eMedicine Specialties > Infectious Diseases > Lower Respiratory Tract Infections

Nosocomial Pneumonia: Treatment & Medication

Author: Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Contributor Information and Disclosures

Updated: May 28, 2009

Treatment

Medical Care

Patients with nosocomial pneumonia (NP; also known as hospital-acquired pneumonia [HAP] or health care–associated pneumonia [HCAP]) usually require ventilatory support at some point and usually need supplemental oxygen therapy.

Before empiric antimicrobial therapy is initiated, an attempt should be made to rule out mimics of nosocomial pneumonia. If mimics of nosocomial pneumonia can be excluded with a reasonable degree of certainty, then empiric therapy for nosocomial pneumonia is appropriate.

The precise pathogen that causes a given case of nosocomial pneumonia is usually unknown. Therefore, empiric antimicrobial therapy is the only practical approach. Delaying therapy until the pathogen is identified is not recommended. For empiric coverage of nosocomial pneumonia, monotherapy is as effective as combination therapy for early nosocomial pneumonia.

For proven pseudomonal nosocomial pneumonia, double-drug coverage with a high degree of antipseudomonal activity and a low resistance potential should be used. Optimal combinations include meropenem or doripenem plus either levofloxacin or aztreonam. Alternately, antipseudomonal penicillin (eg, piperacillin) in combination with levofloxacin, meropenem, aminoglycoside, or aztreonam may provide equal efficacy.

Principles of appropriate empiric antibiotic coverage in nosocomial pneumonias

Direct empiric coverage against common nosocomial pathogens P aeruginosa, Klebsiella species, E coli, and MRSA. Coverage against P aeruginosa also covers other nosocomial pneumonia pathogens.

Enterobacter species, S maltophilia, and Burkholderia cepacia: Enterobacter species usually do not cause nosocomial pneumonia. S maltophilia and B cepacia are common colonizers of respiratory secretions but rarely, if ever, cause nosocomial pneumonia in most hosts; however, they are potential pathogens in patients with bronchiectasis or cystic fibrosis.

Oropharyngeal anaerobes are unimportant from a therapeutic standpoint, as they are not typically isolated in nosocomial pneumonia.

Empiric monotherapy versus combination therapy

The optimal empiric monotherapy for nosocomial pneumonia consists of ceftriaxone, ertapenem, levofloxacin, or moxifloxacin. Monotherapy may be acceptable in patients with early-onset HAP. Avoid monotherapy with ciprofloxacin, ceftazidime, or imipenem, as they are likely to induce resistance potential. Late-onset HAP, ventilator-associated pneumonia (VAP), or HCAP requires combination therapy using an antipseudomonal cephalosporin, beta-lactam, or carbapenem plus an antipseudomonal fluoroquinolone or aminoglycoside plus an agent such as linezolid or vancomycin to cover MRSA.

Optimal combination regimens for proven P aeruginosa nosocomial pneumonia include (1) piperacillin/tazobactam plus amikacin or (2) meropenem plus levofloxacin, aztreonam, or amikacin. Avoid using ciprofloxacin, ceftazidime, gentamicin, or imipenem in combination regimens, as combination therapy does not eliminate the resistance potential of these antibiotics. When selecting an aminoglycoside for a combination therapy regimen, amikacin once daily is preferred to gentamicin or tobramycin to avoid resistance problems. When selecting a quinolone in a combination therapy regimen, use levofloxacin, which has very good anti– P aeruginosa activity (equal or better than ciprofloxacin at a dose of 750 mg).

Consultations

  • Consult an infectious disease specialist to assess the microbiology of the specimens obtained from the patient, to rule out the mimics of nosocomial pneumonia, and to administer empiric or specific empirical antimicrobial therapy.
  • Consult a pulmonologist to help with mechanical ventilation (often required in patients with nosocomial pneumonia).
  • Other consultations include the following:
    • Rheumatologist, if the patient appears to have lupus or SLE pneumonitis
    • Cardiologist, if the patient has heart failure
    • Oncologist for possible pulmonary infiltrates caused by a lymphangitic spread of a malignancy

Diet

  • Most patients with nosocomial pneumonia are intubated and are instructed to receive nothing by mouth (NPO).

Activity

  • Most patients with nosocomial pneumonia are intubated and are limited to bed rest.

Medication

Ordinarily, nosocomial pneumonia (NP; also known as hospital-acquired pneumonia [HAP] or health care–associated pneumonia [HCAP]) is treated for 14 days. If the patient indeed has nosocomial pneumonia and the appropriate antimicrobial therapy is administered, chest radiography shows significant improvement in the pulmonary infiltrate during the 2 weeks of antimicrobial therapy. Pulmonary infiltrates that are unchanged after a 2-week course of therapy suggest that the infiltrates may not be infectious in origin. Start a diagnostic workup to consider other infectious diseases that do not respond to antibiotics (eg, herpesvirus type 1 [HSV-1] pneumonitis) or noninfectious diseases (eg, bronchogenic carcinomas).

Antibiotics

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


Cefepime (Maxipime)

A fourth-generation cephalosporin with good gram-negative coverage similar to ceftazidime; however, better gram-positive coverage than ceftazidime is equivalent in its coverage of P aeruginosa. This drug may be more active than ceftazidime against Enterobacter species because of its enhanced stability against beta-lactamases.

Adult

2 g IV q12h

Pediatric

50 mg/kg IV q8h

Probenecid at a high dose decreases cefepime clearance; vancomycin, polymyxin B, colistin, loop diuretics, and aminoglycosides increase the risk of nephrotoxicity

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adjust dose in patients with severe renal insufficiency


Meropenem (Merrem)

A carbapenem, not a beta-lactam antibiotic. Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell wall synthesis. Effective against most gram-positive and gram-negative bacteria. Has slightly increased activity against gram-negative bacteria and a slightly decreased activity against staphylococci and streptococci when compared to imipenem.

Adult

1 g IV q8h (normal renal function)

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Probenecid may inhibit renal excretion and increase meropenem levels

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication


Piperacillin (Pipracil)

Antipseudomonal penicillin. Acts on bacterial cell walls. Greatest degree of antipseudomonal activity among the antipseudomonal penicillins. Inhibits biosynthesis of cell wall mucopeptides and stage of active multiplication; has antipseudomonal activity. Used in combination with other antibiotics.

Adult

4 g IV q8h (normal renal function)

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Tetracyclines may decrease effects; piperacillin at high concentrations may physically inactivate aminoglycosides; probenecid may increase levels of piperacillin; coadministration with aminoglycosides has synergistic effects

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May interfere with platelet function in patients requiring surgery; caution in renal impairment and in history of seizures


Aztreonam (Azactam)

A monobactam, not a beta-lactam antibiotic, inhibits cell wall synthesis during bacterial growth. Active against gram-negative bacilli.

Adult

2 g IV q8h (normal renal function)

Pediatric

<10 years: Not established
>10 years: Administer as in adults

Tetracyclines may reduce effects of this medication

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal insufficiency


Amikacin (Amikin)

Used for gram-negative bacterial coverage of infections resistant to gentamicin and tobramycin. Effective against P aeruginosa. Irreversibly binds to 30S subunit of bacterial ribosomes, blocks recognition step in protein synthesis, and causes growth inhibition. Use patient's ideal body weight for dosage calculation.

Adult

15 mg/kg/d IV/IM divided bid; not to exceed 1.5 g/d regardless of higher body weight

Pediatric

Administer as in adults

Coadministration with other aminoglycosides, penicillins, cephalosporins, and amphotericin B increases nephrotoxicity; enhances effects of neuromuscular blocking agents; causes respiratory depression; irreversible hearing loss may occur with coadministration of loop diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not intended for long-term therapy; caution in patients with renal failure (not on dialysis), hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission


Levofloxacin (Levaquin)

Second-generation quinolone. Acts by interfering with DNA gyrase in bacterial cells. This is a bactericidal and is highly active against gram-negative and gram-positive organisms including P aeruginosa. For pseudomonal infections and infections caused by multidrug-resistant gram-negative organisms.

Adult

750 mg PO/IV q24h (normal renal function)

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; levofloxacin reduces therapeutic effects of phenytoin; probenecid may increase levofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy


Piperacillin and tazobactam sodium (Zosyn)

Antipseudomonal penicillin plus beta-lactamase inhibitor. Inhibits biosynthesis of cell wall mucopeptide and is effective during stage of active multiplication.

Adult

4.5 g (piperacillin 4 g and tazobactam 0.5 g) IV q6h

Pediatric

<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; effects when administered concurrently with aminoglycosides are synergistic; 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

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Perform CBC count prior to initiation of therapy and at least weekly during therapy; monitor for liver function abnormalities by measuring AST and ALT levels during therapy; exercise 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


Doripenem (Doribax)

Carbapenem antibiotic. Elicits activity against a wide range of gram-positive and gram-negative bacteria. Indicated as a single agent for complicated intra-abdominal infections caused by susceptible strains of E coli, Klebsiella pneumoniae, P aeruginosa, Bacteroides caccae, B fragilis, Bacteroides thetaiotaomicron, Bacteroides uniformis, Bacteroides vulgatus, Streptococcus intermedius, Streptococcus constellatus, and Peptostreptococcus micros.

Adult

500 mg IV q8h infused over 1 h
CrCl 30-49: 250 mg IV q8h
CrCl 11-29: 250 mg IV q12h

Pediatric

<18 years: Not established
>18 years: Administer as in adults

Carbapenems may decrease valproic acid serum concentration, causing increased seizure risk; probenecid reduces renal clearance of doripenem, resulting in increased doripenem concentration; does not inhibit or induce major CYP450 enzymes

Documented hypersensitivity to doripenem or other carbapenems or demonstrated anaphylactic reactions to beta-lactams

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Clostridium difficile –associated diarrhea has been reported with nearly all antibacterial agents and must be considered if patient presents with diarrhea; common adverse effects (ie, >5%) include headache, nausea, diarrhea, rash, and phlebitis; decrease dose with renal insufficiency

More on Nosocomial Pneumonia

Overview: Nosocomial Pneumonia
Differential Diagnoses & Workup: Nosocomial Pneumonia
Treatment & Medication: Nosocomial Pneumonia
Follow-up: Nosocomial Pneumonia
Multimedia: Nosocomial Pneumonia
References
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Further Reading

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Keywords

nosocomial pneumonia, NP, hospital-acquired pneumonia, HAP, healthcare-associated pneumonia, health care–associated pneumonia, HCAP, ventilator-associated pneumonia, VAP

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Contributor Information and Disclosures

Author

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Wesley W Emmons, MD, FACP, Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE
Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, Section of Infectious Diseases, University of Oklahoma College of Medicine
Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology
Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist  Speaking and teaching

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center
Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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