Nursing Home Acquired Pneumonia 

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Nursing Home Acquired Pneumonia 

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Nursing home–acquired pneumonia (NHAP) is defined as pneumonia occurring in a resident of a long-term care facility or nursing home. NHAP is one of the most common infectious diseases in long-term care facilities and is a significant cause of mortality and morbidity among residents of such facilities. [1, 2] NHAP primarily affects elderly people and shows no sex or race predilection. Dysphagia has been identified as a risk factor. [3] NHAP more closely resembles community-acquired pneumonia (CAP) than nosocomial pneumonia (NP) and is considered diagnostically and therapeutically synonymous with CAP. NHAP is a common diagnosis but is proven in only 33% of patients. Types of pneumonia and their radiologic characteristics are summarized in the table below.

Table 1. Comparison of Characteristics of Nursing Home–Acquired Pneumonia, Community-Acquired Pneumonia, and Nosocomial Pneumonia (Open Table in a new window)

Type of Pneumonia

Most Common Pathogens

Uncommon Pathogens

Appearance on Chest Radiograph

Length of Stay, days

NHAP

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Legionella

Chlamydophila pneumoniae [4]

Focal sequential/lobar ± consolidation ± pleural effusion

No cavitation

7-10

CAP

S pneumoniae

H influenzae

M catarrhalis

Legionella

Mycoplasma

Focal sequential/lobar ± consolidation ± pleural effusion

No cavitation

7-10

NP

Pseudomonas aeruginosa

Klebsiella

Escherichia coli

Serratia

Necrotizing pneumonia and cavitation with P aeruginosa and Klebsiella

Bilateral infiltrates without cavitation or pleural effusion

10-21

Go to Community-Acquired Pneumonia and Nosocomial Pneumonia for more complete information on these topics.

The pathophysiology of NHAP is the same as that of CAP. NHAP may result when a patient aspirates oropharyngeal contents into 1 or more lung segments or lobes. NHAP may also occur if a distant focus of infection hematogenously disseminated to the lungs.

Aspiration pneumonia, whether community-acquired or acquired in a nursing home, results microbiologically from aspirated anaerobic oropharyngeal flora. Hundreds of species of oropharyngeal anaerobes may be cultured from patients with aspiration pneumonia. However, oropharyngeal anaerobes are not like Bacteroides fragilis, which is the primary anaerobe below the diaphragm and is sensitive to nearly all antibiotics. Patients with CAP or NHAP do not require specific anti– B fragilis coverage.

In aspiration pneumonia, the location of the lung lesion is related to the position of the patient at the time of aspiration. Because most patients are supine when they aspirate, most lung infiltrates observed on chest radiographs and most cases of aspiration pneumonia localize to segments of the right lung.

If aspiration occurs when patients are lying on their right side, the pulmonary infiltrates most likely involve the right upper lobe. If patients are lying on their left side, the most likely location of the infiltrates is the left upper lobe. If patients are supine and the aspiration is massive, bilateral infiltrates involving multiple lung segments or lobes are possible and may produce a radiologic appearance indistinguishable from left ventricular failure or acute respiratory distress syndrome. Position-related lobar involvement is summarized in the table below.

Table 2. Radiographic Patterns in Aspiration Pneumonia (Open Table in a new window)

Patient Position at Aspiration

Chest Radiograph Lobar Involvement

Supine

Right lower lobe (ie, superior or posterior segment) or bilateral infiltrates (ie, all lobes)

Right side down

Right upper lobe (ie, axillary segment)

Left side down

Left upper lobe (ie, axillary segment)

Prone

Right middle lobe (ie, lingula)

Sitting upright

Right lower lobe (ie, basilar segments)

Hematogenously acquired pneumonia is not common among patients with CAP or NHAP. Hematogenously acquired pneumonia presents with bilateral symmetrical perihilar infiltrates, as opposed to the localized segmental or lobar distribution characteristic of pneumonia acquired via primary inhalation.

The degree of impaired lung function resulting from NHAP depends on the extent of aspiration and the patient’s preexisting physiologic and anatomic lung function. The histologic changes in lung parenchyma resulting from NHAP are the same as those observed from CAP (ie, no cavitation, necrosis, or blood vessel invasion). As with CAP, resolving NHAP restores the lung function that existed prior to acquiring pneumonia.

Keep patients who are predisposed to aspiration pneumonia in a semiupright position at night. Additionally, take care when feeding patients who have an empiric gag reflex or neurologic disorder that depresses consciousness or interferes with swallowing.

Dysphagia has been identified as a risk factor, so nurses and other healthcare workers should be vigilant for signs of dysphagia to help prevent NHAP. [3]

Patients may report fever, cough, chest pain, or rapid respiration.

Patients with chronic bronchitis are particularly prone to developing pneumonia

Patients with aspiration NHAP often have a history of central nervous system (CNS) or esophageal disease, or they have a decreased gag reflex that predisposes them to recurrent aspiration.

Most, but not all, patients are febrile. Fever, when present, may be low grade.

Physical examination findings in the chest include rales over the involved lung segments, with or without signs of consolidation or pleural effusion.

Fever and leukocytosis are more common in patients with NHAP than in patients with noninfectious mimics of NHAP, but these findings are nonspecific. Fever greater than or equal to 102°F and accompanied by pulmonary symptoms suggests NHAP, especially when accompanied by a productive cough. However, in elderly patients, who are the usual residents of long-term care facilities, the febrile response may be blunted. Therefore, the absence of fever or the presence of a low-grade fever is unhelpful in differentiating NHAP from its mimics.

The diagnosis of NHAP rests on excluding the mimics of pneumonia and on the presence of characteristic findings on chest radiographs. Most patients from long-term care facilities who are transferred to acute care hospitals do not have NHAP. The most common causes of diagnostic confusion in patients with NHAP are noninfectious cardiac and pulmonary disorders.

The most common of these is congestive heart failure (CHF), an exacerbation of which can cause shortness of breath, which mimics the presentation of NHAP. Many elderly patients are unable to raise sputum, making the absence of a productive cough an inadequate determination to differentiate NHAP from CHF.

The clinical presentation of patients with asymptomatic acute myocardial infarctions—fever, shortness of breath, and chest pain—may also mimic that of patients with NHAP.

Other conditions that may mimic NHAP include the following:

Preexisting lung disease

Pulmonary emboli

Bronchogenic malignancies

Collagen-vascular diseases affecting the lungs (eg, systemic lupus erythematosus [SLE])

Pulmonary drug reactions

Pulmonary hemorrhage

Chronic obstructive pulmonary disease

Bronchiolitis obliterans organizing pneumonia (BOOP)

Pleural effusions occasionally cause confusion in the diagnosis of pneumonia. Bacterial pneumonias, particularly infections with S pneumoniae and H influenzae, may be accompanied by pleural effusion. However, pleural effusions without associated infiltrates are not pneumonia.

Bilateral pleural effusion rarely, if ever, results from an infectious etiology. The presence of bilateral pleural effusions with unilateral or bilateral pulmonary infiltrates suggests a noninfectious etiology, and the workup should be designed accordingly.

Do not assume that all patients with respiratory symptoms and infiltrates on their chest radiographs have pneumonia. Consider that patients may have one of the many mimics of pneumonia before embarking on a course of empiric antimicrobial therapy. If a physician treats a patient with empiric antimicrobial therapy when the patient has a treatable noninfectious cause for his or her pulmonary infiltrates, the patient may suffer because cardiac or noninfectious pulmonary conditions require other, nonantimicrobial, measures.

Many physicians perform a suboptimal workup for NHAP, omitting sputum Gram stains and culture studies.

Obtain blood cultures from all patients with CAP and NHAP.

Blood culture findings are usually positive if infection with S pneumoniae or H influenzae is causing the patient’s pneumonia.

The yield of positive blood cultures in NHAP is lower than in CAP, which may represent a difference in the time each culture was taken. Patients with CAP who are admitted to an acute care facility usually have blood cultures drawn in the emergency department or soon after admission. Patients who are transferred to an acute care hospital from a long-term care facility may not have blood cultures drawn for many hours or days after the onset of pneumonia. These factors may account for the difference in culture yields.

Blood cell counts are not helpful diagnostically, because the results are nonspecific. Leukocytosis with a left shift is due to stress to the individual, which may occur with NHAP, an acute myocardial infarction, pulmonary emboli, dehydration, or any cause of stress. Therefore, the clinician should not assume that leukocytosis with a left shift is diagnostic of NHAP.

Stain sputum using a Gram stain and perform culture studies in patients with a productive cough who do not have chronic bronchitis. Sputum culture in chronic bronchitis usually shows normal or mixed flora, which is unhelpful to the clinician.

For sputum specimens to be useful in determining the etiology of the pneumonia, they must be of good quality and must reflect the lower respiratory tract flora. A poor specimen collection, as evidenced by the presence of epithelial squamous cell contamination and a relative lack of polymorphonuclear neutrophils or multiple organisms, suggests that the specimen is invalid and unreliable.

Multiple pathogens are not a feature of NHAP. Dual infections are rare in NHAP and CAP.

Aspiration pneumonia due to anaerobic pharyngeal flora is the only polymicrobial respiratory tract infection that is considered community or nursing home acquired. The presence of a single causative pathogen generally excludes anaerobic aspiration pneumonia in patients with CAP or NHAP.

Chest radiography is the primary tool for ruling out the mimics of pneumonia and any new or preexisting lung disorders. Patients with NHAP have a segmental or lobar distribution of infiltrates. Patients with congestive heart failure (CHF) have a redistribution of vasculature to the upper lobes, usually accompanied by cardiomegaly. Verify cardiomegaly by physical examination. If CHF is present, it usually is accompanied by an S3 gallop rhythm.

Preexisting chest radiographs may reveal previous interstitial lung disease that may mimic the appearance of NHAP.

Noninfectious infiltrates observed on chest radiographs are frequently misdiagnosed as NHAP.

If the resolution of the chest radiograph is insufficient to differentiate NHAP, consider obtaining a chest computed tomography (CT) scan.

Go to Imaging in Typical Bacterial Pneumonia and Imaging in Atypical Bacterial Pneumonia for more complete information on these topics.

Patients with pleural effusions unrelated to a nephrotic syndrome, uremia, hypoalbuminemia, cirrhosis, or heart failure require diagnostic thoracentesis. Physicians should test the thoracentesis fluid using Gram stain and culture studies, as well as pH, glucose, protein, cell count, and differential. This procedure may reveal the causal pathogen if blood culture results are negative and if sputum is not available.

Histologic findings in NHAP include local polymorphonuclear neutrophil infiltration of infected lung areas, without cavitation, necrosis, or blood vessel invasion.

Obtain an electrocardiogram (ECG) and cardiac enzyme levels in patients who may have a cardiac explanation for their pulmonary symptoms, as evidenced by their history, physical, or chest radiograph findings. ECG and cardiac enzyme levels are helpful in ruling out silent myocardial infarctions, which are not uncommon in elderly patients.

Bacterial blood gas analysis or lung scanning may be useful in ruling out pulmonary emboli as a cause of the patient’s pulmonary symptoms.

If considering Legionnaires disease, a cause of clusters of outbreaks of NHAP, obtain liver function tests.

Patients presenting with extrapulmonary findings in a chronic care facility may have NHAP caused by C pneumoniae infection. In such patients, C pneumoniae immunoglobulin M and immunoglobulin G titers may be diagnostic. Immunoglobulin A may also help to clarify if a patient is experiencing a relapse or a reinfection with Chlamydophila.

C pneumoniae infection usually occurs as part of an outbreak; it should be readily recognizable in the nursing home setting, because the infection occurs in clusters and is characterized by extrapulmonary features that distinguish it from Legionnaires disease and other bacterial causes of NHAP.

Patients with NHAP typically do not require specialist consultations; however, when attempting to rule out mimics of pneumonia in patients who are transferred to acute care facilities, consider consultation with an infectious diseases specialist.

Patients with preexisting lung disorders may benefit from consultation with a pulmonologist.

Patients with an exacerbation of previous cardiac problems or new cardiac problems benefit from consultation with a cardiologist.

Patients do not require dietary alterations. Clinicians usually advise bed rest for patients with NHAP, with gradual transition to ambulation as tolerated.

Transferring a patient with NHAP to an acute care facility simply to receive intravenous antibiotics is usually not necessary. Such transfer may be appropriate if there is a diagnostic question or if the patient requires oxygen therapy, pulmonary toilet, or adjustment of cardiac drugs. Make certain that the pneumonia is resolving and that the patient is clinically stabilized before returning him or her to the long-term care facility.

Empyema may complicate pneumonia. Diagnose empyema with thoracentesis and treat patients with appropriate antimicrobial therapy and chest tube drainage.

Renal function decreases with age, and most patients in long-term care facilities are elderly; therefore, consider their creatinine clearance rate when calculating antimicrobial dosing.

The initial dose of renally cleared antibiotics in patients with renal insufficiency is the same as that administered to individuals without renal insufficiency; however, physicians should decrease the maintenance dose in proportion to the degree of renal dysfunction. If using hepatically cleared antibiotics (eg, doxycycline) that primarily have a nonrenal mode of elimination, no dosing adjustment is necessary in elderly patients with impaired renal function.

If the physician suspects NHAP and the mimics of pneumonia can be ruled out, early appropriate empiric therapy is the critical component of medical management. Promptly instituting empiric antimicrobial therapy significantly decreases the likelihood of mortality and morbidity associated with NHAP and CAP. Direct antimicrobial coverage against the most likely pathogens (ie, S pneumoniae, H influenzae, M catarrhalis).

Select antibiotics that have the appropriate spectrum and minimal resistance potential, have excellent safety profiles, are cost effective, and are available in intravenous and oral formulations.

Antimicrobial therapy may be administered intravenously, but this is frequently difficult for elderly patients in long-term care facilities, which may lack intravenous teams and adequate nursing staff. Elderly patients frequently have poor venous access, further complicating the problem. Intramuscular administration is not recommended. Therefore, an appropriate oral antimicrobial is ideal for early treatment of NHAP. Further weakening of the patient’s condition may require transfer to an acute care hospital.

Patients with severe NHAP who are transferred to acute care facilities may require initial intravenous antimicrobial administration. Alternatively, oral administration in the acute care facility is acceptable and equivalent to intravenous antibiotic therapy. Patients started on intravenous antimicrobial therapy in the nursing home or the hospital should be switched to an equivalent oral antimicrobial therapy after 48-72 hours of clinical improvement. After patients are on oral therapy and their cardiopulmonary status stabilizes, transfer them back to the long-term care facility.

The duration of therapy usually is 2 weeks, depending on the patient’s host defenses and underlying cardiopulmonary status. Consider extending antimicrobial therapy for a few days in more severe cases, but do not automatically prolong therapy simply because persisting pulmonary infiltrates are observed on chest radiographs, a low-grade fever is present, or the patient has minimal leukocytosis if necessary. Use oral formulations for extended therapy.

Pulmonary infiltrates that do not resolve after 2 weeks of appropriate antimicrobial therapy suggest that the infiltrates are not infectious, and the physician should initiate further diagnostic studies to determine the cause. Pulmonary infiltrates resolve more slowly than their appearance on chest radiographs indicates; however, as long as the infiltrates are resolving and the patient is improving clinically, the patient does not need to remain in the acute care facility until the infiltrates clear from the radiographs.

Prognosis depends on the host immune system, the patient’s preexisting cardiopulmonary reserve status, and the extent of the patient’s lobar involvement resulting from the NHAP.

Patients who are predisposed to aspiration are at high risk for re-aspiration, owing to the same factors that caused the initial aspiration. Treat these patients with the same antibiotics for each episode. The recurrence of pneumonia is not the result of antibiotic failure but is instead the result of the underlying factors predisposing to aspiration.

Hutt E, Radcliff TA, Oman KS, Fink R, Ruscin JM, Linnebur S, et al. Impact of NHAP guideline implementation intervention on staff and resident vaccination rates. J Am Med Dir Assoc. 2010 Jun. 11(5):365-70. [Medline].

Mills K, Graham AC, Winslow BT, Springer KL. Treatment of nursing home-acquired pneumonia. Am Fam Physician. 2009 Jun 1. 79(11):976-82. [Medline].

Hollaar VRY, van der Putten GJ, van der Maarel-Wierink CD, Bronkhorst EM, de Swart BJM, de Baat C, et al. Nursing home-acquired pneumonia, dysphagia and associated diseases in nursing home residents: A retrospective, cross-sectional study. Geriatr Nurs. 2017 Sep – Oct. 38 (5):437-441. [Medline].

Troy CJ, Peeling RW, Ellis AG, Hockin JC, Bennett DA, Murphy MR, et al. Chlamydia pneumoniae as a new source of infectious outbreaks in nursing homes. JAMA. 1997 Apr 16. 277(15):1214-8. [Medline].

Buehrens PE. Effectiveness of oral antibiotic treatment in nursing-home acquired pneumonia. J Am Geriatr Soc. 1995 Dec. 43(12):1443; author reply 1443-4. [Medline].

Crossley KB, Thurn JR. Nursing home-acquired pneumonia. Semin Respir Infect. 1989 Mar. 4(1):64-72. [Medline].

Cunha BA. Doxycycline for nursing home acquired pneumonia (NHAP). Scand J Infect Dis. 2009. 41(1):77-8, author reply 76. [Medline].

Cunha BA. Nursing Home-Acquired Pneumonia (NHAP). Cunha BA. Pneumonia Essentials. 3rd ed. 2010. 106-110.

Degelau J, Guay D, Straub K, Luxenberg MG. Effectiveness of oral antibiotic treatment in nursing home-acquired pneumonia. J Am Geriatr Soc. 1995 Mar. 43(3):245-51. [Medline].

Ewig S, Klapdor B, Pletz MW, Rohde G, Schütte H, Schaberg T, et al. Nursing-home-acquired pneumonia in Germany: an 8-year prospective multicentre study. Thorax. 2012 Feb. 67(2):132-8. [Medline].

Kaku N, Yanagihara K, Morinaga Y, Izumikawa K, Nagashima S, Kakeya H, et al. The definition of healthcare-associated pneumonia (HCAP) is insufficient for the medical environment in Japan: a comparison of HCAP and nursing and healthcare-associated pneumonia (NHCAP). J Infect Chemother. 2013 Feb. 19(1):70-6. [Medline].

Klapdor B, Ewig S, Schaberg T, Rohde G, Pletz MW, Schütte H, et al. Presentation, etiology and outcome of pneumonia in younger nursing home residents. J Infect. 2012 Jul. 65(1):32-8. [Medline].

Lim WS, Macfarlane JT. A prospective comparison of nursing home acquired pneumonia with community acquired pneumonia. Eur Respir J. 2001 Aug. 18(2):362-8. [Medline].

Loeb M. Epidemiology of community- and nursing home-acquired pneumonia in older adults. Expert Rev Anti Infect Ther. 2005 Apr. 3(2):263-70. [Medline].

Ma HM, Ip M, Hui E, Chan PK, Hui DS, Woo J. Role of atypical pathogens in nursing home-acquired pneumonia. J Am Med Dir Assoc. 2013 Feb. 14(2):109-13. [Medline].

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Phares CR, Russell E, Thigpen MC, Service W, Crist MB, Salyers M. Legionnaires’ disease among residents of a long-term care facility: the sentinel event in a community outbreak. Am J Infect Control. 2007 Jun. 35(5):319-23. [Medline].

Troy CJ, Peeling RW, Ellis AG, Hockin JC, Bennett DA, Murphy MR. Chlamydia pneumoniae as a new source of infectious outbreaks in nursing homes. JAMA. 1997 Apr 16. 277(15):1214-8. [Medline].

Minnaganti VR, Patel PJ, Cunha BA. Nursing Home Acquired Pneumonia (NHAP): Community Acquired or Nosocomial. Infectious Disease Practice. 2000. 24:20-23.

Type of Pneumonia

Most Common Pathogens

Uncommon Pathogens

Appearance on Chest Radiograph

Length of Stay, days

NHAP

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Legionella

Chlamydophila pneumoniae [4]

Focal sequential/lobar ± consolidation ± pleural effusion

No cavitation

7-10

CAP

S pneumoniae

H influenzae

M catarrhalis

Legionella

Mycoplasma

Focal sequential/lobar ± consolidation ± pleural effusion

No cavitation

7-10

NP

Pseudomonas aeruginosa

Klebsiella

Escherichia coli

Serratia

Necrotizing pneumonia and cavitation with P aeruginosa and Klebsiella

Bilateral infiltrates without cavitation or pleural effusion

10-21

Patient Position at Aspiration

Chest Radiograph Lobar Involvement

Supine

Right lower lobe (ie, superior or posterior segment) or bilateral infiltrates (ie, all lobes)

Right side down

Right upper lobe (ie, axillary segment)

Left side down

Left upper lobe (ie, axillary segment)

Prone

Right middle lobe (ie, lingula)

Sitting upright

Right lower lobe (ie, basilar segments)

Shirin A Mazumder, MD Associate Professor of Medicine, Director of Infectious Disease Fellowship Program, Division of Infectious Diseases, Department of Internal Medicine, University of Tennessee Health Science Center College of Medicine, University of Tennessee Methodist Physicians

Shirin A Mazumder, MD is a member of the following medical societies: American College of Physicians, American Medical Association, HIV Medicine Association, Infectious Diseases Society of America, Memphis Medical Society, Society for Healthcare Epidemiology of America, Tennessee Medical Association

Disclosure: Nothing to disclose.

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

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, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Ronald A Greenfield, MD Professor, Department of Internal Medicine, 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; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching

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

Disclosure: Medscape Reference Salary Employment

Nursing Home Acquired Pneumonia 

Research & References of Nursing Home Acquired Pneumonia |A&C Accounting And Tax Services
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Nursing Home Acquired Pneumonia 

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