**4. Risk factors and pathophysiology**

Multiple different etiologies for development of DSWI have been invoked over time. For example, most infections were traditionally thought to arise as a result of breaks in proper surgical technique, prompting strict guidelines for sterile surgical technique. In addition, secondary involvement the mediastinum from remote sites such as leg incisions or the pulmonary tree has also been suggested as a mechanism for DSWI. The "endogenous pathway," seeding of the mediastinum from other host sources, does appear to be important in the development of *S. aureus* mediastinitis. To illustrate, Jakob et al showed that nasal carriage of *S. aureus* was an independent predictor of sternal infection postoperatively [28], while others have demonstrated that application of mupirocin to the nares of *S. aureus* colonized individuals can help reduce postoperative infection [29]. More recently, other factors have been recognized as important contributors to cardiac surgical site infections. For instance, the appropriate timing of perioperative antibiotics and strict perioperative glucose control are both associated with reduced surgical wound infectious complications [30, 31].

Several different patient-related factors have been repeatedly implicated in the development of DSWI, most consistently obesity and diabetes mellitus [5, 6, 32, TABLE 4]. Eklund et al and others have observed that increasing severity of obesity elevates the risk for surgical site infection in a step-wise fashion [6, 13, 33]. Furthermore, when obesity is described in terms of percentage body fat, the relationship between obesity and surgical site infection is nearly linear and appears more accurate than use of body mass index as a descriptor of obesity [34]. Potential explanations for relationship between obesity and DSWI include technical problems

The classification by Jones et al differs from that of El Oakley and Wright in that it is more descriptive anatomically and physiologically [26, TABLE 3]. Three different "types" of sternal infection are described, encompassing both superficial and deep infections, and based on the degree of underlying tissue involvement with infection. We have preferred the use of this classification system as it is simpler to use since it based strictly on features observed or encountered at the time of initial sternal exploration. In addition, Type 3b is physiologically meaningful since it denotes the patient who is systemically ill from the sternal wound process. In our own institutional experience of 222 adult cardiac surgical patients treated for postoperative DSWI, approximately 50% of patients exhibited

Class Depth of Involvement Description

1a Superficial Skin/subcutaneous tissue dehiscence 1b Superficial Exposed deep fascia, sutures intact 2a Deep Exposed bone, stable wired sternotomy

3a Deep Exposed necrotic or fractured bone,

sternotomy

unstable, heart exposed

2b Deep Exposed bone, unstable wired

3b Deep Types 2 or 3 with septicemia Table 3. Mediastinal wound classification system modified from Jones et al [26]. Although anatomic involvement by infection in distinguished, the presence of septicemia is the most

Multiple different etiologies for development of DSWI have been invoked over time. For example, most infections were traditionally thought to arise as a result of breaks in proper surgical technique, prompting strict guidelines for sterile surgical technique. In addition, secondary involvement the mediastinum from remote sites such as leg incisions or the pulmonary tree has also been suggested as a mechanism for DSWI. The "endogenous pathway," seeding of the mediastinum from other host sources, does appear to be important in the development of *S. aureus* mediastinitis. To illustrate, Jakob et al showed that nasal carriage of *S. aureus* was an independent predictor of sternal infection postoperatively [28], while others have demonstrated that application of mupirocin to the nares of *S. aureus* colonized individuals can help reduce postoperative infection [29]. More recently, other factors have been recognized as important contributors to cardiac surgical site infections. For instance, the appropriate timing of perioperative antibiotics and strict perioperative glucose control are

Several different patient-related factors have been repeatedly implicated in the development of DSWI, most consistently obesity and diabetes mellitus [5, 6, 32, TABLE 4]. Eklund et al and others have observed that increasing severity of obesity elevates the risk for surgical site infection in a step-wise fashion [6, 13, 33]. Furthermore, when obesity is described in terms of percentage body fat, the relationship between obesity and surgical site infection is nearly linear and appears more accurate than use of body mass index as a descriptor of obesity [34]. Potential explanations for relationship between obesity and DSWI include technical problems

both associated with reduced surgical wound infectious complications [30, 31].

septicemia (Jones 3b) upon initial presentation [14].

important feature clinically.

**4. Risk factors and pathophysiology** 


Table 4. Compiled analyses for underlying risk factors associated with sternal wound infection. Obesity and diabetes mellitus are consistently shown to be independent predictors of poststernotomy mediastinitis.

during surgery owing to the patient's size, increased bleeding, increased deadspace in the wound, and ineffective or inadequate dosing of perioperative antibiotics [6, 9].

Although multiple mechanisms for sternal wound complications are proposed, it is widely accepted that reduced sternal perfusion, often by virtue of internal mammary artery (IMA) harvesting for use as a vascular conduit in coronary artery revascularization, is one of the most important causes of sternal nonhealing and infection [1-6, 8, 26], especially when both IMAs are harvested for bypass graft surgery [5]. Therefore, more cases of DSWI appear to occur after coronary artery bypass grafting or after combined procedures that include coronary artery surgery [7, 35]. Other viable explanations for DSWI etiology include poor bone stock from osteoporosis, malnutrition, and other factors; poorly performed sternotomy leading to sternal fractures and/or costosternal disassociation; and other patient related factors including peripheral vascular disease and lung disease [8, 36]. Several other factors have been implicated in the development of DSWI but may not be manifest in the context of a retrospective review or randomized trial because the numbers are too low. For example, it is generally accepted that postoperative steroids or chronic immunosuppression increases risk for DSWI, but this has been difficult to demonstrate in even large database reviews [13, 37]. Finally, Risnes et al have demonstrated in a review of over 18,000 consecutive patients undergoing coronary artery surgery in Norway, the major preventable risk factor associated with the development of DSWI was the amount of blood product transfusion perioperatively [12].

Sternal Wound Complications Following Cardiac Surgery 289

as a "sternal stripe" indicated present of air between the two sternal halves. The lateral displacement of one or more sternal wires, secondary to tearing of the wire through one side of the sternum, has been a frequently noted finding in the case of poststernotomy infection [37]. More recently, chest computed tomography has been suggested as the procedure of choice for assessing sternal wound infection when a diagnosis cannot be established by clinical examination alone [45, 46]. Mediastial fluid collections, free gas bubbles, soft tissue swelling, pleural effusions, sternal dehiscence, and subcutaneous fluid collections have been the predominant CT findings in cases of DSWI [47], but these features appear to be more specific

Mediastinal infection negatively impacts early, mid-term, and long-term survival after adult heart surgery [2, 7-12]. While it is intuitive that clinically serious DSWI reduces 30-day and/or in-hospital survival relative to similar patients not suffering this complications, the effect of DSWI on long-term survival is especially insulting since many patients referred for heart surgery expect to gain a survival advantage compared with other treatment options

Prior to the development of modern protocols for DSWI management, which include thorough sternal debridement and use of vascularized flaps to repair the mediastinal defect resulting from debridement, early mortality from DSWI exceeded 50% [50]. In the "modern era," reported rates of in-hospital or 30-day DSWI mortality for range from 7% to over 30% [11,14, 35, 42, 51, 52]. In our own recent experience, early mortality for DSWI is approximately 16% [14]. Therefore, despite many advancements in intensive care medicine, DSWI continues to be a deadly complication. Death in the early period is typicaly the result of sepsis or other infectious complications including multiorgan failure [12]. Morisaki et al. recently demonstrated methicillin-resistent *S. aureus* infection to be an independent risk

factor for in-hospital mortality in their cohort of poststernotomy DSWI patients [53].

Patients surviving infectious complications and the acute insult of DSWI exhibit reduced mid-term survival compared with controls. For example, one-year mortality for DSWI following CABG is significantly increased compared with similar patients who did not develop DSWI [2, 8, 10]. Milano et al and Braxton et al both demonstrated a doubling of mid-term mortality among patients with DSWI after CABG compared with controls [9, 54]. Karra et al examined predictors of one-year mortality after treatment for DSWI and found that delay in closing the mediastinal defect; age over 65 years; need for ICU care prior to sternal debridement; and methicillin-resistent *S. aureus* infections were each independently

Long-term survival has consistently been demonstrated to suffer in patients with a history of poststernotomy DSWI [5, 8, 9, 12, 35, 52, 54-56, Figure 1]. For example, Filsoufi et al reviewed nearly 5,800 adult heart surgery patients at a single institution over 8 years and found DSWI to be associated with significantly reduced 5-year survival compared with patients who did not develop DSWI [35]. Similarly, Risnes et al reviewed their experience of over 18,000 cardiac surgical patients with a mean follow-up of over 10 years. Long-term survival for patients whose course was complicated by DSWI was <50% compared with >70% for patients without DSWI, and DSWI was independently associated with reduced long-term survival after cardiac surgery [HR 1.59; 95% CI 1.16 – 2.70, p = 0.003] [12]. Similar

and sensitive for DSWI presenting more than 3 weeks after surgery [48].

**7. Morbidity and mortality** 

associated with mortality [7].

data have been also been reported by Toumpoulis et al. [55].

for their underlying heart disease [49].

Several risk analyses are available to estimate the individual patient's propensity for developing DSWI. For example, using Society of Thoracic Surgery National Cardiac Database information, Fowler et al created a model to estimate the risk for systemic infection after coronary artery bypass surgery using patient characteristics available preoperatively [13]. The Fowler model also provides for inclusion of important intraoperative details known to influence postoperative infection including the need for intra-aortic balloon counterpulsation and prolonged cardiopulmonary bypass times [13]. Although the model devised by Fowler et al was based on various cases of major infection after coronary artery surgery, including DSWI, the authors did validate the model as predictive of infection in a test population from the STS Database, and the model was also recently validated in a different cohort of patients from the UK as being predictive of DSWI [38]. The EuroSCORE system also has been shown to predict infection and associated mortality with acceptable discrimination [39].
