Surgical Site Infections in Breast Surgery – A Primer for Plastic Surgeons

Surgical site infections (SSIs) are one of the most common complications of breast surgery. The United States Centers for Disease Control and Prevention has developed criteria that define SSI as infection related to an operative procedure that occurs at or near the surgical incision within 30 days of the procedure or within 90 days if prosthetic material is implanted at surgery. SSIs are often localized to the incision site (superficial/deep incisional SSI) but can also extend into deep tissues.¹ In the case of breast surgery, they can lead to removal of the implant, resection of the nipple-areolar complex, prolonged bed rest, late start of neoadjuvant therapy, and a compromised aesthetic result.

The purpose of this primer is to provide an overview of SSIs, their etiology, risk factors, and current treatment modalities in relation to breast surgery.^2-3 The goals are to increase awareness of SSIs among plastic surgeons and to promote further research into potential risk factors and management strategies. 

SSIs can be classified as follows:⁴

• Superficial incisional SSI. In these infections, the skin or subcutaneous tissue is involved and they occur within 30 days postoperatively. In addition, at least one of the following additional criteria must be fulfilled:
  • Presence of purulent drainage from incision with or without diagnostic laboratory testing (culture).
  • Presence of isolated organisms from aseptically obtained fluid or tissue culture in incision.
  • Presence of at least 1 sign or symptom of clinical infection: localized pain, edema, erythema, or warmth, and the superficial incision is deliberately opened by a surgeon (unless culture of incision is negative).
  • Diagnosis of a superficial incisional SSI by a surgeon or attending physician.

• Deep incisional SSI. This type of infection involves deep soft tissues, such as fascia or muscle within the incision, and occurs within 30 days postoperatively without implant or within 1 year if an implant is in place and the infection appears to be directly related to surgical procedure. At least one of the following additional criteria must also be fulfilled:
  • Presence of purulent drainage from the incision but not from the organ/space of the site.
  • Dehiscence or deliberate opening by the surgeon from the deep incision when the patient has at least one of the following signs or symptoms of clinical infection: fever greater than 100.4°F (38.0°C), localized pain or edema, unless a culture shows no growth.
  • Presence of abscess or other evidence of infection involving the deep incision found during examination of incision, reoperation, or pathologic or radiologic examination.
  • Diagnosis of a deep incisional SSI by a surgeon or attending physician.

• Organ/space SSI. This type of SSI involves any part of the anatomy other than the incision and occurs within 30 days postoperatively without implant or within 1 year if an implant is in place and the infection appears to be directly related to the surgical procedure. In addition, at least one of the following criteria must be fulfilled:
  • Presence of purulence from a drain that was placed via stab incision into the organ/space (infection of drain site is not an SSI).
  • Presence of isolated organisms from aseptically obtained fluid or tissue from the organ/space.
  • Abscess or other evidence of infection involving the deep incision found during examination of incision, reoperation, or pathologic or radiologic examination.
  • Diagnosis of an organ/space SSI by a surgeon or attending physician.

If both superficial and deep layers are involved, or if an organ/space SSI drains through the incision, the classification will be deep incisional SSI.^5-7 

In the US, SSIs are second in frequency only to urinary tract infections, and the main pathogens involved are Staphylococcus aureus (30.4%), coagulase-negative staphylococci (CoNS; 11.7%), Escherichia coli (9.4%), Escherichia faecalis (5.9%), Pseudomonas aeruginosa (5.5%), Enterobacter spp (4.0%), and Klebsiella spp (4.0%).⁸ While S aureus represents the main cause of surgical wound infections, CoNS account for the main cause of infections associated with prosthetic devices.

Two large groups of staphylococci can be distinguished: coagulase-positive staphylococci (essentially, S aureus) and CoNS, which include Staphylococcus epidermidis and Staphylococcus lugdunensis, among others. The distinction is made on the basis of the bacterium’s ability to synthesize coagulase, a surface enzyme capable of transforming fibrinogen into fibrin and creating a coating that allows the pathogen to evade the immune system. In addition to this virulence factor, S aureus also possesses the genes that code for biofilm formation. This characteristic is shared with the CoNS, which, despite their low virulence compared with coagulase-positive staphylococci, remain important pathogens, especially in infections associated with prosthetic devices. This ability to colonize surfaces of different natures and survive in a state of quiescence makes staphylococci the most frequent cause of device-associated infections and explains, at least in part, the high frequency of recurrence.⁹

Coagulase-Positive Staphylococci

About 25% to 50% of healthy people are persistently or transiently colonized by S aureus; in this regard, the bacterium can be considered part of the normal human flora. The most commonly colonized sites are the nostrils and the skin (especially when injured), followed by the oropharynx, armpit, vagina, and perineum. In most patients who develop S aureus infection, the strain in question is the one that colonizes them. Transmission occurs more frequently following transient colonization of the hands of hospital staff or, in fewer cases, through aerosols and nasal secretions from highly colonized patients.

Staphylococci are classifiable as opportunistic germs. To cause disease, most of the following events must occur: contamination and colonization of tissue surfaces; establishment of a local infection, invasion, or evasion of the host’s immune system; and metastatic diffusion.⁹S aureus is thought to be responsible for a significant percentage of device-associated infections. The clinical picture is characteristic and differs from that of typical CoNS infections due to the acute course with which it manifests itself and the greater tendency to progress rapidly, with formation of purulent collections at the level of the device.

CoNS

Although they are much less virulent than S aureus, CoNS are among the most common causes of prosthetic device-associated infections.

S epidermidis, which is normally found on the skin and in the oropharynx, is most frequently involved in device-associated infections. The peculiarity of S epidermidis lies in its ability to synthesize the glycocalyx that facilitates the formation of the biofilm on the surface of the device. The biofilm acts as a barrier, protecting bacteria from host defense mechanisms and antibiotics.¹⁰

The clinical course that marks the infection with CoNS is often subtle, with slow progression and often limited systemic signs and symptoms. Signs of local infection with erythema, purulent discharge, and pain may be present. Fever is often but not always present and can be associated with modest leukocytosis and elevation of inflammatory markers (eg, C-reactive protein and erythrocyte sedimentation rate).¹¹

Mupirocin and Chlorhexidine Gluconate

As already stated, S aureus is the main culprit among the pathogens responsible for SSIs. Traditionally, attempts have been made to prevent horizontal patient-to-patient transmission, but it has been shown that about 80% of S aureus infections classified as SSIs originate from the patient’s own bacterial flora. The high costs in terms of mortality and morbidity associated with this phenomenon and the widespread problems related to the increase in resistance to antibiotic therapies (ie, methicillin and vancomycin) have led the World Health Organization to recommend preoperative use of mupirocin ointment 2% in patients known to be nasal carriers of S aureus, either alone or in combination with body wash containing 2% chlorhexidine gluconate.¹² This was initially recommended only for high-risk surgeries (eg, cardiac surgery and orthopedic procedures), but in recent years it has been extended to other surgeries, probably due to the low cost of the protocol and the high number of studies attesting to its value in reducing the incidence of SSIs.¹²

Preoperative Antibiotic Prophylaxis

Despite the attention to ensuring maximum sterility during the surgery, contamination of the surgical field is possible by microorganisms of both exogenous (ie, environment, surgical instruments, operators) and endogenous (ie, the patient’s own bacterial microflora) origin. It is therefore of fundamental importance to pay attention to the preparation and perioperative management of the patient by using prophylactic antibiotic regimens to prevent these contaminations from giving rise to infections.

Perioperative antibiotic therapy for SSI prevention is based on the following assumptions: the selected antimicrobial should cover the most probable pathogens; a single antimicrobial agent is almost always effective in prophylaxis; the half-life must be long enough to ensure adequate tissue antibacterial coverage for the duration of the intervention; the first dose should be administered intravenously (IV) just before proceeding with skin incision; a second dose should be administered if surgery lasts longer than 3 hours or twice the half-life of the drug; additional postsurgical doses are useless after 24 hours.

Timing of antibiotic administration must be based on its pharmacokinetics; administration before the 120-minute interval preceding the start of the procedure or, on the contrary, a delayed administration occurring after the start of surgery  makes antibiotic tissue concentrations inadequate for the prevention of infection. For short-lived antibiotics, such as cefazolin, cefoxitin, and penicillins in general, the optimal administration should take place no earlier than 60 minutes before the surgery.¹² With the exception of colorectal, abdominal, or penetrating trauma operations, a single agent has been shown to be effective in a surgical prophylactic regimen. In the former cases, a combination therapy should be considered.

Immediate 2-stage tissue expander breast reconstruction is classified as a “clean intervention with prosthesis.” This makes it prudent to use at least the first preoperative dose in all patients due to the high risk related to the surgical factor itself. International guidelines recommend the administration of cefazolin 1 g IV during the induction of anesthesia or vancomycin 1 g if the patient is allergic to cephalosporins or in the presence of methicillin-resistant microorganisms. 

Maximum sterility of the surgical field is required. This reduces the risk of microbial contamination and is the cornerstone of infection prevention. Lack of adherence to established practices for sterility control during invasive procedures has been associated with the occurrence of SSIs.¹³ The sterile field should be prepared as close to the time of use as possible. The likelihood of contamination and development of microorganisms increases with time as dust and other particles in the environment settle on horizontal surfaces. Particles can also intrude as a result of personnel movements, settling on open sterile material.^14-15

Antiseptic agents for the preparation of the operating field should be selected according to patient characteristics and, if there are no contraindications, should always contain alcohol (this has great bactericidal power but should be combined with another antiseptic because the persistence of its antiseptic effect is relatively short).¹⁶

The most commonly used antiseptic solutions are iodopovidone and chlorhexidine gluconate in either aqueous or alcohol solutions. Iodopovidone may cause dermatitis or irritant reactions and is not indicated for patients allergic to iodine, although anaphylactic reactions to iodopovidone are extremely rare.¹⁷ Chlorhexidine gluconate triggers allergic reactions in sensitive individuals, ranging from mild local symptoms to severe anaphylaxis.

Antiseptic solutions should be distributed in concentric circles starting from the incision area and expanding outwards while avoiding areas that have been already treated. The area should then be dried with sterile towels and marked off with sterile drapes. The demarcated area must be large enough to protect new incisions or drainage sites away from the main incision.¹³ 

Before placement of the breast implant, the surgeon should change gloves to reduce bacterial contamination and rinse the implant with an antiseptic for biofilm mitigation.^18-19 In the case of breast augmentation using the periareoral approach, the Keller funnel can be employed to decrease the contact of the implant with skin and ducts.²⁰ 

SSIs consist of a heterogeneous group of pathological processes though with common features:

• Pathogens enter an environment that is normally sterile through an interruption in the epithelial barrier formed upon the surgical act.

• Establishment and perpetuation of the infection are the result of a complex interaction between pathogens’ virulence factors and host defense systems that are unable to cope with them.

It is therefore possible to identify 2 kinds of risk factors: those associated with the traits of the patient (individual factors) and those intrinsic to the surgical/therapeutic act (surgical factors).

Individual Risk Factors

Any tissue insult during a surgical procedure triggers a physiological cascade of events (inflammation) aimed at healing the damaged tissue. During the acute phase, there is a predominance of neutrophils that are gradually replaced by macrophages in the later phase. The activation of other systems may lead to systemic manifestations (the acute phase response). The global activation of these mechanisms serves to destroy, dilute, or wall off the injurious agent(s) and the consequences of the injury (necrotic cells and tissue) in an attempt to heal the damaged tissue. 

Both systemic and local factors influence the quality of the response and conditions, such as immunosuppression, ongoing medical therapies, malnutrition, and other comorbidities that make the individual more susceptible to infections. Immunosuppression can stem from underlying diseases or be intrinsically linked with surgery. Among the main variables that may influence the patient’s postoperative course are age, smoking, body mass index (BMI), diabetes mellitus, immunocompromised state, chemotherapy, or local regional radiotherapy.²¹

Surgical Risk Factors

Among the surgical factors that can cause or, on the contrary, prevent infections of the surgical site, there are particular devices employed in breast reconstruction. Specifically, the placement of a tissue expander or a breast implant and its permanence increase the infective risk. Also, the volumetric size of the device seems to be directly correlated with an increased infective risk. This may be explained by the fact that larger devices are placed in larger breasts, which are common in women with higher BMIs. 

In general, every prosthetic device or foreign body potentially promotes infectious phenomena. Suture threads, hemostatic devices, and surgical drains constitute a communication between the surgical site and the external environment. However, in the case of abscess formation at the surgical site, surgical drains function in promoting the removal of cellular debris and contaminated fluids; this reduces the bacterial load and thus favors the host response (therapeutic function). Combining the use of drains with antibiotic therapy guarantees the best chance of therapeutic success. At the same time, the prophylactic role of surgical drains is still a matter of debate. On the one hand, they help prevent complications, such as hematomas and seromas; on the other, drains left in place for prolonged periods have never been demonstrated to reduce the rate of infections. Instead, they may actually promote the onset of infection through different mechanisms: the formation of the biofilm is promoted by the presence of a drain, and the drained material can be mobilized retrogradely through the drain and be deposited again in the sterile surgical site, especially if the drain is left in for a prolonged period.

Finally, another infective risk factor is associated with the mastectomy technique used in the reconstructed breast. Some studies have shown high infective rates in prosthetic breast reconstruction following skin-sparing mastectomy and in those reconstructions in which mastectomy is accompanied by axillary dissection.²² 

Despite the use of sterile technique, the administration of reasonable empirical therapies, and, when possible, use of targeted therapies at the time of identification of the etiopathologic agent, infectious complications may still arise. Approximately 50% of infected tissue expanders and breast implants require reintervention or removal of the implanted device. Due to the often-nuanced nature of the clinical manifestations, it is very important to maintain a watchful eye with regards to any local or systemic clinical signs and symptoms.²³

The medical approach to infectious complication may range in degree of invasiveness. Oral or IV antibiotic therapy may be sufficient in some cases, whereas other patients may require more aggressive washing procedures of the prosthetic pocket, surgical toilet, or definitive or temporary removal of the infected device.²³

Medical Therapy

The administration of targeted antibiotic therapies at the time of diagnosis would represent the ideal medical treatment in the clinical management of the infection. What happens, however, is that the identification of the pathogen through culture tests and the determination of its relative sensitivity to antibiotics requires at least 48 to 72 hours, hence the need to initiate reasoned empirical antibiotic therapy based on the epidemiology of the possible pathogens involved and on the characteristics of the patient. In immunocompromised patients, the antibiotic treatment cannot be delayed beyond the third day after the clinical presentation. The therapy may be considered definitive when a host response to infection is observed, or when a final antibiotic therapy is administered based on the antibiogram.²³

It is of fundamental importance to identify “high infectious risk” patients; this is possible based on the evaluation of such variables as age, immune response, nutritional status, acute response to infection, and the presence of comorbid conditions. Within the authors’ operating unit, Scott Spear’s guidelines are used for the management of patients undergoing implantation of breast prosthetic devices who are variably exposed to the threat of infection.²³ In most cases, the infection is confined to the area of surgical incision. If the infection is localized at the superficial level and there is no evidence of systemic manifestations, antibiotic therapy is not required. If, instead, there is a severe or extensive local reaction, the administration of antibiotic therapy is advisable.²³

As previously stated, in the case of clean wounds far from the perineum or associated with intestinal interventions, the pathogens most likely to be involved are S aureus or some streptococcal species. In these cases, the administration of cefazolin 1 g every 6 hours appears to be appropriate. The same cannot be said for wounds near the perineal region that are considered to be contaminated or for wounds arising from abdominal operations, which often require combined antibiotic therapies with the aim of counteracting both aerobic and anaerobic pathogens. For more aggressive infections with evidence of tissue necrosis or severe systemic manifestations, an antibiotic therapy based on an aminoglycoside, a third-generation cephalosporin, or a quinolone combined with clindamycin or metronidazole is advised.²³

Surgical Therapy

The surgeon who is confronted with a case of prosthetic infection that does not respond to systemic antibiotic therapy must take a series of surgical precautions to manually reduce the severity of the infective process. The first approach in the surgical treatment of a postoperative infection is to open the wound. If possible, the incision should be made on the mastectomy scar or, if dehiscence of the wound is observed, the incision should be enlarged to form a flap encompassing the infected margins. Surgical debridement of the pocket should then be performed and the collected biological material sent for culture (ie, swab, capsulectomy). The expander/implant should then be removed from the pocket and subsequently washed repeatedly with a chlorhexidine solution. The surgeon must establish whether to replace the implant or perform a layered closure, which would then be followed by irrigation with 2 vials of rifampicin solution.²³

To reduce the risk of infection, a prophylactic antibiotic therapy should be administered before and after the operation. Infections can be classified as early infections when they arise before the 30th postoperative day whereas late infections are those that arise after this cutoff date. Infections may drastically worsen the aesthetic outcome and even require a new intervention, rendering it necessary to also remove the expander/implant—a complication that forces a delay of the entire reconstructive process by a few months.²³ 

SSIs are common complications of breast reconstruction. Although multiple etiological agents, risk factors, and treatment options have been identified, more research is required, particularly given the potential success with avoidance of risk factors and early intervention. 

Authors: Domenico Costanzo, MD¹; Antonella Romeo, MD² 

Affiliations: ¹Humanitas Research Hospital, Humanitas University, Pieve Emanuele, Italy; ²Università degli Studi di Roma “Tor Vergata,” Rome, Italy  

Correspondence: Domenico Costanzo, MD; domenico.costanzo@mail.com

Availability of data and material: The datasets collected and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Ethics: The principles outlined in the Declaration of Helsinki have been followed in this study.

Disclosures: The authors disclose no relationship with any commercial source related directly or indirectly to this scientific paper.