Chest Wall Infections Following Open Heart Surgery
Michael A. Wait
INTRODUCTION
Epidemiology
The majority of coronary artery bypass grafting (CABG) and valvular repair or replacement operations are performed through a median sternotomy incision. This procedure was first reported in the journal Lancet in 18971 by the British surgeon Herbert Meyrick Nelson Milton at the Kasr El Aini Hospital in Cairo for the treatment of tuberculous lymphadenopathy; later, it was reintroduced by Ormand Julian in 1957 to replace the more painful and disfiguring bilateral anterior thoracotomy for open heart surgery and then in 1964 for CABG.2 The two most catastrophic complications of the median sternotomy soon followed—dehiscence and deep sternal wound infection (DSWI) with mediastinitis.3 Indeed, Milton’s second patient suffered fatal sternotomy dehiscence. The overall incidence of deep sternotomy wound infection or dehiscence is relatively uncommon, ranging from 0.1% to 5%. Oakley et al provided a review in 1996 in which centers reported incidences from 0.1% to 2%. The National Nosocomial Infection Surveillance (NNIS) system of the Centers for Disease Control and Prevention (CDC) in 1997 reported a sternal infection rate of 3.7%. More recently, the Society of Thoracic Surgeons (STS) Databank, a prospective registry, which has recorded outcome events of over 6 million cardiac surgical procedures since 1989, reports a DSWI incidence of 0.4%.4
The morbidity and mortality rate of DSWI is substantial. Mortality rates for DSWI as high as 30% have been reported5 and are dependent upon the virulence of the infecting agent, patient comorbidities, and treatment modality used to effect healing of such an infection. DSWI morbidity includes suffering, chronic debility, reoperation, prolonged hospital stay (9-20 days), and cost.6 Patients with DSWI experience on average an additional hospital cost of $20,000 in the first year in 1999 dollars; infected patients who died experienced an additional $60,547 more than those who survived. In 2008, an effort to control hospital costs and compel physicians to prevent DSWI was initiated by the Centers for Medicare & Medicaid Services (CMMS); acting in concert with the Deficit Reduction Act of 2006, CMMS established a list of hospital-acquired conditions (HAC) which, when acquired during hospitalization (ie, not present on admission), do not qualify the facility for additional payment (http://www.cms.gov/HospitalAcqCond/downloads/HACFactsheet.pdf).
Mediastinitis following CABG is one of the 12 listed HACs in this government action.
Risk Factors
Risk factors associated with a deep sternotomy wound infection can be categorized as occurring in the preoperative,7,8 intraoperative, and postoperative phase of care; risk factors can also be considered modifiable and unmodifiable (Table 94.1).
Preoperative risk factors are primarily those related to patient conditions and comorbidities. Operative factors that contribute to wound infection are listed in Table 94.1. Antibiotic prophylaxis is proven to prevent surgical site infections. However, the timing of antibiotic prophylaxis more than 60 minutes before incision or more than 30 minutes after incision and variance of antibiotic choice to a nonrecommended prophylaxis agent is associated with DSWI. Use of bone wax as a topical hemostatic agent on the sternal bone marrow, intra-aortic balloon pump use, indiscriminate use of the Bovie electrocautery device, undrained fluid collections (especially blood), cardiopulmonary bypass time, total operative time, and operation in addition to CABG—such as a valve-CABG procedure—also contribute to the risk of DSWI.8 Postoperative factors include the following: shock, need for a postop tracheostomy, poorly controlled hyperglycemia.
Interest was generated from the observation that patients who were on statin agents experienced fewer wound infections. Although the preoperative administration of statins has been demonstrated in cohort studies to reduce the incidence of all infections, they were not specifically linked to a statistically significant reduction in specific infections, such as DSWI.9
Blood transfusion following cardiac surgery has also been associated with increased infection risk,10 which was not mitigated by the use of leukocyte-depleted blood products.11 A tiered-level effect was observed in a study published by Murphy et al12; in a stepwise fashion, the infection rate was 3.9% in patients receiving up to 2 units of packed red blood cells, 6.9% for those receiving 3 to 5 units, and as high as 22% in those receiving 6 units of blood or more. Logistic regression analysis showed that the most significant predictor of infection was transfusion amount; the increased risk of infection was postulated to be related to transfusion-mediated immunomodulation. Relevant to blood transfusions, the independent effect of preoperative anemia has been evaluated but not demonstrated to directly affect the rate of sternal wound complications.13
TABLE 94.1 Patient and Operative Risk Factors Influencing Surgical Site Infections | ||||
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Hemoglobin A1c influences the risk of developing a wound infection. A single-center study from UT Southwestern Medical Center demonstrated that every 1% increase in preoperative hemoglobin A1c is associated with a 13% relative risk increase for a wound infection.14 In addition, perioperative glycemic control—independent of hemoglobin A1c—influences the incidence of sternotomy wound infections and mediastinitis.15
The effect of single versus bilateral internal thoracic artery harvesting on the incidence of severe sternal wound complications has been extensively studied. In the Arterial Revascularization Trial,16 patients were randomly assigned to undergo single (N = 1554) versus bilateral (N = 1548) internal thoracic artery grafting during CABG procedures; 23% of patients enrolled were diabetic. Although not a primary end-point of this trial, sternal wound complications (1.9% vs 3.5% in the single versus bilateral graft group, respectively) and sternal wound reconstruction (0.6% vs 2.0% in the single versus bilateral graft group, respectively) were not statistically different.
PATHOGENESIS
Infectious sternotomy incision complications can be classified as superficial or deep according to the STS guidelines and the 1988 CDC definitions for nosocomial infections17; superficial wound infections (SWI) are those limited to the epidermis, dermis, and superficial subcutaneous adipose. Additionally, SWI must include at least one of the following:
purulent drainage is present;
an organism is isolated from the incision;
at least one of the following symptoms is present: tenderness, swelling, redness, or heat;
the incision is opened by a surgeon; or
diagnosis is made by the surgeon or attending physician.
Infections involving the pectoralis fascia, sternal wires, sternal bone, or mediastinum collectively represent deep sternal wound infections (DSWI). DSWI must satisfy at least one of the following criteria:
an organism is isolated from a culture of mediastinal fluid or tissue;
evidence of mediastinitis is seen during operation or by histopathologic examination;
one of the following is present; fever greater than 38 °C, chest pain, sternal instability, and there is either purulent drainage from the mediastinum or an organism isolated from blood culture or culture of drainage of the mediastinal area. If organisms from common skin flora (coagulase-negative Staphylococci, diphtheroids, Bacillus species, Propionibacterium species) were isolated, two positive cultures with the same strain are required.17
SWI are more common than DSWI and can be adequately treated with local wound care, oral or parenteral antibiotics, and limited wound debridement. If during debridement of an infected sternotomy incision, the sternal wires become exposed, by definition it is classified as a DSWI.
Sternotomy wound infections more commonly follow CABG procedures than valve procedures, suggesting that the use of the internal thoracic artery causes devascularization of the ipsilateral hemisternum, which contributes to wound separation and necrosis, and subsequently progresses to a DSWI. Foreign bodies such as bone marrow wax are widely held to be a major contributory operative factor leading to DSWI. Bone wax is a hydrophobic derivative of petroleum by way of paraffin oil, combined with sterilized Cera Alba (the common honeybee) wax, and is used as a bone marrow hemostatic agent during sternotomy incisions for open heart surgery. Bone wax as a hemostatic agent works by mechanical occlusion of transected vessels in cancellous bone. Although highly efficacious, bone wax nonetheless behaves as a foreign body.18
The morbidity and mortality rate of patients who suffer DSWI is considerably higher than in those patients who do
not experience DSWI; Tewarie et al reported a 20% mortality rate with infection (vs 0% without),19 and Levi et al reported a 30% mortality rate for DSWI, which occurred in 0.67% of their study population.5 Hospital length of stay was extended by 12 to 18 days for those cases which occurred during the same index hospitalization as the open heart procedure.20
not experience DSWI; Tewarie et al reported a 20% mortality rate with infection (vs 0% without),19 and Levi et al reported a 30% mortality rate for DSWI, which occurred in 0.67% of their study population.5 Hospital length of stay was extended by 12 to 18 days for those cases which occurred during the same index hospitalization as the open heart procedure.20
The microbiology of DSWI is predominantly but not exclusively bacterial; Staphylococcus aureus, Staphylococcus epidermidis, and α-hemolytic Streptococcus continue to predominate, with Gram-negative aerobic and anaerobic bacteria contributing to a lesser extent.21 Predominant anaerobes include Prevotella sp., Porphyromonas sp., Peptostreptococcus sp., Propiobacter sp., and Bacteroides fragilis. From a study by Ford et al, a higher proportion of Gram-negative bacteria (75% of cases) and fungal (9%) relative to Gram-positive bacteria (16%) were seen in patients whose only identifiable risk factor was prolonged intubation, mechanical ventilation, nasogastric suction, and time to enteral nutrition.22 They concluded that gut translocation as a consequence of disuse was the major contributing factor in those infections.