Pleural Effusion Medication

Updated: Dec 28, 2018
  • Author: Kamran Boka, MD, MS; Chief Editor: Guy W Soo Hoo, MD, MPH  more...
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Medication

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. Antimicrobial 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 pre-existing 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.

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.

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.

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.

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.

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.

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.

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.

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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