Deep Sternal Wound InfectionEdit

Deep sternal wound infection (DSWI) is a serious, potentially life-threatening complication that can arise after sternotomy, most commonly in patients undergoing cardiothoracic procedures such as coronary artery bypass grafting. Infections in this region involve the sternum and adjacent mediastinal tissues and frequently require a combination of aggressive antimicrobial therapy and surgical intervention. Early recognition and coordinated care by cardiothoracic surgeons, infectious disease specialists, and wound care teams are associated with improved outcomes. DSWI is distinct from superficial sternal wound infections, which are limited to the skin and subcutaneous tissues; when the sternum and mediastinal structures are involved, the condition is referred to as deep sternal wound infection or mediastinitis in clinical practice.

The incidence of DSWI varies with patient population and procedural risk, but contemporary reports generally place it in the low single digits, with higher rates in redo sternotomies, obesity, diabetes mellitus, chronic kidney disease, chronic obstructive pulmonary disease, smoking, and prolonged operative times. Mortality and morbidity are substantial, reflecting the difficulty of eradicating infection in the presence of necrotic bone and the need for major reconstructive procedures in many cases. Outcomes have improved over time with standardized diagnostic criteria, antibiotic regimens, and advances in wound management and reconstruction.

Epidemiology

DSWI is most often encountered after median sternotomy, the standard approach in many cardiothoracic surgery such as coronary artery bypass grafting.
Reported incidence ranges from roughly 0.5% to several percent, depending on patient risk factors and institutional practices.
Risk factors include advanced age, diabetes mellitus, obesity, chronic lung or kidney disease, immune compromise, emergency or redo surgeries, prolonged mechanical ventilation, and perioperative hemodynamic instability.
The microbiology is frequently polymicrobial, with common pathogens including Staphylococcus aureus (including MRSA in some settings), coagulase-negative staphylococci, Enterococcus species, and Gram-negative bacilli such as Pseudomonas aeruginosa.

Pathophysiology

Infection typically begins at the sternotomy incision and can progress to involve the sternum (osteomyelitis) and the mediastinal tissues.
Necrosis of tissue, impaired blood supply to the sternum, and the presence of prosthetic material or grafts can create a nidus for bacterial proliferation.
Involvement of the mediastinum raises the risk of sepsis and empyema, requiring aggressive source control in addition to antimicrobial therapy.
Biofilm formation on hardware or sternal wires can complicate eradication and necessitate hardware management.

Classification

In clinical practice, DSWI is distinguished from superficial sternal wound infections by depth of involvement (sternum and mediastinal tissues vs skin/subcutaneous tissue).
Mediastinitis is a related term often used when infection extends into the mediastinal space; imaging and intraoperative findings help determine the extent and guide management.
Classification schemes used in literature and guidelines may reference timing (early postoperative vs. late infections) and the presence of conduit infection, hardware involvement, or osteomyelitis.

Risk factors

Diabetes mellitus and poor glycemic control
Obesity and metabolic syndrome
Redo sternotomy or multiple prior cardiac procedures
Renal insufficiency or dialysis dependence
Chronic obstructive pulmonary disease and impaired pulmonary function
Immunosuppression (e.g., steroids, chemotherapy)
Smoking and poor tissue perfusion
Prolonged operative times, low cardiac output states, or intraoperative complications
Use of bilateral internal mammary arteries in CABG, which can influence sternal perfusion in some patients

Microbiology

The infectious profile is often polymicrobial.
Common pathogens include:
- Staphylococcus aureus (including MRSA strains in settings with high prevalence)
- coagulase-negative staphylococci
- Enteric Gram-negative bacteria
- Pseudomonas aeruginosa
Culture data from wound drainage, mediastinal tissue, or explanted hardware guide targeted antimicrobial therapy.

Diagnosis

Clinical suspicion arises from fever, chest pain, wound drainage, sternal instability or click, and erythema extending beyond the wound margins.
Laboratory markers such as leukocytosis and elevated inflammatory markers (e.g., C-reactive protein) support the diagnosis but are not specific.
Imaging, particularly computed tomography (CT) of the chest, helps assess mediastinal involvement, chest wall destruction, and presence of empyema.
Microbiological cultures from wound sites, mediastinal tissue, or any drained collections are essential for guiding therapy.
Distinction from superficial wound infections is important, as management differs markedly with deeper infection and potential mediastinal involvement.

Diagnosis and classification terminology (linking to related topics)

Median sternotomy trauma and postoperative care are discussed in median sternotomy resources.
The mediastinal infection spectrum intersects with mediastinitis discussions in thoracic practice.
Management planning often involves concepts from debridement and regional tissue transfer, including muscle flap techniques such as pectoralis major flap or latissimus dorsi flap.

Management

Management requires rapid source control, appropriate antimicrobial therapy, and clearance of infection with reconstruction when needed. A multidisciplinary approach improves outcomes.

Antibiotic therapy
- Start empiric broad-spectrum coverage to address likely Gram-positive organisms (including MRSA in high-prevalence areas) and Gram-negative bacilli.
- Typical empiric regimens may include vancomycin plus a broad-spectrum beta-lactam or antipseudomonal agent (for example, a regimen that could involve piperacillin-tazobactam or cefepime).
- Once culture results are available, tailor therapy to the identified pathogens and susceptibility patterns.
- Consider the role of rifampin in certain hardware-associated infections, used in combination with other agents and with attention to drug interactions and resistance concerns.
- Duration is guided by the extent of infection and reconstruction; typical courses range from 4 to 6 weeks, with longer durations if there is osteomyelitis or retained hardware.
- See also antibiotics and pathogen-specific guidelines for tailored regimens.
Source control and surgical management
- Urgent surgical debridement of necrotic tissue is essential to remove infected material and vascularized tissue that wicks infection.
- Infected sternal wires and nonviable osseous tissue may need removal or replacement; persistent instability often necessitates reconstructive strategies.
- Techniques to restore chest wall integrity and fill dead space include regional muscle flaps such as the pectoralis major flap or other regional flaps like the latissimus dorsi flap or omental flap.
- Negative pressure wound therapy (negative pressure wound therapy) is commonly used as a bridge to definitive closure or in staged reconstruction, helping manage wound exudate, edema, and tissue perfusion.
- In selected cases, sternal plating or mesh-based stabilization may complement soft-tissue reconstruction and improve chest wall stability.
- Reoperations for infection control and flap advancement often involve coordination with plastic or reconstructive surgery teams.
Reconstruction and rehabilitation
- Muscle flap–based reconstruction provides vascularized tissue to the infected sternum and mediastinal space, enhances healing, and lowers reinfection risk.
- Reconstructive choices depend on defect size, prior surgeries, comorbidities, and tissue availability. Options include bilateral pectoralis major advancement flaps, latissimus dorsi flaps, or omental flaps when feasible.
- Rehabilitation focuses on respiratory function, chest wall mechanics, and prevention of recurrent wound problems.

Prevention

Preoperative optimization of comorbidities (e.g., strict glycemic control in diabetes) reduces infection risk.
Perioperative antibiotic prophylaxis should be aligned with guidelines and timed appropriately relative to incision.
Sterile technique, meticulous hemostasis, and minimization of operating room contamination are essential.
Perioperative nasal decolonization for MRSA carriers, when indicated, may reduce infection risk.
Intraoperative and postoperative strategies to optimize tissue perfusion, oxygenation, and hemodynamic stability contribute to better outcomes.
Postoperative care includes careful wound surveillance, early mobilization, pulmonary hygiene, and smoking cessation resources when applicable.