ICU Infections
KEY POINTS
1 Antibiotic choices should be reassessed on a daily basis, keeping in mind that antibiotics rarely, if ever, reverse the effects of any infection in less than 48 to 72 h. Antibiotic choices should be trimmed to the simplest effective combination as clinical response and culture data become available.
2 The speed with which an infectious diagnosis is pursued and the invasiveness of the techniques used generally should parallel the severity of illness of the patient. Stable patients with functioning immune systems and good physiologic reserves require less-aggressive diagnostic approaches, whereas critically ill, unusually vulnerable and fragile patients require rapid, definitive diagnosis.
3 When several equally effective alternatives exist to treat the same infection, choose the combination with the best side effect and cost profile. Oral therapy and parenteral dosing of a long-acting antibiotic on an infrequent schedule are the best methods of reducing antibiotic costs.
4 Antibiotics should be selected based on culture results, if available, and on microscopic examination of body fluid specimens if not. In the absence of diagnostic material, the clinical history and presumed site of infection should be the primary determinants of antibiotic selection.
5 For the unstable, infected or septic patient, broad-spectrum empiric antibiotic therapy should be instituted after obtaining appropriate cultures. As a rule, for such patients, it is best initially to give too many rather than too few antibiotics—second chances to choose the appropriate therapy may not arise.
▪ SUSPECTING INFECTION
Infection may be suspected on the basis of localizing signs (e.g., swelling, erythema, wound discharge) or localizing symptoms (e.g., pain, dyspnea, cough) but most commonly is considered because of the presence of fever or leukocytosis. Fever afflicts at least half of all patients during their stay in the intensive care unit (ICU) and often is an important clue to the presence of infection. The magnitude and pattern of fever, typically defined as a temperature exceeding 101°F (38°C) to 101.4°F (38.5°C), are often accorded undue significance; fever characteristics actually have little diagnostic value. It is essential to recognize that not all fever is due to infection. Several diseases as deadly as disseminated infection can induce fever. Prominent among them are heat stroke, neuroleptic malignant syndrome, and the endocrine disorders of hyperthyroidism, adrenal insufficiency, and pheochromocytoma. Noninfectious causes of febrile syndromes are discussed in detail in Chapter 28.
For some patients, diagnosis of infection is difficult because both localizing and generalized signs are unimpressive. Patients infected with human immunodeficiency virus (HIV) often have minimal tissue inflammation when infected. Elderly patients and patients with hypothyroidism and renal failure often have reduced fever responses compared to younger patients. Both neutropenia and immunosuppressive drug therapy tend to reduce the local response to infection, making erythema, pain, swelling, and pus formation less likely.
▪ COMMON SCENARIOS
Three categories account for most infections seen in the ICU: primary bacterial infections that prompt admission (e.g., pneumonia, urinary tract infection [UTI], meningitis); nosocomial infections (e.g., catheter-related sepsis, nosocomial pneumonia); and infections of the immune-compromised host. The broad topic of infection cannot be addressed comprehensively in a single chapter of reasonable length; therefore, the discussion that follows focuses on the most common and serious infections occurring in the ICU. Patient characteristics profoundly influence the likely site of infection and the likely organisms responsible. The selection
of antimicrobials must take allergies and organ dysfunctions into account. Furthermore, individual hospitals have different spectra of bacteria causing a particular clinical syndrome, and even within a single hospital antibiotic susceptibility can vary widely among units. Therefore, practitioners must have a thorough knowledge of the patient being treated, the likely pathogens, and the antimicrobial susceptibility pattern of the hospital in which they practice.
of antimicrobials must take allergies and organ dysfunctions into account. Furthermore, individual hospitals have different spectra of bacteria causing a particular clinical syndrome, and even within a single hospital antibiotic susceptibility can vary widely among units. Therefore, practitioners must have a thorough knowledge of the patient being treated, the likely pathogens, and the antimicrobial susceptibility pattern of the hospital in which they practice.
Antimicrobial options are constantly evolving. In recent years, for example, entirely new antibiotic categories have been exploited and better-tolerated formulations of long-established drugs have been commercially released. In the former category are drugs directed at organisms resistant to most standard agents, such as linezolid, daptomycin, and quinupristin-dalfopristin for methicillin-resistant Staphylococcus aureus (MRSA) and vancomycinresistant Enterococcus. Others include new antifungal agents, such as caspofungin for invasive Aspergillus and Candida infections. Nephrotoxicity of traditional amphotericin desoxycholate has been attenuated by its lipid complex, cholesteryl complex, and liposomal variants. Voriconazole, a modified triazole, now offers a well-tolerated alternative to amphotericin that can be given orally as well as parenterally in the treatment of aspergillosis. Modifications within well-established antimicrobial categories have extended their spectra and/or limited their side effects. For example, fluoroquinolones (e.g., levofloxacin, gatifloxacin, and moxifloxacin) offer potent competition to traditional drugs in the treatment of typical and atypical pneumonia. Although allergic sensitivity, renal insufficiency, hepatic dysfunction, bleeding tendency, or other vital organ dysfunction may restrict the options, almost always, there is more than one potentially effective antimicrobial combination for any given infection. Suggestions that follow for antibiotic therapy are based on the most common pathogens and their usual susceptibility patterns while considering the frequency and severity of side effects and ease and cost of administration. “Broad-spectrum” effectiveness is both a luxury and a liability, as the desire to cover a large number of potential pathogens comes at a high price. Indiscriminate use of broad-spectrum antibiotics is rapidly producing multidrug-resistant bacteria. MRSA and penicill-inresistant Pneumococcus are now pandemic. New and menacing pathogens such as multiresistant Enterococcus and Acinetobacter are recognized with increasing frequency, and unless patterns of antibiotic use change, it is likely such infections will grow in importance. Antibiotics are the only class of drugs that, when misused, can injure not only the patient being treated but nearby patients and patients admitted to the ICU in the future. For example, the routine use of vancomycin to treat diarrhea or to cover for Gram-positive pathogens may inadvertently “select out” organisms resistant to this useful drug. These highly resistant organisms then lurk in the ICU, ready to infect subsequent patients.
▪ URINARY TRACT INFECTIONS
Pathogenesis
The urinary tract is the most common site of ICU infection, accounting for almost 40% of all infections. Although UTIs usually are inconsequential, the mortality rate for a bacteremic UTI approaches 30%. Risk factors for UTI include presence of a urinary catheter, female gender, diabetes, and advanced age. Colonization of urinary catheters occurs at a rate of about 5% to 10% per day, and most ICU-acquired UTIs occur in such colonized patients. Presumably, the colonized catheter permits retrograde passage of pathogenic bacteria into the bladder where they proliferate. Urinary catheter composition (Teflon rather than rubber) may reduce the infective hazard; however, there is no evidence that routine changing of the catheter or external application of antibiotic ointment decreases risk. Keys to preventing nosocomial UTI are sterile catheter insertion, early catheter removal, and maintaining a closed drainage system.
Diagnosis
The diagnosis of UTI is all but certain when greater than 105 bacteria/mL are isolated from culture of freshly collected urine. This level of bacteriuria correlates well with the presence of more than one organism per high-power field of unspun urine. Unfortunately, fewer bacteria do not exclude the presence of infection. True infections have been documented with colony counts as low as 102/mL. Escherichia coli, the most common bacterial isolate, occurs in about 30% of UTIs. Enterococcus and Pseudomonas are each recovered about 15% of the time in the ICU population. Klebsiella and Proteus species represent less-common isolates. Contrary to previous teaching, in many cases, pure cultures of Staphylococcus epidermidis represent infection, not contamination. In the absence of frank pyuria or quantitative culture data, it is difficult to differentiate
colonization from infection in critically ill patients with indwelling catheters. In the tenuous patient with bacteriuria, it is probably best to err on the side of brief, organism-directed antibiotic therapy. For more resilient patients in the ICU, treatment of asymptomatic bacteriuria may be deferred safely.
colonization from infection in critically ill patients with indwelling catheters. In the tenuous patient with bacteriuria, it is probably best to err on the side of brief, organism-directed antibiotic therapy. For more resilient patients in the ICU, treatment of asymptomatic bacteriuria may be deferred safely.
Recovery of Candida species in urine is a common event. The choice of therapy for isolated candiduria should be based on a clinical judgment regarding whether the patient is “colonized” or “infected.” Unfortunately, there are few reliable signs to distinguish these conditions. A clinical picture of sepsis, with recovery of Candida from blood cultures as well as urine, suggests disseminated infection that should be treated with intravenous antifungals such as amphotericin B, fluconazole, or caspofungin. Conversely, finding small numbers of yeast in an asymptomatic patient with an indwelling urinary catheter rarely requires systemic treatment (except expedited removal of the catheter). The most difficult situation occurs when large numbers of yeast or clumps of hyphal forms are found in the urine of an asymptomatic patient or a patient with only modest fever. Although suggestive of invasive infection, such patients usually respond promptly to fluconazole (oral or intravenous), especially if the urinary catheter can be removed. Without evidence of infection elsewhere, parenteral amphotericin B probably should be reserved for immunocompromised patients or those with limited physiologic reserves. Bladder irrigation with amphotericin B is time consuming, expensive, of uncertain benefit, and confounding to accurate assessment of urine output. Fluconazole has all but eliminated bladder irrigation.
Pyocystis, an invasive infection of the bladder wall, may complicate oliguria or anuria, especially in patients requiring hemodialysis. In this setting, reduced urine flow allows bacteria to proliferate to massive numbers within the bladder. For oliguric patients with obscure fever, the bladder should be catheterized and the urine sediment should be examined. In the appropriate setting, murky, turbid, culture-positive urine establishes the diagnosis.
Treatment
The aggressiveness of therapy should parallel the clinical severity of the acute syndrome and the underlying illness. As a rule, presumed UTIs should be treated aggressively because patients in the ICU often have impaired immunity (diabetes, HIV infection, immunosuppressive therapy); numerous indwelling devices (e.g., vascular catheters, prosthetic heart valves, pacemakers); and marginal physiologic reserves. The treatment of UTI includes the promotion of urine flow and drainage, removal of urinary catheters (when feasible), and antibiotic therapy. Not all patients with bacteriuria require prolonged courses of expensive, broadspectrum, intravenous antibiotics. Otherwise stable immunocompetent patients can be treated successfully using enteral antibiotics (e.g., ampicillin, trimethoprim-sulfamethoxazole, quinolones). Oral therapy is not appropriate for septic patients or patients with obstructive uropathy or a focal complication (e.g., renal abscess). The need for two drug coverage of pseudomonal infections in non-immunocompromised patients is uncertain, but two drugs effective against Pseudomonas should be given to patients with abnormal immunity. (These include intravenous aminoglycosides and antipseudomonal penicillins, fluoroquinolones, or thirdgeneration cephalosporins.) If Enterococcus or Staphylococcus is deemed likely (based on the urine Gram stain or culture), vancomycin probably should be first-line therapy. Rarely, when the infection is life threatening and the possibility of vancomycin resistance is high, linezolid is an appropriate choice. Urine concentrations of renally excreted antibiotics often are dramatically higher than those used in sensitivity testing; therefore, UTIs often can be cured using an antibiotic to which the bacteria are found to be “resistant” in vitro. Because drainage bags provide important pathogen reservoirs, manipulations of the closed drainage system should be undertaken only when necessary and conducted with sterile technique. Furthermore, drainage bags should not be raised above the level of the bladder, as often occurs during patient transport. Doing so, even briefly, produces urinary stasis and retrograde flow of potentially highly contaminated urine.
▪ PNEUMONIA
Pathogenesis
Pneumonia-producing organisms usually enter the lower respiratory tract in aspirated upper airway secretions. Hematogenous seeding is a much less-common mechanism. Unless the inoculum is very large, glottic closure, cough, and mucociliary clearance normally provide an effective mechanical defense (Table 26-1). Even when mechanical barriers fail, infection usually is averted by
effective cellular (neutrophil and macrophage) and humoral immunity (antibody secretion). Unfortunately, both mechanical and immune defenses are jeopardized commonly in critically ill patients, even in those without a recognizable immune deficiency. Common conditions that allow proliferation of organisms leading to pneumonia are listed in Table 26-2. The organism causing pneumonia is highly dependent on where the infection was acquired and on individual patient characteristics.
effective cellular (neutrophil and macrophage) and humoral immunity (antibody secretion). Unfortunately, both mechanical and immune defenses are jeopardized commonly in critically ill patients, even in those without a recognizable immune deficiency. Common conditions that allow proliferation of organisms leading to pneumonia are listed in Table 26-2. The organism causing pneumonia is highly dependent on where the infection was acquired and on individual patient characteristics.
TABLE 26-1 CONDITIONS PROMOTING LUNG INOCULATION | ||||||||||||||||
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Diagnosis
In the community, a patient with acute onset of fever, dyspnea, chest discomfort, and cough productive of purulent sputum is likely to be suffering from bacterial pneumonia. Leukocytosis with a predominance of neutrophils and distinct (new) infiltrate(s) on chest radiograph are strong supporting data. Sputum that demonstrates an overwhelming predominance of neutrophils, intracellular organisms, and the predominance of a single morphologic bacterial form further strengthens the case. Finally, the diagnosis is established unequivocally by recovering the same organism from blood and sputum or pleural fluid cultures. The presentation is not always so classic, even with community-acquired pneumonia: fever may be mild, infiltrates may be subtle, and self-medication with antibiotics often obscures a bacteriologic diagnosis.
TABLE 26-2 CONDITIONS ALLOWING PROLIFERATION OF MICROORGANISMS IN LUNG | ||||||||||||||
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In the ICU, making a correct clinical diagnosis of pneumonia can be difficult for several reasons. Fever and leukocytosis are nonspecific, and patients often have several potential nonpulmonary sites to explain these findings. In addition, the radiographic infiltrates that suggest pneumonia are mimicked by atelectasis, aspiration pneumonitis, pulmonary embolism and infarction, pleural effusion, and pulmonary edema. Computed tomography (CT) sharpens discrimination but may not settle the issue. Finally, widespread use of antibiotics inhibits the ability to recover a single pathogenic organism, and even when sputum cultures are positive, small numbers of colonizing bacteria are usually recovered.
Causative Organism
The organisms causing pneumonia differ dramatically, depending on site of acquisition—community versus hospital. Common causes of communityacquired pneumonia and their clinical associations are shown in Table 26-3. In the community, streptococci, especially Pneumococcus and, Haemophilus influenzae, Mycoplasma, and viruses are the most common pathogens in otherwise “healthy” adults. Many underlying conditions vary this spectrum, however. In addition to the organisms listed, patients with alcoholism, diabetes, or heart failure are predisposed to infection with Klebsiella, Legionella, enteric Gram-negative rods, and Staphylococcus. When aspiration is likely (e.g., alcoholism, drug abuse, esophageal disorders), Bacteroides and other anaerobes are more prevalent. S. aureus frequently is recovered from patients with “postin-fluenza” pneumonia, and Pseudomonas species and Staphylococcus are common etiologic organisms among patients with cystic fibrosis. In fact, staphylococcal disease including MRSA is now frequently encountered in patients with severe communityacquired pneumonia. Pneumonia acquired in
chronic nursing care facilities or within 3 weeks of hospital discharge is likely to be caused by organisms usually recovered in hospital-acquired infections.
chronic nursing care facilities or within 3 weeks of hospital discharge is likely to be caused by organisms usually recovered in hospital-acquired infections.
For pneumonias that develop after the first few days in the ICU, a different, hospital-specific spectrum predominates. Such infections are frequently polymicrobial. Gram-negative rods (Pseudomonas aeruginosa, Klebsiella species, Enterobacter species, Actinetobacter species, E. coli, Proteus, and Serratia) cause approximately 50% of all ICU pneumonias. Which Gram-negative organism predominates at a given hospital has a great deal to do with antibiotic pressure placed on the environment. Acinetobacter, for example, represents a significant threat in some hospitals, but by no means all. Interestingly, Acinetobacter species infections have been exceedingly common among servicemen injured in Iraq. S. aureus causes another 10% to 20% of infections and its incidence appears to be rising. The predominance of Gram-negative rods and Staphylococcus seen in the hospitalized patient is explained partially by the rapid rate at which the oropharynx of the critically ill patient becomes colonized. Almost all critically ill patients are colonized with nonnative Gram-negative bacteria (many of which are antibiotic resistant) by the third hospital day.
TABLE 26-3 CLINICAL ASSOCIATIONS IN COMMUNITY-ACQUIRED PNEUMONIA | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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All too often, a specific pathogen cannot be identified, despite good sampling methods and symptoms compatible with acute pneumonia. Polymicrobial causation mixed aerobic/anaerobic infection, Mycoplasma, Chlamydia, Legionella, and viral agents become more likely candidates under these conditions. Fungal pneumonia (Candida/Torulopsis species, Aspergillus, or Mucor) must be considered in the neutropenic or severely debilitated patient (<500 neutrophils/mm3) but it occurs only rarely in the immunocompetent patient. When lung involvement occurs in the immunocompetent patient, it usually is the result of hematogenous seeding with Candida in a predisposed host. For some patients with chronic destructive lung diseases (e.g., chronic obstructive pulmonary disease [COPD], healed cavitary tuberculosis), Aspergillus can produce a primary invasive pneumonia.
Patients infected with HIV present a unique set of problems. When the CD4 T cell counts are normal, patients infected with HIV are susceptible to the same organisms as any other adult in the risk categories outlined in Table 26-3. As the CD4
count declines, and especially as it falls below 200 cells/mm3, the spectrum of infecting organisms broadens. Although routine bacterial pathogens still predominate, Pneumocystis carinii (jiroveci), Mycobacterium tuberculosis, atypical mycobacteria, and fungal infections become more likely. There is a rough correlation between the CD4 count and the infecting organism, but the linkage is not sufficiently strong to forgo detailed evaluation for presumptive diagnosis. Potential pathogens also are influenced by the prior use of prophylactic therapy. Oral trimethoprim-sulfamethoxazole prophylaxis, for example, has dramatically reduced the incidence of Pneumocystis and Toxoplasmosis infections.
count declines, and especially as it falls below 200 cells/mm3, the spectrum of infecting organisms broadens. Although routine bacterial pathogens still predominate, Pneumocystis carinii (jiroveci), Mycobacterium tuberculosis, atypical mycobacteria, and fungal infections become more likely. There is a rough correlation between the CD4 count and the infecting organism, but the linkage is not sufficiently strong to forgo detailed evaluation for presumptive diagnosis. Potential pathogens also are influenced by the prior use of prophylactic therapy. Oral trimethoprim-sulfamethoxazole prophylaxis, for example, has dramatically reduced the incidence of Pneumocystis and Toxoplasmosis infections.
Regardless of the patient substrate, the choice of initial therapy for a bacterial pneumonia is always accompanied by some uncertainty, even in the presence of a Gram stain “typical” of a specific organism. Historical features can help immensely in sorting through the diagnostic possibilities. For example, the sudden onset of chills, pleurisy, rigors, and high temperature are characteristic features for community-acquired Pneumococcus in a young adult. On the other hand, these findings may be inconspicuous in an older person, in whom confusion or stupor often predominate. A history of seizures, drug abuse, alcoholism, or swallowing disorder focuses attention on aspiration. Recent travel history, occupational or recreational exposure, and concurrent family illnesses can help diagnose an unusual organism (Table 26-4). In the absence of intrinsic cardiac conduction abnormality or intense β-blockade, a pulse rate that fails to rise in proportion to fever (pulse-temperature dissociation) suggests an “intracellular pathogen” such as Legionella, Rickettesia, Mycoplasma, Q fever, psittacosis, virus, or tularemia. Mycoplasma often has accompanying pharyngitis, myringitis, or conjunctivitis. Contrary to popular teaching, extrapulmonary symptoms (diarrhea, central nervous system disease) are no more common in Legionnaires disease than in other bacterial pneumonia.
Unlike community-acquired pneumonia, nosocomial pneumonia offers few historical clues to diagnosis. Occasionally, however, a skin rash, gingival disease, or purulent sinus drainage helps narrow the possibilities. Numerous classic radiographic features have been described, including lobar consolidation without air bronchograms (central obstruction), bulging fissures (Klebsiella), infiltrate with ipsilateral hilar adenopathy (histoplasmosis, tularemia, tuberculosis), widespread cavitation (Staphylococcus, Aspergillus), and sequential progression to multilobar involvement (Legionella). These findings are not sufficiently consistent, however, to be of real value in con firming the diagnosis.
TABLE 26-4 CLUES TO UNUSUAL CAUSES OF PNEUMONIA | ||||||||||||||||||||||||
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Diagnostic techniques
Although the history provides clues to the etiologic organism, laboratory studies are the cornerstone of the workup. Leukopenia often results from overwhelming infections, particularly those that are due to Staphylococcus, Pneumococcus, or Gram-negative organisms. A differential count that is not significantly left-shifted suggests the possibility of virus, Mycoplasma, or Legionella. Cultures of blood and pleural fluid (when present) must be obtained, and if positive, they are the most convincing evidence of a causative organism. Unfortunately, such specimens are usually nondiagnostic, even in seriously ill patients, and sampling of pulmonary secretions becomes the primary diagnostic modality.
The aggressiveness of the diagnostic evaluation should parallel the severity of the illness. In an otherwise healthy young person with a lobar pneumonia and good oxygenation, empiric therapy or treatment based on Gram stain alone is acceptable. For the septic, profoundly hypoxemic or immunocompromised patient, however, a
more systematic evaluation is often prudent. When performed correctly, stain and culture of pulmonary secretions or alveolar lavage fluid remain the most likely techniques to yield a diagnosis. For patients with severe communityacquired pneumonia, high-quality sputum often is obtained immediately after endotracheal intubation because forceful coughing and suctioning at this time often yield copious lung secretions not yet contaminated by ICU colonization. Expectorated sputum is appropriate for analysis and culture only if there is a high ratio of inflammatory to epithelial cells. Apart from the Gram stain, direct immunofluorescent antibody staining for Legionella and tuberculosis are other useful methods for processing the expectorated sample that can yield an immediate, but presumptive, diagnosis. Inhalation of a hypertonic aerosol, particularly if given via an ultrasonic nebulizer, can stimulate a productive cough in patients otherwise unable to expectorate. When adequate sputum is not expectorated, nasotracheal suctioning can be helpful. Transtracheal aspiration has been all but abandoned with wide availability of fiberoptic bronchoscopy.
more systematic evaluation is often prudent. When performed correctly, stain and culture of pulmonary secretions or alveolar lavage fluid remain the most likely techniques to yield a diagnosis. For patients with severe communityacquired pneumonia, high-quality sputum often is obtained immediately after endotracheal intubation because forceful coughing and suctioning at this time often yield copious lung secretions not yet contaminated by ICU colonization. Expectorated sputum is appropriate for analysis and culture only if there is a high ratio of inflammatory to epithelial cells. Apart from the Gram stain, direct immunofluorescent antibody staining for Legionella and tuberculosis are other useful methods for processing the expectorated sample that can yield an immediate, but presumptive, diagnosis. Inhalation of a hypertonic aerosol, particularly if given via an ultrasonic nebulizer, can stimulate a productive cough in patients otherwise unable to expectorate. When adequate sputum is not expectorated, nasotracheal suctioning can be helpful. Transtracheal aspiration has been all but abandoned with wide availability of fiberoptic bronchoscopy.
Properly performed on well-selected patients, fiberoptic bronchoscopy is a valuable technique for evaluation of pneumonic infection. In general, bronchoscopic procedures should be reserved for those who are seriously ill, immunocompromised, or unresponsive to conventional therapy. The safety and ease of bronchoscopy are facilitated by the presence of an endotracheal tube. When a decision is made to perform bronchoscopy, bronchoalveolar lavage and protected brush sampling from the involved region are both reasonable alternatives. Of these, lavage methodology is perhaps more popular, as it is relatively easier, and the protected brush seldom conflicts with or adds to its accuracy. If the lavage specimen yields a predominance of polymorphonuclear leukocytes and more than 103 to 104 organisms/mL are isolated, infection with the recovered organism is likely. Fewer bacteria suggest an active infection but also may be seen with a partially treated bacterial pneumonia. Blind suctioning, conducted with or without lavage through a wedged catheter (“mini-BAL”), can be performed proficiently by respiratory therapists or trained nurses. In the setting of diffuse pneumonia, this is a low-cost and generally effective sampling option. Only bronchoscopy, however, offers the directed sampling so often necessary.
Performing transbronchial biopsies to obtain tissue for histologic examination and/or culture is more hazardous in mechanically ventilated patients. Moreover, empirically chosen antibiotics are usually effective in addressing potential pathogens in patients who are immune competent. Although not performed commonly because of the risk of pneumothorax, transbronchial biopsy may be attempted when tissue recovery is essential, oxygenation can be well maintained, and coagulopathy is not present. In this setting, the only diagnostic alternatives are open or thoracoscopic lung biopsy. (The latter may not be feasible because of altered anatomy, high ventilation requirements, or refractory hypoxemia.) The risk of developing a pneumothorax while on the mechanical ventilator must be balanced against the potential yield and the clinician’s ability to promptly recognize and evacuate the air leak. (Note that the incidence of pneumothorax is 100% after open lung biopsy.) In addition, there are situations in which a diagnosis can be made only by tissue biopsy. Open lung biopsy is rarely necessary for patients with intact host defenses, and the value in even compromised hosts is arguable. Transthoracic needle aspiration often yields an adequate specimen but exposes the patient to attendant risks of pneumothorax and bleeding.
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