Pleural Effusion Medication

  • Author: Jeffrey Rubins, MD; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: May 21, 2012
 

Medication Summary

Pharmacologic management of pleural effusion depends on the condition’s etiology. For example, medical management includes nitrates and diuretics for congestive heart failure and pulmonary edema, antibiotics for parapneumonic effusion and empyema, and anticoagulation for pulmonary embolism.

In patients with parapneumonic effusions, empyemas, and effusions associated with esophageal perforation and intra-abdominal abscesses, antibiotics should be administered early when these conditions are suspected.

Antibiotic selection should be based on the suspected causative microorganisms and the overall clinical picture. Considerations include the patient's age, comorbidities, duration of the illness, setting (community vs nursing home), and local organism sensitivities. Various effective single agents and combination antimicrobial therapies exist. Coverage should generally include anaerobic organisms. Options may include clindamycin, extended-spectrum penicillins, and imipenem. Depending on the patient's clinical condition, infectious disease consultation may be appropriate.

Particular attention must be given to potential drug interactions, adverse effects, and preexisting conditions.

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Antibiotics, Other

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

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Ampicillin and sulbactam (Unasyn)

 

This combination of ampicillin and a beta-lactamase inhibitor interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. It is an alternative to amoxicillin when the patient is unable to take medication orally.

Ampicillin/sulbactam covers skin, enteric flora, and anaerobes. It is not ideal for nosocomial pathogens.

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Imipenem and cilastatin (Primaxin)

 

This drug combination is used for the treatment of multiple organism infections for which other agents do not have wide-spectrum coverage or are contraindicated due to their potential toxicity.

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Piperacillin and tazobactam sodium (Zosyn)

 

This consists of antipseudomonal penicillin plus a beta-lactamase inhibitor. It inhibits biosynthesis of the cell wall mucopeptide and is effective during the active multiplication stage.

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Clindamycin (Cleocin)

 

Clindamycin is a lincosamide for the treatment of serious skin and soft-tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). Clindamycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer ribonucleic acid (tRNA) from ribosomes, arresting RNA-dependent protein synthesis.

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Piperacillin

 

Piperacillin inhibits biosynthesis of cell-wall mucopeptides and the active multiplication stage; it has antipseudomonal activity.

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Vasodilators

Class Summary

These agents are used for their ability to decrease preload.

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Nitroglycerin (Nitrostat, Nitro-Bid, Nitro-Dur, Nitrolingual)

 

Nitroglycerin is a first-line therapy for patients who are not hypotensive. It provides excellent and reliable preload reduction. Higher doses provide mild afterload reduction. Nitroglycerin has a rapid onset and offset (both within minutes), allowing rapid clinical effects and rapid discontinuation of effects in adverse clinical situations.

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Diuretics

Class Summary

Loop diuretics decrease plasma volume and edema by causing diuresis.

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Furosemide (Lasix)

 

Furosemide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.

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Anticoagulants, Hematologic

Class Summary

Anticoagulants prevent recurrent or ongoing thromboembolic disorders by inhibiting thrombogenesis.

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Heparin

 

Heparin augments the activity of antithrombin III and prevents the conversion of fibrinogen to fibrin. It does not actively lyse but is able to inhibit further thrombogenesis. Heparin prevents reaccumulation of a clot after spontaneous fibrinolysis. When unfractionated heparin is used, the activated partial thromboplastin time (aPTT) should not be checked until 6 hours after the initial heparin bolus because an extremely high or low value during this time should not provoke any action.

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Contributor Information and Disclosures
Author

Jeffrey Rubins, MD  Professor of Medicine, University of Minnesota Medical School; Director, Palliative Medicine, Hennepin County Medical Center

Jeffrey Rubins, MD is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Harold L Manning, MD Professor, Departments of Medicine, Anesthesiology and Physiology, Section of Pulmonary and Critical Care Medicine, Dartmouth Medical School

Harold L Manning, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Stephen P Peters, MD, PhD, FACP, FAAAAI, FCCP, FCPP Professor of Genomics and Personalized Medicine Research, Internal Medicine, and Pediatrics, Associate Director, Center for Genomics and Personalized Medicine Research, Director of Research, Section on Pulmonary, Critical Care, Allergy and Immunologic Diseases, Wake Forest University School of Medicine

Stephen P Peters, MD, PhD, FACP, FAAAAI, FCCP, FCPP is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society, and Sigma Xi

Disclosure: See below for list of all activities None None

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Large, malignant, right-sided pleural effusion.
Chest radiograph showing left-sided pleural effusion.
Left lateral decubitus film showing freely layering pleural effusion.
Lung entrapment with right hydropneumothorax and pleural drain in place
Massive right pleural effusion with shift of mediastinum towards left
Right pleural effusion after partial drainage showing decrease in shift of mediastinum towards left
Anteroposterior, upright chest radiograph shows bilateral pleural effusions and loss of bilateral costophrenic angles (meniscus sign). Image courtesy of Allen R. Thomas, MD.
Chest radiograph, lateral view, shows loss of bilateral, posterior costophrenic angles. Image courtesy of Allen R. Thomas, MD.
Posteroanterior, upright chest radiograph shows isolated, left-sided pleural effusion and loss of left, lateral costophrenic angle. Image courtesy of Allen R. Thomas, MD.
 
 
 
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