Treatment of Postoperative Pulmonary Infections

Symposium on Surgical Infections and Antibiotics

Treatment of Postoperative Pulmonary Infections

John G. Bartlett, M.D.*

Pulmonary infection represents a major cause of postoperative complications. Therapeutic principles are the same as with other forms of pulmonary infection but there are two noteworthy factors to be emphasized from the outset. First, relatively unusual pulmonary pathogens are often responsible. Second, expectorated sputum culture is of little value in establishing the responsible organism. The implication of these observations is that specialized procedures are often required for an accurate etiological diagnosis. When empirical therapy is necessary, antimicrobials should be selected with a view toward covering possible multiple pathogens.

PREDISPOSING CONDITIONS Aspiration There are several factors which predispose surgical patients to aspiration. These include general anesthesia, nasogastric feeding tubes, protracted vomiting, and local anesthesia of the upper airways. Although aspiration is a commonly recognized postoperative complication, there is considerable confusion regarding the pathophysiology and treatment of the pulmonary consequences. We feel that aspiration may be divided into three distinct syndromes according to the composition of the inoculum (Table 1).2 Greatest attention in the surgical literature has been devoted to the chemical pneumonitis which follows gastric acid aspiration as described by Mendelson.12 Characteristic features are the precipitous onset of acute dyspnea, bronchospasm, hypoxia, frothy sputum and chest x-rays showing mottled densities in one or both lower lobes. The most important facet of therapy is to correct hypoxia. Additional important measures are tracheal suction to maintain a clear airway, intravenous fluids and early institution of short term corticosteroids. Infection plays essen'Associate Professor of Medicine, Tufts-New England Medical Center, Boston, Massachusetts; Veterans Administration Hospital, Boston, Massachusetts

Surgical Clinics of North America- Vol. 55, No.6, December 1975

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Table 1.

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Forms of Aspiration Pneumonia

INOCULUM

PULMONARY REACTION

THERAPY

Gas tric acid

Chemical pneumonitis

Reverse hypoxia Tracheal suction Intravenous fluids Corticosteroids

Oropharyngeal bacteria

Bacterial infection

Antimicrobials

Inert material Fluids Solid particles

Pulmonary obstruction Pulmonary obstruction

Tracheal suction Extraction of particle

tially no role in the immediate events following gastric acid aspiration, but it may complicate the subsequent course. It is our view that antimicrobials should be reserved for cases in which there is evolving evidence for this complication such as significant fever and purulent sputum. A more common form of aspiration pneumonia bears the hallmarks of bacterial infection from the onset. In contrast to acid pneumonitis, the aspiratory event is seldom observed, but the diagnosis can be made when typical symptoms occur in a susceptible host. The usual findings are fever, purulent sputum production and an infiltrate in a dependent pulmonary segment. The bacterial challenge in these cases is composed of oropharyngeal flora. 3 Anaerobic bacteria are the usual culprits in patients who aspirate outside the hospital setting. Among hospitalized patients, likely pathogens include anaerobic bacteria, aerobic gram-negative bacilli and Staph. aureus. The third form of aspiration involves substances which have no inherent toxic effect on the lung. Airway obstruction may result with sufficient volumes of inert fluids and this requires immediate tracheal suction. Solid particle aspiration may also produce bronchial obstruction necessitating removal by bronchoscopy.

Atelectasis Atelectasis is a common postoperative complication which generally responds to mechanical measures without antimicrobials. However, pneumonitis often supervenes if atelectasis persists for more than two to three days.9 Clues to a superimposed infection are fever of greater than 101°F., leukocytosis, purulent sputum production, and a pulmonary infiltrate rather than collapse on chest x-ray. Suspected pathogens in these cases are the same oropharyngeal strains discussed for aspiration pneumonia. Tracheostomy The normal trachea is sterile but it becomes colonized within 24 to 48 hours following tracheostomy. Usually there are multiple species in a single aspirate and common isolates include coliforms, pseudomonads,

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Staph. aureus and Candida.4 Some degree of inflammation is inevitable, most frequently at the stoma, tip of the tube and area of the cuff. Antimicrobials have no effect on the incidence of colonization or mild local inflammatory reactions.u Infectious complications which merit antimicrobial treatment are serious wound sepsis, febrile tracheobronchitis and pneumonitis. Bacterial pathogens in such cases are those which commonly colonize the tracheostomy site. Thus the decision to use antiInicrobials is based on associated clinical findings and agents are selected according to cultures of tracheostomy aspirates. A similar approach is used for patients with endotracheal intubation. Inhalation Therapy Inhalation therapy is a recognized risk factor for pulmonary infections when aerosolizing nebulizers are used. IS This is easily averted by decontaminating the equipment at least once daily. The bacteria involved are those which survive well in water, particularly Pseudomonas, Klebsiella and Serratia. Antimicrobials Surgical patients often receive antimicrobial agents for extrapulmonary infections or as prophylaxis during the perioperative period. Previous studies indicate that these agents do not prevent pulmonary infections in the susceptible host. Instead, they appear to simply select out resistant forms.13

SPECIMENS The time honored method to identify pathogens in pulmonary infections is culture of expectorated sputum. However, several studies have shown that this procedure is of limited diagnostic value.6 • 10. 18 The problem is largely related to the inevitable contaInination of the specimen during passage through the upper airways. Thus, specimens are considered reliable only if they are devoid of the upper respiratory tract flora. Examples include transtracheal aspirates, percutaneous lung puncture aspirates, empyema fluid, thoracotomy specimens and blood cultures. A precautionary note is that antimicrobials may rapidly alter the cultivable flora and, therefore, these specimens should be collected prior to the institution of treatment. Transtracheal aspiration has proved to be a safe and reliable culture source providing the procedure is performed by an experienced person on adult patients with no contraindications (bleeding diathesis, severe hypoxia or severe hemoptysis).6 Percutaneous transthoracic aspiration is the preferred method in children with serious pulmonary infections.8 Bronchoscopy aspirates collected with the usual techniques are considered unreliable due to instrument contamination during passage through the upper airways. This contamination may be partially or completely avoided by inserting vinyl tubing well beyond the tip of the bronchoscope for specimen collection. lo • 18

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ANTIMICROBIAL TREATMENT Selection of Agents According to Pathogens The most common pulmonary pathogens in nonsurgical patients are viruses, Mycoplasma pneumoniae and the pneumococcus. The responsible organism in these patients can usually be predicted according to clinical presentation. Among surgical patients, however, an entirely different array of pathogens is to be anticipated. Despite variations within different predisposing group categories, there is a recurrent theme of aerobic gram-negative bacilli. These organisms seldom cause community-acquired pulmonary infections, but they account for 30 to 50 per cent of those acquired within the hospital setting. 16 The best explanation for this observation is offered by the pharyngeal flora studies of Johanson et al. 7 These investigators showed that aerobic gram-negative bacilli cohabitate the upper airways in only 2 to 3 per cent of normal persons but they are detected in as many as 63 per cent of patients in intensive care units. Factors which correlate with this type of pharyngeal colonization are the severity of the underlying illness and preceding antimicrobial therapy.14 Presumably this represents the source of gram-negative infections of the lowe.r respiratory tract. The current antimicrobial agent of choice for serious infections involving gram-negative bacilli is gentamicin. Once susceptibility tests are available, an alternative agent may often be selected. Some authorities prefer the combination of gentamicin and carbenicillin for pulmonary infections caused by Pseudomonas aeruginosa. Staph. aureus is another important cause of pulmonary infection in surgical patients. Mortality rates of 50 per cent have been reported with recent studies of staphylococcal pneumonia.5 This emphasizes the importance of clinical recognition and early institution of treatment. Antibiotics of choice are penicillinase-resistant penicillins such as nafcillin, oxacillin and methicillin. These three are considered equally effective, although there is a higher incidence of nephrotoxicity with methicillin. The usual alternative agent for penicillin-allergic patients is a cephalosporin. However, due to possible penicillin-cephalosporin cross sensitivity, we would favor an entirely different compound, such as clindamycin, if the penicillin reaction was anaphylaxis or serum sickness. Anaerobic bacteria are frequent pathogens in pulmonary infections related to aspiration. Pencillin G is the preferred antimicrobial with alternative agents being clindamycin or chloramphenicol.1 Most respiratory strains of anaerobes are susceptible to cefazolin17 although there is little in vivo experience to corroborate the in vitro data. Empiric Antimicrobial Selection Optimal treatment of pulmonary infections is based on culture results of reliable specimens. When empirical treatment is used it is necessary to take into account the multiplicity of likely pathogens. For serious infections a two drug regimen is suggested: gentamicin in combination with nafcillin, cefazolin or clindamycin.

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Table 2.

Antimicrobial Parenteral Dosage for Severe Pulmonary Infections AGENT

DOSAGE

Penicillin G Ampicillin Carbenicillin * Nafcillin Cephalothin Cefazolin* Clindamycin Chloramphenicol Gentamicin':'

0.5 to 2 million units every 4 to 6 hours 0.5 to 2 gm. every 4 to 6 hours 5 gm. every 4 hours 1 to 2 gm. every 4 to 6 hours 0.5 to 2 gm. every 4 to 6 hours 0.5 to 1 gm. every 6 to 8 hours 600 mg. every 8 hours 1 gm. every 6 to 8 hours 2.0 mg./kg., then 1.5 mg./kg. every 8 hours

*Dose adjustment required in patients with renal failure.

Dosage and Duration of Treatment Suggested doses of the principal antibiotics used in pulmonary infections are given in Table 2. Parenteral treatment is usually recommended until fever and toxicity subside. At that time an appropriate oral antimicrobial may be substituted and continued to provide a total of seven to ten days of treatment. An exception is staphylococcal pneumonia which is generally treated for four to six weeks. Pulmonary infections associated with cavitation, i.e., lung abscess and necrotizing pneumonia, should also be treated for extended periods. In these cases antimicrobials are continued until the roentgenographic changes have cleared or show only a small stable residual lesion.

REFERENCES 1. Bartlett, J. G.: Treatment of anaerobic pulmonary infections. Ann. Intern. Med., in press. 2. Bartlett, J. G., and Gorbach, S. L.: The triple threat of aspiration. Chest, in press. 3. Bartlett, J. G., Gorbach, S. L., and Finegold, S. M.: The bacteriology of aspiration pneumonia. Amer. J. Med., 56:202-207, 1974. 4. Espinoza, H., Palmer, D. L., Kisch, A. L., Ulrich, J., Eberle, B., and Reed, W. P.: Clinical and immunologic response to bacteria isolated from tracheal secretions following tracheostomy. J. Thorac. Cardiovasc. Surg., 68:432-439,1974. 5. Fisher, A. M., Trever, R. W., Curtin, J. A., Schultze, G., and Miller, D. F.: Staphylococcal pneumonia: A review of 21 cases in adults. New Engl. J. Med., 258:919-928,1958. 6. Hoeprich, P. D.: Etiologic diagnosis of lower respiratory tract infections. Calif. Med., 112:1-8,1970. 7. Johanson, W. G., Pierce, A. K., and Sanford, J. P.: Changing pharyngeal bacterial flora of hospitalized patients: Emergence of gram-negative bacilli. New Engl. J. Med., 281:1137-1140,1969. 8. Klein, J. 0.: Diagnostic lung puncture in the pneumonias of infants and children. Pediatrics, 44:486-492, 1969. 9. Lansing, A. M., and Jamieson, W. G.: Mechanisms of fever in pulmonary atelectasis. Arch. Surg., 87:184-190,1963. 10. Lees, A. W., and McNaught, W.: Non-tuberculous bacterial flora of sputum and of the upper and lower respiratory tract in pulmonary tuberculosis. Lancet, 2:1115-1117, 1959. 11. Lepper, M. H., Kofman, S., Blatt, N., Dowling, H. F., and Jackson, G. G.: Effect of eight antibiotics used singly and in combination on the tracheal flora following tracheotomy in poliomyelitis. Antibiotics and Chemother., 1954, pp. 829-843. 12. Mendelson, C. L.: The aspiration of stomach contents into the lungs dUring obstetric anesthesia. Am. J. Obstet. Gynec., 52:191-205,1946. 13. Petersdorf, R. G., Curtin, J. A., Hoeprich, P. D., Peeler, R. N., and Bennet, I. L., Jr.: A study

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of antibiotic prophylaxis in unconscious patients. New Engl. J. Med., 257:1001-1009, 1957. Pierce, A. K., and Sanford, J. P.: Aerobic Gram-negative bacillary pneumonias. Amer. Rev. Resp. Dis., 110:647-658,1974. Pierce, A. K., and Sanford, J. P.: Bacterial contamination of aerosols. Arch. Intern. Med., 131 :156-162,1973. Sanford, J. P., and Pierce, A. K.: Current infection problems-respiratory, In Proceedings of the International Conference on Nosocomial Infections, Center for Disease Control. Chicago, American Hospital Association, 1973, pp. 77-81. Tally, F. P., Jacobus, N. V., Bartlett, J. G., and Gorbach, S. L.: Susceptibility of anaerobes to cefoxitin and other cephalosporins. Antimicrob. Ag. Chemother., 1975, pp. 128-132. Wanner, A., Amikam, B., and Sackner, M. A.: A technique for bedside bronchofiberoscopy. Chest, 61 :287-288, 1972.

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