Pediatric Pleural Effusion Medication: Antibiotics, Other, Antitubercular Agents, Thrombolytics
Pediatric Pleural Effusion Medication: Antibiotics, Other, Antitubercular Agents, Thrombolytics
The treatment of a transudative, chylous, or hemorrhagic pleural effusion involves treatment of the underlying process. Antibiotics are administered for parapneumonic effusions caused by aerobic and anaerobic organisms. Specific agents should be based on the patient's age and the types of organisms and sensitivities common in the community. Therefore, the list of antibiotics below is only a guide. More than 1 agent may be used for synergy and for polymicrobial infections. Antibiotics may be changed if the organisms and their sensitivities are identified.
Initially, administer antibiotics intravenously while a thoracostomy tube is present until some time after the child is afebrile and improving clinically; then, the IV drugs can be switched to oral medications for 2-4 weeks. Empyema usually requires prolonged antimicrobial therapy.
Antituberculous drugs for tuberculosis-associated effusion should be administered for 6-9 months. Chemotherapeutic agents are used for malignancy. Steroids are indicated for connective-tissue disorders and may be useful for tuberculosis effusion. Fibrinolytic drugs are used to lyse fibrinous strands in loculated empyemas.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Nafcillin is a broad-spectrum penicillin. It is used for methicillin-sensitive S aureus and is the initial therapy for suspected penicillin G–resistant streptococcal or staphylococcal infections. In severe infections, start with parenteral therapy, and change to oral therapy as the condition warrants. Because of thrombophlebitis, particularly in elderly persons, administer parenterally for only 1-2 days; change to oral therapy as indicated clinically.
Oxacillin is a bactericidal antibiotic that inhibits cell-wall synthesis. It is used to treat infections caused by penicillinase-producing staphylococci. Oxacillin may be used to start therapy when a staphylococcal infection is suspected.
Vancomycin can be used for methicillin-resistant S aureus and for S pneumoniae. It is a potent antibiotic against gram-positive organisms and is active against Enterococcus species. Vancomycin is indicated for patients who cannot receive or whose conditions fail to respond to penicillins and cephalosporins or those with infections with resistant staphylococci. To avoid toxicity, the current recommendation is to assay vancomycin trough levels 30 minutes before the fourth dose. Use creatinine clearance (CrCl) to adjust the dose in renal impairment.
Penicillin G is used to treat S pneumoniae infection and anaerobic bacteria. It interferes with synthesis of cell-wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.
Cefotaxime is a third-generation cephalosporin. It can be used for S pneumoniae or H influenzae infection. Cefotaxime arrests bacterial cell-wall synthesis, inhibiting bacterial growth.
Ceftriaxone is a third-generation cephalosporin; it can be used for S pneumoniae or H influenzae infection. Ceftriaxone arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
Clindamycin can be used for S pneumoniae infection and anaerobes and as alternative drug for methicillin-resistant S aureus. 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, causing RNA-dependent protein synthesis to arrest.
Linezolid prevents the formation of a functional 70S initiation complex, which is essential for the bacterial translation process. It is bacteriostatic against enterococci and staphylococci and bactericidal against most strains of streptococci. Linezolid is used as an alternative in patients who are allergic to vancomycin and for the treatment of vancomycin-resistant enterococci.
These agents are used for the treatment of drug-susceptible tuberculosis infection. Recommendations include 6-9 months of therapy. The 6-month regimen includes either 2 months of isoniazid (INH), rifampin, and pyrazinamide once per day, followed by 4 months of INH and rifampin daily, or 2 months of INH, rifampin, and pyrazinamide daily, followed by 4 months of INH and rifampin twice weekly under directly observed therapy (DOT).
For drug-resistant tuberculosis, initial treatment should include 4 drugs until susceptibility is determined. Therapy should last 12-18 months.
Isoniazid offers the best combination of effectiveness, low cost, and minor adverse effects. It is a first-line drug unless resistance or another contraindication is known. Therapeutic regimens of less than 6 months have an unacceptably high relapse rate. Coadministration of pyridoxine is recommended if peripheral neuropathies secondary to INH therapy develop. Prophylactic doses of 6-50 mg/d are recommended.
Rifampin is for use in combination with at least 1 other anti-tuberculosis drug. It inhibits RNA synthesis in bacteria by binding to the beta subunit of DNA-dependent RNA polymerase, which in turn blocks RNA transcription. Cross-resistance may occur. Treat the patient for 6-9 months or until 6 months have elapsed from conversion to negative sputum cultures.
This is a pyrazine analog of nicotinamide that may be bacteriostatic or bactericidal against M tuberculosis, depending on the concentration of drug attained at the site of infection. The mechanism of action is unknown. In drug-susceptible patients, administer pyrazinamide for the initial 2 months of a regimen lasting 6 months or longer. Treat drug-resistant cases with individualized regimens.
Streptomycin is administered for the treatment of susceptible mycobacterial infections. It is used in combination with other anti-tuberculosis drugs (eg, INH, ethambutol, rifampin).
Fibrinolytic drugs may lyse the fibrinous strands in loculated empyemas and thereby clear the lymphatic pores and restore pleural fluid circulation.
Tissue plasminogen activator binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin, thereby initiating local fibrinolysis. Alteplase's serum half-life is 4-6 minutes, but the half-life is lengthened when alteplase is bound to fibrin in a clot. Circulating plasma levels are not expected to reach pharmacologic concentrations after intrapleural administration.
Dagnachew (Dagne) Assefa, MD, FAAP Pediatric Pulmonologist, Respiratory Center for Children, Morristown Memorial Hospital
Dagnachew (Dagne) Assefa, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, American Academy of Sleep Medicine
Coauthor(s)
Arthur B Atlas, MD Assistant Clinical Professor, Department of Pediatrics, University of Medicine and Dentistry of New Jersey
Arthur B Atlas, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Sleep Medicine, American College of Chest Physicians, American Lung Association, American Thoracic Society, Medical Society of New Jersey
Disclosure: Received grant/research funds from astra zeneca for none.
Chief Editor
Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society
Acknowledgements
Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine
Girish D Sharma, MD Associate Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center
Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
References
Upright chest radiograph in a 3-year-old child with dyspnea and fever obtained 1 day before the development of the pleural effusion reveals pneumonia on the left side.
Upright chest radiograph in a 3-year-old child with dyspnea and fever reveals a large opacity on the left, with obliteration of the left costophrenic angle and a fluid stripe.
Left lateral decubitus image in a 3-year-old child with dyspnea and fever reveals minimal layering of the fluid, which indicates a loculated effusion.
Upright posteroanterior chest radiograph of a child with a right-sided pleural effusion.
Lateral view in a child with right-sided pleural effusion reveals a pleural effusion and a fluid level.
Right lateral decubitus radiograph in a child with a right-sided pleural effusion. Image reveals partial layering of the fluid in the right side.
Posteroanterior view in a patient with reaccumulated pleural effusion in the left side of the chest.
Left lateral view in a patient with reaccumulated pleural effusion on the left side of the chest reveals layering of the effusion.
Anteroposterior view of the chest reveals a large chylothorax on the right side of the chest in a neonate.
Anteroposterior view in a neonate reveals reaccumulation of the chylothorax in the right hemithorax after a chest tube has been removed.
Right lateral decubitus radiograph in a neonate reveals layering of the chylothorax effusion after a chest tube has been removed.
Ultrasonogram of the pleural effusion in a 3-year-old child with dyspnea and fever reveals many septa (arrowheads) and several large, loculated portions of fluid (arrows).
Ultrasonogram of the effusion in a 3-year-old child with dyspnea and fever reveals several fluid loculations (arrows) separated by septa (arrowheads). The lung is seen under the effusion.
CT scan of the chest in a 3-year-old child with dyspnea and fever reveals a left-sided effusion and underlying parenchymal infiltrate and atelectasis.
Medication Summary
The treatment of a transudative, chylous, or hemorrhagic pleural effusion involves treatment of the underlying process. Antibiotics are administered for parapneumonic effusions caused by aerobic and anaerobic organisms. Specific agents should be based on the patient's age and the types of organisms and sensitivities common in the community. Therefore, the list of antibiotics below is only a guide. More than 1 agent may be used for synergy and for polymicrobial infections. Antibiotics may be changed if the organisms and their sensitivities are identified.
Initially, administer antibiotics intravenously while a thoracostomy tube is present until some time after the child is afebrile and improving clinically; then, the IV drugs can be switched to oral medications for 2-4 weeks. Empyema usually requires prolonged antimicrobial therapy.
Antituberculous drugs for tuberculosis-associated effusion should be administered for 6-9 months. Chemotherapeutic agents are used for malignancy. Steroids are indicated for connective-tissue disorders and may be useful for tuberculosis effusion. Fibrinolytic drugs are used to lyse fibrinous strands in loculated empyemas.
Antibiotics, Other
Class Summary
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Nafcillin
Nafcillin is a broad-spectrum penicillin. It is used for methicillin-sensitive S aureus and is the initial therapy for suspected penicillin G–resistant streptococcal or staphylococcal infections. In severe infections, start with parenteral therapy, and change to oral therapy as the condition warrants. Because of thrombophlebitis, particularly in elderly persons, administer parenterally for only 1-2 days; change to oral therapy as indicated clinically.
Oxacillin
Oxacillin is a bactericidal antibiotic that inhibits cell-wall synthesis. It is used to treat infections caused by penicillinase-producing staphylococci. Oxacillin may be used to start therapy when a staphylococcal infection is suspected.
Vancomycin (Vancocin)
Vancomycin can be used for methicillin-resistant S aureus and for S pneumoniae. It is a potent antibiotic against gram-positive organisms and is active against Enterococcus species. Vancomycin is indicated for patients who cannot receive or whose conditions fail to respond to penicillins and cephalosporins or those with infections with resistant staphylococci. To avoid toxicity, the current recommendation is to assay vancomycin trough levels 30 minutes before the fourth dose. Use creatinine clearance (CrCl) to adjust the dose in renal impairment.
Penicillin G aqueous (Pfizerpen)
Penicillin G is used to treat S pneumoniae infection and anaerobic bacteria. It interferes with synthesis of cell-wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms.
Cefotaxime (Claforan)
Cefotaxime is a third-generation cephalosporin. It can be used for S pneumoniae or H influenzae infection. Cefotaxime arrests bacterial cell-wall synthesis, inhibiting bacterial growth.
Ceftriaxone (Rocephin)
Ceftriaxone is a third-generation cephalosporin; it can be used for S pneumoniae or H influenzae infection. Ceftriaxone arrests bacterial growth by binding to 1 or more penicillin-binding proteins.
Clindamycin (Cleocin)
Clindamycin can be used for S pneumoniae infection and anaerobes and as alternative drug for methicillin-resistant S aureus. 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, causing RNA-dependent protein synthesis to arrest.
Linezolid (Zyvox)
Linezolid prevents the formation of a functional 70S initiation complex, which is essential for the bacterial translation process. It is bacteriostatic against enterococci and staphylococci and bactericidal against most strains of streptococci. Linezolid is used as an alternative in patients who are allergic to vancomycin and for the treatment of vancomycin-resistant enterococci.
Antitubercular Agents
Class Summary
These agents are used for the treatment of drug-susceptible tuberculosis infection. Recommendations include 6-9 months of therapy. The 6-month regimen includes either 2 months of isoniazid (INH), rifampin, and pyrazinamide once per day, followed by 4 months of INH and rifampin daily, or 2 months of INH, rifampin, and pyrazinamide daily, followed by 4 months of INH and rifampin twice weekly under directly observed therapy (DOT).
For drug-resistant tuberculosis, initial treatment should include 4 drugs until susceptibility is determined. Therapy should last 12-18 months.
Isoniazid
Isoniazid offers the best combination of effectiveness, low cost, and minor adverse effects. It is a first-line drug unless resistance or another contraindication is known. Therapeutic regimens of less than 6 months have an unacceptably high relapse rate. Coadministration of pyridoxine is recommended if peripheral neuropathies secondary to INH therapy develop. Prophylactic doses of 6-50 mg/d are recommended.
Rifampin (Rifadin)
Rifampin is for use in combination with at least 1 other anti-tuberculosis drug. It inhibits RNA synthesis in bacteria by binding to the beta subunit of DNA-dependent RNA polymerase, which in turn blocks RNA transcription. Cross-resistance may occur. Treat the patient for 6-9 months or until 6 months have elapsed from conversion to negative sputum cultures.
Pyrazinamide
This is a pyrazine analog of nicotinamide that may be bacteriostatic or bactericidal against M tuberculosis, depending on the concentration of drug attained at the site of infection. The mechanism of action is unknown. In drug-susceptible patients, administer pyrazinamide for the initial 2 months of a regimen lasting 6 months or longer. Treat drug-resistant cases with individualized regimens.
Streptomycin
Streptomycin is administered for the treatment of susceptible mycobacterial infections. It is used in combination with other anti-tuberculosis drugs (eg, INH, ethambutol, rifampin).
Thrombolytics
Class Summary
Fibrinolytic drugs may lyse the fibrinous strands in loculated empyemas and thereby clear the lymphatic pores and restore pleural fluid circulation.
Alteplase (Activase, Cathflo Activase, TPA)
Tissue plasminogen activator binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin, thereby initiating local fibrinolysis. Alteplase's serum half-life is 4-6 minutes, but the half-life is lengthened when alteplase is bound to fibrin in a clot. Circulating plasma levels are not expected to reach pharmacologic concentrations after intrapleural administration.
Dagnachew (Dagne) Assefa, MD, FAAP Pediatric Pulmonologist, Respiratory Center for Children, Morristown Memorial Hospital
Dagnachew (Dagne) Assefa, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, American Academy of Sleep Medicine
Coauthor(s)
Arthur B Atlas, MD Assistant Clinical Professor, Department of Pediatrics, University of Medicine and Dentistry of New Jersey
Arthur B Atlas, MD is a member of the following medical societies: American Academy of Pediatrics, American Academy of Sleep Medicine, American College of Chest Physicians, American Lung Association, American Thoracic Society, Medical Society of New Jersey
Disclosure: Received grant/research funds from astra zeneca for none.
Chief Editor
Michael R Bye, MD Professor of Clinical Pediatrics, State University of New York at Buffalo School of Medicine; Attending Physician, Pediatric Pulmonary Division, Women's and Children's Hospital of Buffalo
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society
Acknowledgements
Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine
Girish D Sharma, MD Associate Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center
Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland
Disclosure: Nothing to disclose.
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
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Upright chest radiograph in a 3-year-old child with dyspnea and fever obtained 1 day before the development of the pleural effusion reveals pneumonia on the left side.
Upright chest radiograph in a 3-year-old child with dyspnea and fever reveals a large opacity on the left, with obliteration of the left costophrenic angle and a fluid stripe.
Left lateral decubitus image in a 3-year-old child with dyspnea and fever reveals minimal layering of the fluid, which indicates a loculated effusion.
Upright posteroanterior chest radiograph of a child with a right-sided pleural effusion.
Lateral view in a child with right-sided pleural effusion reveals a pleural effusion and a fluid level.
Right lateral decubitus radiograph in a child with a right-sided pleural effusion. Image reveals partial layering of the fluid in the right side.
Posteroanterior view in a patient with reaccumulated pleural effusion in the left side of the chest.
Left lateral view in a patient with reaccumulated pleural effusion on the left side of the chest reveals layering of the effusion.
Anteroposterior view of the chest reveals a large chylothorax on the right side of the chest in a neonate.
Anteroposterior view in a neonate reveals reaccumulation of the chylothorax in the right hemithorax after a chest tube has been removed.
Right lateral decubitus radiograph in a neonate reveals layering of the chylothorax effusion after a chest tube has been removed.
Ultrasonogram of the pleural effusion in a 3-year-old child with dyspnea and fever reveals many septa (arrowheads) and several large, loculated portions of fluid (arrows).
Ultrasonogram of the effusion in a 3-year-old child with dyspnea and fever reveals several fluid loculations (arrows) separated by septa (arrowheads). The lung is seen under the effusion.
CT scan of the chest in a 3-year-old child with dyspnea and fever reveals a left-sided effusion and underlying parenchymal infiltrate and atelectasis.
