and

IV wounds (inflamed or infected wounds or where there has

been a major break in sterile surgical technique) should receive

therapeutic antibacterials.

1.3 Clinical Features

The 1992 CDC definitions of nosocomial infections give

clear guidelines for diagnosing SSI.[31] Though there is no va-

lidated, gold standard definition for surgical wound infection,

these guidelines, which were based on the 1988 CDC defini-

tions,[35] have been widely adopted in the US, Europe and

Australia.[36,37] Superficial surgical site skin infection can be

diagnosed if it involves skin, subcutaneous tissues, or muscle

above the fascial layer at the incision site, it occurs within

30 days of surgery, and at least one of the following is present:

� Purulent discharge from the incisional wound.

� Organisms are isolated on culture of aseptically obtained

wound fluid or tissue.

� One or more of the following is present: pain, tenderness,

localized swelling, redness, heat.

� The surgeon deliberately reopens the wound (unless culture

of the incision is negative).

� The treating doctor diagnoses a superficial incisional SSI.

In a literature review of 90 prospective studies from 20 dif-

ferent countries on wound infection, Bruce et al.[36] found that

evenwith the use of guidelines, the definition of wound infection

is subject to considerable inter- and intra-observer variation.

1.4 Pathogens Involved

The most frequent source of microbial contamination of

surgical skin wounds is from endogenous cutaneous ormucosal

flora.[1,4] Staphylococcus aureus and Streptococcus pyogenes are

the most common pathogens causing wound infection in kera-

tinized skin (table II).[20,33,38] Other microorganisms causing

SSI include coagulase-negative staphylococci, Enterococcus

spp., Pseudomonas aeruginosa, and Enterobacter spp.[39]

S. viridans is commonly found in the oral cavity.[34] Other

pathogens commonly involving mucosal sites include S. aureus

and S. pyogenes.[20,33,38] S. aureus, enterococci, and Escherichia

coli are the pathogens that most frequently cause perineal SSIs.[34]

Many different bacteria have been encountered in cases of

endocarditis, but streptococcal and staphylococcal bacteria

account for 80–90% of the cases.[34] Joint prosthesis infections

are predominantly caused by S. aureus and S. epidermidis.[1]

1.5 Medical Risk Factors

Evidence suggests that poor nutritional status is a risk factor

for postoperative wound infection.[40,41] Obesity may also be an

independent risk factor for SSI.[42] A prospective study invol-

ving >5000 wounds showed no increased risk of infection fol-

lowing cutaneous surgery for patients taking warfarin and

aspirin, or for smokers.[18] More recently, a 5-year observa-

tional study involving 439 smokers (having 646 skin excisions)

and 3759 nonsmokers (having 6578 skin excisions) found no

increased risk of infection, postoperative bleeding, or wound

dehiscience in smokers.[43]

SSI rates have been found to be higher in those with diabetes

mellitus.[28] A recent large, prospective trial compared out-

comes in 196 known diabetic patients having 551 procedures

with 4001 people without diabetes.[44] Diabetes was confirmed

as an independent risk factor for infection. The earlier smaller

Table I. Wound classification based on 1985 Centers for Disease Control

classification of wounds[31,32]

Class Skin condition Body location/surgicaltechnique

Antibacterial

recommendations

I Clean Sterile procedure No prophylaxis

II Clean

contaminated

Oral cavity, nasal

mucosa, perineum, axilla;

sterile procedure

Prophylaxis only if

immunocompromised

III Contaminated Traumatic wounds,

non-purulent

inflammation;

non-sterile procedure

Therapeutic

antibacterials

IV Infected Gross contamination,

devitalized tissue, foreign

body contamination

Therapeutic

antibacterials

Table II. Common bacterial pathogens in surgical site infections

Infective site Infective microorganisms

Oral cavity and nasal

mucosa

Streptococcus viridans, Staphylococcus aureus,

Streptococcus pyogenes

Perineum S. aureus, Enterococcus spp., Escherichia coli

Skin elsewhere S. aureus, S. pyogenes

Heart valves Streptococcal and staphylococcal spp.

Joint prosthesis S. aureus, S. epidermidis

Antibacterial Prophylaxis in Dermatologic Surgery 37


study by Dixon et al.,[18] which did not show this correlation,

was not multivariate in analysis.

1.6 Surgical Risk Factors

Potential sources of microbial contamination of the surgical

wound include the patient’s skin, flora of the skin and nares of

the operating team, the surgical apparel, the surgeons’ gloves,

and airborne organisms in the operating theater.[1] Paying

careful attention to aseptic technique, including preoperative

hand washing practice, procedures for sterilizing instruments,

and wound preparation, as well as using hats, gloves, and

masks, and reducing traffic in the operating theater, are all

recognized to be important in combating SSIs.[1,37] Little re-

search has been done in this area, though it has been shown that

using correct hand washing technique for at least 2 minutes

prior to surgery significantly lowers the microbial count.[37]

A recent study, in which data were collected by interviewing

hospital theater nurses, has shown that existing guidelines and

recommendations for preventing SSIs in operating theaters can

frequently be overlooked.[45] However, research shows that

simply implementing active surveillance in hospital operating

theaters is an effective strategy for reducing SSIs.[46]

A Cochrane review on preoperative hair removal found that

shaving is associated with statistically significantly more SSIs

than both clipping (three trials, 3139 patients) and the use of

depilatory creams (seven trials, 1213 patients).[47] There was no

significant statistical difference in infection rates when com-

paring shaving with not removing the hair at all. Furthermore,

shaving the day before surgery compared with on the day of

surgery made no statistically significant difference to the risk of

SSI. Though the studies included in this Cochrane review in-

volved many types of surgery at different anatomic sites, given

the consistency of the findings, the results may also be relevant

to SSI prevention in dermatologic surgery.

Studies confirm that surgical wound infection rate is higher

for more complex reconstructive techniques than for simple

surgery.[18,19,29,48] Dixon et al.[18] showed an infection rate

of 0.54% for simple excisions, 2.94% for flaps, and 8.7%for grafts in 5091 dermatologic surgical procedures. Rogues

et al.[19] showed an infection rate of 1.6% for simple excisions

and 4.3% for reconstructive procedures (90.2% of which were

skin flaps) in 3491 surgical skin procedures. Another study

measuring wound infection in 464 facial skin excisions found

that complex surgical procedures had a significantly greater

infection rate than simple excisions regardless of the facial

site.[29] Given the higher infection rate for more complex skin

surgery, simple reconstruction is preferable wherever possible.

No study has compared the SSI rate with surgical technique

in skin flap surgery, but poor flap reconstruction design

may influence infection rate. Therefore, it is prudent to avoid

excessive tissue injury and high-tension closures while ensuring

adequate blood supply to the flap during skin surgery.

Studies have established the need for satisfactory control of

hemostasis to help prevent SSI. Two prospective multivariate

analyses, one with 3788 surgical skin procedures and the other

with 3491, have shown that hemorrhagic complications in both

simple and complex dermatologic surgical procedures are an

independent risk factor for SSI.[19,48]

2. Outcome of the Review

2.1 Aims of the Review

The purpose of this article is to review the literature and

current guidelines for prophylaxis of SSI, bacterial endocar-

ditis, and infection of prostheses.

2.2 SSI Prophylactic Agents

2.2.1 Dressings and Topical Agents Containing Silver for

Treatment and Prevention

Although silver has been recognized for centuries to have

antimicrobial properties, its use in wound care is relatively re-

cent.[49] A Cochrane review found no statistically significant

difference with the use of silver dressings in chronic wounds

and the authors concluded that there was insufficient evidence

to recommend the use of silver-containing dressings or topi-

cal agents for treating infected or contaminated chronic

wounds.[50] Though there is some evidence that silver dressings

help prevent infection in acute wounds, further trials are needed

to support their widespread clinical use.[51] A recent prospective,

randomized controlled study involving routine infra-inguinal

revascularization leg incisions found that the use of a silver

dressing (Acticoat�; Smith & Nephew Healthcare Limited,

London, UK) immediately following surgery was associated

with significantly fewer complications than the use of a con-

ventional dressing (p < 0.02).[52]

2.2.2 Honey for Treatment and Prevention

Honey, which has been used for millennia in wound healing,

has recently become popular as an antimicrobial agent.[53]

Case reports have found honey-impregnated dressings to be

helpful even for methicillin-resistant S. aureus-infected chronic

wounds.[54,55] A study involving 368 chronic venous ulcers



randomly assigned to application of either manuka honey-

impregnated dressings or non-honey dressings found no

difference in the healing rate over a 12-week study period.[56] In

clean, non-complicated surgical wounds, the role of topical

honey as prophylaxis against SSI has not been properly as-

sessed in a randomized controlled trial.

2.2.3 Oral Antibacterial Prophylaxis

Recent prospective studies categorizing wound infections

according to body site and surgical technique have identified

patients who may be at higher risk of infection following der-

matologic surgery.[10,18,20,22,27-29,57] Taking the evidence from

these studies into account, we suggest the administration of

prophylactic antibacterials for certain anatomical sites and

surgical procedures (table III). However, there are no published

large, randomized controlled trials measuring the effectiveness

of prophylactic oral antibacterials.

One study, with an overall infection rate of 1.47%, involved

5091 surgical skin excisions in 2424 patients, none of whom

received prophylactic antibacterials.[18] Surgical procedures

with an infection rate >5% were skin grafts (8.7%), and wedge

excisions on the ear or lip (8.57%). Anatomic sites with a sig-

nificantly higher infection rate were all areas below the knee

(6.92%), and the groin (10%). A study of 857 skin procedures in

tropical north Queensland, Australia, with an overall infection

rate of 8.7%, found location on lower extremities to be an in-

dependent risk factor for wound infection.[28] The infection

rates in this study were 14% on the thighs and 15% on the legs

and feet. Other studies have found higher infection rates below

the knee,[27,58] and in the groin.[22]

Another prospective study measured infection rates for

surgery on the face in 464 surgical procedures.[29] With an

overall infection rate of 1.5%, a significantly higher SSI rate was

found in auricular (5%) and nasal areas (6.5%). Furthermore,

complex surgery for skin cancers on the nose and ear had a

3-fold greater infection rate than complex surgery elsewhere on

the face, which suggests that intrinsic factors may make these

surgical sites more susceptible to infection. Other studies have

identified the nose[57] and ear[10,20] as high-risk sites for surgical

wound infection.

Prophylactic antibacterials will be most effective if present at

the surgical site at the time of incision and should, therefore, be

administered prior to the procedure.[59-61] Bacteria introduced

during the surgical procedure reside and multiply in the wound

coagulum. Since it is difficult for antibacterials to gain access to

the coagulum, multiplying bacteria remain relatively protected

there unless antibacterials are present prior to its formation.[3]

Antibacterial prophylaxis, whether oral or intravenous, should be

administered 30–60 minutes prior to dermatologic surgery.[1,2]

There have been no large-scale, prospective trials comparing

different prophylactic antibacterial regimens. However, based

on the organisms most likely to cause infection, the penicilli-

nase-resistant penicillins or first-generation cephalosporins are

generally the oral antibacterials of choice for SSI prophylaxis

(table IV).[1,2,4] Wright et al.[2] recommended either cefalexin 2 g

or dicloxacillin 2 g administered orally 30–60 minutes before

the surgical procedure for most dermatologic surgery. Given

the resident bacteria, amoxicillin 2 g is the oral antibacterial

of choice for procedures breaching the oral[1,2] or nasal[2]

mucosa. In penicillin-allergic patients, regardless of whether the

oral or nasal mucosa is breached, clindamycin 600mg, azithro-

mycin 500mg or clarithromycin 500mg should be given orally

30–60 minutes preoperatively.[2] For patients unable to take

medication orally, cefazolin or ceftriaxone 1 g can be given

intramuscularly or intravenously. For penicillin-allergic patients,

clindamycin 600mg intramuscularly or intravenously is

advocated.[2]

2.2.4 Topical Antibacterial Prophylaxis

There is evidence that postoperative, moist, occlusive wound

dressings may help to prevent infections,[62-64] as well as result

in more rapid wound healing.[62] With evidence that short-term

wound dressings make no difference to wound infection

rates,[23,65] the benefits of a dressing may be associated with

leaving it intact for longer periods.[66,67] More recently, a review

Table III. Anatomic sites and surgical procedures associated with higher

infection rates where prophylactic antibacterials may be helpful

Below the knee

Groin

Skin grafts at any site

Wedge excision on the ear and lip

Flap surgery on the nose and ear

Table IV. Recommended antibacterials for prevention of surgical site infec-

tions in dermatologic surgery, to be given 30–60 minutes prior to surgery

Surgical site Antibacterial

restrictions

Antibacterial Oral dose

Keratinized skin Nil Cefalexin

Dicloxacillin

2 g

2 g

Oral mucosa Nil Amoxicillin 2 g

Any (including oral) Penicillin

allergy

Clindamycin

Azithromycin

Clarithromycin

600mg

500mg

500mg



of 14 studies looking at the evidence relating to moist wound

healing and its influence on infection rates found no statistically

significant evidence that occlusive dressings reduced sub-

sequent SSI.[68]

Some clinicians advocate the use of antibacterial ointments

on wounds after closure.[69-71] It has also been suggested that

ointment that does not contain antibacterials may be equally

effective in preventing infection.[33] A randomized controlled

trial involving 1249 wounds in 922 patients compared bacitra-

cin (antibacterial) and petrolatum (non-antibacterial) ointment

under occlusive wound dressings and found no statistically

significant difference in healing time or infection rates in the

two groups.[27] Even below the knee, where wound infection rates

were greatest, the antibacterial ointment had no benefit over

petrolatum ointment. On the basis of these results, the authors

postulated that it was the ointment rather than the presence of a

topical antibacterial that was beneficial in wound healing.

Campbell et al.[10] also found no statistically significant

difference in wound infection rates when using antibacterial or

non-antibacterial ointments. The 147 auricular wounds left to

heal by secondary intent were randomized to either gentamicin

or petrolatum ointment. Of the 12 (8.33%) patients who de-

veloped inflammatory chondritis, ten had been in the genta-

micin intervention group, which led the authors to conclude

that petrolatum may be less irritating than gentamicin.

A large, prospective, controlled trial randomized 1801 sur-

gical skin wounds to no ointment, paraffin (non-antibacterial)

ointment, ormupirocin (antibacterial) ointment prior to the use

of an occlusive dressing.[72] Wounds were assessed at suture

removal and again at 6–9 months following surgery. There was

no statistical difference in infection rates between the three

groups (1.4%with no ointment, 1.6% for paraffin, and 2.3% for

mupirocin). Furthermore, there was no statistical difference in

healing time, wound discomfort, aesthetic outcome, pain level,

or patient satisfaction between the groups, though the incidence

of wound edge necrosis was higher with mupirocin.[72] In ad-

dition, allergic contact dermatitis is a rare but well documented

adverse effect of topical antibacterials.[73] In light of these find-

ings, antibacterial ointment is not indicated for clean surgical

wounds.

A recent, prospective, controlled trial taking place in north

Queensland, Australia, involving 973 wounds measured the

effect of a single prophylactic application of topical chlor-

amphenicol following ‘high risk sutured wounds after minor

surgery’.[74] More patients developed wound infection in the

paraffin ointment control group (11%) than the treatment

group (6.6%). The authors concluded that, though statistically

significant, this result was not clinically relevant.

2.2.5 Use of Prophylactic Mupirocin Ointment in Staphylococcus

aureus Nasal Carriers

Nasal carriage of S. aureus is a significant risk factor for

developing infection following surgery.[75] Compared with non-

carriers, S. aureus carriers are 2–9 times more likely to acquire

SSIs.[76-78] A recent Cochrane review of pooled studies com-

paring mupirocin with placebo or with no treatment found

statistically fewer S. aureus infections after the use of intranasal

mupirocin.[79] These studies looked at several types of infection

including bacteremia and various SSIs. It remains to be shown

in randomized, placebo-controlled trials whether eradication of

S. aureus nasal carriage has any effect in dermatologic surgery.

2.2.6 Intraincisional Antibacterial Prophylaxis

It has been shown that intraincisional antibacterials can help

prevent postoperative infection.[80,81] Huether et al.[80] found

lower infection rates (0.7%) in delayed closure Mohs proce-

dures when intraincisional clindamycin, administered with the

local anesthetic, was used compared with infection rates in

control patients who received anesthetic alone (2.4%). With the

intraincisional antibacterial use, common gastrointestinal ad-

verse effects associated with the oral route are not encountered.

It may also be that systemic antibacterial absorption is mini-

mized with the intraincisional route, which would result in less

antimicrobial resistance than with the oral route. Though no

published data have confirmed an increased risk of topical

contact dermatitis with the use of intraincisional antibacterials,

this is a potential problem. Further prospective randomized

studies using intraincisional antibacterials for prophylaxis in

appropriate patients are needed to help determine the effec-

tiveness and risks of this route of administration.

2.2.7 Prophylaxis of Bacterial Endocarditis

Studies have shown that skin surgery is an insignificant risk

for endocarditis and hence prophylaxis is generally not re-

commended.[1,3,82] Though the incidence of bacteremia fol-

lowing dermatologic surgery is low, there have been reported

cases of bacterial endocarditis even without evidence of cuta-

neous infection.[83] However, most reported cases of bacterial

endocarditis are not associated with surgery or invasive pro-

cedures.[84,85] Furthermore, infective endocarditis can occur

despite prophylaxis, with approximately one-third of cases

being caused by bacteria that may not be sensitive to re-

commended antibacterial regimens.[34]

In 1997, the AHA guidelines for the prevention of bacterial

endocarditis recommended that even for high-risk patients,

endocarditis prophylaxis was not necessary for ‘‘incision or



biopsy of surgically scrubbed skin.’’[84] This rather limited de-

scription of dermatologic surgery did not address specific sur-

gical circumstances such as prolonged procedures and instances

where mucosal surfaces are breached.

The latest 2007 AHA guidelines address these gaps and now

recommend the use of endocarditis prophylactic antibacterials

in high-risk patients having dermatologic surgery involving the

oral mucosa or infected skin.[11] Endocarditis antibacterial

prophylaxis in high-risk patients undergoing Mohs surgery is

not warranted unless it involves the oral mucosa or infected

skin. The 2007 AHA guidelines has seen the definition of high-

risk bacterial endocarditis patients limited to those with pre-

vious endocarditis, prosthetic heart valves, congenital heart

disease, and transplanted hearts that develop valvulopathy.[11]

TheAHA recommends that high-risk patients should receive

an antibacterial that is active against the organisms most likely

to cause the bacterial endocarditis that colonize the surgical

site.[11,84] For keratinized skin the most likely pathogens are

S. aureus and b-hemolytic streptococcus, and coverage with a

penicillin or cephalosporin is recommended. Vancomycin or

clindamycin can also be given to high-risk individuals having

surgery involving infected skin. For the oral mucosa, where the

antibacterial must prevent S. viridans endocarditis, amoxicillin

2 g is the antibacterial of choice. For those with penicillin

allergy, the AHA is now recommending azithromycin, clin-

damycin, or clarithromycin, which are associated with less

gastrointestinal upset, in place of erythromycin for mucosal

surgery endocarditis prophylaxis. It is recommended by the

AHA that oral antibacterials given for endocarditis prophy-

laxis are taken 30 minutes to 1 hour prior to surgery.[11]

2.2.8 Prophylaxis of Prosthesis Infection

There is little research work published on prophylaxis of

prosthetic infection. Most of what is published relates to dental

and urologic procedures rather than dermatologic surgery.[1]

The ADA/AAOS published results following a detailed lit-

erature review in 1997 and concluded that antibacterial joint

prosthesis prophylaxis was not warranted for most dental

procedures.[86] However, the 2003 ADA/AAOS advisory

statement does recommend considering antibacterial prophy-

laxis for identified patient groups at high risk of hematogenous

total joint infection for oral procedures where bleeding is an-

ticipated, and for acute orofacial infection.[12]

High-risk patients include those who have had a total joint

replacement within the preceding 2 years, those who have had

previous prosthetic joint infections and patients with certain co-

morbidities who have had a total joint replacement at any time.

The high-risk co-morbidities include insulin-dependent (type 1)

diabetes, malignancy, immunosuppression, HIV, malnourish-

ment, and hemophilia. For these patients, antibacterial pro-

phylaxis should be considered for any procedure breaching the

mucosa, including a lip wedge resection.

The administration of a mucosal anesthetic is considered a

lower risk bacteremic procedure[12] and it might be advisable

for the cutaneous surgeon to consider antibacterial prosthetic

prophylaxis in high-risk patients when administering a nerve

block administered by the intraoral route.

It is recognized by the ADA/AAOS that bacteremias asso-

ciated with acute infections can cause late prosthetic implant

infections,[12] and this has been emphasized by other au-

thors.[2,13,14] It may therefore be prudent to consider aggressive

treatment of any skin infection in high-risk patients, not only to

give symptomatic relief but also to help prevent whole joint

prosthesis infection.

The recommended prophylactic antibacterial regimen is

cefalexin, cefradine, or amoxicillin 2 g orally 1 hour prior to the

procedure.[12] For patients with penicillin allergy, clindamycin

600mg is advocated 1 hour prior to surgery.[12]

Antibacterial prophylaxis is not indicated for patients with

pins, plates, or screws.[12]

3. Conclusion and Recommendations

Antibacterial prophylaxis for SSI is generally not re-

commended for clean surgical wounds, which are usually as-

sociated with low infection rates. Certain body areas (such as

below the knee and the groin) and constructive surgical pro-

cedures (such as wedge resections on the ear or lip, flaps on the

nose or ear, and grafts anywhere) are associated with higher

infection rates and may warrant the use of prophylactic anti-

bacterials. This may be especially true for diabetic patients who

are known to be at higher risk of SSI anyway. However, in-

discriminate use of antibacterials may be associated with ad-

verse effects, anaphylactic reactions, and the emergence of

multidrug-resistant organisms. Prospective controlled trials

using prophylactic oral antibacterials for prevention of wound

infection for high-risk surgical sites and high-risk constructive

surgery are needed.

There is insufficient evidence with regard to the effectiveness

of intraincisional prophylactic antibacterials. Administration

by this route may give fewer adverse effects and produce less

antibacterial resistance, and as such further research in this area

is warranted. Most studies show that topical antibacterial

ointment and sterile paraffin ointment do not prevent SSIs in

clean dermatologic surgery. Evidence shows that honey- and



silver-impregnated dressings make no difference in chronic

wounds. Further research is needed to establish the role of these

dressings in the prevention of acute SSI after skin surgery.

Bacterial endocarditis prophylaxis is recommended in the

revised 2007 AHA guidelines in high-risk patients having der-

matologic surgery involving the oral mucosa or infected

skin.[11] The 2003 ADA/AAOS statement advises consideration

of joint prosthesis infection prophylaxis in specified high-risk

groups with an acute orofacial infection or undergoing surgery

breaching the oralmucosa.[12] In high-risk patients with awhole

joint prosthesis, it may be prudent to consider aggressive

treatment of any skin infection not only to give symptomatic

relief but also to help prevent whole joint infection as a con-

sequence of bacteremia.

In addition, antibacterial prophylaxis may be warranted for

high-risk cardiac and whole joint prosthesis patients under-

going dermatologic surgery associated with higher rates of

infection (below the knee, in the groin, flaps on the ear and

nose, wedge excisions or grafts). This would not only give

prophylaxis against an SSI but would also provide prophylaxis

against bacterial endocarditis or prosthesis infection. This

recommendation is not in current guidelines.

Acknowledgments

No sources of funding were used to assist in the preparation of this

review. The authors have no potential conflicts of interest that are directly

relevant to the contents of this review.

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Correspondence: Dr Helena Rosengren, Skin Cancer Research Group, School

of Public Health, TropicalMedicine and Rehabilitation Sciences, James Cook

University, 101 Angus Smith Drive, Townsville, QLD 4811, Australia.

E-mail: [email protected]



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Antibacterial Prophylaxis in Dermatologic Surgery