ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Postoperative mediastinitis after cardiac surgery

Postoperative mediastinitis after cardiac surgery
Literature review current through: May 2024.
This topic last updated: Nov 21, 2022.

INTRODUCTION — Mediastinitis refers to infection involving the mediastinum, the region in the middle of the thorax bordered by the sternum and costal cartilages anteriorly, the thoracic vertebral bodies posteriorly, and the lungs and pleurae on each side. Prior to the development of modern cardiovascular surgery, most cases of mediastinitis arose from either esophageal perforation or from contiguous spread of odontogenic or retropharyngeal infections. Rarely, primary infections of the mediastinum developed as a result of penetrating trauma or hematogenous spread of infection. However, in modern practice, most cases of mediastinitis are a postoperative complication of cardiovascular or other thoracic surgical procedures.

The clinical features, diagnosis, and medical management of postoperative mediastinitis are reviewed here. The surgical management of sternal wound complications is discussed in detail separately. (See "Surgical management of sternal wound complications".)

PATHOGENESIS — The pathogenesis of postoperative mediastinitis is complex and multifactorial. The most important factor is intraoperative wound contamination, usually from the patients’ endogenous flora, but occasionally from exogenous contamination of the surgical field. Such contamination occurs in virtually all patients during the long time interval that sternotomy wounds remain open during cardiac surgery. The degree and type of contamination in combination with host factors, such as the adequacy of local blood supply, nutrition, and immunologic status, affect the risk of infection. In a small number of patients, the contamination leads to infection, even if meticulous care is exercised by the surgical team.

A number of other preoperative, intraoperative, and postoperative factors play a role in the pathogenesis of postoperative mediastinitis and are outlined in greater detail below. Some of these include preoperative skin colonization with potentially pathogenic or highly resistant organisms, disruption of the blood supply to the sternum during surgery, tissue trauma due to electrocautery, and early postoperative wound disruption (eg, from coughing).

EPIDEMIOLOGY

Incidence — The incidence of postoperative mediastinitis ranges from 0.25 to 5 percent, with the incidence in most centers being between 1 and 2 percent [1-5]. However, the risk may be considerably higher in certain subsets of patients. As an example, the rates have ranged from 2.5 to 7.5 percent in patients undergoing heart transplantation [6,7], and may be higher if cardiac assist devices are used [8]. (See 'Risk factors' below.)

The incidence rate of postoperative mediastinitis has remained stable over the years. In a retrospective cohort of more than 45,000 patients who underwent coronary artery bypass surgery from 2006 to 2015, the overall incidence of postoperative mediastinitis was 0.78 percent and remained stable over time [9].

Risk factors — Various risk factors have been described for adult and pediatric postoperative sternal wound infection

In adults [3,5,10-21]:

Preoperative risk factors:

-Nasal colonization with Staphylococcus aureus

-Diabetes mellitus or perioperative hyperglycemia

-Obesity

-Heart failure and left ventricular dysfunction

-Peripheral artery disease

-Tobacco use

-Prior cardiac surgery

-End-stage renal disease requiring hemodialysis

-Chronic obstructive pulmonary disease

-Need for an intra-aortic balloon pump

-Hair removal with razor versus electric clippers

Intraoperative/surgical risk factors:

-Emergent or urgent surgery

-Mobilization of the internal mammary arteries

-Prolonged perfusion time and aortic cross clamp time

-Prolonged surgical procedure (greater than five hours)

Postoperative risk factors:

-Return to the operating room (eg, control bleeding)

-Respiratory failure requiring prolonged mechanical ventilation

-Prolonged intensive care unit stay

-Poor glycemic control

Although a general lack of consensus exists as to which risk factors are most important, diabetes and obesity are frequently cited as the two key risk factors for developing postoperative mediastinitis [22]. In one review of >10,000 cardiac procedures, the rate of mediastinitis was almost three times as high in patients with body mass index (BMI) >30 as in those with BMI <25 [23].

In children [4,24-26]:

Preoperative risk factors:

-Younger age (<1 years highest risk)

-Higher American Society of Anesthesiologists score

-Preoperative infection or upper respiratory infection

Intraoperative/surgical risk factors:

-Prolonged perfusion time and aortic cross clamp time

-Prolonged surgical procedure

Postoperative risk factors:

-Respiratory failure requiring prolonged mechanical ventilation

-Prolonged intensive care unit stay

-Presence of intracardiac pacing wires for >3 days

-Receipt of >2 red blood cell transfusions

-Open-chest and return to operating room to control bleeding

Risk factors for sternal wound complications (including poor wound healing and infection) are discussed in further detail separately. (See "Surgical management of sternal wound complications", section on 'Risk factors for sternal wound complications'.)

Risk indices — Several risk indices for sternal wound infections following cardiac surgery have been described [10,11,14,27,28]. A preoperative scoring system based on a 3-point scale evaluated in a cohort of 4987 patients may be the most useful for predicting the risk of postoperative mediastinitis [14]. In this study, points were assigned for diabetes (1 point), a BMI >29 but <35 kg/m2 (1 point) and a BMI of 35 kg/m2 or greater (2 points). Each point in the scoring system approximately doubled the risk for postoperative surgical-site infection. Subsequent validation of this risk index was noted in a separate study of 269 cases of surgical site infections after coronary artery bypass surgery [28]. These risk indices are primarily used in analyzing quality improvement or comparative outcome data.

MICROBIOLOGY — The majority of patients with postoperative mediastinitis have monomicrobial infections. In two reviews with a total of 350 patients with postoperative mediastinitis, 290 (83 percent) had a single pathogen isolated from their mediastinum or blood [1,29].

Virtually any organism can cause mediastinitis, however, Staphylococcus aureus remains the most common cause. In a prospective review of 316 patients with mediastinitis occurring less than 30 days after sternotomy, the most common microorganisms isolated were [29]:

Methicillin-susceptible S. aureus (MSSA) (45 percent)

Methicillin-resistant S. aureus (MRSA) (16 percent)

Gram-negative bacilli (17 percent)

Coagulase-negative staphylococci (13 percent)

Streptococci (5 percent)

Postoperative mediastinitis due to MSSA appears to occur more often in the setting of preoperative nasal MSSA colonization, whereas postoperative mediastinitis due to MRSA appears to occur via nosocomial transmission between patients. This was illustrated in a study of 17 cases of mediastinitis observed among 1432 cardiac surgery patients [30]. Among the nine cases due to MSSA, seven had an identical isolate in preoperative nasal and surgical site cultures (as demonstrated by pulsed field gel electrophoresis [PFGE]). Among the eight cases due to MRSA, none had an identical isolate by PFGE, and the same MRSA clone was implicated in all of these cases.

Rarely, postoperative mediastinitis is due to unusual organisms such as fungi [31,32], Legionella [33], Mycoplasma hominis [34], Nocardia [35], Mycobacterium chimaera and Mycobacterium abscessus (associated with contaminated heater-cooler devices used in bypass surgery) [36-38], and Mycobacterium tuberculosis [39]. (See "Candida infections of the abdomen and thorax", section on 'Mediastinitis' and "Overview of nontuberculous mycobacterial infections", section on 'M. chimaera associated with cardiac surgery'.)

CLINICAL FEATURES

Time to presentation — The majority of patients with postoperative mediastinitis develop evidence of infection within 7 to 14 days of surgery; however, in some cases, the onset may be delayed for months. In one report, for example, the time to onset ranged from 3 to 417 days after surgery; however, the median was seven days, and two-thirds of patients presented within two weeks of surgery [40]. Similar findings were noted in another series, in which the onset of infection occurred more than one month after surgery in only 4 of 34 cases [1]. Gram-negative postoperative mediastinitis tends to occur earlier following surgery than gram-positive postoperative mediastinitis [41].

Signs and symptoms — Postoperative mediastinitis may follow a fulminant or more subacute clinical course. Most often, patients present with fever and localizing signs of infection such as erythema/cellulitis, tenderness, purulent wound drainage, and in some cases, sternal instability. In one study, for example, sternal wound drainage and/or cellulitis were present in 29 of 34 patients (85 percent) with postoperative mediastinitis [1]. More subtle presentations may manifest as sepsis without associated external signs of infection and clinicians must maintain a high index of suspicion for mediastinitis. Other local exam findings that may be seen include crepitus and edema of the chest wall, and Hamman's sign (a crunching sound that is synchronous with the heart beat and heard by chest auscultation).

Although signs of sternal wound infection can precede or follow the recognition of mediastinitis, fever and systemic symptoms appear first in most patients. (See "Surgical management of sternal wound complications", section on 'Wound assessment'.)

Laboratory features — Almost all patients with postoperative mediastinitis have leukocytosis, but this is a nonspecific finding. C-reactive protein and procalcitonin are also typically elevated. Because bacteremia may be the first sign of postoperative mediastinitis, the possibility of mediastinitis should be considered carefully during the evaluation of all bacteremic patients following cardiac or thoracic surgery.

Bacteremia is common in postoperative mediastinitis, occurring in 57 percent of patients with postoperative mediastinitis in one report [40]. As an example, a study including 266 febrile patients post-cardiac surgery found that the presence of S. aureus bacteremia had a 73 percent sensitivity, 98 percent specificity, 90 percent positive predictive value, and 93 percent negative predictive value for postoperative mediastinitis [42]. Another series identified mediastinitis as the underlying cause of bacteremia in 16 of 27 (59 percent) of patients with positive blood cultures in the early postoperative period [43].

Radiographic features — The two hallmark imaging findings of mediastinitis are:

Localized mediastinal fluid

Pneumomediastinum (ie, gas bubbles in the mediastinum)

Computed tomography is better than plain radiography in demonstrating these findings.

Gas bubbles and mediastinal fluid collections may be normal findings after surgery, but they usually disappear within 21 days [44]. Thus, persistent gas or fluid collections more than three weeks after surgery can be useful and important diagnostic clues if they are accompanied by other signs of infection. Gas bubbles are present in slightly more than half of patients with postoperative mediastinitis. In such cases, gas may be related to abscess formation or esophageal injury.

Mediastinal widening on chest radiograph, which is a radiologic hallmark of non-postoperative mediastinitis, is rarely seen in patients with mediastinitis following cardiac surgery [45]. Other abnormalities that are rarely seen include air fluid levels in the mediastinum or subcutaneous tissue, and mediastinal air on lateral chest radiographs.

DIAGNOSIS — The diagnosis of postoperative mediastinitis should be suspected in patients who present with a characteristic clinical pattern of fever, leukocytosis, and external exam findings of infection such as erythema/cellulitis, tenderness, purulent wound drainage, or sternal instability. When mediastinitis is suspected, patients should have two sets of blood cultures obtained via venipuncture and should undergo computed tomography (CT) of the chest with and without contrast to evaluate for enhancing pleural or loculated fluid collection, enlarged brachiocephalic lymph nodes, or presence of gas bubbles [46]. The presence of positive blood cultures and/or concerning mediastinal fluid collections or gas should prompt a return to the operating room for further exploration. The diagnosis can be definitively made through microbiologic, anatomic, or histopathologic evidence collected at the time of repeat surgery. We recommend that intraoperative mediastinal tissue be sent for bacterial, fungal, and mycobacterial culture. Fungal and mycobacterial cultures are important in establishing a microbiologic diagnosis for immunocompromised patients as they are at greater risk for atypical pathogens. Furthermore, in light of prior outbreaks of M. chimaera and M. abscessus associated with heater-cooler use, clinicians should maintain a high level of suspicion for an infection due to nontuberculous mycobacteria in patients with negative routine bacterial cultures.

The United States Centers for Diseases Control and Prevention has proposed a definition of mediastinitis that requires patients to meet at least one of the three criteria below [47]:

Patient has organism(s) identified from mediastinal tissue or fluid by a culture or nonculture based microbiologic testing method, which was performed for purposes of clinical diagnosis or treatment.

Patient has evidence of mediastinitis on gross anatomic or histopathologic exam.

Patient has at least one of these signs or symptoms (fever [>38.0°C], chest pain, or sternal instability) and at least one of the following: purulent drainage from mediastinal area or mediastinal widening on imaging test.

This definition allows for the clinical diagnosis of mediastinitis to be made in situations where the patient has a clinical presentation consistent with mediastinitis but microbiologic or histopathologic evidence is not available.

The diagnosis may be more difficult to establish in patients with fever and leukocytosis but who lack signs of local sternal wound infection. In these situations, we also recommend two sets of blood cultures obtained via venipuncture and CT of the chest with and without contrast. If fevers and leukocytosis persist, alternative nosocomial infections and causes of fever have been ruled out, blood cultures remain negative, and no new localizing signs of sternal wound infection appear, CT scan findings of fluid collection or gas bubbles should prompt further discussion with the surgical team regarding the utility of mediastinal needle aspiration versus exploratory surgery.

The timing of the CT scan plays an important role in the discussion. The later CT imaging is performed after surgery, the more likely the findings are to be diagnostically useful. In one study, for example, CT had a sensitivity of 100 percent but a specificity of only 33 percent for postoperative mediastinitis if performed before postoperative day 17; however, both the specificity and sensitivity were 100 percent when CT scan was performed later [44]. In another study, the presence of mediastinal fluid collections or free gas bubbles before 21 days had a sensitivity and specificity of 100 and 39 percent, respectively for mediastinitis. After 21 days, the sensitivity remained 100 percent and the specificity increased to 85 percent [48].

One group reported on their experience using needle aspiration in 49 patients with suspected postoperative mediastinitis [49]. A 21-gauge needle was placed through the margins of the prior sternotomy site and an aspirate was performed at an approximate depth of one centimeter. If the initial aspirate did not obtain fluid, aspirates were repeated at two other portions of the sternal wound. This approach yielded the same organism as was subsequently found during a later debridement in all 23 patients diagnosed with true mediastinitis; cultures and Gram stain of aspirates were negative in 24 of 26 patients without mediastinitis. Furthermore, performing a needle aspiration to help diagnose mediastinitis resulted in a significantly shorter delay in diagnosis, reduction in the length of mechanical ventilation and intensive care unit stay when compared with 20 patients who did not undergo aspiration. Although this report suggests that sternal puncture is safe and reliable, the sensitivity, specificity, and safety of this technique require validation by others, and this procedure is not commonly done in most centers.

Another study examined the utility of blood cultures in diagnosing postoperative mediastinitis in a large number of patients undergoing open heart surgery via a median sternotomy [50]. In this cohort of 5500 patients, the detection of S. aureus bacteremia had a likelihood ratio (LR) of 25 for the presence of mediastinitis (95% CI 14.7-44.4). Forty-six of 60 patients (77 percent) who had bacteremia due to S. aureus within 90 days of cardiac surgery developed mediastinitis due to the same organism. Curiously, bacteremia due to other organisms did not have the same prognostic significance: only 15 of 126 patients (12 percent) with non-S. aureus bacteremia developed mediastinitis (LR 1.0, 95% CI 0.6-1.7). Patients with negative blood cultures were significantly less likely to have mediastinitis (LR 0.45, 95% CI 0.35-0.58).

Cultures of epicardial pacing wires may be of some utility in patients who present with early-onset postoperative mediastinitis. In one report, such cultures had a sensitivity of 75 percent and a specificity of 83 percent [51]. Although the positive predictive value of a single culture was only 12 percent, the negative predictive value of an individual culture was 99 percent. When S. aureus was isolated from such cultures, the specificity, sensitivity, and positive predictive value were even higher. In our experience, however, these cultures are rarely practical because pacing wires have often been removed by the time mediastinitis manifests or because the diagnosis is obvious from the typical clinical findings.

TREATMENT — Treatment of mediastinitis requires a combination of surgical debridement and antimicrobial therapy.

Surgical management — Surgical debridement is the mainstay of therapy for postoperative mediastinitis followed by an immediate closure, or an interval of open wound care followed by delayed primary or flap closure [2,32]. The surgical management of sternal wound complications is discussed separately. (See "Surgical management of sternal wound complications".)

For patients who have an open sternal wound following debridement for post-sternotomy mediastinitis, topical negative pressure wound therapy, or vacuum-assisted closure (VAC), is commonly used prior to subsequent delayed pectoral flap or omental flap repair. In a systematic review of studies that evaluated the outcome of negative pressure wound therapy compared to other wound management strategies for post-sternotomy mediastinitis, most studies observed that negative pressure wound therapy was associated with clinical benefits, such as decreased hospital stay, decreased rates of reinfection, and in a few studies, decreased early mortality [52]. The comparable efficacy of this modality versus conventional treatment (debridement followed by delayed closure with open dressings or immediate closure with closed irrigation) was also evaluated in a separate retrospective study of 90 patients who developed mediastinitis after coronary artery bypass surgery [53]. Negative pressure wound therapy was associated with a lower ninety day mortality (8.5 versus 23.2 percent with conventional treatment) and higher overall one-year survival (91.5 versus 76.7 percent). These results should be interpreted with caution, however, as all these studies are observational (and predominantly retrospective), and there was substantial variability in the actual wound management strategies used for comparison.

The management of the open sternal wound, including the use of negative pressure wound therapy or open dressings, is discussed separately. (See "Surgical management of sternal wound complications", section on 'Management of the open sternum'.)

Antimicrobial therapy — Systemic antimicrobial therapy should be instituted as soon the diagnosis of mediastinitis is suspected or established and after blood cultures have been obtained. Initial empiric therapy should consist of broad coverage against gram-positive cocci, including methicillin-resistant staphylococci, and gram-negative bacilli. We recommend a regimen consisting of intravenous vancomycin plus ceftazidime or cefepime pending further culture data. The regimen should be adjusted as soon as the results of cultures of blood and mediastinal or deep sternal wound drainage become available.

The optimal duration of therapy for postoperative mediastinitis is not well defined and largely depends on how patients are surgically managed after diagnosis. Postoperative mediastinitis commonly presents with an associated deep sternal wound infection and osteomyelitis. Sternal wires in the infected area are typically removed and the bone is debrided as much as possible; however, the remaining bone may serve as a residual site of infection. As such, we recommend treating for a total of four to six weeks for underlying osteomyelitis. As usual, parenteral therapy is preferred for the treatment of osteomyelitis, except in cases where an oral antibiotic with excellent bone penetration is an option (eg, ciprofloxacin for Pseudomonas aeruginosa or another gram-negative organism). In the rare cases where patients undergo complete sternal resection and pectoralis flap repair, two to three weeks of antibiotic therapy may be sufficient. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

Residual sternal wires or the presence of chronically infected bone may serve as a nidus for infection and both patients and clinicians should monitor for signs or recrudescence of infection. Presence of a draining sinus tract should signal the need for additional debridement and removal of potentially involved sternal wires.

PREVENTION — The issue of antibiotic prophylaxis and S. aureus decontamination to prevent surgical site infections such as postoperative mediastinitis is discussed in detail separately. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Cardiac surgery' and "Overview of control measures for prevention of surgical site infection in adults", section on 'S. aureus decolonization'.)

Summarized briefly:

Routine antimicrobial prophylaxis should be administered within 60 minutes before the initial incision. There are conflicting recommendations for repeat dosing during and shortly after the completion of surgery.

The usual drugs of choice are intravenous cefazolin or cefuroxime. Intravenous vancomycin is preferred if the patient is previously colonized with MRSA or is allergic to penicillins or cephalosporins, or if surgery is performed in a hospital in which MRSA and/or coagulase-negative staphylococci are a common cause of postoperative infection. Details on dosing and administration are found elsewhere. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults", section on 'Cardiac surgery'.)

Routine preoperative S. aureus screening and decolonization has not been definitively proven to be effective is discussed in detail separately. (See "Overview of control measures for prevention of surgical site infection in adults", section on 'S. aureus decolonization'.)

The use of gentamicin-collagen sponges does not appear to reduce the 90-day sternal wound infection rate among patients with diabetes and/or high body mass index [54].

Similarly, the use of vancomycin paste does not appear to reduce rates of deep sternal wound infection based on one study [55].

Technical factors that are important for preventing sternal wound infection include appropriate choice of sternal wiring (or suture) technique with proper alignment of the sternal edges and meticulous hemostasis that avoids the excessive use of electrocautery. These issues are discussed further separately.

PROGNOSIS — Since the widespread use of advanced surgical management techniques, mortality rates have ranged from 1 to 14 percent, improved over prior reported rates of 12 to 50 percent [5]. In one study including 83 patients with mediastinitis, the mortality during the first 90 days after surgery was 12 percent (compared with 6 percent for 6376 patients without mediastinitis) [12]. In addition, the interval mortality between one and two years after surgery remained higher in the patients with mediastinitis (8 versus 2 percent). Another study suggested that the risk of death following mediastinitis remains higher than in uninfected controls for up to 10 years (49 versus 71 percent) [4]. The majority of deaths in both groups was attributed to cardiac causes, but the proportion of cardiac deaths was higher in patients who had mediastinitis [4].

A prospective study of 316 consecutive cases of postoperative mediastinitis identified patient risk factors for intensive care unit mortality [29]. Independent risk factors present on admission were age greater than 70 years, operation other than coronary artery bypass grafting alone, severity of the underlying medical condition (McCabe class 2/3), APACHE II score, and organ failure. After introducing day three variables into the logistic regression model, the additional independent risk factors for death were mechanical ventilation still required on day three and persistently positive blood cultures.

A study of 183 patients with postoperative mediastinitis published in 2006 found that death occurred in 51 patients (33 percent); median time to death was 37 days [56]. Independent predictors of death included:

Delay >3 days in sternal closure after debridement (Hazard Ratio [HR] 6.3)

Age >65 (HR 2.3)

Stay in ICU before sternal debridement (HR 5.6)

Serum creatinine >2 mg/dL before debridement (HR 2.5)

Infection due to MRSA (HR 2.1)

Treatment with antibiotics with in vitro activity against the infecting pathogen within 7 days of debridement was associated with decreased mortality risk (HR 0.4)

Mortality is higher among patients with MRSA than MSSA infection [57-59]. This was illustrated in a series of 41 patients with mediastinitis; 15 with MRSA and 26 with MSSA [57]. MRSA mortality rates were higher than MSSA mortality rates at one month (40 versus 15 percent), one year (48 versus 21 percent) and three years (74 versus 21 percent). However, these results should be interpreted with caution since the underlying characteristics of patients with MRSA infections are often substantially different from those of typical patients who acquire infections due to MSSA.

Postoperative mediastinitis is also associated with substantial morbidity including the need for additional surgery, increased length of stay, and increased cost. The length of stay for affected patients is ranged from 38 to 51 days and the total cost of care by two- to threefold compared with control patients [3]. Another study of 436 sternal wound infections contributed to 2600 additional hospital days and USD $20,000 cost per case [60].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Deep sternal wound infection".)

SUMMARY AND RECOMMENDATIONS

Microbiology Most contemporary cases of mediastinitis occur as a postoperative complication of cardiothoracic surgical procedures. The majority of infections are caused by a single organism. Although a wide array of bacterial, mycobacterial, and fungal organisms can cause mediastinitis, Staphylococcus aureus remains the most commonly isolated pathogen. (See 'Introduction' above and 'Microbiology' above.)

Risk factors A variety of preoperative, intraoperative, and postoperative risk factors for the development of postoperative mediastinitis exist. (See 'Risk factors' above.)

Clinical features The vast majority of patients with postoperative mediastinitis present with fever and leukocytosis or other signs of sepsis, chest pain or sternal instability, local signs of sternal wound infection, or purulent discharge. Bacteremia is common. The infection typically manifests within two weeks following the surgery, although the onset of symptoms can occasionally occur months later. Hallmark findings on computed tomography are localized mediastinal fluid and a pneumomediastinum. (See 'Clinical features' above.)

Diagnosis The diagnosis is made clinically in a patient presenting with signs and symptoms consistent with postoperative mediastinitis. Computed tomography is more useful in supporting the diagnosis when performed later than two weeks postoperatively. Finding pus in the mediastinum during subsequent surgical debridement can confirm the clinical diagnosis. (See 'Diagnosis' above.)

Treatment The treatment of mediastinitis involves a combination of antimicrobial therapy and surgical debridement with either immediate or delayed closure. An empiric antimicrobial regimen should include broad coverage against both gram-positive cocci (including methicillin-resistant S. aureus) and gram-negative bacilli and can later be adjusted based on culture and susceptibility data. The duration of therapy generally ranges from two to six weeks and depends on the extent of surgical debridement performed as well as presence of associated deep sternal wound infection and underlying osteomyelitis. (See 'Treatment' above.)

Prevention and prognosis Strategies to prevent postoperative mediastinitis include perioperative antibiotics, naso- and oropharyngeal chlorhexidine decontamination, and surgical techniques that ensure alignment of sternal edges and meticulous hemostasis. Mediastinitis is associated with an excess postoperative mortality that can persist for years following the procedure. (See 'Prevention' above and 'Prognosis' above.)

ACKNOWLEDGMENT — UpToDate gratefully acknowledges John G Bartlett, MD, who contributed as Section Editor on earlier versions of this topic and was a founding Editor-in-Chief for UpToDate in Infectious Diseases.

  1. Fariñas MC, Gald Peralta F, Bernal JM, et al. Suppurative mediastinitis after open-heart surgery: a case-control study covering a seven-year period in Santander, Spain. Clin Infect Dis 1995; 20:272.
  2. El Oakley RM, Wright JE. Postoperative mediastinitis: classification and management. Ann Thorac Surg 1996; 61:1030.
  3. Loop FD, Lytle BW, Cosgrove DM, et al. J. Maxwell Chamberlain memorial paper. Sternal wound complications after isolated coronary artery bypass grafting: early and late mortality, morbidity, and cost of care. Ann Thorac Surg 1990; 49:179.
  4. Risnes I, Abdelnoor M, Almdahl SM, Svennevig JL. Mediastinitis after coronary artery bypass grafting risk factors and long-term survival. Ann Thorac Surg 2010; 89:1502.
  5. Abu-Omar Y, Kocher GJ, Bosco P, et al. European Association for Cardio-Thoracic Surgery expert consensus statement on the prevention and management of mediastinitis. Eur J Cardiothorac Surg 2017; 51:10.
  6. Baldwin RT, Radovancevic B, Sweeney MS, et al. Bacterial mediastinitis after heart transplantation. J Heart Lung Transplant 1992; 11:545.
  7. Sénéchal M, LePrince P, Tezenas du Montcel S, et al. Bacterial mediastinitis after heart transplantation: clinical presentation, risk factors and treatment. J Heart Lung Transplant 2004; 23:165.
  8. Griffith BP, Kormos RL, Hardesty RL, et al. The artificial heart: infection-related morbidity and its effect on transplantation. Ann Thorac Surg 1988; 45:409.
  9. Wojnarski CM, Elgudin Y, Rubelowsky JJ, et al. Emerging trends in mediastinitis: National Veterans Health Administration experience with methicillin-resistant Staphylococcus aureus prevention. J Thorac Cardiovasc Surg 2021; 162:1125.
  10. Kohli M, Yuan L, Escobar M, et al. A risk index for sternal surgical wound infection after cardiovascular surgery. Infect Control Hosp Epidemiol 2003; 24:17.
  11. Russo PL, Spelman DW. A new surgical-site infection risk index using risk factors identified by multivariate analysis for patients undergoing coronary artery bypass graft surgery. Infect Control Hosp Epidemiol 2002; 23:372.
  12. Milano CA, Kesler K, Archibald N, et al. Mediastinitis after coronary artery bypass graft surgery. Risk factors and long-term survival. Circulation 1995; 92:2245.
  13. Ottino G, De Paulis R, Pansini S, et al. Major sternal wound infection after open-heart surgery: a multivariate analysis of risk factors in 2,579 consecutive operative procedures. Ann Thorac Surg 1987; 44:173.
  14. Friedman ND, Bull AL, Russo PL, et al. An alternative scoring system to predict risk for surgical site infection complicating coronary artery bypass graft surgery. Infect Control Hosp Epidemiol 2007; 28:1162.
  15. Trick WE, Scheckler WE, Tokars JI, et al. Modifiable risk factors associated with deep sternal site infection after coronary artery bypass grafting. J Thorac Cardiovasc Surg 2000; 119:108.
  16. Wilson SJ, Sexton DJ. Elevated preoperative fasting serum glucose levels increase the risk of postoperative mediastinitis in patients undergoing open heart surgery. Infect Control Hosp Epidemiol 2003; 24:776.
  17. Grossi EA, Esposito R, Harris LJ, et al. Sternal wound infections and use of internal mammary artery grafts. J Thorac Cardiovasc Surg 1991; 102:342.
  18. Dodds Ashley ES, Carroll DN, Engemann JJ, et al. Risk factors for postoperative mediastinitis due to methicillin-resistant Staphylococcus aureus. Clin Infect Dis 2004; 38:1555.
  19. Perrault LP, Kirkwood KA, Chang HL, et al. A Prospective Multi-Institutional Cohort Study of Mediastinal Infections After Cardiac Operations. Ann Thorac Surg 2018; 105:461.
  20. Tanner J, Melen K. Preoperative hair removal to reduce surgical site infection. Cochrane Database Syst Rev 2021; 8:CD004122.
  21. Muñoz P, Hortal J, Giannella M, et al. Nasal carriage of S. aureus increases the risk of surgical site infection after major heart surgery. J Hosp Infect 2008; 68:25.
  22. Bryan CS, Yarbrough WM. Preventing deep wound infection after coronary artery bypass grafting: a review. Tex Heart Inst J 2013; 40:125.
  23. Eklund AM, Lyytikäinen O, Klemets P, et al. Mediastinitis after more than 10,000 cardiac surgical procedures. Ann Thorac Surg 2006; 82:1784.
  24. Costello JM, Graham DA, Morrow DF, et al. Risk factors for surgical site infection after cardiac surgery in children. Ann Thorac Surg 2010; 89:1833.
  25. Kagen J, Lautenbach E, Bilker WB, et al. Risk factors for mediastinitis following median sternotomy in children. Pediatr Infect Dis J 2007; 26:613.
  26. Mangukia CV, Agarwal S, Satyarthy S, et al. Mediastinitis following pediatric cardiac surgery. J Card Surg 2014; 29:74.
  27. Roy MC, Herwaldt LA, Embrey R, et al. Does the Centers for Disease Control's NNIS system risk index stratify patients undergoing cardiothoracic operations by their risk of surgical-site infection? Infect Control Hosp Epidemiol 2000; 21:186.
  28. Chen L, Anderson D, Kaye K, Sexton DJ. Validating a new predictive instrument for surgical site infections following cardiac bypass surgery. Presented at the Annual IDSA Meeting. San Diego, CA. October 4-7, 2007.
  29. Trouillet JL, Vuagnat A, Combes A, et al. Acute poststernotomy mediastinitis managed with debridement and closed-drainage aspiration: factors associated with death in the intensive care unit. J Thorac Cardiovasc Surg 2005; 129:518.
  30. San Juan R, Chaves F, López Gude MJ, et al. Staphylococcus aureus poststernotomy mediastinitis: description of two distinct acquisition pathways with different potential preventive approaches. J Thorac Cardiovasc Surg 2007; 134:670.
  31. Pertowski CA, Baron RC, Lasker BA, et al. Nosocomial outbreak of Candida albicans sternal wound infections following cardiac surgery traced to a scrub nurse. J Infect Dis 1995; 172:817.
  32. Glower DD, Douglas JM Jr, Gaynor JW, et al. Candida mediastinitis after a cardiac operation. Ann Thorac Surg 1990; 49:157.
  33. Lowry PW, Blankenship RJ, Gridley W, et al. A cluster of legionella sternal-wound infections due to postoperative topical exposure to contaminated tap water. N Engl J Med 1991; 324:109.
  34. Sielaff TD, Everett JE, Shumway SJ, et al. Mycoplasma hominis infections occurring in cardiovascular surgical patients. Ann Thorac Surg 1996; 61:99.
  35. Wenger PN, Brown JM, McNeil MM, Jarvis WR. Nocardia farcinica sternotomy site infections in patients following open heart surgery. J Infect Dis 1998; 178:1539.
  36. Kohler P, Kuster SP, Bloemberg G, et al. Healthcare-associated prosthetic heart valve, aortic vascular graft, and disseminated Mycobacterium chimaera infections subsequent to open heart surgery. Eur Heart J 2015; 36:2745.
  37. Sax H, Bloemberg G, Hasse B, et al. Prolonged Outbreak of Mycobacterium chimaera Infection After Open-Chest Heart Surgery. Clin Infect Dis 2015; 61:67.
  38. Baker AW, Lewis SS, Alexander BD, et al. Two-Phase Hospital-Associated Outbreak of Mycobacterium abscessus: Investigation and Mitigation. Clin Infect Dis 2017; 64:902.
  39. Wang TK, Wong CF, Au WK, et al. Mycobacterium tuberculosis sternal wound infection after open heart surgery: a case report and review of the literature. Diagn Microbiol Infect Dis 2007; 58:245.
  40. Bor DH, Rose RM, Modlin JF, et al. Mediastinitis after cardiovascular surgery. Rev Infect Dis 1983; 5:885.
  41. Peghin M, Pompei E, Vendramin I, Tascini C. Gram-negative bacteria as a cause of mediastinitis after cardiac surgery. Curr Opin Infect Dis 2021; 34:710.
  42. San Juan R, Aguado JM, López MJ, et al. Accuracy of blood culture for early diagnosis of mediastinitis in febrile patients after cardiac surgery. Eur J Clin Microbiol Infect Dis 2005; 24:182.
  43. Kohman LJ, Coleman MJ, Parker FB Jr. Bacteremia and sternal infection after coronary artery bypass grafting. Ann Thorac Surg 1990; 49:454.
  44. Exarhos DN, Malagari K, Tsatalou EG, et al. Acute mediastinitis: spectrum of computed tomography findings. Eur Radiol 2005; 15:1569.
  45. Sarr MG, Gott VL, Townsend TR. Mediastinal infection after cardiac surgery. Ann Thorac Surg 1984; 38:415.
  46. Foldyna B, Mueller M, Etz CD, et al. Computed tomography improves the differentiation of infectious mediastinitis from normal postoperative changes after sternotomy in cardiac surgery. Eur Radiol 2019; 29:2949.
  47. Centers for Disease Control and Prevention. CDC/NHSN surveillance definitions for specific types of infections. https://www.cdc.gov/nhsn/pdfs/pscmanual/17pscnosinfdef_current.pdf (Accessed on April 10, 2017).
  48. Yamashiro T, Kamiya H, Murayama S, et al. Infectious mediastinitis after cardiovascular surgery: role of computed tomography. Radiat Med 2008; 26:343.
  49. Benlolo S, Matéo J, Raskine L, et al. Sternal puncture allows an early diagnosis of poststernotomy mediastinitis. J Thorac Cardiovasc Surg 2003; 125:611.
  50. Fowler VG Jr, Kaye KS, Simel DL, et al. Staphylococcus aureus bacteremia after median sternotomy: clinical utility of blood culture results in the identification of postoperative mediastinitis. Circulation 2003; 108:73.
  51. Maroto LC, Aguado JM, Carrascal Y, et al. Role of epicardial pacing wire cultures in the diagnosis of poststernotomy mediastinitis. Clin Infect Dis 1997; 24:419.
  52. Yu AW, Rippel RA, Smock E, Jarral OA. In patients with post-sternotomy mediastinitis is vacuum-assisted closure superior to conventional therapy? Interact Cardiovasc Thorac Surg 2013; 17:861.
  53. Deniz H, Gokaslan G, Arslanoglu Y, et al. Treatment outcomes of postoperative mediastinitis in cardiac surgery; negative pressure wound therapy versus conventional treatment. J Cardiothorac Surg 2012; 7:67.
  54. Bennett-Guerrero E, Ferguson TB Jr, Lin M, et al. Effect of an implantable gentamicin-collagen sponge on sternal wound infections following cardiac surgery: a randomized trial. JAMA 2010; 304:755.
  55. Lander HL, Ejiofor JI, McGurk S, et al. Vancomycin Paste Does Not Reduce the Incidence of Deep Sternal Wound Infection After Cardiac Operations. Ann Thorac Surg 2017; 103:497.
  56. Karra R, McDermott L, Connelly S, et al. Risk factors for 1-year mortality after postoperative mediastinitis. J Thorac Cardiovasc Surg 2006; 132:537.
  57. Mekontso-Dessap A, Kirsch M, Brun-Buisson C, Loisance D. Poststernotomy mediastinitis due to Staphylococcus aureus: comparison of methicillin-resistant and methicillin-susceptible cases. Clin Infect Dis 2001; 32:877.
  58. Engemann JJ, Carmeli Y, Cosgrove SE, et al. Adverse clinical and economic outcomes attributable to methicillin resistance among patients with Staphylococcus aureus surgical site infection. Clin Infect Dis 2003; 36:592.
  59. Reddy SL, Grayson AD, Smith G, et al. Methicillin resistant Staphylococcus aureus infections following cardiac surgery: incidence, impact and identifying adverse outcome traits. Eur J Cardiothorac Surg 2007; 32:113.
  60. Mossad SB, Serkey JM, Longworth DL, et al. Coagulase-negative staphylococcal sternal wound infections after open heart operations. Ann Thorac Surg 1997; 63:395.
Topic 7014 Version 34.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟