Prevention

Prevention of surgical site infections involves meticulous aseptic technique, appropriate timing of prophylactic antimicrobials, tight perioperative glucose control, and strict adherence to a hand hygiene policy.

Diagnosis

Surgical site infections typically present with localized cellulitis (erythema, warmth, and tenderness) and purulent discharge. With deep infections there may be sternal instability, chest pain, and systemic upset. Wound swabs and blood cultures (two sets) should be obtained before antimicrobials are given. If mediastinitis is suspected, a contrast computed tomography (CT) scan of the chest may be performed to confirm the diagnosis.¹⁸ However, most surgeons elect to proceed directly to reexploration, as it is diagnostic, provides tissue or pus for culture, and is therapeutic.

Microbiology

Staphylococci, either S. aureus or a coagulase-negative staphylococcus (mainly S. epidermidis), are responsible for the majority of postoperative sternal wound infections, with gram-negative bacilli accounting for most of the remainder.^19–21 More than 50% of leg wound infections are polymicrobial; multiple enteric gram-negative organisms are commonly identified.¹⁹ Polymicrobial mediastinal infection implies a serious breach of aseptic technique, such as that which may occur during lifesaving chest reopening in the ICU. Mediastinitis due to perforation of the esophagus or trachea is also likely to be polymicrobial, commonly involving enteric gram-negative bacilli and oropharyngeal streptococci, gram-negative coccobacilli, and anaerobes.

Treatment

For superficial cellulitis, oral antimicrobial therapy for 5 to 7 days is usually sufficient. If pus is draining from the wound, the skin sutures may be removed to facilitate drainage. If there is copious pus, sternal instability, severe pain, or systemic upset, intravenous antimicrobials should be given and reexploration considered. At the completion of reexploration, the sternum is usually rewired over multiple mediastinal drains. The drains may be continuously irrigated with antimicrobial or antiseptic solution for several days.²² If there is extensive necrosis of the sternum and mediastinal tissues, closure of the sternum may be delayed. Once infection has settled and granulation tissue has formed, the wound may be closed directly or, more commonly, via a muscle flap reconstruction.²³ Right ventricular laceration is a rare but usually fatal complication of open sternal wounds.²⁴ A vacuum-assisted closure device may be used to promote the healing of open sternal (and leg) wounds and is an effective bridge between débridement and delayed definitive closure.²⁵ Intravenous antimicrobials should be continued for at least 2 weeks; a longer course may be indicated if there are ongoing signs of infection or osteomyelitis or if a prosthetic valve is in situ. Infected leg wounds occasionally require surgical débridement and either delayed closure or closure by secondary intention (i.e., by the formation of granulation tissue).

Definitions and Causes

Pleural space infections include complicated exudative pleural effusions and empyema. Pleural effusions may be classified as transudative or exudative on the basis of their biochemistry (Table 35-3).²⁶ Transudative effusions are due to disturbances in the capillary Starling forces (see Equation 1-12) caused by conditions such as heart failure and liver cirrhosis. Transudative fluid is typically clear, low in protein, and acellular. Exudative effusions are due to inflammation or infection and are associated with conditions such as bacterial pneumonia (parapneumonic effusions), tuberculosis, connective tissue disorders, lung or pleural malignancy, pulmonary embolism, and postpericardectomy syndrome (see Chapter 20). Exudative effusions may be further classified as simple or complicated (see Table 35-3). Simple exudative effusions result from increased permeability of the pleura to protein and fluid, and they do not necessarily imply infection. Complicated exudative effusions result from invasion of the pleural space by microorganisms. They are characterized by a high neutrophil count, high lactate dehydrogenase concentration (due to neutrophil lysis), and a low glucose concentration and pH (due to anaerobic glucose utilization by bacteria and neutrophils).²⁷ The fluid is cloudy because of the presence of cellular debris. Activation of the coagulation cascade leads to fibrin deposition and the formation of loculations within the effusion. Undrained, complicated effusions can lead to empyema, which is defined as pus within the pleural space. There is marked fibroblast activity, which leads to thickening and fibrosis of the pleura.

Table 35-3 Chemistries of Transudative Pleural Effusions, Exudative Pleural Effusions (Simple and Complicated), and Empyema

Rights were not granted to include this table in electronic media. Please refer to the printed book.

From Maskell NA, Butland RJ: BTS guidelines for the investigation of a unilateral pleural effusion in adults. Thorax 58(suppl 2): ii8-ii17, 2003; Chapman S, Davies RJ: Recent advances in parapneumonic effusion and empyema. Curr Opin Pulmon Med 10:299-304, 2004; Light RW, MacGregor MI, Luchsinger PC, et al: Pleural effusions: the diagnostic separation of transudates and exudates. Ann Intern Med 77: 507-513, 1972.

Even when there is active infection, bacteria are not commonly seen on gram stain or grown from fluid sampled from a complicated effusion or empyema. Neutrophils and other inflammatory cells rapidly clear bacteria from the pleural space, which may reduce the number of bacteria to below the threshold visible on microscopy. Treatment with antimicrobials prior to fluid sampling may affect staining of bacteria for microscopy and may also inhibit microorganism growth in vitro. Some pathogenic microorganisms, notably anaerobes, are fastidious (i.e., have complicated nutritional requirements), which makes it difficult to grow them in vitro.

Community-acquired bacterial pneumonia is the most common cause of empyema. Sometimes empyema arises spontaneously, commonly in patients with lung disease but occasionally in young, healthy people. In the latter case, the causative organism is often one of the Streptococcus milleri group. Other causes of empyema include subdiaphragmatic infection (e.g., cholecystitis); postoperative infection (e.g., mediastinitis or bronchopleural fistula); esophageal perforation (e.g., following surgery or perforation by a foreign body); and infections related to chest trauma or intercostal drain sites.

Diagnosis

Patients with complicated effusions and empyema are typically systemically unwell and show signs of sepsis. They may have productive cough, chest pain, and respiratory distress. The appearances of chest radiographs are variable. Free-flowing effusions produce characteristic changes on erect and supine films (see Chapter 6). Loculated effusions or pleural thickening may produce nondependent pleural-based opacities (Fig. 35-1). There may be signs of the underlying cause of empyema, such as consolidation of the lung (pneumonia) or an air fluid level (bronchopleural fistula). Ultrasound scanning is useful to confirm the presence and volume of fluid in the pleural space, to identify septations, and to guide diagnostic thoracocentesis.²⁸ Thickening and enhancement of the parietal pleura in conjunction with pleural collection as seen on contrast-enhanced CT scan are strongly suggestive of empyema (Fig. 35-2).²⁹ CT scanning may also identify the cause. Septations are not easily seen on CT scans.

Figure 35.1 Erect chest radiograph of a left-sided nondependent pleural collection consistent with empyema.

Figure 35.2 Transverse CT scan of a right-sided, loculated empyema. The parietal pleura (arrows) is thickened. Both an anterior and a posterior pleural collection are seen, along with a thinner collection laterally.

Microbiology

Causative microorganisms include Streptococci species (S. pneumoniae, S. milleri group, viridans group); S. aureus; enteric gram-negative bacilli (particularly Klebsiella pneumoniae and Escherichia coli); Pseudomonas aeruginosa; Haemophilus influenzae; and anaerobes.³⁰ With hospital-acquired empyema, similar microorganisms are identified, but it is more common to find Enterococcus species, MRSA, S. milleri, and multi-drug-resistant gram-negative bacilli (particularly P. aeruginosa).³⁰ Occasionally, Candida species are responsible for empyema.

Treatment of Exudative Effusions

Simple parapneumonic effusions usually resolve spontaneously with treatment of the underlying pneumonia. In general, thoracocentesis should be performed in all parapneumonic effusions because clinical differentiation between simple and complicated effusions is unreliable.³¹ Effusions in patients with hypoalbuminemia, heart failure, or atelectasis are at low risk for infection and do not require sampling (but may need draining if they are large). Effusions in patients with either pneumonia or sepsis and effusions that are associated with thickening of the parietal pleura on CT scan or loculations on ultrasound scanning should be sampled.³¹

If thoracocentesis reveals a complicated effusion, it should be drained to prevent progression to empyema.³² If the effusion is relatively free-flowing, tube thoracostomy using a large-bore tube (e.g., 36F) is appropriate. If there are numerous septations or there has not been substantial radiographic resolution of the effusion within 24 hours of tube thoracostomy, intrapleural fibrinolytic therapy may be considered. With this technique, 100,000 IU of urokinase or 250,000 IU of streptokinase in 100 ml of 0.9% saline is instilled into the chest cavity and the tube clamped for 1 to 4 hours. This can be repeated once or twice a day for 2 to 4 days. Systemic fibrinolysis does not occur. The value of intrapleural fibrinolytic therapy, in terms of radiographic and clinical improvement, has been demonstrated in a number of small studies. However, in a recent large, randomized trial, intrapleural streptokinase was not associated with a reduced need for surgery or with improved survival rates.³³ Thus, if the technique is not rapidly effective, patients should undergo surgery. Antimicrobial therapy for complicated effusions is the same as for empyema, described subsequently.

Treatment of Empyema

Once a fluid sample has been obtained by needle thoracocentesis, intravenous antimicrobials should be commenced empirically. For community-acquired empyema, amoxicillin/clavulanic acid or a secondgeneration cephalosporin (e.g., cefuroxime) combined with metronidazole may be used.³⁴ An alternative for patients allergic to penicillins is clindamycin plus a fluoroquinolone (e.g., ciprofloxacin). For hospital-acquired empyema, a carbapenem plus vancomycin is appropriate.³⁴ Antimicrobial therapy should be adjusted on the basis of culture and sensitivity results, but empiric cover against anaerobes should continue because these organisms are commonly present but frequently are not isolated on culture. Aminoglycosides have poor penetration into empyemas and are best avoided. Following drainage of an empyema, antimicrobial therapy should continue for a minimum of 3 weeks.³⁴

Effective drainage of an organized empyema in which there are extensive loculations and pleural thickening requires surgery. There are two main approaches: (1) open thoracotomy and decortication; (2) video-assisted thoracoscopic débridement. The latter is a relatively new technique that appears to be safe and effective in experienced hands.^35,36 During surgery, loculations must be broken down, pus drained, and any thickened visceral pleura excised (decortication) to allow the collapsed lung to reexpand. Specimens for culture should be obtained at the time of surgery and their results used to guide antimicrobial therapy. Decortication of a chronically organized empyema can result in substantial perioperative blood loss. Postoperatively there may be marked systemic inflammatory response, including fever, tachycardia, third-space fluid losses, and vasodilatation. Positive-pressure ventilation may be difficult because of air leaks, acute lung injury, and poor reexpansion of the affected lung.

Postpneumonectomy Empyema

Empyema that occurs within the first few weeks after pneumonectomy is usually caused by a bronchopleural fistula. Patients present with fever, cough, purulent or hemorrhagic sputum, respiratory distress and, occasionally, sepsis and acute respiratory failure. Chest radiographs typically demonstrate increased air content and reduced fluid levels within the pleural space. There may be soiling of the nonoperative lung demonstrated by pulmonary infiltrates on the chest radiograph (see Fig. 12-6). Empyema that occurs more than 3 months after pneumonectomy is usually due to hematogenous spread of infection into the pleural space. Patients typically present subacutely with malaise, flulike symptoms, low-grade fever, and weight loss.

The diagnosis of a bronchopleural fistula is usually confirmed by bronchoscopy or a contrast-enhanced CT scan of the chest. Alternatively, methylene blue can be instilled into the pleural space and recovered from the sputum. Needle aspiration of the thoracic space is rarely helpful in the acute setting, but if it is undertaken, it should be guided by ultrasound. Two sets of blood cultures should be obtained before starting antimicrobial therapy. Causative organisms and empiric antimicrobial therapy are as described for hospital-acquired empyema. In particular, antimicrobials against MRSA and P. aeruginosa must be administered until culture results are available. Surgical treatment of a bronchopleural fistula is described in Chapter 12.

Pathophysiology and Risk Factors

The initiating event of infective endocarditis is the formation of fibrin-platelet thrombus on damaged endothelium or prosthetic material.³⁸ With bacteremia, microorganisms seed on the thrombus. Bacterial replication and further thrombosis lead to the formation of infected vegetations (see Fig. 7-11). Clinical disease may take several weeks to develop following a bacteremic episode. Infection may result in localized tissue destruction, which can cause valve regurgitation, abscesses, or fistulae. Abscesses (see Fig. 7-14) and fistulae typically involve the aortic root. Very occasionally, large vegetations cause valve stenosis. There may be systemic emboli, including cerebral and pulmonary emboli. Pulmonary emboli arise from right-sided vegetations, whereas cerebral emboli arise from left-sided vegetations. Systemic embolization resulting from right heart lesions can occur in a patient with an intracardiac shunt or a patent foramen ovale. Right-sided lesions are associated with injection drug use. The risk for infective endocarditis with various cardiac lesions is summarized in Table 10-7; congenital cardiac lesions and rheumatic heart disease underlie most cases.

Microbiology

Gram-positive microorganisms are responsible for the majority of cases of infective endocarditis. They include (1) streptococci, particularly viridans streptococci (e.g., Streptococcus sanguis, S. mutans, S. mitis); β-hemolytic streptococci (e.g., S. pyogenes, S. agalactiae); and nonhemolytic streptococci (e.g., S. bovis); (2) staphylococci, particularly Staphylococcus aureus and coagulase-negative staphylococci (primarily S. epidermidis); (3) enterococci (e.g., Enterococcus faecium, E. faecalis). Viridans streptococci and S. aureus cause most cases of native valve endocarditis, whereas S. aureus and coagulase-negative staphylococci are important causes of prosthetic valve endocarditis occurring early after implantation (Table 35-4). Less common (<10%) causes of infective endocarditis include gram-negative bacilli, fungi, and the HACEK group of microorganisms. The HACEK group are fastidious, slow-growing, gram-negative coccobacilli from the oropharynx which, although constituting only 3% to 4% of infective endocarditis, are increasing in prevalence. They are composed of Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae. As much as one third of cases of infective endocarditis are culture-negative.

Table 35-4 Common Causative Microorganisms in Native and Prosthetic Valve Infective Endocarditis

Diagnosis

The diagnosis of infective endocarditis rests on clinical, microbiologic, and echocardiographic criteria, as outlined in Table 35-5.^37,39 Infective endocarditis should be suspected in any at-risk patient who develops a febrile illness. Three sets of blood cultures should be obtained between 30 and 60 minutes apart, and an echocardiogram should be performed (see material under Investigations). Blood samples should be incubated for at least 1 week because fastidious bacteria and fungi can occasionally be grown after the standard incubation period of 5 days.

Table 35-5 Modified Duke Criteria for Diagnosing Infective Endocarditis

* See text for details.

** The term persistently positive blood cultures is defined as at least two blood cultures drawn more than 12 hours apart, or three of three or a majority of four or more blood cultures drawn over the span of at least 1 hour.

† An echocardiogram is positive when any of the following are seen: (1) a discrete, echogenic, oscillating intracardiac mass located at the site of endocardial injury; (2) a periannular abscess; (3) a new dehiscence of a prosthetic valve.

Clinical Features

Infective endocarditis may have an acute or a subacute course. The acute form is commonly caused by S. aureus. Signs of sepsis are common, and valvular destruction and abscess formation (with aortic valve involvement) occur early. More commonly, infective endocarditis has a subacute course with symptoms of fever, malaise, and musculoskeletal pain extending over several weeks. Acute valvular regurgitation is less common with subacute endocarditis.

Signs of cardiac involvement include a new or changing murmur, abnormalities of cardiac conduction, or clinical features of heart failure and valvular regurgitation. First-degree heart block with a progressively lengthening PR interval strongly suggests an aortic root abscess.

Neurologic complications occur in about one third of patients. They may take the form of a generalized encephalopathy—thought to be due to multiple microemboli—or of a focal neurologic deficit due to a macroembolus with or without cerebral abscess formation. Brain CT scanning may reveal asymptomatic cerebral abscesses. Mycotic aneurysms may involve the large arteries.

A variety of peripheral embolic, vascular, and immunologic phenomena may be identified. Petechiae are small purplish spots that may be present in the conjunctiva, the mucous membranes of the mouth, and on the skin—commonly on the fingertips. Splinter hemorrhages are red or brown linear marks under the fingernails or toenails. Osler nodes are small painful pink nodules on the pads of the fingers and toes. Janeway lesions are nontender red-blue macular lesions on the palmar surface of the hands and feet. Roth spots are superficial retinal hemorrhages that may be seen on fundoscopy. Circulating immune complexes can cause polyarthritis or glomerulonephritis. However, renal dysfunction is more likely to be due to heart failure or sepsis than to glomerulonephritis. Splenomegaly is common. Pain localized to a specific region (e.g., liver, bone, soft tissue) may represent an embolic abscess.

Investigations

Normochromic normocytic anemia, leukocytosis, and elevated acute-phase reactants (fibrinogen, C-reactive protein, and the erythrocyte sedimentation rate) are common findings. In addition to blood cultures and an echocardiogram (see earlier discussion under Diagnosis), a chest radiograph, and an electrocardiogram should be obtained in all patients. Transesophageal echocardiography may be required to diagnose small vegetations and to fully delineate aortic root abscesses or fistulae. A contrast CT scan of the brain, abdomen, or chest should be performed if there are clinical signs of systemic embolization. Suspected bony emboli may be confirmed by a radionuclide bone scan.

Treatment

If infective endocarditis is suspected clinically and the presentation is acute, empiric antimicrobial treatment (see subsequent material) should be started as soon as blood cultures have been obtained. If the presentation is subacute, it may be reasonable to await the results of blood cultures before starting antimicrobials. Continued pyrexia despite appropriate antimicrobial therapy suggests an undrained abscess. This should be investigated by a repeat echocardiogram, chest, abdominal and pelvic CT scan and, if indicated, a radionuclide bone scan.

Surgery is indicated in the following circumstances:

Antimicrobial therapy alone is usually successful in infective endocarditis due to Streptococcus species. However, when due to S. aureus, fungi, or gram-negative microorganisms such as Serratia species and P. aeruginosa, surgery is commonly required.

Risk factors for systemic embolization include vegetations greater than 10 mm diameter or highly mobile lesions attached to the anterior leaflet of the mitral valve.³⁸ Given that more than 50% of systemic emboli involve the central nervous system, early surgery should be considered in patients with large or mobile vegetations, particularly if they are caused by S

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