Lung abscess literally means a collection of pus within a de-stroyed portion of the lung; thus there are numerous possible causes of such a lesion (Table 6). As uscd cliniclly, however, the term "lung abscess" refers to a pulmonary infection with parenchymal necrosis, generally caused by bacteria other than mycobacteria. Lung abscesses are usually solitary, but occasionally multiple dis-crete lesions are observed. Numerous small abscesses confined to a given region of the lung are sometimes referred to as "necrotizing pneumonia. "Because they share a common pathogenesis, there is considerable overlap among aspiration pneumonia, lung abscess, and necrotizing pneumonia, and each of these may lead to and coexist with an empyema(a collection of pus within the pleural space).

Etioloay As indicated in the following Table, many different underlying processes can lead to the formation of a lung abscess. By far the most important are necrotizing pulmonary infections, and of these, anaerobic bacteria are responsible for the majority. These or-ganisms account for essentially all "putrid" lung abscesses and nearly all that have been classified as "nonspecific" or "primary". Most of these infections involve multiple bacterial species, which may in-dude aerobic organisms , The dominant bacteria are Fusobacterium nucleatum, Bacteroides melaninogenicus, B. intermedius, pep-tostreptococcus, aerobic streptococci, and microaerophilic strepto-cocci.

Pneumonia, particularly cases caused by Staphylococcus aureus and Klebsiella pneumoniae, may also be complicated by abscess formation. Less frequent but well-documented agents of lung abscess include Streptococcus pyogenes(group A beta-hemolytic streptococci), Streptococcus pneumoniae (especially type 3), Streptococcus milleri, Haemophilus influenzae (type B),Pseudo-monas aeruginosa, Pseudomonas pseudomallei(me-lioidosis), Ac-tinomyces (actinomycosis), Legionella, Nocar-dia, Paragonimus Westermani (lung fluke), and Entamoeba histolytica (amebiasis), Enteric gram-negative bacilli other than K. pneumoniae may cause lung abscess, but this occurs almost exclusively in debilitated patients with severe associated medical-surgical conditions. Necrotizing alveolitis is a separate entity diagnosed by micro-scopic examination and usually caused by P. aeruginosa; sometimes these microabscesses coa-lesce to form radiographically detectable cavities.

Pathogenesis The formation of an anaerobic lung abscess nearly always involves two coexisting abnormalities: 1. peri-odontal infection, such as gingivitis or pyorrhea, which pro-vides the inoculum; and 2.aspiration, which provides access to the lung parenchyma. The usual causes for aspiration are those that compromise consciousness and the gag reflex, such as al-coholism, drug addiction, general anesthesia, seizure disorder, sedative use, or neurologic disorders. Other factors predispos-ing to aspiration include dysphagia resulting from esophageal disorders or neurologic deficits; disruption of the usual me-chanical barriers, as with nasogastric intubation, tracheosto-my, or nasogastric feeding tubes; or pharyngeal anesthesia, as seen with dental procedures or surgery involving the upper air-way. Most healthy persons periodically aspirate smalt inocula from the upper airways, but these are readily cleared by the normal cough reflex and other pulmonary defense mechanisms without deleterious consequences. Patients who develop aspira-tion pneumonia and lung abscesses presumably do so because of the relatively large inocula of bacteria and failure of the usual protective mechanisms.

The initial lesion is pneumonitis, or "aspiration pneumo-nia". which typically involves dependent pulmonary segments, e.g., those favored by gravitational flow. The dependent pul-monary segments in patients who aspirate in the recumbent po-sition are the superior segments of the lower lobes or posterior segments of the upper lobes. Aspiration in the upright or semi-upright position favorg involvement of the basilar segments of the lower lobes. Patients who have a defined period of known or probable aspiration demonstrate with sequential radiographs that 7 to 14 days are usually required for the appearance of typical air-fluid level on chest radiograph.

Clinical Manifestations Patients with anaerobic abscess-es tend to have indolent symptomatology with medical com-plaints dating for 2 or more weeks before presentation. The usual symptoms are fever, malaise, cough sputum production, and pleuritic pain. The frequent observation of weight loss and anemia provides testimony to the chronicity of the infection. There may be "chilliness", but frank rigors are rare, and their presence suggests organisms other than anaerobes. The cough often becomes more productive at the time of cavitation, and it is at this time that the patient is most likely to note the onset of putrid sputum, which is considered diagnostic of anaerobic infection. Putrid sputum is found in 60 per cent of patients with a confirmed anaerobic etiology. Many patients will also note that the suputm has an unusually noxious taste. Most pa-tients have a historyof compromised consciousness or other rish factors for aspiration, and many have periodontal infec-tion. Nevertheless, about 10 per cent of patients with anaero-bic lung abscesses have no identifiable predisposing condition. Occasional patients with anaerobic lung abscesses are edentu-lous; the incidence of underlying bronchogenic neoplasms seems particularly high in this group. Patients with lung ab-scesses due to S. aureus, gramnegative bacilli, and amebae usually have a more fulminant course, with the precipitous on-set of symptoms. Other features that may be noted in this group include chills, the lack of putrid discharge, and the ab-sence of the usual associated findings. The physical findings in the early phases of disease are those of pneumonia, with or without a pleural effusion. At a later stage there may be am-phoric or cavernous breath sounds, pleural effusions are com-mon, and approximately 25 per cent of patients have an associ-ated empyema.

Diagnosis The diagnosis of lung abscess is usually estab-lished on the basis of a chest radiograph showing a parenchy-mal infiltrate with a cavity containing an air-fluid level. The differential diagnosis of this roentgenographic finding is includ-ed in the above Table(Table 6). Certain roentgenographic fea-tures may provide clues to the presence of an infected cyst, bulla, or sequestration. Massive pulmonary fibrosis with necrosis from occupational exposure is usually distinctive. A loculated empyema with an air-fluid level may be differentiated from lung abscess with computed tomography.

Studies for an etiologic agent are often hampered by the limitations of bacteriologic analysis of expectorated sputum. These specimens are useful in detecting mycobacteria, pathogenic fungi, and parasites, and they may be used for cytologic studies. However, routine aerobic cultures often give

TABLE 6 DIFFERENTIAL DIAGNOSIS OF

A CAVITARY LESION IN THE LUNG

Treatment The most important facets of the treatment are the administration of appropriate antibiotics and adequate drainage of any associated empyema. Physiotherapy with pos-rural drainage should be utilized when possible; however, this must be done with considerable caution in patients with large lung abscesses because of the possibility of spillage of purulent contents, with extensive involvement of other lobes.

The drugs of choice for the treatment of abscesses caused by aerobic pyogenie microorganisms, Mycobacterium tubercu-losis, fungi, and Entamoeba histolytica are reviewed in detail elsewhere in this volume. For aspiration-related lung abscess involving anaerobic bacteria, the three antimicrobial regimens recommended are penicillin, clindamycin, or penicillin plus metronifamodazole. Penicillin has traditionally been regarded as the favored drug on the basis of its long, well-established track record. There is considerable variation in the dosage rec-ommendations, but most authorities recommend doses of 10 to 20million units given intravenously per day. This is continued until the patient is afebrile and clinically improved, at which time treatment is changed to intramuscular or oral penicillin using penicillin G, penicillin V, ampicillin, or amoxicillin in doses of 500 to 750 mg three or four times daily. Some author-ities suggest an arbitrarily selected total duration of treatment of 3 to 6 weeks, whereas others continue treatment until the chest radiograph changes have cleared or there is only a small, stable residual lesion. The latter criterion commonly requires 2 to 4 months or longer but may be necessary to prevent relaps-es.

Clindamycin is active against most penicillin-resistant anaer-obes that are found in 20 to 25 per cent of cases, includ-ing many or most strains of B. melaninogenicus, B. fragilis, B. ruminicola, and B. ureolyticus. Some regard clindamycin as the preferred agent for all lung abscesses due to anaerobic bac-teria; others advocate it only for patients who fail to respond to penicillin, have a contraindication to penicillin, or have a seri-ous infection with a fulminant course. The usual regimen is 600 mg given intravenously every 6 to 8 hours until the patient is afebrile and clinically improved, followed by 300 mg orally four times daily. An alternative regimen is penicillin G(above doses) combined with metronidazole (2 mg orally per day in two to four divided doses). Metronidazole is active against nearly all clinically important anaerobes, but penicillin must be added owing to the probable importance of aerobic and mi-croaerophilic streptococci.

The necessity to treat the aerobic components of mixed aerobic-anaerobic infections is controversial, but this is gener-ally advo-cated for patients who are seriously ill of fail to re-spond to clindamycin. In such cases, most penicillins are con-sidered equally effective against oral anaerobes, including peni-cillin G, penicillin V, anpicillin, amoxicillin, ticarcillin, and piperacillin. However, antistaphylococcal penicillins , such as nafcillin or oxacillin, are considered inferior and unacceptable. Cephalosporins are considered nearly equivalent to penicillins in terms of in vitro activity, although the clinical experience is limited, Imipenem and any combination of a betalactam-beta-lactamase inhibitor are considered almost universally active a-gainst clinically important anaerobes. The activity of tetracy-clines and erythromycin is variable. Quinolones and trimetho-prim-sulfamethoxazole are un-acceptable for infections caused by anaerobic bacteria.

Patients with lung abscesses involving S. aureus should be treated with a penicillinase-resistant penicillin or a first-genera-tion cephalosporin. Vancomycin is the preferred agent for meth-icillin-resistant strains of S. aureus. This agent or clin-damycin may be used for patients with a contraindication to beta-lactam antibiotics. Penicillin G is the preferred agent for infections involving group A beta-hemolytic streptococcal infec-tion. Anti-biotic selection for infections involving gram-nega-tive bacilli requires in vitro sensitivity data. This usually con-sists of an aminoglycoside combined with an expanded-spec-trum penicillin, such as ticarcillin for P. aeruginosa or a cephalosporin for Enter-obacteriaceae. Sulfonamides are pre-ferred agents for Nocardia infections.

The expected response to antimicrobial agents is subjec-tive improvement with decreased fever within 3 to 7days and elimination of fever within 7 to 14 days. The putrid odor of the sputum, when initially present, usually resolves in 3 to 10 days. Delayed response may indicate large cavity size, poor host status, obstruction, erroneous antimicrobial selection, a wrong diagnosis, drug fever, a complicating empyema requir-ing drainage, of an abscess that requires drainage by physio-therapy, bronchoscopy, or surgery. Radiographic response is delayed;in fact, there is often extension of the infiltrate and increased cavity size or new cavity formation during the first week. Chest radiographs should be followed at 2 to 3 week in-tervals with the expectation that infiltrates will clear or there will be a small residual scar or a thin-walled cyst.

Bronchoscopy is indicated in patients with an atypical pre-sen-tation and in those who fail to respond to recommended an-timi-crobial regimens. The major purpose of the procedure is to differentiate cavitating neoplasms and to detect underlying lesions, such as bronchogenic neoplasms, bronchostenosis, or a foreign body. It may also be used to facilitate drainage.

The major indications for surgery are an uncontrollable or life-threatening hemorrhage, a bronchogenic neoplasm, a bronchial obstruction, or a lung abscess that proves absolutely refractory to medical treatment . Medical failures are rare but are most common in patients with an obstructed bronchus, those with extremely large abscesses, those with abscesses that have been present for an extended period before the institution of treatment , and those with infections involving certain bacte-ria such as gram-negative bacilli. The usual surgical procedure is lobectomy. Patients with prohibitive operative risks may benefit from percutaneous drain-age, but care must be taken to avoid contamination of the pleural space.

Prognosis The natural course of lung abscesses was best studied in the prechemotherapeutic era. Treatment at that time was nearly equally divided between conservative manage-ment using postural drainage and supportive care, and surgery. The mortality rate was about 33 per cent in both groups, and another third of patients developed a chronic de-bilitating disease or suffered recurrent symptoms. The avail-ability of the Jackson bronchoscope to facilitate drainage had no important bearing on outcome. The technique of resectional surgery was developed at about the time penicillin became available, and the relative merits of these two approaches as the primary therapeutic modality were widely debated. During the past two decades, however, the majority of patients have been treated with antibiotics alone, including those with "de-layed closure" (i. e. , the persistence of a cavity demonstrated by a chest radiograph at 4 to 6 weeks after the initiation of an-tibiotic therapy), because most of these cavities eventually re-solve if the antibiotics are continued long enough . The mortali-ty rate for aspiration-related lung abscess is currently reported at 5 to 6 per cent. Findings that herald a relatively poor prog-

nosis include 1.large cavity size, particularly cavities greater than 6 cm in diameter; 2.prolonged symptoms prior to presen-tation, especially symptoms for more than 6 weeks; 3.necro-tizing pneumonia characterized by multiple small abscesses in contiguous segments; 4.patients who are elderly, debilitated, or immunologically compromised; 5.abscesses associated with bronchial obstruction; and 6.abscess due to aerobic bacteria, including S. aureus and gram-negative bacilli.

Prevention The major preventive measures are factors used to reduce the incidence or magnitude of aspiration, appro-priate care of periodontal disease, early treatment of pneumo-nia, and adequate courses of antimicrobials to prevent relapses.

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