Community-Acquired Pneumonia (CAP)
Bacterial pneumonia, lower respiratory tract infection
Bacterial pneumonia, lower respiratory tract infection
1. Description of the problem
Community-acquired pneumonia (CAP) is defined as an infection of the alveolar, distal airway and interstitium of the lungs acquired while the patient is in the community.
CAP is associated with significant morbidity, mortality and cost.
Clinical stratification is important in assisting clinicians to admit the patient to the hospital or if severely ill to the ICU.
Approximately 10% of all hospitalized patients require ICU admission, with a mortality rate that ranges between 30% and 60% in this hospital setting.
Early treatment should be instituted, including early antimicrobial therapy and other interventions as in patients with sepsis.
This chapter will focus on CAP in the ICU setting.
The most common symptoms are fever, nonproductive or productive cough, pleuritic chest pain, dyspnea, chills, and rigors.
Patients present less commonly with diarrhea, new-onset or worsening confusion in elderly patients, and headache.
Clinical signs include fever or hypothermia, dullness to percussion, increased tactile and vocal fremitus, egophony, crackles, whispering pectoriloquy and pleural friction rub. Tachypnea > 25/min alone or > 20/min with associated tachycardia (>100/min) and fever has a higher probability of pneumonia.
Key management points
The decision about admission to ward or ICU service should be based on severity of illness.
Two important criteria may assist the clinician in the decision of admission to the ward by using the CURB-65 rule and to the ICU by applying the Infectious Diseases Society (IDSA)/American Thoracic Society (ATS) criteria, respectively.
CURB-65 criteria consist of age > 65 years, altered mental status, serum blood urea > 20 mg/dl, respiratory rate > 30 breaths per minute, diastolic blood pressure < 60mmHg.
Each criterion in CURB-65 has a score of one. Two or more criteria suggest severe CAP and admission to the hospital is recommended. Three or more criteria suggest the need for a higher level of care, including the ICU.
IDSA/ATS criteria define the need for ICU care by applying major and minor criteria for severe CAP:
One of two following major criteria : Need for invasive mechanical ventilation and requiring vasopressors (for septic shock)
Three of the nine minor criteria : Respiratory rate > or = 30/min, PaO2/FIO2 ratio < or = 250, multilobar infiltrates, confusion/disorientation, uremia with a BUN level > or = 20 mg/dL, leukopenia with a WBC count < 4,000 cells/mm3, platelet count < 100,000 cells/mm3, core temperature < 36°C, and hypotension requiring aggressive fluid resuscitation
At least one major or three minor criteria would define severe CAP and the need for ICU admission.
However, both CURB-65 score and ATS criteria should not limit physician clinical judgment to decide about site of care.
CAP is common and an important cause of death from infectious disease. Therefore, early diagnosis should be prioritized.
The most important determinants for hospitalization and assessment of severity in CAP are patient comorbid conditions and/or prior antibiotic use.
CURB-65 criteria and ATS modified score should be used for both severity of illness score and to define ICU admission, respectively.
Attempt to obtain cultures if possible, but more importantly, chest x-ray findings are needed to confirm the diagnosis of pneumonia.
Antibiotics should be given within 8 hours of ER arrival if pneumonia is confirmed in this location.
Since inappropriate antimicrobial choice is associated with higher mortality, risk factors for MDR pathogens such as Pseudomonas infection should be evaluated when empiric therapy for CAP is going to be started.
If aspiration pneumonia is suspected, then symptoms should be watched without antibiotics for 24 hours. If symptoms persist, then antibiotics should be started.
If no clinical (3-7 days) or radiological (4-6 weeks) improvement is seen, other possible processes should be suspected, such as pulmonary abscess, collagen-vascular disease, malignancy, etc.
2. Emergency Management
History and Physical Exam
Measure vital signs
Respiratory rate >30/min in a patient with no underlying disease is a good single clinical parameter that suggests severity of the disease.
Assess oxygenation by pulse oximetry or arterial blood gases.
Confirm adequate vascular access to ensure adequate hydration.
Assess for possible alternative differential diagnosis:
Pulmonary embolism should be considered in patient with pleuritic chest pain, dyspnea and hypoxemia.
Rapid initiation of antimicrobial agents (directly in the ER) and within 6 hours of patient presentation
Laboratory and imaging testing
Complete blood cell count (CBC)
Basic blood chemistry (electrolytes, glucose, creatinine and blood urea nitrogen)
Liver function test
Arterial blood gas (ABG) or pulse oximetry
Blood cultures (collect at least 2 sets of blood cultures) for all patients to be admitted before initiation of antibiotic therapy
Sample with >25 white blood cells (WBCs) and <10 squamous epithelial cells per low-power field is suitable for culture.
C-reactive protein (CRP)
Serologic test initially and in the convalescent stages for Legionella spp, M. pneumoniae, C. pneumoniae, if no CRP available for these pathogens
Urinary antigen for Legionella spp and Streptococcus pneumoniae
Direct rapid viral test by nucleic acid amplification: influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza, rhinovirus
Sputum sample with special stains and culture when indicated for Pneumocystis, fungal pathogens, and
M. tuberculosis infection should be sent if suspected pneumonia in immunocompromised patients or with the presence of cavitation.
Confirmation of pneumonia diagnosis
Lower respiratory tract symptoms in a patient with abnormal chest x-ray is consistent with bacterial pneumonia.
Radiographic findings include the presence of alveolar infiltrates and consolidation, interstitial infiltrates, cavitation, and sometimes a pleural effusion.
If the initial chest x-ray does not confirm pneumonia, a new film should be repeated within 48 hours of presentation in patients with high clinical suspicion for pneumonia. An alternative approach is to consider performing a chest CT scan,
Patients with symptomatic or considerable-size pleural effusions should undergo a diagnostic thoracentesis.
Diagnostic thoracentesis is recommended in patients with a radiographic free-flowing pleural fluid confirmed to be >1 cm on the lateral decubitus chest x-ray (affected side down).
Pleural fluid should be analyzed for Gram’s stain, culture, cell counts, protein, lactate dehydrogenase (LDH), glucose, and pH.
Although there is no evidence that microbiological studies will improve the final outcome in these patients, an attempt to obtain samples to identify the etiologic agent in patients with severe CAP is indicated.
Bronchoscopic sampling should be consider to obtain lower respiratory material for further studies, if other diagnostic tools have not been helpful in confirming the diagnosis and no clinical improvement is seen with the initial empiric therapy.
How do I know this is what the patient has?
The clinician needs to rely on the combination of the following parameters to support the suspected diagnosis of pneumonia:
High clinical suspicion based on signs and symptoms
Confirmatory radiological diagnosis of CAP
Other laboratory parameters such as WBC, uremia, and worsening oxygenation
Clinical response after the initiation of antimicrobial therapy
The differential diagnosis includes:
Chemical aspiration without infection
Acute respiratory distress syndrome
Inflammatory disorders (sarcoidosis, Wegener’s, vasculitis and other rheumatologic disease)
Bronchiolitis obliterans organizing pneumonia (BOOP)
Confirmatory tests include:
Imaging confirmation of a pulmonary infiltrate in a patient with lower respiratory tract symptoms highly confirms the evidence of a pulmonary process, but does not confirm the presence of bacteria in the lower respiratory tract.
Microbiological sampling is recommended for severely ill patients with severe CAP and includes:
Respiratory samples (bronchoscopic or non-bronchoscopic techniques), particularly if the patient requires mechanical ventilation
Legionella and pneumococcal urinary antigen
Consider serological testing on patients with certain risk factors.
Lung biopsy by bronchoscopic or surgical methods is rarely done for final gold standard confirmation.
4. Specific Treatment
Risk for pseudomonas infection needs to be assessed.
If no risk for pseudomonas infection (history of broad-spectrum antibiotic therapy >7 days in the past month, bronchiectasis, malnutrition, human immunodeficiency virus [HIV] infection, chronic immunosuppression – prednisone >10 mg/day, prior P. pseudomonas) first-line therapy:
Beta-lactam (ceftriaxone, 1-2 gr IV q24h or cefotaxime, 1-2 gr IV q6-8h) plus
Quinolone IV (levofloxacin 500-750 mg IV daily; moxifloxacin 400 mg IV daily or gatifloxacin 400 mg daily) or
Azithromycin (1 gr; then, 24 hours later 500 mg IV q24h)
If risk for Pseudomonas infection is present:
Carbapenem: imipenem 500 mg IV q6h or meropenem 1 gr IV q8h or
Antipseudomonal cephalosporin: cefepime 2 gr IV q8h or ceftazidime 2 gr IV q8h or
Piperacillin/tazobactam: 4.5 gr IV q6h
Plus: quinolone IV (levofloxacin 500-750 mg IV daily; moxifloxacin 400 mg IV daily or gatifloxacin 400 mg daily) or
Azithromycin (1 gr; then, 24 hours later 500 mg IV q24h)
If patient severely ill:
Consider adding coverage for methicillin-resistant
S. aureus (MRSA) with vancomycin 1 gr IV q12h until cultures are available.
If aspiration penumonitis is suspected:
Watch symptoms for 24 hours.
If there is persistence of symptoms, consider:
Levofloxacin, moxifloxacin, gatifloxacin, ceftriaxone or cefotaxime (please see doses above)
If poor dental hygiene, putrid sputum or alcoholism history present, consider:
Quinolone, ceftriaxone or cefotaxime (please see doses above) plus
Clindamycin (450 mg PO q6h or 300-900 mg IV q6-12h) or
Metronidazole (500 mg q12h PO) or
Piperacillin/tazobactam 4.5 g IV q6h or ampicillin/sulbactam 1.5-3 gr IV q6h or
Imipenem (500 mg IV q6h)
Combination of therapy with beta-lactam plus macrolide or fluoroquinolone
Intermediate resistance to penicillin (<2 mg/dl): third-generation cephalosporin, or respiratory fluoroquinolone
High level of resistance to penicillin (>2 mg/dl): respiratory fluoroquinolone, linezolid, vancomycin
Staphylococcus aureus methicillin-susceptible (MSSA)
Third-generation cephalosporin, respiratory fluoroquinolone or clindamycin
Staphylococcus aureus methicillin-resistant (community acquired – MRSA)
Vancomycin or linezolid
Atypicals: Chlamydophila pneumoniae, Mycoplasma pneumoniae and Legionella spp
Respiratory fluoroquinolone, macrolide or doxycycline (nor for Legionella spp)
Beta-lactamase producer: third-generation cephalosporin, beta-lactam/beta-lactamase inhibitors or a fluoroquinolone, newer macrolide (clarithromycin or azithromycin), or doxycycline
Enterobacteriaceae including E. coli, Klebsiella pneumoniae, Klebsiella oxytoca, Proteus mirabilis
Third-generation cephalosporin, beta-lactam/beta-lactamase inhibitors or a fluoroquinolone
Intravenous anti-pseudomonal beta-lactam/beta-lactamase inhibitor plus either intravenous aminoglycoside or intravenous ciprofloxacin/levofloxacin, plus intravenous macrolide if aminoglycoside used, but not with the use of ciprofloxacin/levofloxacin
Coxiella burnetii or Chlamydophila psittaci
Macrolide or tetracycline
Oseltamivir or zanamivir (cover both influenza A and B)
Consider using combination therapy for severely ill patients.
What do I do about particularly refractory cases?
Look for complications such as:
Complicated pleural effusions
If same area, consider bronchial obstruction from a tumor or foreign body.
If different area and no history of COPD, consider HIV infection, immunodeficiency.
Consider aspiration or bronchiectasis.
5. Disease monitoring, follow-up and disposition
Expected response to treatment
A decrease in mortality rates has been associated with early and appropriate antibiotic therapy.
Patients generally stabilize within 3 to 7 days and should be monitored for:
Improvement in temperature and WBCs
Culture results and decrease of antibiotic therapy accordingly
Stability of comorbid conditions such as COPD, renal failure, etc.
Possible S. aureus superinfection
If no clinical improvement in the acute setting or eventually no radiographic improvement after several weeks (see below), suspect the following:
Resistant pathogens such as MRSA are being treated with antibiotics different to vancomycin or linezolid.
Collagen vascular disease
Other infectious pathogens are involved, such as M. tuberculosis, pneumocystis or fungal infection
Malignancy/obstructing bronchus secondary to malignancy
Presence of undrained infectious focus (empyema, brain abscess, endocarditis, splenic abcess, osteomyelitis)
Repeating a careful physical exam
Repeat cultures: urine, blood, sputum, chest XR, +/- CT chest
Bronchial alveolar lavage (BAL) for microbiological and cytology studies
Radiographic resolution of CAP must be ensured.
Half of patients with lung cancer have evidence of cancer abnormalities on initial chest XR, but the other half could manifest as failure of chest XR findings to resolve after an episode of CAP.
Therefore, patients older than 40 years and all tobacco smokers should have a follow-up chest XR after an episode of CAP, as follows:
6 weeks: if <50 years old, nonsmoker, and without underlying lung disease.
8-12 weeks: elderly with COPD..
Pneumonia is the product of proliferation of microbial pathogens and a response of the host to them in the alveolar space.
The most common mechanism for infection is when microorganisms gain access to the alveolar space after aspiration from the oropharynx. However, they can be inhaled as contaminated droplets or less commonly by hematogenous spread.
Host barriers such as hairs and turbinates of the nares, branching architecture of the tracheobronchial tree (mucociliary clearance and local antibacterial factors), gag reflex and cough can be overcome when microorganisms are small enough to be inhaled to the alveolar space.
Alveolar macrophages are very efficient in killing and clearing pathogens that once engulfed can be eliminated by the mucociliary system or lymphatics.
If the function of alveolar macrophages is exceeded, then pneumonia becomes manifested that is mainly due to the activation of an inflammatory response rather than proliferation of microorganisms.
Eighth leading cause of death overall.
Most common cause of death from infectious disease in the United States.
More common among African Americans and men than among whites and women.
Hospitalized mortality rate depends on severity of illness but the higher mortality rate is seen in ICU patients admitted with CAP.
Most hospitalizations and severity assessments are determined by chronic comorbid conditions and/or prior antibiotic use (past 3 months).
Chronic obstructive pulmonary disease (COPD) (50%), alcoholism, chronic heart disease and diabetes mellitus are the most common associated comorbidities.
Half of CAP cases that require hospital admission are due to Streptococcus pneumoniae.
Patients with severe CAP most commonly die from refractory hypoxemia, refractory shock and multiorgan failure.
Inpatient mortality is estimated to be around 8%, with half of the cases due to pneumonia and half to comorbid illnesses.
Respiratory failure, sepsis and heart disease are the most common immediate causes of death.
P. aeruginosa has the highest mortality (>50%).
Dementia, immunosuppression, active cancer, systolic hypotension, male gender and multilobar infiltrates are factors other than pneumonia that are independently associated with mortality in CAP.
Presence of aspiration should be considered an independent predictor for both pneumonia- and comorbid conditions-related mortality.
Approximately 10% to 15% of patients will have another episode of pneumonia in the next 2 years.
Special considerations for nursing and allied health professionals.
What's the evidence?
“Pneumonia and Influenza death rates – United States, 1979-1994”. MMWR. vol. 44. 1995. pp. 535-7.
Advance report of final mortality statistics 1992. 1994.
Niederman, MS. “Guidelines for the management of adults with community-acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention”. Am J Respir Crit Care Med. vol. 163. 2001. pp. 1730-54.
Woodhead, M. “Guidelines for the management of adult lower respiratory tract infections”. Eur Respir J. vol. 26. 2005. pp. 1138-80.
Mandell, LA. “Update of practice guidelines for the management of community-acquired pneumonia in immunocompetent adults”. Clin infect Dis. vol. 37. 2003. pp. 1405-33.
Tejerina, E. “Prognosis factors and outcome of community-acquired pneumonia needing mechanical ventilation”. J Crit Care. vol. 20. 2005. pp. 230-8.
Marrie, TJ. “Factors associated with death among adults < 55 years of age hospitalized for community-acquired pneumonia”. Clin Infect Dis. vol. 36. 2003. pp. 413-21.
Mortensen, EM. “Causes of death for patients with community-acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team cohort study”. Arch Intern Med. vol. 162. 2002. pp. 1059-64.
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- 1. Description of the problem
- 2. Emergency Management
- 3. Diagnosis
- 4. Specific Treatment
- 5. Disease monitoring, follow-up and disposition
- Special considerations for nursing and allied health professionals.
- What's the evidence?