Updated: Nov 7, 2007
A lung abscess is a subacute infection in which an area of necrosis forms in the lung parenchyma. It usually is in a dependent section of the lung, more often involves the right lung than the left, and is most commonly seen after aspiration of oropharyngeal secretions. Lung abscesses have a slow, insidious presentation and usually develop 1-2 weeks after the initial aspiration event.
Empyema is defined as pus in the pleural space. It typically is a complication of pneumonia. However, it can also arise from penetrating chest trauma, esophageal rupture, complication from lung surgery, or inoculation of the pleural cavity after thoracentesis or chest tube placement. An empyema can also occur from extension of a subdiaphragmatic or paravertebral abscess.
A lung abscess involves the lung parenchyma, while an empyema involves the pleural space. In many patients with pneumonia, a sterile simple parapneumonic effusion develops in the pleural space. If this pleural effusion becomes infected, it is labeled a complicated parapneumonic effusion, while the presence of frank pus in the pleural space defines an empyema. The development stages of an effusion can be divided into 3 phases: exudative, fibropurulent, and organizational. The initial effusion develops from increased pulmonary interstitial fluid along with progressive capillary vascular permeability. A simple effusion is frequently sterile and resolves with antibiotic treatment of the underlying pulmonary infection. In 5-10% of the patients with a pleural effusion, the effusion becomes infected and neutrophils buildup. This inflammatoryresponse also causes the production of chemokines, cytokines, oxidants, and protease mediators. This more complicated parapneumonic effusion needs both antibiotics and some form of surgical drainage or alternative treatment modality to remove the purulent effusion. In these more complicated effusions, fibrinolysis and activation of the coagulation cascade leads to the production of fibrin with subsequent adhesions and loculated fluid collections. This process ultimately can cause pleural fibrosis and impairment of lung expansion.
An estimated 60,000 pleural infections are diagnosed annually in the United States.
The mortality rate for lung abscesses is approximately 4-7% but varies with the type of material aspirated. Aspiration of fluids with mixed gram-negative flora has a mortality rate approaching 20%, while aspiration of acidic materials has an even higher rate. The fatality rate for complicated parapneumonic effusions is estimated to be as high as 15%.
Complicated effusions and empyema are more common in elderly persons and during childhood. An increase has occurred in the incidence of empyema in the pediatric population. Lung abscess is more common in elderly persons.
The patient's history may reveal the following findings:
The physical examination may reveal the following findings:
| Pleural Effusion | Pneumonia, Viral |
| Pneumonia, Aspiration | Tuberculosis |
| Pneumonia, Bacterial | |
| Pneumonia, Immunocompromised | |
| Pneumonia, Mycoplasma |
Sarcoidosis
Treatment of lung abscesses or empyema is performed in-hospital, with consultations involving internists, thoracic surgeons, or both. Many clinicians advocate administering intrapleural fibrinolytics in patients with empyemas to assist in the breakdown of fibrin bands that can cause loculation of the empyema and to allow for better chest tube drainage of the infected material. However, randomized clinical trials have given conflicting results about the benefits of fibrinolytic therapy on outcomes. A recent meta-analysis that included 575 patients showed no benefit for the use of fibrinolytic therapy based on clinical outcomes of death or need for surgery when compared with control groups. If chest tube drainage and fibrinolytic treatment are unsuccessful, many authors recommend video-assisted thoracic surgery (VATS) rather than the more traditional open thoracotomy. VATS is less invasive and well tolerated, and outcomes compare favorably with open thoracotomy.
In the pediatric population, Avansino et al performed a meta-analysis comparing nonoperative (antibiotics and either thoracentesis and/or tube thoracostomy) with operative therapy (antibiotics and either VATS or thoracotomy) in patients with an empyema.1 Their results suggest that, with operative therapy, the in-hospital mortality rate, reintervention rate, length of stay, time with tube thoracostomy, and time of antibiotic therapy are lower compared with nonoperative treatment.
Lung abscesses typically respond well to antibiotic therapy, but when that therapy is unsuccessful, the consulting clinician might consider percutaneous catheter drainage or endoscopic surgical resection of the involved area of the lung.
Lung abscesses are treated with a prolonged course of parenteral antibiotics that target organisms found in aspiration pneumonia. The initial choice of antibiotics frequently is empiric, beginning with clindamycin, cefoxitin, ticarcillin, or piperacillin/tazobactam, although penicillin has been very effective when the organism is sensitive. Some authors advocate adding coverage for Klebsiella as well. Subsequent therapy should be based on sputum or blood culture results.
An empyema is treated with parenteral antibiotics and prompt chest tube drainage. Empiric therapy for an empyema is frequently with imipenem or piperacillin/tazobactam until a definitive organism is identified on pleural fluid cultures and sensitivities are obtained. Antibiotic coverage for anaerobic organisms is also recommended since anaerobes frequently coexist but are more difficult to isolate. For an empyema secondary to aspiration pneumonia or a parapneumonic process, choose antibiotics that are active against mouth flora, S aureus and Streptococcus species. For an empyema secondary to penetrating chest trauma, administer antibiotics that have coverage for skin flora. If MRSA is suspected, include vancomycin in the treatment plan. Pleural fluids or sputum specimens that are obtained should be cultured for M tuberculosis as well.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Lincosamide for the treatment of serious skin and soft-tissue staphylococcal infections. Also effective against aerobic and anaerobic streptococci (except enterococci). Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.
600 mg IV q6-8h
25-40 mg/kg/d IV divided tid/qid
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis
Second-generation cephalosporin indicated for infections with gram-positive cocci and gram-negative rod. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond.
2 g IV q6-8h
80-160 mg/kg/d IV divided q4-6h
Probenecid may increase effects; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis
Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms; traditional drug for the treatment of lung abscess, but its spectrum of activity is narrow.
2 million U IV q4h
150,000 U/kg/d IV divided q4h
Probenecid can increase effects; coadministration of tetracyclines can decrease effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function
Inhibits biosynthesis of cell wall mucopeptide and is effective during active growth stage. Antipseudomonal penicillin plus beta-lactamase inhibitor that provides coverage against most gram-positive bacteria, most gram-negative bacteria, and most anaerobes.
3.1 g IV q4-6h
75 mg/kg IV q6h
Tetracyclines may decrease effects of ticarcillin; high concentrations of ticarcillin may physically inactivate aminoglycosides if administered in same IV line; synergistic effects when administered concurrently with aminoglycosides; probenecid may increase penicillin levels
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with oral penicillin during acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBC prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; caution in patients with hepatic insufficiencies; perform urinalysis and BUN and creatinine determinations during therapy, and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication.
3.375 g IV q6h
<12 years: Not established
>12 years: Administer as in adults
Tetracyclines may decrease effects of piperacillin; high concentrations of piperacillin may physically inactivate aminoglycosides if administered in same IV line; synergistic effects when administered concurrently with aminoglycosides; probenecid may increase penicillin levels; high-dose parenteral penicillins may result in increased risk of bleeding
Documented hypersensitivity; severe pneumonia, bacteremia, pericarditis, emphysema, meningitis, and purulent or septic arthritis should not be treated with an oral penicillin during the acute stage
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Perform CBC prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; caution in patients with hepatic insufficiencies; perform urinalysis and BUN and creatinine determinations during therapy, and adjust dose if values become elevated; monitor blood levels to avoid possible neurotoxic reactions
For treatment of multiple organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of potential for toxicity.
Base initial dose on severity of infection and administer in equally divided doses; dose may range from 250-500 mg IV q6h for a maximum of 3-4 g/d
Alternatively, 500-750 mg IM q12h or intra-abdominally
<12 years: Not established; 15-25 mg/kg/dose IV q6h suggested for >3 mo
Fully susceptible organisms: Not to exceed 2 g/d
Infections with moderately susceptible organisms: Not to exceed 4 g/d
>12 years: Administer as in adults
Coadministration with cyclosporine may increase CNS side effects of both agents; coadministration with ganciclovir may result in generalized seizures
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in renal insufficiency; avoid use in children <12 y
Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or whose conditions are unresponsive to penicillins and cephalosporins or have infections with resistant staphylococci. For abdominal-penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes. To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients with renal impairment.
500 mg to 2 g/d IV divided tid/qid
40 mg/kg/d IV divided tid/qid
Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that associated with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal failure and neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2 h or as PO or IP administration; red man syndrome is not an allergic reaction
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aspiration, lung abscess, pleural pus, penetrating chest trauma, esophageal rupture, inoculation of the pleural cavity, thoracentesis, chest tube placement, subdiaphragmatic abscess, paravertebral abscess, poor dentition, absent gag reflex, septic emboli, vasculitic disorders, cavitating lung malignancies, pulmonary cystic disease, needle compression, polymicrobial oral flora, Bacteroides species, Fusobacterium species, Peptostreptococcus species, Staphylococcus aureus, S aureus, MRSA, Mycobacterium tuberculosis, M tuberculosis, skin flora, Staphylococcus epidermis, S epidermis, pleural effusion
Mark Zwanger, MD, MBA, Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University
Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association
Disclosure: Nothing to disclose.
Mark S Slabinski, MD, FACEP, FAAEM, Vice President, EMP Medical Group
Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Paul Blackburn, DO, FACOEP, FACEP, Program Director, Department of Emergency Medicine, Maricopa Medical Center; Assistant Professor, Department of Surgery, University of Arizona
Paul Blackburn, DO, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Medical Association, and Arizona Medical Association
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.