Doi:10.1053/j.semtcvs.2004.01.004

Methods for Reduction of Sternal Wound
Infection
Francis Fynn–Thompson, MD, and Thomas J. Vander Salm, MD
Deep sternal wound infections continue to be an uncommon but potentially devastating complication
of cardiac surgical procedures. Numerous risk factors have been identified but only a few can be
characterized as modifiable. These risk factors and their modifications are reviewed in the following
article.
2004 Elsevier Inc. All rights reserved.
Although the overall incidence of postopera- identifyandhighlightanumberofthesemodifi- able risk factors: antibiotic prophylaxis; preoper- heart surgery continues to be low, the prevention ative preparation; intraoperative management; and subsequent management of the complication still poses a daunting task for every cardiac sur-geon. The reported incidence ranges from 1.3%to 5% in most recent series and with a high Microbiology
associated mortality rate of 9.8% to 14%.1-3 Inaddition to the increased mortality, the condition The microbial etiology of sternal wound infec- also carries with it a high morbidity, resulting in tions can be varied and include Gram-positive prolonged hospitalization and the associated in- and Gram-negative bacteria as well as fungi.
crease in cost. The average cost of hospitalization However, numerous recent studies have demon- for a patient with a sternal infection is approxi- strated that the most common causative patho- mately three times that of patients without gens involved in sternal wound infections are Staphylococcus epidermis and Staphylococcus aureus,both from the normal flora of the skin.9-11 That Postoperative sternal infection exists along a these organisms account for over half of postop- spectrum of presentations from sterile wound de- erative mediastinitis suggests that skin flora, in- hiscence to suppurative mediastinitis, and its troduced into the wound at the time of operation, pathogenesis is complex and multifactorial. How- is a major and potentially modifiable risk fac- ever, a number of specific patient and procedure related risk factors have been delineated.5-8 Often regarded as a relatively benign organ- These include obesity, diabetes, reoperation, in- ism, S. epidermis (coagulase-negative staphylococ- creased duration of the operation, coronary ar- cus) has emerged as the most common sternal tery bypass grafting, use of bilateral internal tho- infection pathogen and often presents with only racic arteries, postoperative inotropic support, minimal signs of systemic infection. It often has a and the need for multiple blood transfusions.
slow and late onset of up to 3 weeks.12 Interest- While most of these risk factors are not amenable ingly, this organism appears more frequently in to intervention, others can be modified with a association with sternal instability.7,9 The pro- consequent reduction of sternal wound complica- posed mechanism for this association is that the tions. The purpose of this review is to attempt to deep sternal infection originates from a minorcutaneous or subcutaneous infection and thenspreads into the mediastinal space when sternal From the Division of Cardiothoracic Surgery, Massachusetts Gen- eral Hospital, Boston, MA , and North Shore Medical Center, Salem, dehiscence disrupts the mechanical barrier be- tween the mediastinum and the presternal tis- Address reprint requests to Thomas J. Vander Salm, MD, North sues. A superficial, self-contained pocket of infec- Shore Medical Center, 81 Highland Avenue, Salem, MA 01970. tion with coagulase-negative staphylococci that 2004 Elsevier Inc. All rights reserved.
1043-0679/04/1601-0012$30.00/0 would otherwise be benign can thus progress into Seminars in Thoracic and Cardiovascular Surgery, Vol 16, No 1 (Spring), 2004: pp 77-80 S. aureus is the other major pathogen. It has attempt to eliminate the S. aureus and reduce the been increasingly associated with colonization of risk of sternal infection.13,17 Perioperative appli- the nasal passages of patients, leading to specific cation of nasal mupirocin eradicates 95% to 100% dissemination in the operating room.10,13 of S. aureus up to 1 year postoperatively,18 and Another major group of bacteria involved in demonstrates a 67% reduction of infection in a the genesis of deep sternal infections is aerobic mupirocin treated group as compared with a ret- Gram-negative rods. The etiology of these infec- tions is likely to be entirely different from those caused by staphylococci. These Gram-negative mediastinal infections are associated with a more Hyperglycemic Control
complicated postoperative course and concomi- In diabetic patients, it is has been demonstrated tant nosocomial infection.6,9 These include pneu- that aggressive and intensive blood sugar control monia from prolonged mechanical ventilation, is associated with improved survival following urinary tract infections, and intraabdominal sep- sis. Aggressive treatment of these comorbid con- erative hyperglycemia have been identified as in- ditions should also reduce the risk of mediastini- dependent risk factors for deep sternal wound infections.19,20 The study by Furnary and cowork- ers demonstrated that continuous insulin infu- Antibiotic Prophylaxis
sion (glucose kept in range 150-200 mg/mL) when compared with intermittent subcutaneous The perioperative administration of antibiotics is insulin, led to a significant reduction in the inci- a universal but not extensively studied compo- dence of deep sternal wound infections (0.8% nent of prophylaxis against sternal wound infec- tions. Two significant conclusions form the basis of most prophylactic antibiotic regimens.14 First, antibiotic prophylaxis significantly reduces the prevalence of sternal infections when compared Sternal Stability and Closure
with placebo. Second, increasing the duration of Techniques
prophylaxis beyond 36 to 48 hours does not fur- Numerous studies now support the emerging con- ther reduce sternal infection rates. The 1999 con- cept that sternal instability is a major risk factor sensus paper from the Hospital Infection Control in the development of sternal wound infec- Practices Advisory Committee (HICPAC) recom- tions.9,10,22,23 It is postulated that this increased mends treatment consistent with those two con- infection rate seen with unstable sternal fixation clusions.15 Common practice in many hospitals is is due to increased bone movement, which dam- to use a second-generation cephalosporin, with ages local tissue, leads to tissue necrosis, and vancomycin substituted for it in penicillin-aller- creates a milieu for bacterial growth at the time gic patients or for valve operations, and modu- of transient inoculation.9,24 In contrast, stable lated by hospital-specific antibiotic sensitivities.
bony fixation reduces the amount of tissue The incidence of nasal colonization with S. trauma and promotes more rapid vascularization aureus in the normal population is reported to range from 10% to 15%.11 Such colonization in- A careful and precise midline sternotomy re- creases the risk of sternal wound infections.11,13,16 duces the risk of later sternal instability and Proposed mechanisms for the transfer of nasal S. dehiscence.23 A paramedian sternotomy predis- aureus to the sternal wound include direct spread poses to sternal instability regardless of the clo- from the nose to hands to the incision, and he- matogenous spread caused by endotracheal tube The orthopedic surgery literature documents trauma to the nose.13 Elegant DNA fingerprint that fracture instability increases the risk of in- analysis demonstrates the genotype of S. aureus fection. In a study by Worlock, rabbit tibial frac- isolates recovered from the patient’s sternum tures were stabilized with either a dynamic com- and nose often were identical. This observation led to the use of topical nasal antibiotics in the intramedullary rod (unstable group).24 These preoperative and early postoperative period in fractures were then inoculated with S. aureus. The infection rate was double in the unstable group The routine application of bone wax as a he- mostatic agent following sternotomy has also In primates, Sargent and colleagues, tested been implicated in promoting sternal infections the hypothesis that rigid fixation enhanced ster- with a reduced bacterial inoculum required to nal bone healing.25 They compared interrupted produce sternal osteomyelitis in the presence of wire suture technique with compression miniplates bone wax.35 This infection predilection appears to (their model for rigid fixation) in skeletally ma- be caused by local inhibition of osteogenesis and ture baboons. By carefully studying sternal har- intense local inflammation. An alternative to vests from each group, they were able to show bone wax is the use of topical vancomycin and that at 4 weeks, clinical stability was superior powdered absorbable gelatin (Gelfoam®) mixed with rigid fixation and resulted in increased new with topical thrombin to form a hemostatic paste.
bone formation across the osteotomy gap. Rigid When applied to cut sternal edges, this paste was fracture stabilization promulgates earlier bone not only hemostatic but was also shown to reduce healing and therefore greater resistance to infec- Multiple techniques of sternal closure include the use of simple cerclage wires, figure-of-eight Multiple practices and techniques easily can be wires, figure-of-eight stainless steel cables, stain- altered to reduce the incidence of sternal and less-steel plates, sternal screws with a central lumen for wire placement, bone staples to but-tress cerclage wires, thermoreactive clips, andintercostal weaving of wires to buttress cerclage References
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