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Mediastinal Infection after Cardiac Surgery
COLLECTIVE REVIEW
Mediastinal Infection after Cardiac Surgery Michael G. Sarr, M.D., Vincent L. Gott, M.D., and Timothy R. Townsend, M.D. ABSTRACT Mediastinitis is an uncommon complication after cardiac surgery; however, its associated morbidity and mortality demand early recognition and emergency therapy. This review is intended to emphasize certain features of the incidence, pathogenesis, and bacteriology of this complication in patients undergoing cardiopulmonary bypass through a median sternotomy. The diagnosis and treatment of mediastinitis after cardiac surgical procedures, as well as methods of prevention, are also reviewed. Mediastinitis after cardiac surgical procedures remains a devastating complication. Localized mediastinal suppuration, generalized sepsis, and the possibility of local or metastatic spread of infection to prosthetic materials used in the cardiac repair [l-41 are all serious consequences, each minimized only by optimal prevention, early diagnosis, and emergency therapy. The last twenty years have witnessed a remarkable change in the spectrum of this disease. Concurrently, understanding of the physiology and pathophysiology of cardiopulmonary bypass (CPB) has expanded markedly, yielding a more comprehensive insight into the prevention of this complication.
Incidence of Postoperative Mediastinitis While the incidence of superficial wound infection after median sternotomy is no different than after other thoracic incisions [5], the incidence of mediastinitis after cardiac surgical procedures, when defined as suppuration involving the anterior mediastinal space, ranges from 0.4 to 5.0% (Table 1).Our most recent experience at the Johns Hopkins Hospital (1982) revealed an 0.7% incidence of mediastinitis after cardiac procedures. The most comprehensive series is that of Culliford and coworkers [6], who found an incidence of 1.5% in 2,594 patients undergoing cardiac procedures at the New York University Medical Center between 1971 and 1975. There appears to be no difference in the incidence of mediastinitis after the three major categories of cardiac surgical procedures (see Table 1).After coronary artery bypass grafting, the incidence has ranged from 1.2 to 2.5%. It may be even greater when the internal mammary artery (IMA) is used for coronary revascularization [7, 81. When both IMAs are used, the incidence of sternal and mediastinal sepsis may be as high as 8% [6]. Operations for congenital heart anomalies have a lower incidence of mediastinal sepsis, while valve replaceFrom the Departments of Surgery and Hospital Epidemiology, Johns Hopkins Hospital, Baltimore, MD. Address reprint requests to Dr.Sarr, Department of Surgery, Johns Hopkins Hospital, Baltimore, MD 21205.
415
ments fall in between. Double valve replacement or coronary artery bypass grafting combined with valve replacement [9] seems to manifest a higher infection rate.
Predisposing Factors Many factors in the perioperative and postoperative periods have been implicated as predisposing to an increased incidence of postoperative mediastinitis. Postoperative hemorrhage with the formation of mediastinal hematoma [2] appears to be a major complication leading to a high risk of mediastinal infection. In the New York University study [6], 53% of the 39 patients with mediastinitis experienced greater than 1,250 ml of blood loss following the cardiac procedure. Postoperative resternotomy (usually for hemorrhage), especially under emergency conditions [6], has been recognized repeatedly as a factor contributing to a higher incidence of “wound complications” [lo, 111 and mediastinitis [8]. Culliford, Engelman, Bryant, and their colleagues [6, 9, 121 found that 18 to 42% of patients with mediastinal infection had undergone early reexploration for hemorrhage. Prolonged operative time also may be a factor in development of mediastinal infection [13]. Engelman and co-workers [9] analyzed 17 patients with postoperative mediastinitis; the majority had undergone prolonged operations ranging from 6 to 17 hours. Nine were operated on for longer than 10 hours; CPB time exceeded 3 hours in 12 patients. Similarly, the larger New York University study [6] found that 53% of those patients in whom mediastinal infection later developed had been on bypass in excess of 3 hours. The sternotomy itself predisposes to sternal and mediastinal infection. Introduction of the safer, more precise Stryker saw has lessened the incidence of wound complications seen after use of the Gigli saw, the Tenon saw, or the Lebsche knife [13]. More secure sternal approximation has played an equally integral role in minimizing wound complications. Early studies found a higher incidence of sternal dehiscence when the sternal edges were approximated with silk instead of wire [5] or a less stable nylon band closure [ll, 141. Disruption of sternal approximation during external cardiac massage in the early postoperative period has been associated with a two to four times greater incidence of wound complications [lo, 111, mediastinitis [9], and chronic sternal infections [6]. A history of previous sternotomy appears to increase the incidence of postoperative hemorrhage and other wound complications [6, 15, 161. Culliford and co-workers [6] found that 33% of their patients in whom chronic osteochondritis or costochondritis developed following median sternotomy had a previous history of sternotomy.
416 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
Table I . Incidence of Mediastinal and Sternal Infection after Cardiac Surgical Procedures Utilizing Cardiopulmonary Bypass
Reference Ochsner et a1 [71] Grmoljez et al [8] Johns Hopkins Hospital (1982) [this review] Sutherland et a1 [17] Jurkiewicz et a1 [86] Culliford et a1 (61 Engelman et a1 [9] Thurer et a1 [62] Orringer et a1 [76] Jimenez-Martinezet a1 [26]
No. of
Patients 750 1,500 824
904 3,239 2,594 1,042 645 212 257
Specific Incidence (%)
Overall
Incidence
Repair CHD
Valve
Replacement
(%)
CABG
0.4 0.7 0.7
...
...
...
1.2 0.2
0.5
...
0.1 1.5
...
1.4
1.5 1.5 1.6 2.2
...
... ...
... ...
0.4 0.7 3.2 2.2"
2.2 1.4
...
5.0
1.9 2.5
... ... ...
...
...
... ...
"Total repair of tetralogy of Fallot prior to 1971. CABG = coronary artery bypass grafting; CHD = congenital heart disease.
Postoperative cardiopulmonary complications can also predispose to development of mediastinitis [lo-121. Although some studies failed to show an increased incidence of wound complications [ l l ] or mediastinitis [8, 171 in the presence of a low cardiac output state, in the two largest series [6, 91 half of the patients with mediastinal infection had experienced a low cardiac output syndrome in the early postoperative period. In patients with preoperative or postoperative pneumonitis, mediastinitis has developed with the same organism isolated from the pulmonary secretions [9]. Tracheostomy with prolonged artificial ventilation has been associated with mediastinal sepsis [HI. When the procedures are performed simultaneously, the tracheostomy and sternotomy wounds can be seen to communicate, thus allowing a portal of entry for pathogens into the anterior mediastinum. The relationship between use of the IMA for coronary bypass and subsequent mediastinitis is a topic of controversy. In 1974, Kay and co-workers [19] reported a series of 814 IMA grafts in 628 patients with a hospital mortality approaching only 1.7%;no mention was made of sternal infection, dehiscence, or mediastinitis. Previously, Green [20] had reported his series of 146 patients with IMA grafts; there were only 2 cases of "sternal dehiscence" and 3 of sepsis but, again, no specific mention of mediastinal or sternal infection. Other groups [9, 17, 211 denied an increased incidence of mediastinal or sternal infection with use of the IMA graft. However, some theoretical [7] and retrospective [6, 81 studies suggest an increased incidence of mediastinitis with use of the IMA. Arnold [7] evaluated the vascular supply of the sternum by utilizing dye injection techniques in cadavers before and after mobilization of the IMAs. He demonstrated that tributaries of the IMA form anterior and posterior periosteal plexuses that constitute
the primary vascular supply to the sternum. After mock IMA dissection, these periosteal plexuses fail to opacify with injection of dye into the mobilized IMA. Use of the IMA for coronary bypass might lead to relative ischemia of the sternotomy closure, especially when both IMAs are mobilized. Hutchinson and colleagues [22] acknowledged Arnold's results but noted only four sternal infections (two "major" and two "minor") in 222 patients after IMA bypass, an incidence of 1.8%.Grmoljez and associates [8] found an increased incidence of mediastinitis when comparing IMA grafts with saphenous vein grafts (2.5% versus 0.5%, respectively). The most provocative study emerged from the New York University group [6]. Review of 954 patients undergoing coronary revascularization showed an incidence of mediastinitis of only 1.1% after saphenous vein bypass; after single (385) or double (45) IMA grafts, the incidence rose to 2.3 and 8.5%, respectively. Sternal ischemia and a higher incidence of hemorrhage following IMA mobilization were incriminated as the factors predisposing to mediastinal infection.
Pathogenesis The very mechanics of cardiac surgical procedures subject the patient to myriad potential portals of entry for bacterial pathogens. Permanent foreign graft materials in direct contact with the bloodstream predispose to the initiation of infection. In addition, the debilitated status of many cardiac patients preoperatively and their sometimes precarious hemodynamic state postoperatively lower the body's inherent defenses [I, 231. Many studies have investigated the incidence of sepsis, wound complications, and mediastinitis in patients undergoing procedures requiring CPB. Although an early report of 611 patients failed to demonstrate differences in incidence of infectious complications related to CPB [5], most studies
417 Collective Review: Sarr, Gott, and Townsend Mediastinal Infection after Cardiac Surgery
have shown a higher rate [13, 24-27]. Speculation concerning the mechanisms of infection have focused on intraoperative bacterial contamination and lowered host defenses exposed to minimal numbers of invading microorganisms.
lntraoperative Factors Bacteriological surveillance of the operating room, its personnel, and the mechanics of CPB has implicated intraoperative contamination as a not uncommon factor in the development of postoperative sepsis [28-311. Contamination of the heart-lung machine has been investigated in considerable depth. Geldof and Brom [30] obtained positive blood cultures from the heart-lung machine immediately after bypass in 16 of 657 patients (2.4%).Signs of postoperative sepsis developed in 4 of these patients, 3 of whom manifested unequivocal septic foci preoperatively. Frater and Santos [32] demonstrated a significant incidence of preoperative urinary and nasopharyngeal bacterial colonization in patients having cardiac surgical procedures, suggesting that preoperative sepsis or colonization may contribute to intraoperative contamination of the heart-lung machine. Ankeney and Parker [28] studied 393 patients undergoing CPB. Positive cultures occurred in 19%, either from the heart-lung machine tubing prior to initiation of CPB or from the coronary suction system, the arterial line, or some other source in direct contact with the perfusion blood. The greatest incidence of positive cultures was recovered from the coronary suction system 129, 33, 341. Prosthetic valve endocarditis developed in 4 patients, 3 of whom had the identical organism cultured intraoperatively from the perfusion blood. Blakemore and associates [29] evaluated 32 patients prospectively; although prebypass cultures were negative, positive cultures were obtained from the heart-lung machine in fourteen instances. Identical organisms were cultured from distant sites postoperatively in 7 patients; serious infection developed in 2. Kluge and co-workers [35] followed 66 patients prospectively at the University of Maryland. Although prebypass cultures from the heart-lung machine were negative, 47 patients (71%) had positive intraoperative cultures; 20% had positive cultures from multiple sites. The prosthetic valve proved culture positive in an astonishing 50% of patients, the cardiotomy site in 64%, the donor blood bag in 4%, and the heart-lung machine in only 3%. Although just 2 patients had a "serious infection," the implications of this study and others remain disconcerting. Operating room personnel and anesthesia equipment are potential vectors of intraoperative contamination. Hairston and Lee [l] found a high incidence of Staphylococcus epidermidis in random cultures of anesthesia equipment. Lathrop and Wise and their associates [34, 361 investigated a cluster of nosocomial infections with S. epiderrnidis at one hospital and demonstrated nasal colonization with this organism in 80% of operating room personnel. At the end of the operative procedure,
the inner surface of 90% of the surgical gloves proved culture positive and 80% of the wounds prior to closure grew staphylococci. Blakemore and colleagues [29] monitored intraoperative levels of airborne bacteria near the wound. They found a direct relationship between the number of people in the operating room and the number of "colony forming units," a measure of airborne bacteria. The lowest counts were obtained before and after the operation when there was minimal physical activity. Identical organisms were cultured from the perfusion blood. The spectrum of bacteria isolated from intraoperative cultures has proven quite diverse [28, 29, 35, 371. Diphtheroids and S. epidermidis remain by far the most common isolates, while gram-negative organisms occur less frequently.
Postoperative Factors The postoperative setting provides numerous portals of entry for access of bacterial pathogens into the bloodstream and mediastinum. Hematogenous seeding is recognized as a source of both sternal osteomyelitis and spontaneous mediastinitis [38]. Current techniques of hemodynamic monitoring require intravenous and intraarterial catheters. Surveillance of intravenous catheters has revealed a 20 to 30% incidence of positive cultures [32, 35, 39-42], often with associated infectious complications. Urinary catheters, mediastinal and pleural drainage tubes, and endotracheal tubes also serve as well-recognized potential sources of sepsis [32, 35,431. A number of studies [44-461 have linked specific epidemics of nosocomial infections to the use of contaminated equipment in the postoperative setting. For instance, a case of mediastinitis secondary to Pseudomonas cepacia was traced to contamination of a detergent used to clean pressure transducers [47]. Rosendorf and co-workers [48] compared the incidence of cutaneous gram-negative colonization and postoperative infection in 22 patients undergoing cardiac procedures. Only 9% manifested preoperative colonization of the nose, throat, axilla, or groin; however, 91%became colonized in the postoperative period, usually in the intensive care unit. Common isolates were Escherichia coli and Klebsiella, Pseudomonas, and Enterobacter organisms. The hands of nursing personnel grew gram-negative organisms in 70% of random culturesmost commonly Pseudomonas. Similarly, respiratory care equipment was often contaminated. Three of the 22 patients experienced an infectious complication with an organism identical to that cultured from a site of cutaneous colonization. These studies suggest that gramnegative infection probably originates from a source in the postoperative period, while gram-positive infection is more likely related to intraoperative contamination. Effects of Cardiopulmonary Bypass Cardiopulmonary bypass causes alterations in host defenses by affecting phagocytic function as well as the humoral and cellular immune systems. An early study
418 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
showed a depression in the mean phagocytic index for clearance of gold 198 colloid in rats undergoing CPB using a bubble oxygenator [49]. Subramanian and coworkers [50] demonstrated a decreased clearance of intravenously administered Klebsielh organisms in dogs after CPB. Early reports of circulating phagocytes noted striking decreases in serum bacteriocidal and phagocytic capacity [51] and in reduction of nitroblue tetrazolium [52]. These abnormalities varied directly with CPB perfusion time [53, 541 and returned to normal in the first few postoperative days. Rheological stresses and surface effects during CPB produce structural damage to elements borne by blood. Morphological alterations in leukocytes [52], destruction of mononuclear cells [53, 551, derangement of oxygen and glycogen metabolism [53], damage to lysosomal membranes [56], and an overall leukopenia [52,53] during CPB have been observed. Goodman and colleagues [25] postulate a diminished bone marrow reserve postoperatively. Of greater importance is the obligate denaturation of proteins that occurs at the surface interface of nonmembrane oxygenators [57]. A decrease in complement factors and immunoglobulin levels occurs immediately after CPB and for as long as 7 days postoperatively [51, 52, 581. Pruitt and associates [59] postulated that denaturation of gammaglobulin at the gas-liquid interface activates complement, thereby depleting its factors and thus depressing host immune defenses. In addition, Salo [60] demonstrated depressed cell-mediated immunity related to CPB in the postoperative period. Hopefully, refinement of techniques of CPB will eliminate alterations in immune function [61].
Bacteriology of Mediastinitis The most common pathogen causing postoperative mediastinal infection remains staphylococcus. Gramnegative organisms, primarily E . coli, Klebsiellu, Serrutiu, Proteus, and Enterobucter, are less common etiological agents in the development of mediastinitis. Mixed infections with both gram-positive and gram-negative isolates are found in up to 40% of patients [2, 6, 9, 17, 621. Although Bucteroides frugilis has been implicated in at least 2 cases of mediastinitis [63, 641, the potential of other anaerobes as primary pathogens remains unknown because most studies were conducted prior to the advent of efficient anaerobic culture techniques. Cundidu species have been cultured occasionally from areas of mediastinal suppuration [6, 91, but these organisms have proven to be a more common pathogen in the chronic cartilaginous infections [6, 651. The most important finding has been the emergence of S. epidermidis as a primary pathogen in postoperative mediastinitis, probably due in part to routine use of "prophylactic" antistaphylococcal, penicillinaseresistant antibiotics. The incidence of prosthetic valve endocarditis fell dramatically with the advent of methicillin [4, 28, 66, 67, 681. But with continued use, about 30% of all S. epidermidis isolates in large centers [6, 9, 68, 691 have become resistant to many antibiotics. For instance, Engelman and colleagues [9] used antistaphy-
lococcal agents to treat their patients, yet 6 of 17 cases of mediastinitis (35%)were caused by S. epidermidis. Similarly, the more recent study by the New York University group [6] reported that more than one-half of the staphylococcal infections were caused by S. epidermidis. Gram-negative mediastinal infections have also been influenced by prophylactic antibiotics [24, 671. Bryant and co-workers [12] used either chloramphenicol or streptomycin (as well as a penicillin) prophylactically in patients undergoing cardiac surgical procedures. Gramnegative mediastinal sepsis occurred in 5 patients; in 3, the infection proved resistant to the prophylactic agents employed.
Diagnosis Most commonly, mediastinitis is seen between 4 and 30 days postoperatively and usually within two weeks of the original procedure [8, 9, 12, 17, 26, 62, 64, 70, 711. Rare cases have been recognized as long as 60 and 145 days postoperatively [6, 261. Mediastinal infection after open-heart procedures can be clinically obvious or obscure. Wound drainage is the most common presentation in 70 to 90% of patients [8, 9, 12, 261. Although occasionally present in the absence of sternal instability [9], drainage is pathognomonic when seen to bubble through an unstable sternotomy wound through a sinus tract [26]. Sternal instability or frank dehiscence alone is not diagnostic of underlying infection; many cases of these entities prove sterile and require only rewiring [ll, 721. A widened mediastinum sometimes can be appreciated on chest radiograph [73]; however, this finding is unreliable as a criterion for mediastinitis following cardiac surgical procedures. Only occasionallywill the patient complain of dysphagia [73] or, with associated osteochondritis or costochondritis, of inordinant sternal tenderness [6]. Mediastinitis can also present as occult sepsis, devoid of any objective wound or sternal abnormalities. Three of 19 patients in one series [26] and 1 of 17 patients in another [9] were seen with occult sepsis. Persistent fever [12, 261 or leukocytosis [6, 91 can suggest mediastinal infection; however, these and similar indirect clues remain only suggestive, since they are frequent postoperative findings in patients having cardiac surgical procedures [74]. The sole objective diagnostic procedure short of reexploration has been mediastinal needle aspiration. Two techniques have been described-the subxiphoid, retrosternal approach [26] and the anterior transsternotomy approach [6]. Gram stain and cultures are confirmative. Best surgical results, of course, follow early diagnosis. A more aggressive use of mediastinal aspiration may diagnose mediastinal infection earlier, before wound drainage or sternal dehiscence appear.
Treatment Treatment of postoperative mediastinitis requires immediate drainage, debridement, and parenteral antibiotic therapy. Mortality is extremely high in patients
419 Collective Review: Sarr, Gott, and Townsend Mediastinal Infection after Cardiac Surgery
Table 2. Treatment of Postoperative Mediastinitis after Cardiac Surgery: Results of Open and Closed Methods Redebridement Reference
No. of
Mortality
Patients
(%)
10 13 7
20 45
15 15 14 27 16
33 7 14
Required
Development of Chronic Infection (%)
OPEN METHOD
Grmoljez et a1 [8] Sutherland et a1 [17] Culliford et a1 [6]
...
100
... ...
... ... 43
CLOSED METHOD
Engelman et a1 [9] Barois et a1 [75]
Thurer et a1 [62] Culliford et a1 [6] Jimenez-Martinezet a1 [26]
...
13
treated with antibiotics but without surgical drainage. Unfortunately, even with aggressive treatment, mortality remains high, and the morbidity and prolonged hospitalization prove considerable. Two approaches to the surgical management of postoperative mediastinitis have been described that differ only in the timing of sternal closure. The ”open” method [3] involves debridement and open packing of the mediastinal and sternal wounds with the option of a delayed or staged secondary closure. The advantage of this technique is that a potentially undrained space no longer exists. Active debridement continues through dressing changes during convalescence. However, frequent dressing changes are required and hospitalization is prolonged. Complete healing can take as long as sixteen months [8] and may require a skin graft. Lifethreatening hemorrhage from exposed mediastinal vessels is a potentially disastrous complication [26, 64, 75, 761. Moreover, the loss of sternal apposition impairs respiratory function secondary to inadequate chest support [26]. Two studies [8, 171 reported mortality of 20% and 45% when this “open“ method of therapy was employed (Table 2). Grmoljez and co-workers [8] treated 10 patients; all required at least one formal redebridement, and 5 required two or more subsequent procedures. Culliford and colleagues [6] adopted this method only for treatment of more advanced cases of mediastinal suppuration or for chronically infected patients. In their 39 patients, the ”open” method was required in only 7 patients; in 3 of these patients, chronic osteochondritis or costochondritis developed. In contrast, treatment of mediastinitis by the ”closed” method was reported in 1963 by Shumaker and Mandelbaum [771. This technique involves surgical drainage, debridement, and thorough intraoperative irrigation of the wound, after which the sternal edges are reapproximated over one or more fenestrated infusion catheters
13 66
...
...
20 21 7 19
...
and usually two or more larger drainage catheters. The subcutaneous wound has been left open and packed [62, 64, 711 or closed primarily with or without a drain [6, 9, 12, 261. Postoperatively, the mediastinum is irrigated continuously with saline solution [78], Dakin’s solution [75], or an antibiotic solution until cultures of the effluent turn negative, usually within one to three weeks. The antibiotic solutions employed have included neomycin [6, 12, 47, 64, 65, 791, bacitracin [6, 9, 12, 641, penicillin [77], nafcillin [80], polymyxin B [9, 121, kanamycin [2, 261, povidone-iodine [62, 64, 811, amphotericin B [2, 91, framycetin [75], and cephalothin and ampicillin [9]. Ochsner and colleagues [71] suggest adding streptokinase-streptodornase to the irrigation solution. Advantages of the “closed” method are obvious. Hospitalization is shortened; in one series, all patients were discharged less than 30 days after the initial drainage procedure [26]. Closure of the sternum returns stability to the thorax, thereby facilitating respiratory toilet. Moreover, frequent and sometimes hazardous dressing changes are avoided, emotional trauma is minimized, and the cosmetic result is improved. However, the ”closed” technique is not without complications. Closing the sternal wound creates a potentially undrained cavity, and reexploration for loculated sepsis has been required in 13 to 66% of patients [9, 751. The mediastinal catheters have eroded adjacent tissues, occasionally leading to life-threatening hemorrhage [64]. Antibiotic solutions may predispose to superinfection, possibly exacerbated by the indwelling mediastinal catheters [64]. A common superinfecting organism has been Candida [9, 65, 751. Indeed, several groups [6, 12, 641 have recognized a higher incidence of chronic osteochondritis and costochondritis caused by this organism after continuous closed-chest mediastinal irrigation. One must also watch for signs of systemic toxicity of the irrigant [9] (e.g., neomycin [82, 83, 841, framycetin [75],
420 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
and povidone-iodine [Sl]). The volume of effluent from the drainage tubes must closely match the volume of irrigant. Results have proven encouraging (see Table 2). After Shumaker and Mandelbaum’s [77] successful treatment of 2 cases, Bryant and co-workers [12], Jimenez-Martinez and colleagues [26], and Engelman and associates [9], using a variety of antibiotic irrigants, reported success in 80%, 88%, and 67% of patients, respectively. Thurer’s group [62] and others [64,811 suggested irrigation with dilute povidone-iodine because this agent is effective against both bacteria and fungi; results proved acceptable without evidence of Candida superinfection. Although others have reported the successful treatment of infected prosthetic materials by the closed method without removal of the prosthesis [12, 80, 811, this must be unusual. Indeed, in some patients, removal of the infected foreign material was required to eradicate local sepsis [85]. With either method of treatment, optimal supportive measures are mandatory. Parenteral antibiotics remain compulsory; many authors recommend continuing these agents for three months, while others institute oral, single-agent coverage for up to nine months [75]. The importance of providing adequate nutrition cannot be overemphasized [6]. Occasionally, all attempts at local treatment fail and total excision of the sternum and infected costal cartilage becomes necessary. Under these conditions, Lee and colleagues [70] have used a pedicled, omental flap to cover the great vessels and associated suture lines; others have used pectoralis major muscle flaps [86-881. A full-thickness skin flap may be rotated for external coverage. In terms of survival, presentation within the first postoperative month confers a better prognosis than late development of mediastinal infection [6]. Renal failure [9] or prolonged ventilatory support [171 portends a dismal chance of survival. Prosthetic valve endocarditis has also been recognized as a complication of mediastinal suppuration [l-4, 751. Interestingly, patency of coronary bypass grafts evaluated one year postoperatively was not affected in those patients who had mediastinitis [8, 62, 64, 781.
Prevention The key to control of postoperative mediastinal infection lies in optimizing its prevention, a subject addressed by much of the present literature. Recognition and containment of nosocomial infection, meticulous operative technique, surveillance of postoperative care, and the rational use of perioperative antibiotics represent the obvious avenues of prevention. Intraoperative surveillance of infection control, including cognizance of airborne as well as personnel and surface contamination [34, 361, requires regular review by all involved. Elaborate, highly effective air filtration systems have been designed [89, 901; however, their cost-effectiveness has not been determined. Recognition of epidemics of nosocomial infection led to the evolution
of adequate precautions to prevent bacterial contamination [34, 44-47]. Primary areas of concern include the respiratory care systems and physical isolation policies of the intensive care unit. Special consideration should be given to the permanent physical isolation of chronically infected patients and their nursing teams to minimize cross-contamination (481. Surveillance of the changing spectrum of nosocomial infection has proven of preventive importance. Emergence of bacteria resistant to the usual antibiotics must be anticipated and recognized early [69]. For instance, S. epidermidis has emerged as a dangerous pathogen; at present only 70% of in-hospital isolates remain sensitive to the synthetic penicillinase-resistant derivatives [6, 9, 681. Preoperative preparation of the patient may minimize postoperative complications. Optimizing nutritional status, immunological competence, and respiratory function, as well as the eradication of foci of low-grade infection (especially of dental, respiratory, and genitourinary origin) are requisite preoperative adjuncts [91]. Scrubbing with a hexachlorophene detergent cleanser such as pHisoHex, or with defatting agents, or both prior to application of the iodine-containing skin preparation is considered important by some [6, 171. Similarly, under emergency conditions skin preparation and wound isolation, however hasty, prior to resternotomy seem important in minimizing the increased risk of infection following such procedures. Careful surgical technique and meticulous hemostasis are of paramount importance [2, 111. Ochsner and colleagues [71] stress the role of a precise, midline sternal osteotomy, which prevents cartilaginous exposure and minimizes subsequent sternal fracture. Equally essential is a mechanically stable sternal closure [ll, 171. Placement of wires through the costochondral cartilage [6, 651 should be avoided [92]. Many methods have been described to maximize sternal stability if the sternal edges are fractured, friable, or otherwise unstable [ll, 93-98]. The importance of careful apposition of the sternal periosteum and the sternalis muscle have been stressed [6]. Use of bone wax, a potential foreign body, is best avoided whenever possible. One group suggests removal of the xiphoid for fear of cartilaginous necrosis and subsequent infection [13]. Routine pericardial closure remains controversial [99]; two studies [6, 1001 support pericardial closure or approximation of mediastinal fat to prevent the spread of infection from the anterior wound to the myocardium, cardiotomy site, or prosthetic material. Ongoing educational programs directed at the paramedical and nursing staff should reinforce techniques of aseptic care and thereby lessen the incidence of local or hematogenous wound contamination. Early endotracheal extubation and removal of vascular, mediastinal, and urinary catheters will minimize the incidence of bacteremia. If prolonged ventilatory support is required, consideration should be given to the use of cricothyroidotomy instead of routine tracheostomy; the
421 Collective Review: Sam, Gott, and Townsend Mediastind Infection after Cardiac Surgery
former approach lessens the risk of wound communication and subsequent contamination of the anterior mediastinum [18, 1011. Prophylactic Antibiotics Introduction of effective prophylatic antibiotics added a new dimension to the prevention of infection after cardiac surgery. Prior to this, the incidence of postoperative prosthetic valve endocarditis approached 4% [4, 1021. With the introduction of antistaphylococcalprophylaxis, the incidence of fatal endocarditis has fallen dramatically [4, 28, 66, 681. Prophylactic antibiotics lowered the incidence of other infectious complications as well [69]. Merli and colleagues [lo31 found a 50% decrease in postoperative infections with oxacillin and hetacillin prophylaxis. Sutherland and associates [ 171 compared prophylactic antibiotics with placebo in the prevention of mediastinal sepsis. They found a slight but not significant difference in the incidence of mediastinitis. Unfortunately, serum levels of antibiotics were not assessed. To be effective as a prophylactic agent, serum levels of antibiotic must be adequate at the time of contamination. Brenner [lo41 monitored 6 patients given 1 gm of cephalothin the evening before and the morning of operation; inadequate serum levels of cephalothin were found in all patients while on CPB. Kluge and coworkers [lo51 and others [54, 106, 1071 demonstrated that bacteriocidal serum concentrations of cephalothin are maintained throughout the perioperative period only if the drug is administered immediately before operation. Goldman and co-workers [37] found that wound infections developed in 3 of 11patients with no detectable serum cephalothin activity at the end of operation, while only 2 of 175 patients with adequate levels had similar infections. With routine antibiotic prophylaxis, the spectrum of postoperative pathogens has also changed [12, 23, 671. Emergence of the resistant strain of S. epidermidis represents an example of this phenomenon [6, 9, 68, 691. Fekety and co-workers [24] demonstrated a predominance of gram-positive pathogens after penicillin prophylaxis and gram-negative organisms with methicillin prophylaxis. Obviously, the prophylactic agent must be subject to change according to local trends in bacteriological surveillance. At present, cephalothin or one of the newer cephalosporins appears to be the recommended antibiotic for prophylaxis in many centers [24, 37, 54, 69, 106, 108-1101.
References Hairston P, Lee WH Jr: Management of infected prosthetic heart valves. Ann Thorac Surg 9:229, 1970 Ibarra F, Alonso-lej F Mediastinite et dehiscence sternale comme complication de la stemotomie mediane. Ann Chir Thorac Cardiovasc 13:35, 1974 Norman JC (ed): Cardiac Surgery. New York, AppletonCentury-Crofts, 1972 Stein PD, Harken DE, Dexter L: The nature and preven-
tion of prosthetic valve endocarditis. Am Heart J 71:393, 1966 5. Nelson JC, Nelson RM: The incidence of hospital wound infection in thoracotomies. J Thorac Cardiovasc Surg 54:586, 1967 6. Culliford AT, Cunningham JN Jr, Zeff RH, et al: Sternal and costochondral infections following open-heart surgery: a review of 2,594 cases. J Thorac Cardiovasc Surg 72:714, 1976 7. Amold M: The surgical anatomy of sternal blood supply. J Thorac Cardiovasc Surg 64:596, 1972 8. Grmoljez PF, Bamer HH, Willman VL, Kaiser GC: Major complications of median sternotomy. Am J Surg 130:679, 1975 9. Engelman RM, Williams CD, Gouge TH, et al: Mediastinitis following open-heart surgery: review of two years’ experience. Arch Surg 107772, 1973 10. Brown AH, Braimbridge MV, Panagopoulous P, Sibar EF: The complications of median sternotomy. J Thorac Cardiovasc Surg 58:189, 1969 11. Sanfelippo PM, Danielson GK: Complications associated with median sternotomy. J Thorac Cardiovasc Surg 63:419, 1972 12. Bryant LR, Spencer FC, Trinkle JK: Treatment of median sternotomy infection by mediastinal irrigation with an antibiotic solution. Ann Surg 169:914, 1969 13. Hehrlein FW, Herrman H, Kraus J: Complications of median sternotomy in cardiovascular surgery. J Thorac Cardiovasc Surg 13:390, 1972 14. LeVeen HL, Piccone VA: Nylon-band chest closure. Arch Surg 96:36, 1968 15. Londe S, Sugg W L The challenge of reoperation in cardiac surgery. Ann Thorac Surg 17157, 1974 16. Macmanus Q, Okies J, Phillips SJ, Starr A: Surgical considerations in patients undergoing repeat median sternotomies. J Thorac Cardiovasc Surg 69:138, 1975 17. Sutherland RD, Martinez HE, Guynes WA, Miller L: Postoperative chest wound infections in patients requiring coronary bypass: a controlled study evaluating prophylactic antibiotics. J Thorac Cardiovasc Surg 73:944, 1977 18. Pierce WS, Tyers GFO, Waldhausen JA: Effective isolation of a tracheostomy from a median sternotomy wound. J Thorac Cardiovasc Surg 66:841, 1973 19. Kay EB, Naraghipour H, Beg RA, et al: Internal mammary artery bypass graft-long-term patency rate and followup. Ann Thorac Surg 18:269, 1974 20. Green G E Internal mammary artery-to-coronary artery anastomosis: three-year experience with 165 patients. Ann Thorac Surg 14:260, 1972 21. Tector AJ, Davis L, Gabriel R, et al: Experience with internal mammary artery grafts in 298 patients. Ann Thorac Surg 22:515, 1976 22. Hutchinson JE 111, Green GE, Mekhjian HA, Kemp HG: Coronary bypass grafting in 376 consecutive patients with three operative deaths. J Thorac Cardiovasc Surg 677, 1974 23. Firor WB: Infection following open-heart surgery with special reference to the role of prophylactic antibiotics. J Thorac Cardiovasc Surg 53:371, 1967 24. Fekety FR Jr, Cluff LE, Sabiston DC Jr, et al: A study of antibiotic prophylaxis in cardiac surgery. J Thorac Cardiovasc Surg 57757, 1969 25. Goodman JS, Schaffner W, Collins HA, et al: Infection after cardiovascular surgery. N Engl J Med 278:117, 1968
422 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
26. Jimenez-Martinez M, Arguero-Sanchez R, Perez-Alavarez JJ, Mina-Castaneda P: Anterior mediastinitis as a complication of median sternotomy incisions: diagnostic and surgical considerations. Surgery 67929, 1970 27. Kittle CF, Reed WA: Antibiotics and extracorporeal bypass. J Thorac Cardiovasc Surg 41:34, 1961 28. Ankeney JL, Parker RF: Staphylococcal endocarditis following open-heart surgery related to positive intraoperative blood cultures. In Brewer LA 111 (ed): Prosthetic Heart Valves. Springfield, IL, Thomas, 1968, pp 719-730 29. Blakemore WS, McGarrity GJ, Thurer RJ, et al: Infection by air-borne bacteria with cardiopulmonary bypass. Surgery 70830, 1971 30. Geldof WCP, Brom AG: Infections through blood from heart-lung machine. Thorax 27395, 1972 31. Yeh TJ, Anabtawi IN, Cornett VE, et al: Bacterial endocarditis following open-heart surgery. Ann Thorac Surg 329, 1967 32. Frater R W , Santos GH. Sources of infection in open heart surgery. NY State J Med 74:2386, 1974 33. Ankeney JL: Discussion of Amoury RA, Bowman FO Jr, Malm JR: Endocarditis associated with intracardiac prosthesis. J Thorac Cardiovasc Surg 51:48, 1966 34. Lathrop GD, Brockett RM, Blouse LE: Epidemiological surveillance for Staphylococcus qiidermidis infections related to cardiopulmonary bypass. Zentralbl Bakteriol [B] 241:108, 1978 35. Kluge RM, Calia FM, McLaughlin JS, Hornick RB: Sources of contamination in open-heart surgery. JAMA 230:1415, 1974 36. Wise RI, Sweeney FJ Jr, Haupt GJ, Waddell MA: The environmental distribution of Staph. aureus in an operating suite. Ann Surg 149:30, 1959 37. Goldman DA, Hopkins CC, Karchmer AW, et al: Cephalothin prophylaxis in cardiac valve surgery. J Thorac Cardiovasc Surg 73470, 1977 38. Wilensky AO, Samuels SS: Osteomyelitis of the sternum. Ann Surg 83:206, 1926 39. Bernard RW, Stahl WM, Chase RM Jr: Subclavian vein catheterization: a prospective study. Ann Surg 173:191, 1971 40. Borja A R Current status of infraclavicular subclavian vein Catheterization: review of the English literature. Ann Thorac Surg 13:615, 1972 41. Glover JL, OByrne SA, Jolly L: Infusion catheter sepsis: an increasing threat. Ann Surg 173:148, 1971 42. Konold P, Ullmank U, Schrader CP, Kieninger G: Klinische und bakteriologische beobachtungen bei intravenous eingefuhrten kathetern. Dtsch Med Wochenschr 99:1009, 1974 43. MacArthur BS, Ackerman NB: The significance of Serrutiu as an infectious organism. Surg Gynecol Obstet 146:49, 1978 44. Reyes LH, Ratzan KR, Rheinlander HF: Serrutiu murcescens bacteremia originating from a catheter line in the left atrium after mitral valve replacement. J Thorac Cardiovasc Surg 65:241, 1973 45. Richards NM, Levitsky S: Outbreak of Serrutiu murcescens infections in a cardiothoracic surgical intensive care unit. Ann Thorac Surg 19:503, 1975 46. Sanders CV Jr, Luby JP, Johanson WG, et al: Serrutiu marcescens infections from inhalational therapy medications: nosocomial outbreak. Ann Intern Med 73:15, 1970 47. Weinstein RA, Jones EL, Schwarzmann SW, Hatcher CR Jr: Sternal osteomyelitis and mediastinitis after open-heart
operation: pathogenesis and prevention. Ann Thorac Surg 2 1 4 2 , 1976 48. Rosendorf LL, Daicoff G, Baer H: Sources of Gramnegative infection after open-heart surgery. J Thorac Cardiovasc Surg 67195, 1974 49. Subramanian V, McLeod J, Gans H: Effect of extracorporeal circulation on reticuloendothelial function: I. Experimental evidence for impaired reticuloendothelial function following cardiopulmonary bypass in rats. Surgery 64:775, 1968 50. Subramanian VA, Gay WA Jr, Dineen P A P Effect of cardiopulmonary bypass on in vivo clearance of live Klebsiellu aerogens. Surg Forum 28535, 1977 51. Hairston P, Manos JP, Graber CD, Lee WH Jr: Depression of immunologic surveillance by pump-oxygenator perfusion. J Surg Res 9:587, 1969 52. Silva J Jr, Hoeksema H, Fekety FR Jr: Transient defects in phagocytic fiinctions during cardiopulmonary bypass. J Thorac Cardfovasc Surg 67:175, 1974 53. Kusserow B, Larrow R, Nichols J: Perfusion and surfaceinduced injury in leukocytes. Fed Proc 30:1516, 1971 54. Austin TW, Coles JC, McKechnie P, et a1 Cephalothin prophylaxis and valve replacement. Ann Thorac Surg 23:333, 1977 55. Lundstrom M, Olsson P, Unger P, Ekestrom S: Effect of extracorporeal circulation on hematopoesis and phagocytosis. J Cardiovasc Surg 4:664, 1963 56. Replogle RL, Gazzaniga AB, Gross RE: Use of corticosteroids during cardiopulmonary bypass: possible lysosome stabilization. Circulation 33:Suppl 1:86, 1966 57. Lee WH Jr, Krumhaar D, Fonkalsrud EW, et al: Denaturation of plasma proteins as a cause of morbidity and death after intra-cardiac operations. Surgery 50:29, 1961 58. Parker DJ, Cantrell JW, Karp RB, et al: Changes in serum complement and immunoglobulins following cardiopulmonary bypass. Surgery 71:824, 1972 59. Pruitt KM, Stroud RM, Scott J W Blood damage in the heart lung machine. Proc SOCExp Biol Med 137714, 1971 60. Salo M: Effect of anaesthesia and open-heart surgery on lymphocyte responses to phytohemagglutinin and conconavalin A. Acta Anaesth Scand 22471, 1978 61. Vervloet AFC, Edwards MJ, Edwards ML: Minimal apparent blood damage in Lande Edwards membrane oxygenator at physiologic gas tensions. J Thorac Cardiovasc Surg 60774, 1970 62. Thurer RJ, Bognolo D, Vargus A, et al: The management of mediastinal infection following cardiac surgery. J Thorac Cardiovasc Surg 68:962, 1974 63. Cerat GA, McHenry MC, Loop FD: Median sternotomy wound infection and anterior mediastinitis caused by B . fragilis. Chest 69:231, 1976 64. Moseley PW, Ochsner JL, Mills NL, Chapman J: Management of an infected Hancock prosthesis after repair of truncus arteriosus. J Thorac Cardiovasc Surg 73:306, 1977 65. Williams CD, Cunningham JN, Falk EA, et al: Chronic infection of the costal cartilages after thoracic surgical procedures. J Thorac Cardiovasc Surg 66592, 1973 66. Herr R, Starr A, McCord CW, Wood JA: Special problems following valve replacement: embolus, leak, infection, red cell damage. Ann Thorac Surg 1:403, 1965 67. Killen DA, Collins HA, Koenig MG, Goodman JS: Prosthetic cardiac valves and bacterial endocarditis. Ann Thorac Surg 9:238, 1970 68. Slaughter L, Moms JE, Starr A. Prosthetic valvular endocarditis. Circulation 471319, 1973
423 Collective Review: Sarr, Gott, and Townsend Mediastinal Infection after Cardiac Surgery
69. Myerowitz I'D, Caswell K, Lindsay WG, Nicoloff DM: Antibiotic prophylaxis for open-heart surgery. J Thorac Cardiovasc Surg 73:625, 1977 70. Lee AB Jr, Schimert G, Shatkin S: Total excision of the sternum and thoracic pedicle transposition of the greater omentum: useful strategems in managing severe mediastinal infection following open-heart surgery. Surgery 80433, 1976 71. Ochsner JL, Mills NL, Woolverton WC: Disruption and infection of the median sternotomy incision. J Cardiovasc Surg 13:394, 1972 72. Stoney WS, Alford WC Jr, Burrus GR, et al: Median sternotomy dehiscence. Ann Thorac Surg 26:421, 1978 73. Webb WR, Burford TH: Management of acute mediastinitis. Am Surg 28:309, 1962 74. Bell DM, Goldman DA, Hopkins CC, et al: Unreliability of fever and leukocytosis in the diagnosis of infection after cardiac valve surgery. J Thorac Cardiovasc Surg 75:87, 1978 75. Barois A, Grosbuis S, Simon N, et al: Treatment of mediastinitis in children after cardiac surgery. Intensive Care Med 4:35, 1978 76. Orringer MB, Murray GF, Haller JA, Gott VL: Median sternotomy and outflow patch infections in total repair of tetralogy of Fallot. J Thorac Cardiovasc Surg 63:442, 1972 77. Shumaker HB Jr, Mandelbaum I: Continuous antibiotic irrigation in the treatment of infection. Arch Surg 86:384, 1963 78. Carlson RG: Discussion of [9] 79. Cheanvechai C, Travisano F, Effler DB: Treatment of infected sternal wounds. Cleve Clin Q 39:43, 1972 80. Stewart S: The infected mediastinum: successful treatment in the presence of externalcardiac material. J Thorac Cardiovasc Surg 73:801, 1977 81. Macmanus Q, Okies JE: Mediastinal wound infection and aorto-coronary graft patency. Am J Surg 132:558, 1976 82. Davis JE, Siemsen AW, Anderson R W Uremia, deafness, and paralysis due to irrigating antibiotic solutions. Arch Intern Med 125:135, 1970 83. Gruhl VR: Renal failure, deafness, and brain lesions following irrigation of the mediastinum with neomycin. Ann Thorac Surg 11:376, 1971 84. Leach W: Ototoxicity of neomycin and other antibiotics. J Laryngol Otol 76:774, 1962 85. Engelman RM, Saxena A, Levitsky S: Delayed mediastinal infection after ventricular aneurysm resection (case report). Ann Thorac Surg 25:470, 1978 86. Jurkiewicz MJ, Bostwick J 111, Hester TR, et al: Infected median sternotomy wound: successful treatment by muscle flaps. Ann Surg 191:738, 1980 87. Herrera HR, Ginsburg ME: The pectoralis major, myocutaneous flap and omental transposition for closure of infected median stemotomy wounds. Plast Reconstr Surg 70465, 1982 88. Nahai F, Morales L Jr, Bone DK, Bostwick J 111: Pectoralis major muscle turnover flaps for closure of the infected sternotomy wound with preservation of form and function. Plast Reconstr Surg 70:471, 1982 89. Bechtol CO: Environmental bacteriology in the unidirectional (vertical) operating room. Arch Surg 114:784, 1979
90. Nelson CL: Environmental bacteriology in the unidirectional (horizontal) operating room. Arch Surg 114:778, 1979 91. Baffes TG, Blazek WV, Fridman JL, et al: Postoperative infections in 1,136 consecutive cardiac operations. Surg 68:791, 1970 92. Sanfelippo PM, Danielson G K Nylon bands for closure of median sternotomy incisions: an unacceptable method. Ann Thorac Surg 13:404, 1972 93. Bowen TE, Brott WH, Green DC, et al: Thoracic traction for median sternotomy dehiscence. Ann Thorac Surg 25:148, 1978 94. Lambert CJ, Mitchell BF, Adam M, Shiekh S: A modified technique for secure median sternotomy closure. Surgery 69:393, 1971 95. Robicsek F, Daugherty HK, Cook JW: The prevention and treatment of sternum separation following open-heart surgery. J Thorac Cardiovasc Surg 73:267, 1977 96. Taber RE: Discussion of [6] 97. Taber RE, Madaras J: Prevention of stemotomy wound disruptions by the use of figure-of-eight pericostal sutures. Ann Thorac Surg 8:367, 1969 98. Uretzky G, Borman JB, Appelbaum A, Merin G: A new method of sternal reclosure. Ann Thorac Surg 2782, 1979 99. Asanza L, Rao G, Voleti C, et al: Should the pericardium be closed after an open-heart operation? Ann Thorac Surg 22:532, 1976 100. Timmis HH: Reconstruction of the anterior mediastinum after median sternotomy. Arch Surg 97736, 1968 101. Boyd AD, Romita MC, Conlan AA, et al: A clinical evaluation of cricothyroidotomy. Surg Gynecol Obstet 149:365, 1979 102. Hatcher CR Jr, Tyras DH: Complications from cardiac prostheses: infection, thrombosis, and emboli. In Sabiston DC Jr, Spencer FC (eds): Gibbon's Surgery of the Chest. Third edition. Philadelphia, Saunders, 1976, p 1211 103. Merli M, Cattani C, Pellegrini A, Pratelli EM: The role of prophylactic antibiotic therapy in cardiac surgery. J Cardiovasc Surg (Torino) 14:131, 1973 104. Brenner EJ: Metabolism of antibiotics during cardiopulmonary bypass for open-heart surgery. Antimicrob Agents Chemother 1968, p 373 105. Kluge RM, Calia FM, McLaughlin JS, Hornick RB: Serum antibiotic concentrations pre- and post-cardiopulmonary bypass. Antimicrob Agents Chemother 4:270, 1973 106. Eigel P, Tschirkov A, Satter P, Knothe H: Assays of cephalosporin antibiotics administered prophylactically in open-heart surgery. Infection 6:23, 1978 107. Williams DJ, Steele TW: Cephalothin prophylaxis assay during cardiopulmonary bypass. J Thorac Cardiovasc Surg 71:207, 1974 108. Archer GL, Polk RE, Duma RJ, Lower R Comparison of cephalothin and cefamandole prophylaxis during insertion of prosthetic heart valves. Antimicrob Agents Chemother 13:924, 1978 109. Conte JE, Cohen SN, Roe BB, Elashoff RM: Antibiotic prophylaxis and cardiac surgery. Ann Intern Med 76:943,1972 110. Pien FD, Michael NL, Mamiya R, et al: Comparative study of prophylactic antibiotics in cardiac surgery. J Thorac Cardiovasc Surg 77:908, 1979
Mediastinal Infection after Cardiac Surgery Michael G. Sarr, M.D., Vincent L. Gott, M.D., and Timothy R. Townsend, M.D. ABSTRACT Mediastinitis is an uncommon complication after cardiac surgery; however, its associated morbidity and mortality demand early recognition and emergency therapy. This review is intended to emphasize certain features of the incidence, pathogenesis, and bacteriology of this complication in patients undergoing cardiopulmonary bypass through a median sternotomy. The diagnosis and treatment of mediastinitis after cardiac surgical procedures, as well as methods of prevention, are also reviewed. Mediastinitis after cardiac surgical procedures remains a devastating complication. Localized mediastinal suppuration, generalized sepsis, and the possibility of local or metastatic spread of infection to prosthetic materials used in the cardiac repair [l-41 are all serious consequences, each minimized only by optimal prevention, early diagnosis, and emergency therapy. The last twenty years have witnessed a remarkable change in the spectrum of this disease. Concurrently, understanding of the physiology and pathophysiology of cardiopulmonary bypass (CPB) has expanded markedly, yielding a more comprehensive insight into the prevention of this complication.
Incidence of Postoperative Mediastinitis While the incidence of superficial wound infection after median sternotomy is no different than after other thoracic incisions [5], the incidence of mediastinitis after cardiac surgical procedures, when defined as suppuration involving the anterior mediastinal space, ranges from 0.4 to 5.0% (Table 1).Our most recent experience at the Johns Hopkins Hospital (1982) revealed an 0.7% incidence of mediastinitis after cardiac procedures. The most comprehensive series is that of Culliford and coworkers [6], who found an incidence of 1.5% in 2,594 patients undergoing cardiac procedures at the New York University Medical Center between 1971 and 1975. There appears to be no difference in the incidence of mediastinitis after the three major categories of cardiac surgical procedures (see Table 1).After coronary artery bypass grafting, the incidence has ranged from 1.2 to 2.5%. It may be even greater when the internal mammary artery (IMA) is used for coronary revascularization [7, 81. When both IMAs are used, the incidence of sternal and mediastinal sepsis may be as high as 8% [6]. Operations for congenital heart anomalies have a lower incidence of mediastinal sepsis, while valve replaceFrom the Departments of Surgery and Hospital Epidemiology, Johns Hopkins Hospital, Baltimore, MD. Address reprint requests to Dr.Sarr, Department of Surgery, Johns Hopkins Hospital, Baltimore, MD 21205.
415
ments fall in between. Double valve replacement or coronary artery bypass grafting combined with valve replacement [9] seems to manifest a higher infection rate.
Predisposing Factors Many factors in the perioperative and postoperative periods have been implicated as predisposing to an increased incidence of postoperative mediastinitis. Postoperative hemorrhage with the formation of mediastinal hematoma [2] appears to be a major complication leading to a high risk of mediastinal infection. In the New York University study [6], 53% of the 39 patients with mediastinitis experienced greater than 1,250 ml of blood loss following the cardiac procedure. Postoperative resternotomy (usually for hemorrhage), especially under emergency conditions [6], has been recognized repeatedly as a factor contributing to a higher incidence of “wound complications” [lo, 111 and mediastinitis [8]. Culliford, Engelman, Bryant, and their colleagues [6, 9, 121 found that 18 to 42% of patients with mediastinal infection had undergone early reexploration for hemorrhage. Prolonged operative time also may be a factor in development of mediastinal infection [13]. Engelman and co-workers [9] analyzed 17 patients with postoperative mediastinitis; the majority had undergone prolonged operations ranging from 6 to 17 hours. Nine were operated on for longer than 10 hours; CPB time exceeded 3 hours in 12 patients. Similarly, the larger New York University study [6] found that 53% of those patients in whom mediastinal infection later developed had been on bypass in excess of 3 hours. The sternotomy itself predisposes to sternal and mediastinal infection. Introduction of the safer, more precise Stryker saw has lessened the incidence of wound complications seen after use of the Gigli saw, the Tenon saw, or the Lebsche knife [13]. More secure sternal approximation has played an equally integral role in minimizing wound complications. Early studies found a higher incidence of sternal dehiscence when the sternal edges were approximated with silk instead of wire [5] or a less stable nylon band closure [ll, 141. Disruption of sternal approximation during external cardiac massage in the early postoperative period has been associated with a two to four times greater incidence of wound complications [lo, 111, mediastinitis [9], and chronic sternal infections [6]. A history of previous sternotomy appears to increase the incidence of postoperative hemorrhage and other wound complications [6, 15, 161. Culliford and co-workers [6] found that 33% of their patients in whom chronic osteochondritis or costochondritis developed following median sternotomy had a previous history of sternotomy.
416 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
Table I . Incidence of Mediastinal and Sternal Infection after Cardiac Surgical Procedures Utilizing Cardiopulmonary Bypass
Reference Ochsner et a1 [71] Grmoljez et al [8] Johns Hopkins Hospital (1982) [this review] Sutherland et a1 [17] Jurkiewicz et a1 [86] Culliford et a1 (61 Engelman et a1 [9] Thurer et a1 [62] Orringer et a1 [76] Jimenez-Martinezet a1 [26]
No. of
Patients 750 1,500 824
904 3,239 2,594 1,042 645 212 257
Specific Incidence (%)
Overall
Incidence
Repair CHD
Valve
Replacement
(%)
CABG
0.4 0.7 0.7
...
...
...
1.2 0.2
0.5
...
0.1 1.5
...
1.4
1.5 1.5 1.6 2.2
...
... ...
... ...
0.4 0.7 3.2 2.2"
2.2 1.4
...
5.0
1.9 2.5
... ... ...
...
...
... ...
"Total repair of tetralogy of Fallot prior to 1971. CABG = coronary artery bypass grafting; CHD = congenital heart disease.
Postoperative cardiopulmonary complications can also predispose to development of mediastinitis [lo-121. Although some studies failed to show an increased incidence of wound complications [ l l ] or mediastinitis [8, 171 in the presence of a low cardiac output state, in the two largest series [6, 91 half of the patients with mediastinal infection had experienced a low cardiac output syndrome in the early postoperative period. In patients with preoperative or postoperative pneumonitis, mediastinitis has developed with the same organism isolated from the pulmonary secretions [9]. Tracheostomy with prolonged artificial ventilation has been associated with mediastinal sepsis [HI. When the procedures are performed simultaneously, the tracheostomy and sternotomy wounds can be seen to communicate, thus allowing a portal of entry for pathogens into the anterior mediastinum. The relationship between use of the IMA for coronary bypass and subsequent mediastinitis is a topic of controversy. In 1974, Kay and co-workers [19] reported a series of 814 IMA grafts in 628 patients with a hospital mortality approaching only 1.7%;no mention was made of sternal infection, dehiscence, or mediastinitis. Previously, Green [20] had reported his series of 146 patients with IMA grafts; there were only 2 cases of "sternal dehiscence" and 3 of sepsis but, again, no specific mention of mediastinal or sternal infection. Other groups [9, 17, 211 denied an increased incidence of mediastinal or sternal infection with use of the IMA graft. However, some theoretical [7] and retrospective [6, 81 studies suggest an increased incidence of mediastinitis with use of the IMA. Arnold [7] evaluated the vascular supply of the sternum by utilizing dye injection techniques in cadavers before and after mobilization of the IMAs. He demonstrated that tributaries of the IMA form anterior and posterior periosteal plexuses that constitute
the primary vascular supply to the sternum. After mock IMA dissection, these periosteal plexuses fail to opacify with injection of dye into the mobilized IMA. Use of the IMA for coronary bypass might lead to relative ischemia of the sternotomy closure, especially when both IMAs are mobilized. Hutchinson and colleagues [22] acknowledged Arnold's results but noted only four sternal infections (two "major" and two "minor") in 222 patients after IMA bypass, an incidence of 1.8%.Grmoljez and associates [8] found an increased incidence of mediastinitis when comparing IMA grafts with saphenous vein grafts (2.5% versus 0.5%, respectively). The most provocative study emerged from the New York University group [6]. Review of 954 patients undergoing coronary revascularization showed an incidence of mediastinitis of only 1.1% after saphenous vein bypass; after single (385) or double (45) IMA grafts, the incidence rose to 2.3 and 8.5%, respectively. Sternal ischemia and a higher incidence of hemorrhage following IMA mobilization were incriminated as the factors predisposing to mediastinal infection.
Pathogenesis The very mechanics of cardiac surgical procedures subject the patient to myriad potential portals of entry for bacterial pathogens. Permanent foreign graft materials in direct contact with the bloodstream predispose to the initiation of infection. In addition, the debilitated status of many cardiac patients preoperatively and their sometimes precarious hemodynamic state postoperatively lower the body's inherent defenses [I, 231. Many studies have investigated the incidence of sepsis, wound complications, and mediastinitis in patients undergoing procedures requiring CPB. Although an early report of 611 patients failed to demonstrate differences in incidence of infectious complications related to CPB [5], most studies
417 Collective Review: Sarr, Gott, and Townsend Mediastinal Infection after Cardiac Surgery
have shown a higher rate [13, 24-27]. Speculation concerning the mechanisms of infection have focused on intraoperative bacterial contamination and lowered host defenses exposed to minimal numbers of invading microorganisms.
lntraoperative Factors Bacteriological surveillance of the operating room, its personnel, and the mechanics of CPB has implicated intraoperative contamination as a not uncommon factor in the development of postoperative sepsis [28-311. Contamination of the heart-lung machine has been investigated in considerable depth. Geldof and Brom [30] obtained positive blood cultures from the heart-lung machine immediately after bypass in 16 of 657 patients (2.4%).Signs of postoperative sepsis developed in 4 of these patients, 3 of whom manifested unequivocal septic foci preoperatively. Frater and Santos [32] demonstrated a significant incidence of preoperative urinary and nasopharyngeal bacterial colonization in patients having cardiac surgical procedures, suggesting that preoperative sepsis or colonization may contribute to intraoperative contamination of the heart-lung machine. Ankeney and Parker [28] studied 393 patients undergoing CPB. Positive cultures occurred in 19%, either from the heart-lung machine tubing prior to initiation of CPB or from the coronary suction system, the arterial line, or some other source in direct contact with the perfusion blood. The greatest incidence of positive cultures was recovered from the coronary suction system 129, 33, 341. Prosthetic valve endocarditis developed in 4 patients, 3 of whom had the identical organism cultured intraoperatively from the perfusion blood. Blakemore and associates [29] evaluated 32 patients prospectively; although prebypass cultures were negative, positive cultures were obtained from the heart-lung machine in fourteen instances. Identical organisms were cultured from distant sites postoperatively in 7 patients; serious infection developed in 2. Kluge and co-workers [35] followed 66 patients prospectively at the University of Maryland. Although prebypass cultures from the heart-lung machine were negative, 47 patients (71%) had positive intraoperative cultures; 20% had positive cultures from multiple sites. The prosthetic valve proved culture positive in an astonishing 50% of patients, the cardiotomy site in 64%, the donor blood bag in 4%, and the heart-lung machine in only 3%. Although just 2 patients had a "serious infection," the implications of this study and others remain disconcerting. Operating room personnel and anesthesia equipment are potential vectors of intraoperative contamination. Hairston and Lee [l] found a high incidence of Staphylococcus epidermidis in random cultures of anesthesia equipment. Lathrop and Wise and their associates [34, 361 investigated a cluster of nosocomial infections with S. epiderrnidis at one hospital and demonstrated nasal colonization with this organism in 80% of operating room personnel. At the end of the operative procedure,
the inner surface of 90% of the surgical gloves proved culture positive and 80% of the wounds prior to closure grew staphylococci. Blakemore and colleagues [29] monitored intraoperative levels of airborne bacteria near the wound. They found a direct relationship between the number of people in the operating room and the number of "colony forming units," a measure of airborne bacteria. The lowest counts were obtained before and after the operation when there was minimal physical activity. Identical organisms were cultured from the perfusion blood. The spectrum of bacteria isolated from intraoperative cultures has proven quite diverse [28, 29, 35, 371. Diphtheroids and S. epidermidis remain by far the most common isolates, while gram-negative organisms occur less frequently.
Postoperative Factors The postoperative setting provides numerous portals of entry for access of bacterial pathogens into the bloodstream and mediastinum. Hematogenous seeding is recognized as a source of both sternal osteomyelitis and spontaneous mediastinitis [38]. Current techniques of hemodynamic monitoring require intravenous and intraarterial catheters. Surveillance of intravenous catheters has revealed a 20 to 30% incidence of positive cultures [32, 35, 39-42], often with associated infectious complications. Urinary catheters, mediastinal and pleural drainage tubes, and endotracheal tubes also serve as well-recognized potential sources of sepsis [32, 35,431. A number of studies [44-461 have linked specific epidemics of nosocomial infections to the use of contaminated equipment in the postoperative setting. For instance, a case of mediastinitis secondary to Pseudomonas cepacia was traced to contamination of a detergent used to clean pressure transducers [47]. Rosendorf and co-workers [48] compared the incidence of cutaneous gram-negative colonization and postoperative infection in 22 patients undergoing cardiac procedures. Only 9% manifested preoperative colonization of the nose, throat, axilla, or groin; however, 91%became colonized in the postoperative period, usually in the intensive care unit. Common isolates were Escherichia coli and Klebsiella, Pseudomonas, and Enterobacter organisms. The hands of nursing personnel grew gram-negative organisms in 70% of random culturesmost commonly Pseudomonas. Similarly, respiratory care equipment was often contaminated. Three of the 22 patients experienced an infectious complication with an organism identical to that cultured from a site of cutaneous colonization. These studies suggest that gramnegative infection probably originates from a source in the postoperative period, while gram-positive infection is more likely related to intraoperative contamination. Effects of Cardiopulmonary Bypass Cardiopulmonary bypass causes alterations in host defenses by affecting phagocytic function as well as the humoral and cellular immune systems. An early study
418 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
showed a depression in the mean phagocytic index for clearance of gold 198 colloid in rats undergoing CPB using a bubble oxygenator [49]. Subramanian and coworkers [50] demonstrated a decreased clearance of intravenously administered Klebsielh organisms in dogs after CPB. Early reports of circulating phagocytes noted striking decreases in serum bacteriocidal and phagocytic capacity [51] and in reduction of nitroblue tetrazolium [52]. These abnormalities varied directly with CPB perfusion time [53, 541 and returned to normal in the first few postoperative days. Rheological stresses and surface effects during CPB produce structural damage to elements borne by blood. Morphological alterations in leukocytes [52], destruction of mononuclear cells [53, 551, derangement of oxygen and glycogen metabolism [53], damage to lysosomal membranes [56], and an overall leukopenia [52,53] during CPB have been observed. Goodman and colleagues [25] postulate a diminished bone marrow reserve postoperatively. Of greater importance is the obligate denaturation of proteins that occurs at the surface interface of nonmembrane oxygenators [57]. A decrease in complement factors and immunoglobulin levels occurs immediately after CPB and for as long as 7 days postoperatively [51, 52, 581. Pruitt and associates [59] postulated that denaturation of gammaglobulin at the gas-liquid interface activates complement, thereby depleting its factors and thus depressing host immune defenses. In addition, Salo [60] demonstrated depressed cell-mediated immunity related to CPB in the postoperative period. Hopefully, refinement of techniques of CPB will eliminate alterations in immune function [61].
Bacteriology of Mediastinitis The most common pathogen causing postoperative mediastinal infection remains staphylococcus. Gramnegative organisms, primarily E . coli, Klebsiellu, Serrutiu, Proteus, and Enterobucter, are less common etiological agents in the development of mediastinitis. Mixed infections with both gram-positive and gram-negative isolates are found in up to 40% of patients [2, 6, 9, 17, 621. Although Bucteroides frugilis has been implicated in at least 2 cases of mediastinitis [63, 641, the potential of other anaerobes as primary pathogens remains unknown because most studies were conducted prior to the advent of efficient anaerobic culture techniques. Cundidu species have been cultured occasionally from areas of mediastinal suppuration [6, 91, but these organisms have proven to be a more common pathogen in the chronic cartilaginous infections [6, 651. The most important finding has been the emergence of S. epidermidis as a primary pathogen in postoperative mediastinitis, probably due in part to routine use of "prophylactic" antistaphylococcal, penicillinaseresistant antibiotics. The incidence of prosthetic valve endocarditis fell dramatically with the advent of methicillin [4, 28, 66, 67, 681. But with continued use, about 30% of all S. epidermidis isolates in large centers [6, 9, 68, 691 have become resistant to many antibiotics. For instance, Engelman and colleagues [9] used antistaphy-
lococcal agents to treat their patients, yet 6 of 17 cases of mediastinitis (35%)were caused by S. epidermidis. Similarly, the more recent study by the New York University group [6] reported that more than one-half of the staphylococcal infections were caused by S. epidermidis. Gram-negative mediastinal infections have also been influenced by prophylactic antibiotics [24, 671. Bryant and co-workers [12] used either chloramphenicol or streptomycin (as well as a penicillin) prophylactically in patients undergoing cardiac surgical procedures. Gramnegative mediastinal sepsis occurred in 5 patients; in 3, the infection proved resistant to the prophylactic agents employed.
Diagnosis Most commonly, mediastinitis is seen between 4 and 30 days postoperatively and usually within two weeks of the original procedure [8, 9, 12, 17, 26, 62, 64, 70, 711. Rare cases have been recognized as long as 60 and 145 days postoperatively [6, 261. Mediastinal infection after open-heart procedures can be clinically obvious or obscure. Wound drainage is the most common presentation in 70 to 90% of patients [8, 9, 12, 261. Although occasionally present in the absence of sternal instability [9], drainage is pathognomonic when seen to bubble through an unstable sternotomy wound through a sinus tract [26]. Sternal instability or frank dehiscence alone is not diagnostic of underlying infection; many cases of these entities prove sterile and require only rewiring [ll, 721. A widened mediastinum sometimes can be appreciated on chest radiograph [73]; however, this finding is unreliable as a criterion for mediastinitis following cardiac surgical procedures. Only occasionallywill the patient complain of dysphagia [73] or, with associated osteochondritis or costochondritis, of inordinant sternal tenderness [6]. Mediastinitis can also present as occult sepsis, devoid of any objective wound or sternal abnormalities. Three of 19 patients in one series [26] and 1 of 17 patients in another [9] were seen with occult sepsis. Persistent fever [12, 261 or leukocytosis [6, 91 can suggest mediastinal infection; however, these and similar indirect clues remain only suggestive, since they are frequent postoperative findings in patients having cardiac surgical procedures [74]. The sole objective diagnostic procedure short of reexploration has been mediastinal needle aspiration. Two techniques have been described-the subxiphoid, retrosternal approach [26] and the anterior transsternotomy approach [6]. Gram stain and cultures are confirmative. Best surgical results, of course, follow early diagnosis. A more aggressive use of mediastinal aspiration may diagnose mediastinal infection earlier, before wound drainage or sternal dehiscence appear.
Treatment Treatment of postoperative mediastinitis requires immediate drainage, debridement, and parenteral antibiotic therapy. Mortality is extremely high in patients
419 Collective Review: Sarr, Gott, and Townsend Mediastinal Infection after Cardiac Surgery
Table 2. Treatment of Postoperative Mediastinitis after Cardiac Surgery: Results of Open and Closed Methods Redebridement Reference
No. of
Mortality
Patients
(%)
10 13 7
20 45
15 15 14 27 16
33 7 14
Required
Development of Chronic Infection (%)
OPEN METHOD
Grmoljez et a1 [8] Sutherland et a1 [17] Culliford et a1 [6]
...
100
... ...
... ... 43
CLOSED METHOD
Engelman et a1 [9] Barois et a1 [75]
Thurer et a1 [62] Culliford et a1 [6] Jimenez-Martinezet a1 [26]
...
13
treated with antibiotics but without surgical drainage. Unfortunately, even with aggressive treatment, mortality remains high, and the morbidity and prolonged hospitalization prove considerable. Two approaches to the surgical management of postoperative mediastinitis have been described that differ only in the timing of sternal closure. The ”open” method [3] involves debridement and open packing of the mediastinal and sternal wounds with the option of a delayed or staged secondary closure. The advantage of this technique is that a potentially undrained space no longer exists. Active debridement continues through dressing changes during convalescence. However, frequent dressing changes are required and hospitalization is prolonged. Complete healing can take as long as sixteen months [8] and may require a skin graft. Lifethreatening hemorrhage from exposed mediastinal vessels is a potentially disastrous complication [26, 64, 75, 761. Moreover, the loss of sternal apposition impairs respiratory function secondary to inadequate chest support [26]. Two studies [8, 171 reported mortality of 20% and 45% when this “open“ method of therapy was employed (Table 2). Grmoljez and co-workers [8] treated 10 patients; all required at least one formal redebridement, and 5 required two or more subsequent procedures. Culliford and colleagues [6] adopted this method only for treatment of more advanced cases of mediastinal suppuration or for chronically infected patients. In their 39 patients, the ”open” method was required in only 7 patients; in 3 of these patients, chronic osteochondritis or costochondritis developed. In contrast, treatment of mediastinitis by the ”closed” method was reported in 1963 by Shumaker and Mandelbaum [771. This technique involves surgical drainage, debridement, and thorough intraoperative irrigation of the wound, after which the sternal edges are reapproximated over one or more fenestrated infusion catheters
13 66
...
...
20 21 7 19
...
and usually two or more larger drainage catheters. The subcutaneous wound has been left open and packed [62, 64, 711 or closed primarily with or without a drain [6, 9, 12, 261. Postoperatively, the mediastinum is irrigated continuously with saline solution [78], Dakin’s solution [75], or an antibiotic solution until cultures of the effluent turn negative, usually within one to three weeks. The antibiotic solutions employed have included neomycin [6, 12, 47, 64, 65, 791, bacitracin [6, 9, 12, 641, penicillin [77], nafcillin [80], polymyxin B [9, 121, kanamycin [2, 261, povidone-iodine [62, 64, 811, amphotericin B [2, 91, framycetin [75], and cephalothin and ampicillin [9]. Ochsner and colleagues [71] suggest adding streptokinase-streptodornase to the irrigation solution. Advantages of the “closed” method are obvious. Hospitalization is shortened; in one series, all patients were discharged less than 30 days after the initial drainage procedure [26]. Closure of the sternum returns stability to the thorax, thereby facilitating respiratory toilet. Moreover, frequent and sometimes hazardous dressing changes are avoided, emotional trauma is minimized, and the cosmetic result is improved. However, the ”closed” technique is not without complications. Closing the sternal wound creates a potentially undrained cavity, and reexploration for loculated sepsis has been required in 13 to 66% of patients [9, 751. The mediastinal catheters have eroded adjacent tissues, occasionally leading to life-threatening hemorrhage [64]. Antibiotic solutions may predispose to superinfection, possibly exacerbated by the indwelling mediastinal catheters [64]. A common superinfecting organism has been Candida [9, 65, 751. Indeed, several groups [6, 12, 641 have recognized a higher incidence of chronic osteochondritis and costochondritis caused by this organism after continuous closed-chest mediastinal irrigation. One must also watch for signs of systemic toxicity of the irrigant [9] (e.g., neomycin [82, 83, 841, framycetin [75],
420 The Annals of Thoracic Surgery Vol 38 No 4 October 1984
and povidone-iodine [Sl]). The volume of effluent from the drainage tubes must closely match the volume of irrigant. Results have proven encouraging (see Table 2). After Shumaker and Mandelbaum’s [77] successful treatment of 2 cases, Bryant and co-workers [12], Jimenez-Martinez and colleagues [26], and Engelman and associates [9], using a variety of antibiotic irrigants, reported success in 80%, 88%, and 67% of patients, respectively. Thurer’s group [62] and others [64,811 suggested irrigation with dilute povidone-iodine because this agent is effective against both bacteria and fungi; results proved acceptable without evidence of Candida superinfection. Although others have reported the successful treatment of infected prosthetic materials by the closed method without removal of the prosthesis [12, 80, 811, this must be unusual. Indeed, in some patients, removal of the infected foreign material was required to eradicate local sepsis [85]. With either method of treatment, optimal supportive measures are mandatory. Parenteral antibiotics remain compulsory; many authors recommend continuing these agents for three months, while others institute oral, single-agent coverage for up to nine months [75]. The importance of providing adequate nutrition cannot be overemphasized [6]. Occasionally, all attempts at local treatment fail and total excision of the sternum and infected costal cartilage becomes necessary. Under these conditions, Lee and colleagues [70] have used a pedicled, omental flap to cover the great vessels and associated suture lines; others have used pectoralis major muscle flaps [86-881. A full-thickness skin flap may be rotated for external coverage. In terms of survival, presentation within the first postoperative month confers a better prognosis than late development of mediastinal infection [6]. Renal failure [9] or prolonged ventilatory support [171 portends a dismal chance of survival. Prosthetic valve endocarditis has also been recognized as a complication of mediastinal suppuration [l-4, 751. Interestingly, patency of coronary bypass grafts evaluated one year postoperatively was not affected in those patients who had mediastinitis [8, 62, 64, 781.
Prevention The key to control of postoperative mediastinal infection lies in optimizing its prevention, a subject addressed by much of the present literature. Recognition and containment of nosocomial infection, meticulous operative technique, surveillance of postoperative care, and the rational use of perioperative antibiotics represent the obvious avenues of prevention. Intraoperative surveillance of infection control, including cognizance of airborne as well as personnel and surface contamination [34, 361, requires regular review by all involved. Elaborate, highly effective air filtration systems have been designed [89, 901; however, their cost-effectiveness has not been determined. Recognition of epidemics of nosocomial infection led to the evolution
of adequate precautions to prevent bacterial contamination [34, 44-47]. Primary areas of concern include the respiratory care systems and physical isolation policies of the intensive care unit. Special consideration should be given to the permanent physical isolation of chronically infected patients and their nursing teams to minimize cross-contamination (481. Surveillance of the changing spectrum of nosocomial infection has proven of preventive importance. Emergence of bacteria resistant to the usual antibiotics must be anticipated and recognized early [69]. For instance, S. epidermidis has emerged as a dangerous pathogen; at present only 70% of in-hospital isolates remain sensitive to the synthetic penicillinase-resistant derivatives [6, 9, 681. Preoperative preparation of the patient may minimize postoperative complications. Optimizing nutritional status, immunological competence, and respiratory function, as well as the eradication of foci of low-grade infection (especially of dental, respiratory, and genitourinary origin) are requisite preoperative adjuncts [91]. Scrubbing with a hexachlorophene detergent cleanser such as pHisoHex, or with defatting agents, or both prior to application of the iodine-containing skin preparation is considered important by some [6, 171. Similarly, under emergency conditions skin preparation and wound isolation, however hasty, prior to resternotomy seem important in minimizing the increased risk of infection following such procedures. Careful surgical technique and meticulous hemostasis are of paramount importance [2, 111. Ochsner and colleagues [71] stress the role of a precise, midline sternal osteotomy, which prevents cartilaginous exposure and minimizes subsequent sternal fracture. Equally essential is a mechanically stable sternal closure [ll, 171. Placement of wires through the costochondral cartilage [6, 651 should be avoided [92]. Many methods have been described to maximize sternal stability if the sternal edges are fractured, friable, or otherwise unstable [ll, 93-98]. The importance of careful apposition of the sternal periosteum and the sternalis muscle have been stressed [6]. Use of bone wax, a potential foreign body, is best avoided whenever possible. One group suggests removal of the xiphoid for fear of cartilaginous necrosis and subsequent infection [13]. Routine pericardial closure remains controversial [99]; two studies [6, 1001 support pericardial closure or approximation of mediastinal fat to prevent the spread of infection from the anterior wound to the myocardium, cardiotomy site, or prosthetic material. Ongoing educational programs directed at the paramedical and nursing staff should reinforce techniques of aseptic care and thereby lessen the incidence of local or hematogenous wound contamination. Early endotracheal extubation and removal of vascular, mediastinal, and urinary catheters will minimize the incidence of bacteremia. If prolonged ventilatory support is required, consideration should be given to the use of cricothyroidotomy instead of routine tracheostomy; the
421 Collective Review: Sam, Gott, and Townsend Mediastind Infection after Cardiac Surgery
former approach lessens the risk of wound communication and subsequent contamination of the anterior mediastinum [18, 1011. Prophylactic Antibiotics Introduction of effective prophylatic antibiotics added a new dimension to the prevention of infection after cardiac surgery. Prior to this, the incidence of postoperative prosthetic valve endocarditis approached 4% [4, 1021. With the introduction of antistaphylococcalprophylaxis, the incidence of fatal endocarditis has fallen dramatically [4, 28, 66, 681. Prophylactic antibiotics lowered the incidence of other infectious complications as well [69]. Merli and colleagues [lo31 found a 50% decrease in postoperative infections with oxacillin and hetacillin prophylaxis. Sutherland and associates [ 171 compared prophylactic antibiotics with placebo in the prevention of mediastinal sepsis. They found a slight but not significant difference in the incidence of mediastinitis. Unfortunately, serum levels of antibiotics were not assessed. To be effective as a prophylactic agent, serum levels of antibiotic must be adequate at the time of contamination. Brenner [lo41 monitored 6 patients given 1 gm of cephalothin the evening before and the morning of operation; inadequate serum levels of cephalothin were found in all patients while on CPB. Kluge and coworkers [lo51 and others [54, 106, 1071 demonstrated that bacteriocidal serum concentrations of cephalothin are maintained throughout the perioperative period only if the drug is administered immediately before operation. Goldman and co-workers [37] found that wound infections developed in 3 of 11patients with no detectable serum cephalothin activity at the end of operation, while only 2 of 175 patients with adequate levels had similar infections. With routine antibiotic prophylaxis, the spectrum of postoperative pathogens has also changed [12, 23, 671. Emergence of the resistant strain of S. epidermidis represents an example of this phenomenon [6, 9, 68, 691. Fekety and co-workers [24] demonstrated a predominance of gram-positive pathogens after penicillin prophylaxis and gram-negative organisms with methicillin prophylaxis. Obviously, the prophylactic agent must be subject to change according to local trends in bacteriological surveillance. At present, cephalothin or one of the newer cephalosporins appears to be the recommended antibiotic for prophylaxis in many centers [24, 37, 54, 69, 106, 108-1101.
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tion of prosthetic valve endocarditis. Am Heart J 71:393, 1966 5. Nelson JC, Nelson RM: The incidence of hospital wound infection in thoracotomies. J Thorac Cardiovasc Surg 54:586, 1967 6. Culliford AT, Cunningham JN Jr, Zeff RH, et al: Sternal and costochondral infections following open-heart surgery: a review of 2,594 cases. J Thorac Cardiovasc Surg 72:714, 1976 7. Amold M: The surgical anatomy of sternal blood supply. J Thorac Cardiovasc Surg 64:596, 1972 8. Grmoljez PF, Bamer HH, Willman VL, Kaiser GC: Major complications of median sternotomy. Am J Surg 130:679, 1975 9. Engelman RM, Williams CD, Gouge TH, et al: Mediastinitis following open-heart surgery: review of two years’ experience. Arch Surg 107772, 1973 10. Brown AH, Braimbridge MV, Panagopoulous P, Sibar EF: The complications of median sternotomy. J Thorac Cardiovasc Surg 58:189, 1969 11. Sanfelippo PM, Danielson GK: Complications associated with median sternotomy. J Thorac Cardiovasc Surg 63:419, 1972 12. Bryant LR, Spencer FC, Trinkle JK: Treatment of median sternotomy infection by mediastinal irrigation with an antibiotic solution. Ann Surg 169:914, 1969 13. Hehrlein FW, Herrman H, Kraus J: Complications of median sternotomy in cardiovascular surgery. J Thorac Cardiovasc Surg 13:390, 1972 14. LeVeen HL, Piccone VA: Nylon-band chest closure. Arch Surg 96:36, 1968 15. Londe S, Sugg W L The challenge of reoperation in cardiac surgery. Ann Thorac Surg 17157, 1974 16. Macmanus Q, Okies J, Phillips SJ, Starr A: Surgical considerations in patients undergoing repeat median sternotomies. J Thorac Cardiovasc Surg 69:138, 1975 17. Sutherland RD, Martinez HE, Guynes WA, Miller L: Postoperative chest wound infections in patients requiring coronary bypass: a controlled study evaluating prophylactic antibiotics. J Thorac Cardiovasc Surg 73:944, 1977 18. Pierce WS, Tyers GFO, Waldhausen JA: Effective isolation of a tracheostomy from a median sternotomy wound. J Thorac Cardiovasc Surg 66:841, 1973 19. Kay EB, Naraghipour H, Beg RA, et al: Internal mammary artery bypass graft-long-term patency rate and followup. Ann Thorac Surg 18:269, 1974 20. Green G E Internal mammary artery-to-coronary artery anastomosis: three-year experience with 165 patients. Ann Thorac Surg 14:260, 1972 21. Tector AJ, Davis L, Gabriel R, et al: Experience with internal mammary artery grafts in 298 patients. Ann Thorac Surg 22:515, 1976 22. Hutchinson JE 111, Green GE, Mekhjian HA, Kemp HG: Coronary bypass grafting in 376 consecutive patients with three operative deaths. J Thorac Cardiovasc Surg 677, 1974 23. Firor WB: Infection following open-heart surgery with special reference to the role of prophylactic antibiotics. J Thorac Cardiovasc Surg 53:371, 1967 24. Fekety FR Jr, Cluff LE, Sabiston DC Jr, et al: A study of antibiotic prophylaxis in cardiac surgery. J Thorac Cardiovasc Surg 57757, 1969 25. Goodman JS, Schaffner W, Collins HA, et al: Infection after cardiovascular surgery. N Engl J Med 278:117, 1968
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26. Jimenez-Martinez M, Arguero-Sanchez R, Perez-Alavarez JJ, Mina-Castaneda P: Anterior mediastinitis as a complication of median sternotomy incisions: diagnostic and surgical considerations. Surgery 67929, 1970 27. Kittle CF, Reed WA: Antibiotics and extracorporeal bypass. J Thorac Cardiovasc Surg 41:34, 1961 28. Ankeney JL, Parker RF: Staphylococcal endocarditis following open-heart surgery related to positive intraoperative blood cultures. In Brewer LA 111 (ed): Prosthetic Heart Valves. Springfield, IL, Thomas, 1968, pp 719-730 29. Blakemore WS, McGarrity GJ, Thurer RJ, et al: Infection by air-borne bacteria with cardiopulmonary bypass. Surgery 70830, 1971 30. Geldof WCP, Brom AG: Infections through blood from heart-lung machine. Thorax 27395, 1972 31. Yeh TJ, Anabtawi IN, Cornett VE, et al: Bacterial endocarditis following open-heart surgery. Ann Thorac Surg 329, 1967 32. Frater R W , Santos GH. Sources of infection in open heart surgery. NY State J Med 74:2386, 1974 33. Ankeney JL: Discussion of Amoury RA, Bowman FO Jr, Malm JR: Endocarditis associated with intracardiac prosthesis. J Thorac Cardiovasc Surg 51:48, 1966 34. Lathrop GD, Brockett RM, Blouse LE: Epidemiological surveillance for Staphylococcus qiidermidis infections related to cardiopulmonary bypass. Zentralbl Bakteriol [B] 241:108, 1978 35. Kluge RM, Calia FM, McLaughlin JS, Hornick RB: Sources of contamination in open-heart surgery. JAMA 230:1415, 1974 36. Wise RI, Sweeney FJ Jr, Haupt GJ, Waddell MA: The environmental distribution of Staph. aureus in an operating suite. Ann Surg 149:30, 1959 37. Goldman DA, Hopkins CC, Karchmer AW, et al: Cephalothin prophylaxis in cardiac valve surgery. J Thorac Cardiovasc Surg 73470, 1977 38. Wilensky AO, Samuels SS: Osteomyelitis of the sternum. Ann Surg 83:206, 1926 39. Bernard RW, Stahl WM, Chase RM Jr: Subclavian vein catheterization: a prospective study. Ann Surg 173:191, 1971 40. Borja A R Current status of infraclavicular subclavian vein Catheterization: review of the English literature. Ann Thorac Surg 13:615, 1972 41. Glover JL, OByrne SA, Jolly L: Infusion catheter sepsis: an increasing threat. Ann Surg 173:148, 1971 42. Konold P, Ullmank U, Schrader CP, Kieninger G: Klinische und bakteriologische beobachtungen bei intravenous eingefuhrten kathetern. Dtsch Med Wochenschr 99:1009, 1974 43. MacArthur BS, Ackerman NB: The significance of Serrutiu as an infectious organism. Surg Gynecol Obstet 146:49, 1978 44. Reyes LH, Ratzan KR, Rheinlander HF: Serrutiu murcescens bacteremia originating from a catheter line in the left atrium after mitral valve replacement. J Thorac Cardiovasc Surg 65:241, 1973 45. Richards NM, Levitsky S: Outbreak of Serrutiu murcescens infections in a cardiothoracic surgical intensive care unit. Ann Thorac Surg 19:503, 1975 46. Sanders CV Jr, Luby JP, Johanson WG, et al: Serrutiu marcescens infections from inhalational therapy medications: nosocomial outbreak. Ann Intern Med 73:15, 1970 47. Weinstein RA, Jones EL, Schwarzmann SW, Hatcher CR Jr: Sternal osteomyelitis and mediastinitis after open-heart
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