Updated: Jul 24, 2009
Pneumonia and other lower respiratory tract infections are the leading cause of death worldwide. Other respiratory tract diseases such as croup (laryngotracheobronchitis), bronchiolitis, and bronchitis are beyond the scope of this article and are not discussed further. Approximately 150 million new cases of pneumonia occur annually among children younger than 5 years worldwide, accounting for approximately 10-20 million hospitalizations.1 Although the diagnosis is usually made on the basis of radiographic findings in developed countries, the World Health Organization (WHO) has defined pneumonia solely on the basis of clinical findings obtained by visual inspection and timing of the respiratory rate.2,3,4,5
It is important for the physician to understand that the typical causes and presentations of pneumonia in infants and children are variable, depending upon the child's age and underlying medical condition.
Pneumonia results from inflammation of the alveolar space and may compromise air exchange. While often complicating other lower respiratory infections such as bronchiolitis or laryngotracheobronchitis, pneumonia may also occur via hematogenous spread or aspiration. Most commonly, this inflammation is the result of invasion by bacteria, viruses, or fungi, but it can occur as a result of chemical injury or may follow direct lung injury (eg, near drowning).
Four stages of lobar pneumonia have been described. In the first stage, occurring within 24 hours of infection, the lung is characterized microscopically by vascular congestion and alveolar edema. Many bacteria and few neutrophils are present. The stage of red hepatization (2-3 d), so called because of its similarity to the consistency of liver, is characterized by the presence of many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin within the alveoli. In the stage of gray hepatization (2-3 d), the lung is gray-brown to yellow because of fibrinopurulent exudate, disintegration of red cells, and hemosiderin. The final stage of resolution is characterized by resorption and restoration of the pulmonary architecture. Fibrinous inflammation may extend into the pleural space, causing a rub heard by auscultation, and it may lead to resolution or to organization and pleural adhesions.
Bronchopneumonia, a patchy consolidation involving one or more lobes, usually involves the dependent lung zones, a pattern attributable to aspiration of oropharyngeal contents. The neutrophilic exudate is centered in bronchi and bronchioles, with centrifugal spread to the adjacent alveoli.
In interstitial pneumonia, patchy or diffuse inflammation involving the interstitium is characterized by infiltration of lymphocytes and macrophages. The alveoli do not contain a significant exudate, but protein-rich hyaline membranes similar to those found in adult respiratory distress syndrome (ARDS) may line the alveolar spaces. Bacterial superinfection of viral pneumonia can also produce a mixed pattern of interstitial and alveolar airspace inflammation.
Miliary pneumonia is a term applied to multiple, discrete lesions resulting from the spread of the pathogen to the lungs via the bloodstream. The varying degrees of immunocompromise in miliary tuberculosis, histoplasmosis, and coccidioidomycosis may manifest as granulomas with caseous necrosis to foci of necrosis. Miliary herpesvirus, cytomegalovirus, or varicella-zoster virus infection in severely immunocompromised patients results in numerous acute necrotizing hemorrhagic lesions.
Factors that bypass or inactivate local defenses (eg, tracheostomy tubes, immotile cilia syndrome) predispose the child to pneumonia. The result is loss of surfactant activity with local collapse and consolidation.
Pneumonia may be classified by the causative organism, the anatomic location, or the tissue response.
A WHO Child Health Epidemiology Reference Group publication cited the incidence of community-acquired pneumonia among children younger than 5 years in developed countries as approximately 0.026 episodes per child-year.1
In a prospective multicenter study of 154 hospitalized children with acute community-acquired pneumonia in whom a comprehensive search for etiology was sought, a pathogen was identified in 79% of children. Bacteria accounted for 60%, of which 73% were due to Streptococcus pneumoniae; Mycoplasma pneumoniae and Chlamydia pneumoniae were detected in 14% and 9%, respectively. Viruses were documented in 45% of children. Notably, 23% of the children had concurrent acute viral and bacterial disease.6 In the study, preschool-aged children had as many episodes of atypical bacterial lower respiratory infections as older children. Multivariable analyses revealed that high temperature (38.4°C) within 72 hours after admission and the presence of pleural effusion were significantly associated with bacterial pneumonia.
Thompson et al reported annual influenza-associated hospitalizations in the United States by hospital discharge category, discharge type, and age group.7 After elderly persons, the second highest rates of influenza-associated hospitalizations were in children younger than 5 years.
In a randomized double blind trial, the heptavalent pneumococcal vaccine reduced the incidence of clinically diagnosed and radiographically diagnosed pneumonia among children younger than 5 years by 4% and 20%, respectively.8
The WHO Child Health Epidemiology Reference Group estimated the median global incidence of clinical pneumonia to be 0.28 episodes per child-year.1 This equates to an annual incidence of 150.7 million new cases, of which 11-20 million (7-13%) are severe enough to require hospital admission. Ninety-five percent of all episodes of clinical pneumonia in young children worldwide occur in developing countries.
According to the WHOs Global Burden of Disease 2000 Project, lower respiratory infections were the second leading cause of death in children younger than 5 years (about 2.1 million [19.6%]).
Pneumonia affects children of all races; however, certain conditions that may predispose to pneumonia have racial predilections. For example, cystic fibrosis is far more common in white children. Children with sickle cell anemia are at increased risk for pneumonia as a result of sickling within the pulmonary vasculature and functional asplenia.
Pneumonia in the pediatric population is most common in infants and toddlers and least common in adolescents and young adults.
In children, etiologic agent, age of the patient, and underlying illnesses all affect the historical features of the illness.
Pathogens implicated in pneumonia vary with the age of the child, the underlying patient-specific risk factors, immunization status, and seasonality.
| Acute Respiratory Distress Syndrome | Pneumonia, Aspiration |
| Asthma | Pneumonia, Bacterial |
| Bronchiolitis | Pneumonia, Empyema and Abscess |
| Bronchitis | Pneumonia, Immunocompromised |
| Foreign Body Aspiration | Pneumonia, Mycoplasma |
| Pediatrics, Respiratory Distress
Syndrome | Smoke Inhalation |
| Pertussis |
Very few laboratory studies are particularly useful in the evaluation of the child with pneumonia.
The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
Interferes with synthesis of cell wall mucopeptides during active multiplication resulting in bactericidal activity against susceptible bacteria. Appropriate first-line agent in children in whom pneumococcal disease is strongly suspected. It offers the advantages of being relatively palatable and having a tid-dosing schedule. It has limited activity against gram-negative bacteria due to resistance.
250-500 mg PO tid; not to exceed 1500 mg/d
40 mg/kg/d PO divided tid
5 kg: 62.5 mg PO tid
5-10 kg: 125 mg PO tid
>10 kg: 250 mg PO tid
Reduces the efficacy of oral contraceptives; probenecid increases serum concentrations
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in patients who are allergic to cephalosporin antibiotics; appearance of a rash should be carefully evaluated to differentiate a nonallergic ampicillin rash from a hypersensitivity reaction; rash and GI upset are adverse effects
Inhibits the biosynthesis of cell wall mucopeptide. Bactericidal against sensitive organisms when adequate concentrations are reached and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects. May be used as an alternative to amoxicillin in treatment of outpatients with pneumonia in whom pneumococcal disease is strongly suspected. Penicillin has limited activity against gram-negative bacteria.
250-500 mg PO qid; not to exceed 2000 mg/d
40 mg/kg/d PO divided qid
Probenecid may increase effectiveness by decreasing clearance; tetracyclines are bacteriostatic, causing a decrease in the effectiveness of penicillins when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal impairment and in patients who are allergic to cephalosporin antibiotics; rash and GI upset are adverse effects
Second-generation cephalosporin maintains gram-positive activity that first-generation cephalosporins have; adds activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and Moraxella catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.
250-500 mg PO q12h; 750-1500 mg IV/IM q8h
Suspension: 30 mg/kg/d PO bid
Tablets: 250 mg PO q12h
IV: 150-200 mg/kg/d IV divided q8h
Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patients receiving potent diuretics such as loop diuretics; coadministration with aminoglycosides increase nephrotoxic potential; probenecid increases levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Administer half dose if CrCl is 10-30 mL/min and one-quarter dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy; caution in patients allergic to penicillin; skin rashes and GI upset are adverse effects
Inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins. The tablet should be administered with food.
200 mg/dose PO q12h
10 mg/kg/d PO divided bid
Probenecid increases the serum concentrations of cefpodoxime.
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in penicillin allergy, renal impairment; adverse effects include nausea, vomiting, and diarrhea
Binds to one or more of the penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
250-500 mg/dose PO q12h or 500 mg PO qd
30 mg/kg/d PO divided bid
Probenecid increases effect of cefprozil; coadministration with furosemide and aminoglycosides increases nephrotoxic effects of cefprozil
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in penicillin allergy, renal impairment; adverse effects include nausea, vomiting, and diarrhea
Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.
1-2 g IV/IM qd
50-75 mg/kg/d IV/IM qd; not to exceed 1 g
Probenecid may increase ceftriaxone levels; coadministration with ethacrynic acid, furosemide, and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity; not to be used in hyperbilirubinemic neonates
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in renal impairment; caution in breastfeeding women and in those allergic to penicillin; adverse effects include nausea, vomiting, and diarrhea; not to be used in newborns, as it causes hyperbilirubinemia
Third-generation cephalosporin with gram-negative spectrum. Lower efficacy against gram-positive organisms.
1-2 g IV/IM q6-8h; not to exceed 12 g/d
<50 kg: 100-200 mg/kg/d IV/IM divided q6-8h
>50 kg: Administer as in adults
Probenecid may increase cefotaxime levels; coadministration with furosemide and aminoglycosides may increase nephrotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal impairment; caution in breastfeeding women and in those allergic to penicillin; adverse effects include nausea, vomiting, and diarrhea; associated with severe colitis
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. DOC for adults and children >4 y, unless suspect pneumococcal disease. These agents are effective against many of the atypical organisms. Erythromycin is available in 4 forms: base, stearate, estolate, and ethylsuccinate. Erythromycin estolate causes the least GI distress.
Base: 500 mg PO qid for 7 d
Ethylsuccinate (EES): 800 mg PO qid for 7 d or 400-800 mg PO qid
Base, stearate, or estolate: 250-500 mg PO qid
Newborns: 50 mg/kg/d (base) PO divided qid for 14 d or 30-50 mg/kg/d (base and ethylsuccinate) PO divided q6-8h
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis; may increase the toxicity of ergotamine
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur
Erythromycin is a macrolide antibiotic with a large spectrum of activity. Binds to the 50S ribosomal subunit of the bacteria, which inhibits protein synthesis. Sulfisoxazole expands erythromycin's coverage to include gram-negative bacteria. Sulfisoxazole inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid. Dose is based on the erythromycin component.
250 mg PO qid (unlikely to be prescribed to adults)
<2 months: Not recommended
>2 months: 50 mg/kg/d divided tid/qid
May enhance warfarin's anticoagulation action effects and hemorrhage could occur; thiopental anesthetic effects may be enhanced; risk of nephrotoxicity may increase when administered concurrently with cyclosporine; serum hydantoin levels may increase when administered concurrently with sulfisoxazole; methotrexate-induced bone marrow suppression may be enhanced when administered concurrently with sulfisoxazole; may increase sulfonylurea concentrations and cause hypoglycemia in diabetic patients; tolbutamide bioavailability may be prolonged when administered with sulfamethizole Coadministration with diuretics may increase incidence of thrombocytopenia with purpura; sulfonamides free-drug concentration may be increased when administered concurrently with indomethacin; sulfonamides when used concomitantly with methenamine mandelate may form a precipitate in acidic urine; probenecid and salicylates may displace sulfonamides from plasma albumin resulting in increased free-drug concentrations potentiating its
toxicity; coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment; megaloblastic anemia due to folate deficiency; G-6-PD deficiency
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 liver impairment; GI adverse effects are common (give doses pc); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur; caution in patients with renal dysfunction and HIV; maintain adequate fluid intake to prevent crystalluria and stone formation
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes causing RNA-dependent protein synthesis to arrest.
250-500 mg PO bid
15 mg/kg/d PO divided q12h
Toxicity increases with coadministration of fluconazole and pimozide; clarithromycin effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG CoA-reductase inhibitors; cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Documented hypersensitivity; coadministration of pimozide or cisapride
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; give half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies; abnormal metallic taste, nausea, diarrhea, and abdominal pain are adverse effects; do not refrigerate suspension
Azithromycin inhibits RNA synthesis by binding to 50S ribosomal subunit.
Day 1: 500 mg PO
Days 2-5: 250 mg PO qd
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; do not administer with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients; adverse effects include nausea, vomiting, and diarrhea
Inhibits DNA synthesis and viral replication.
Inhibits activity of both HSV-1 and HSV-2. DOC for treatment of pneumonia in children with herpes viruses (eg, herpes simplex, varicella).
Patients experience less pain and faster resolution of cutaneous lesions when used within 48 h from rash onset.
10 mg/kg/dose IV q8h; infuse over 1 h
Administer as in adults
Concomitant use of probenecid or zidovudine prolongs half-life and increases CNS toxicity of acyclovir
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in renal failure or when using nephrotoxic drugs (rapid IV infusion can cause renal injury)
For treatment of severe lower respiratory tract RSV infections in infants and children with an underlying compromising condition. Inhibits replication of RNA and DNA viruses.
Reconstitute 6 g into 300 mL of sterile water to make a concentration of 20 mg/mL; administer as aerosol q12-18h/d for 3 d up to 7 d for RSV pneumonia
2 g aerosolized over 2 h tid for 3 d using a Viratek small particle aerosol generator (SPAG-2)
Concomitant use of ribavirin and nucleoside analogues may increase risk of developing lactic acidosis; concurrent use with didanosine has been noted to increase the risk of pancreatitis and/or peripheral neuropathy in addition to lactic acidosis
Documented hypersensitivity to ribavirin or any component of the formulation; women of childbearing age who will not use contraception reliably; pregnancy, ClCr <50 mL/min; hemoglobinopathies (eg, thalassemia major, sickle cell anemia); patients with autoimmune hepatitis, anemia, or severe heart disease
X - Contraindicated; benefit does not outweigh risk
Use with caution in patients requiring assisted ventilation because precipitation of the drug in the respiratory equipment may interfere with safe and effective patient ventilation; carefully monitor patients with COPD and asthma for deterioration of respiratory function
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pneumonia in children, symptoms of pneumonia in children, treatment of pneumonia in children, bacterial pneumonia, respiratory syncytial virus, RSV, lower respiratory tract infection, empiric antibiotics, interstitial pneumonia, miliary pneumonia, lobar pneumonia, bronchopneumonia, dyspnea, hypoxemia
Mark I Neuman, MD, MPH, Assistant Professor of Pediatrics, Harvard Medical School; Attending Physician, Division of Emergency Medicine, Children's Hospital Boston
Mark I Neuman, MD, MPH is a member of the following medical societies: Society for Pediatric Research
Disclosure: Nothing to disclose.
Garry Wilkes, MBBS, FACEM, Director of Emergency Medicine, Bunbury Hospital, Western Australia; Medical Director, St John Ambulance, WA Ambulance Service; Adjunct Associate Professor, Edith Cowan University; Clinical Associate Professor, Rural Clinical School, University of Western Australia, Australia.
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Grace M Young, MD, Associate Professor, Department of Pediatrics, University of Maryland Medical Center
Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians
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.
Richard G Bachur, MD, Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston
Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research
Disclosure: Nothing to disclose.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Laura E Ferguson, MD, Brent R King, MD, and Lakshmi V Atkuri, MD, to the development and writing of this article.
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