Asthma, chronic obstructive pulmonary disease, and pneumonia

Asthma

• 1.
  What is asthma and what are the presenting symptoms of asthma exacerbation?

  • Asthma is a chronic inflammatory disorder of the airways, resulting in recurrent episodes of wheezing, breathlessness, chest tightness, and coughing. The airway inflammation contributes to airway hyperreactivity, airflow obstruction, and chronic disease.
• 2.
  In addition to asthma, what should be included in the differential diagnosis of wheezing?

  • Chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), foreign body aspiration, anaphylaxis, epiglottitis, tracheobronchitis, reactive airway disease, viral respiratory infections, and vocal cord dysfunction.
• 3.
  Which aspects of the asthmatic’s history are important to the current exacerbation?

  • Ask questions regarding exposure to common precipitants, such as viral upper respiratory tract infections, allergens, cold, exercise, and possible aspirin or nonsteroidal anti-inflammatory drug use. Also important are duration and severity of symptoms, past history and frequency of sudden exacerbations, prior hospitalizations and intubations, number of recent ED visits, current medications, worsening of symptoms while on or if weaning off corticosteroids, and other comorbidities. Non-Caucasian race and lower socioeconomic standing are also risk factors for severity requiring hospitalization.
• 4.
  Are there any helpful ancillary diagnostic tests?

  • Bedside spirometry provides a rapid, objective assessment of patients and serves as a guide to the effectiveness of therapy. The forced expiratory volume in 1 second (FEV₁) and the peak expiratory flow rate (PEFR) directly measure the degree of large airway obstruction.

    • ■
      FEV₁ or PEFR ⩽70% of predicted (or personal best) indicates mild obstruction
    • ■
      FEV₁ or PEFR 40%–69% of predicted (or personal best) indicates moderate obstruction
    • ■
      FEV₁ or PEFR <40% of predicted (or personal best) indicates severe obstruction
  • Pulse oximetry is a useful and convenient method for assessing oxygenation and monitoring oxygen saturation during treatment. Most other tests, including arterial blood gases, complete blood counts, and electrocardiograms, are not useful in the management of asthma except in cases of active or impending respiratory failure. Chest X-ray may be helpful if the patient does not respond to initial treatment or if a pulmonary complication, such as foreign body obstruction, pneumonia, pneumomediastinum, pneumothorax, or CHF, is suspected.
• 5.
  What are the key objectives when treating an asthma exacerbation? How are they achieved?

  • The key objectives include correction of significant hypoxemia, rapid reversal of airflow obstruction, and reduction of the likelihood of recurrence of severe airflow obstruction.
  • First-line treatment includes β₂-agonists and corticosteroids in moderate exacerbations, and oxygen if needed. Ipratropium should be added when treating severe exacerbations. Relief of airflow obstruction (bronchoconstriction) is usually accomplished by administration of either intermittent or continuous doses of aerosolized β₂-agonists. Studies contain mixed conclusions as to whether there is any added clinical benefit to levalbuterol in comparison to racemic formulations. Current evidence does not suggest an improved benefit from intravenous β₂-agonists compared to aerosol. Early administration of systemic corticosteroids addresses the inflammatory component of acute asthma and has been demonstrated to prevent some hospitalization, although beneficial effects of corticosteroids are often not noted until several hours after administration. High-dose inhaled corticosteroids may have some benefit in the acute setting and can be continued safely by patients already on inhaled steroids. Aerosolized ipratropium should be added if FEV₁ or PEFR is <40% of predicted because studies reveal that they increase pulmonary function modestly and decrease need for hospitalization in these patients. Hypoxemia is usually corrected by administration of supplemental oxygen with a goal of oxygen saturation of 90% to 95%. (See Table 26-1 .) Epinephrine or terbutaline may be administered subcutaneously to patients unable to coordinate aerosolized treatments. Theophylline is not recommended in the acute setting.
• 6.
  How can I determine if my patients are improving?

  • Ask them how they feel, re-examine them, and obtain objective measures of pulmonary function. Either FEV₁ or PEFR (the best of three attempts) should be obtained on presentation and after treatment and compared with the patient’s percent predicted (or personal best) FEV₁ or PEFR, if known, to determine the need for more aggressive therapy or hospitalization.
• 7.
  What measures are available if my patient isn’t responding as expected?

  • Magnesium, heliox, ketamine, and continuous positive-pressure ventilation may offer some benefits when all other treatment modalities have failed and patients remain in severe status after conventional therapy. Magnesium sulfate has been noted to help reverse bronchospasm in conjunction with standard therapy if PEFR is 25% or less of predicted but is not useful in patients with mild or moderate obstruction. Although widely discussed in the literature, the data for ketamine, heliox, and continuous positive-pressure ventilation are less compelling.
  • There are no absolute indications for intubation except for respiratory arrest and coma. Possible indication for intubation includes exhaustion, worsening respiratory distress, persistent or increasing hypercarbia, and changes in mental status. Intubate semielectively, before the crisis of respiratory arrest, because intubation is difficult in patients, who have asthma.
• 8.
  How should I decide whether a patient can be discharged or requires hospitalization?

  • Disposition of patients is usually determined by clinical response after three doses of aerosolized β₂-agonist therapy; ipratropium (if used); and corticosteroids. If patients have clear breath sounds, are no longer dyspneic or are back to baseline, and have an FEV₁ or PEFR 70% of predicted, they may be discharged home. Patients with an incomplete response to treatment, that is, FEV₁ between 50% and 70% of predicted and mild dyspnea, can be considered for discharge after assessing their individual circumstances. Patients with a poor response to bronchodilators, that is, FEV₁ <50% of predicted and who have moderate to severe symptoms after treatment, require hospitalization. If an ED observation capability exists, observation for 4 to 6 hours poststeroid administration will decrease the number of inpatient admissions.
• 9.
  What should be considered at time of discharge?

  • Patients who received corticosteroids acutely should continue oral steroid therapy at home for 3 to 10 days. For courses of less than 1 week, there is no taper required. For a 10-day course, there remains no need to taper if the patients are concurrently taking inhaled formulations. Dosing parameters are controversial, so choose a moderate regimen (about 40–50 mg prednisone per day); Patients not already on controller medications who have mild persistent asthma should be started on low-dose inhaled corticosteroids or oral leukotriene modifiers, such as zafirlukast or montelukast. Long-acting β-agonists, such as salmeterol, should be added to the regimen of patients with moderate persistent asthma who are inadequately controlled on inhaled corticosteroids. All patients should be advised to use their short-acting β-agonists on a regularly scheduled basis for a few days and then as needed. Patient education should be provided at discharge, as well as an appointment for a follow-up visit within several weeks.
• 10.
  Does pregnancy change the management of acute asthma?

  • No. It is important to treat pregnant asthmatics aggressively to prevent maternal hypoxia and subsequent fetal morbidity and mortality. Patients should not be undertreated because of fear of teratogenicity; the risks from respiratory failure and severe acute asthma are greater than from therapy with standard medications. The standard therapy and dosages are the same.

    KEY POINTS: EMERGENCY TREATMENT OF ASTHMA.

    • 1.
      Relieve significant hypoxemia: oxygen.
    • 2.
      Reverse airflow obstruction: β-agonists + ipratropium.
    • 3.
      Reduce the likelihood of recurrence: corticosteroids.
    • 4.
      Provide objective measure of improvement: PEFR or FEV1.
    • 5.
      Adequate discharge planning includes education, medications, and follow-up.

TABLE 26-1.

MEDICATIONS USED TO TREAT ASTHMA AND COPD EXACERBATIONS

Medications	Dosage and Route
Inhaled short-acting b2–agonists
Albuterol Nebulizer solution (5 mg/mL)	2.5–5 mg every 20 minutes for three doses, then 2.5–10 mg every 1–4 hours as needed, or 10–15 mg/hour continuously or 7.5 mg bolus
MDI (90 μg/puff): must be used with spacer device	Four to eight puffs every 20 minutes up to 4 hours, then every 1–4 hours as needed
Systemic (injected) b2-agonists*
Epinephrine 1:1000 (1 mg/mL)	0.3–0.5 mg every 20 minutes for three doses subcutaneously
Terbutaline (1 mg/mL)	0.25 mg every 20 minutes for three doses subcutaneously
Inhaled anticholinergics
Ipratropium bromide nebulizer solution (0.25 mg/mL)	0.5 mg every 30 minutes for three doses then every 2–4 hours as needed
MDI (18 μg/puff): must be used with spacer device	Four to eight puffs as needed
Systemic corticosteroids
Prednisone or prednisolone Methylprednisolone	40–60 mg by mouth 125 mg intravenously

COPD, chronic obstructive pulmonary disease.

^*Exercise extreme caution in patients with known coronary artery disease.

Chronic obstructive pulmonary disease

• 11.
  What is COPD and what are the presenting symptoms of a COPD exacerbation?

  • COPD is a disease characterized by chronic airflow limitation that is not fully reversible, is progressive, and is associated with an abnormal inflammatory response to noxious particles or gases. It is a combination of small airway disease and parenchymal destruction. It includes emphysema and chronic bronchitis and can coexist with asthma. The characteristic symptoms of COPD are cough, sputum production, and dyspnea on exertion. Exacerbations are characterized by increased dyspnea, often accompanied by wheezing and chest tightness, increased cough and sputum, change in color or thickness of sputum, and fever. Smoking, exposure to occupational dusts and chemicals, and air pollution are the most common causes of COPD.
• 12.
  In addition to COPD, what should be included in the differential diagnosis?

  • ■
    In patients who present with wheezing, the differential diagnosis includes asthma, CHF, pneumonia, cardiogenic pulmonary edema, and bronchitis.
  • ■
    In those who present with dyspnea, the differential diagnosis includes myocardial ischemia, pericardial effusion, pneumothorax, pulmonary embolism, pneumonia, asthma, acute respiratory distress syndrome (ARDS), bronchiectasis, pulmonary fibrosis, pleural effusion, tuberculosis, and metabolic disturbances, acidosis and shock.
• 13.
  Which diagnostic tests are helpful in the management of COPD?

  • Pulse oximetry should be used in every patient with COPD. Oxygen saturation less than 90% indicates severe hypoxia. Arterial blood gas measurements often can identify patients with increased and continuing hypoxia, hypercarbia, and respiratory acidosis, especially if compared with the patient’s baseline values. Check theophylline levels if indicated. Chest radiographs are appropriate in COPD exacerbations to help manage complications and concomitant disease. In patients with cor pulmonale, continuous cardiac monitoring may identify any associated arrhythmias. The use of B-type natriuretic peptide (BNP) does not substitute for clinical judgment when trying to differentiate COPD from CHF as a numeric cut-off value that differentiates between the two diseases remains elusive. In contrast to asthma, acute pulmonary function tests are less helpful in the emergency setting because of the difficulty that sick patients with COPD have in performing these tests properly. Differentiation of mild, moderate, and severe COPD relies on the FEV₁ and the ratio of FEV₁/forced vital capacity (FVC) <70%. Making this calculation without formal pulmonary function tests (PFTs) is generally not possible in the ED.
• 14.
  What are the key objectives when treating a COPD exacerbation and how are they achieved?

  • The key objectives are to relieve hypoxemia, alleviate reversible bronchospasm, and treat the underlying etiology of the exacerbation. The cornerstone of initial management is treating the hypoxia with supplemental oxygen with a goal of oxygen saturation of 90% or greater. Despite adequate oxygen saturation, CO₂ retention due to the obstructive nature of the disease can occur insidiously with little change in symptoms. Thus, oxygen administration should be carefully monitored by frequent clinical assessment, continuous pulse oximetry, and arterial blood gases, when needed. Excessive supplemental oxygen in this small subset of patients can cause respiratory arrest secondary to loss of their hypoxemia-induced ventilatory drive. Relief of airflow obstruction (bronchoconstriction) is usually accomplished by administration of either intermittent doses of aerosolized β₂-agonists or anticholinergics, such as ipratropium. Systemic corticosteroids are indicated in severe exacerbations of COPD. The use of methylxanthines (theophylline or aminophylline) remains controversial and should be used when only when there is inadequate response to short-acting bronchodilators.
• 15.
  What about antibiotics?

  • Routine antibiotic coverage is controversial, but the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommend antibiotic therapy for patients with three cardinal symptoms: increased dyspnea, increased sputum volume, and increased sputum purulence or patients that require invasive or noninvasive mechanical ventilation. The antibiotic choices should reflect local antibiotic sensitivity to Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Guidelines for treatment of pneumonia, if present, should be considered.
• 16.
  How can I determine if my patient is improving?

  • Ask the patient how he or she feels, re-examine, and monitor the oxygen saturation. If the patient was able to perform objective measures of pulmonary function, compare FEV₁ or PEFR (the best of three attempts) obtained on presentation with that obtained after treatment.
• 17.
  When should a patient with COPD be intubated?

  • Noninvasive modalities such as continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP) often can obviate the need for intubation by improving gas exchange, decreasing hypoxia, and reducing work of breathing. Noninvasive intermittent ventilation (NIV) has been studied in several randomized controlled trials consistently providing positive results with success rates of 80% to 85%. Any patient unable to tolerate NIV or not responding to NIV with changes in mental status, increased respiratory distress with cyanosis, acute deterioration, respiratory arrest, shock, severe acidosis (pH of 7.25), or hypercapnia (PaCO₂ >60 mm Hg) should be intubated and mechanically ventilated immediately.
• 18.
  How can I decide whether a patient can be discharged or requires hospitalization?

  • Relapse rates remain high because patients with COPD have less respiratory reserve and function that is not quickly reversible. These patients often take longer than an ED visit to recover and require hospitalization. Failure to improve while in the ED, failed outpatient management, and concerning pulmonary infections are reasons for hospitalization. Patients who return to near baseline with improvement from ED treatment and have good social support systems in place may be discharged home with close follow-up.
• 19.
  What should be considered at time of discharge?

  • Patients who received corticosteroids acutely should continue oral steroid therapy at home for up to 10 days. Dosing parameters are controversial, so choose a moderate regimen (about 40–50 mg of prednisone per day); no tapering is required. Patients should continue to use their short-acting rescue medications. Adding inhaled anticholinergics plus longer-acting sympathomimetic bronchodilators may improve lung function and help improve effectiveness of pulmonary rehabilitation. The use of chronic inhaled corticosteroids is most beneficial for patients with an FEV₁ between 1 and 2 L. Antibiotics should be prescribed to patients deemed well enough for discharge who have experienced increase in sputum production, thickness, or change in sputum color. Patients with a PaCO₂ lower than 60 mm Hg at baseline should be evaluated for home oxygen therapy. Patient education should be provided at discharge, as well as an appointment for a follow-up visit within several days.
• 20.
  When is ipratropium bromide contraindicated in the management of patients with asthma or COPD?

  • Ipratropium bromide contains derivatives of soy lecithin and related food products. Patients with soybean or peanut allergies may develop anaphylaxis if exposed to this medication in either metered dose inhaler (MDI) or nebulized forms.

    KEY POINTS: EMERGENCY TREATMENT OF COPD.

    • 1.
      Relieve significant hypoxemia: oxygen.
    • 2.
      Reverse airflow obstruction: β-agonists + ipratropium.
    • 3.
      Consider antibiotics if there are changes in sputum production.
    • 4.
      Patients with COPD have less respiratory reserve and require admission more frequently than patients with asthma.
    • 5.
      CPAP or BiPAP may obviate the need for endotracheal intubation.
    • 6.
      Adequate discharge planning includes education, medications, and careful follow-up.

Pneumonia

• 21.
  Why do I need to know about pneumonia?

  • Pneumonia is the seventh leading cause of death overall and the leading cause of death from infectious disease in the United States. There are approximately 4 to 5 million identified cases of community-acquired pneumonia (CAP) each year, resulting in 1.3 million hospital admissions. The ED serves as the portal of entry for 75% of these admissions. When properly identified and treated as an outpatient, the mortality of CAP decreased from 30% to about 1%. Overall mortality has decreased by 3% since 1990. The role of the emergency physician is to diagnose pneumonia accurately, initiate timely antibiotic therapy, and make an appropriate disposition.
• 22.
  How does a pulmonary infection develop? What predisposes people to it?

  • Pneumonia is an infection of the alveolar spaces of the lung. It commonly develops via inhalation of infectious particles or aspiration of oropharyngeal or gastric contents and less commonly through hematogenous spread of infection, direct invasion from contiguous structures, direct inoculation, and reactivation of prior disease. Table 26-2 lists predisposing factors.
• 23.
  What are differences in presentation of typical pneumonia and atypical pneumonia?

  • ■
    Typical pneumonia presents with the abrupt onset of high fever, cough productive of purulent sputum, shortness of breath, and pleuritic chest pain. Infants may present with fever associated with irritability, tachypnea, intercostal retractions, nasal flaring, and grunting. Cough may be absent in infants. Elderly or debilitated patients may present with nonspecific complaints and findings such as confusion or deterioration of baseline function, rather than classic symptoms. The most common organism is Streptococcus pneumoniae.
  • ■
    Atypical pneumonia has a more insidious onset and includes a prominent cough often with the absence of sputum production. Patients may have only a mild fever and are more likely to have extrapulmonary manifestations such as sore throat, dermatitis, headache, cardiac complications (i.e., pericarditis, myocarditis), hepatitis, and renal disease. There are no consistent clinical or radiographic criteria available to distinguish typical from atypical pneumonia. The most common organism is Mycoplasma pneumoniae.
• 24.
  What are the most common causative agents in CAP and nosocomial pneumonia?

  • The causative organism is unknown in 30% to 50% of patients with CAP. In those patients for whom the causative organism is known, S. pneumoniae is the most common agent (see Table 26-3 ). During hospitalization, exposure to more virulent organisms changes the pattern of infection. Gram-negative bacilli, particularly Klebsiella, Pseudomonas aeruginosa, and Escherichia coli, are responsible for more than 50% of cases. Staphylococcus aureus accounts for another 10% to 20% of hospital-acquired pneumonias and tends to be associated with more severe cases. The remainder of cases is usually due to anaerobic oral flora, S. pneumoniae, Legionella, and Moraxella catarrhalis (each accounting for <10% of cases). Nosocomial acquired pneumonias are rising rapidly and in some cases may account for 17% of pneumonias when patients return to the ED. Patients who develop a hospital-acquired pneumonia have an attributable mortality of 27% to 50%.
• 25.
  What are the presenting signs and symptoms in a patient with pneumonia?

  • Patients with pneumonia usually present with cough, dyspnea, sputum production, fever, and pleuritic chest pain. The physical examination may show evidence of alveolar fluid (inspiratory rales); consolidation (bronchial breath sounds); pleural effusion (dullness and decreased breath sounds); or bronchial congestion (rhonchi and wheezing). Findings consistent with pneumonia include fever, tachypnea, tachycardia, decreased oxygen saturation, and altered mental status associated with severe illness.
• 26.
  What diagnostic studies are useful in the evaluation of pneumonia?

  • Although some providers will treat healthy, low-risk patients with suspected pneumonia empirically, others feel a chest X-ray is mandatory in every patient with a history and symptoms suggestive of pneumonia. It is difficult to identify a set of specific criteria for ordering a chest X-ray but all patients who present with a cough do not need chest radiography. Clinical judgment must be used in the presence of clinical indicators. The American Thoracic Society (ATS) and the Infectious Disease Society of America (IDSA) include radiographic findings as part of their definitions of pneumonia. The IDSA 2007 pneumonia guidelines state in their executive summary that, “In addition to a constellation of suggestive clinical features, a demonstrable infiltrate by chest radiograph or other imaging technique, with or without supporting microbiological data, is required for the diagnosis of pneumonia.”
  • An arterial blood gas may augment the information obtained through pulse oximetry to assess the need for respiratory support. In addition, the following laboratory tests may be used to aid in risk stratification of patients: complete blood count and serum electrolytes. The use of sputum Gram stain and blood cultures is controversial.
• 27.
  What radiographic findings are helpful in making a microbiologic differential diagnosis?

  • X-ray findings may suggest the underlying microbial etiology, but the overlapping variations in radiographic signs between different organisms may lead to misclassification. An X-ray is not diagnostic of a specific pathogen. A chest X-ray is helpful in defining the extent and location of the infiltrate (e.g., perihilar or multilobar involvement). In addition, dehydration and the radiographic manifestations of chronic diseases may obscure the infiltrates of pneumonia (see Table 26-4 ).
• 28.
  How do I determine the disposition of a patient with pneumonia?

  • Once a diagnosis of pneumonia is strongly suspected by history, physical, and X-ray results, the next decision is whether the patient is appropriate for discharge or requires hospital admission. Severity-of-illness scores, such as the CURB-65 criteria (confusion, uremia, respiratory rate, low blood pressure, age 65 years or greater), or prognostic models, such as the pneumonia specific severity of illness (PSI), are useful disposition aids. The PSI uses a combination of 20 parameters to evaluate patients, assign disease severity and mortality risk, and guide disposition. (See TABLE 26-5., TABLE 26-6., TABLE 26-7. .) Because of its prognostic accuracy, effectiveness, and safety as a decision aid, the PSI has become the reference standard for risk stratification. Although there are no clear guidelines for intensive care unit (ICU) admission, several rules have been published. Patients requiring ventilatory assistance or pressors and those who have altered mental status, multilobar or bilateral infiltrates, pleural effusion, age >65, comorbid conditions, respiratory rate >30, heart rate >125, Sat <90%, white blood cell count <3 or >20, blood urea nitrogen (BUN) >11, pH <7.35, and sodium <130 are among the patients who should be considered for an ICU setting.
• 29.
  What treatment should be started in the ED?

  • Supportive care, including oxygen and ventilatory support, should be given as required. Rehydration, antipyretics, and pain control should also be started as indicated. Antibiotic therapy should begin, based on the most likely pathogens, as soon as the diagnosis of pneumonia is made or strongly suspected. Studies have shown a decreased mortality and length of stay in a group of patients admitted for CAP when antibiotics were administered within a range 4 to 8 hours of arrival. All patients being admitted for pneumonia from the ED should have their first dose of antibiotics begun prior to transfer to the floor or ICU.
• 30.
  Which antibiotic should I use?

  • The choice of which antibiotic to begin is based on the site of treatment and suspected pathogens. The suggestions in Table 26-8 should be used in consideration with the clinical picture, recent literature, local preference, and resistance patterns. Increasing evidence has strengthened the recommendation for combination empirical therapy for severe CAP. Presence of comorbidities, such as chronic heart, lung, liver, or renal disease; diabetes mellitus; alcoholism; malignancies; asplenia; and immunosuppressing conditions all influence the empiric choice of antimicrobials.
• 31.
  Has the epidemiology of pneumonia changed in recent years?

  • The epidemiology of CAP continues to change due to a number of constantly changing factors, such as the discovery of new pathogens, changing antibiotic resistance, an aging population, and new tools for fighting infection. Pneumonia due to S. pneumoniae continues to be the most common single agent and is continually evolving resistance to a wider array of antibiotics. Viral and atypical agents are the most rapidly growing causes. Pneumocystis carinii pneumonia and tuberculosis (TB) are significant pathogens, particularly in the developing world. The severe acute respiratory syndrome (SARS) was first described in 2002 in China and subsequently spread worldwide. Influenza virus is predicted to be the next global pandemic. Diagnostic and treatment guidelines are available on the Centers for Disease Control and Prevention (CDC) website at www.cdc.gov.
• 32.
  What is the role of sputum Gram stain and culture?

  • The value of the Gram stain for expectorated sputum is controversial because it is uncertain how accurately expectorated sputum reflects lower respiratory tract secretions and pathology. Gram stain is frequently negative for specific organisms and the results rarely change therapy. Gram stain may be more useful in high-risk or hospitalized patients and should be considered in this group. The use of sputum with other stains (such as acid-fast for TB) and techniques such as direct fluorescent antibody staining have a continuing and developing role but are probably not helpful in ED management of these patients.
• 33.
  Are routine blood cultures helpful in the management of CAP?

  • The utility of blood cultures to determine causative agents in unselected patients with CAP is only 5% to 14% and rarely alters therapy for patients presenting to the ED with pneumonia. More discriminatory use may potentially reduce resource utilization. However, in patients with severe symptoms or significant risk factors, blood cultures may demonstrate uncommon causative organisms or unexpected antibiotic resistance. Currently, guidelines suggest that blood cultures be obtained in the ED prior to initiating antibiotics on hospitalized patients, requiring ICU admission and those with cavitary lesions, leukopenia, active alcohol abuse, severe liver disease, asplenia or pleural effusion.

    KEY POINTS: EMERGENCY TREATMENT OF PNEUMONIA.

    • 1.
      Begin empiric treatment early based on suspected pathogens.
    • 2.
      Calculation of the PSI or CURB-65 score is a reliable predictor of mortality and a tool to assist with disposition decisions.
    • 3.
      Support oxygenation, ventilation, and circulation as indicated by the patient’s condition.
    • 4.
      Recently hospitalized and nursing home patients will be infected with different organisms and require additional antibiotic coverage.
    • 5.
      Consider the presentation typical versus atypical when making therapy decisions.

    WEBSITES.

    http://pda.ahrq.gov/clinic/psi/psi.htm

    www.clevelandclinicmeded.com\diseasemanagement\infectiousdisease\ communitypneumonia.htm

    www.emedicine.com/emerg/topic465.htm

    www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm

TABLE 26-2.

FACTORS PREDISPOSING TO DEVELOPMENT OF PNEUMONIA

Factor	Likely Populations
Impaired swallowing/airway protection	Patients with history of alcohol abuse, CVA, ET and NT intubation, head injury, impaired gag reflex, seizures
Extremes of age	Very young and very old
Underlying pulmonary disease	Pulmonary embolism, COPD, pulmonary foreign body or tumor, pulmonary contusion, atelectasis
Chest wall disorders Prevent good cough and clearing of secretions	Rib fracture, surgical wounds, myopathies affecting chest muscles
Impaired mucociliary clearance mechanisms	Smokers, smog, alcohol, underlying viral infection, chronic lung disease
Impaired immune function	HIV, cancer, chemotherapy, malnutrition, sickle-cell disease, chronic steroid use
Other predisposing risks—these may lead to more severe infections with more virulent organisms	Diabetes, alcoholism, recent antibiotic use, recent hospitalization

COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident; ET, endotracheal; NT, nasotracheal.

Adapted from www.clevelandclinicmeded.com\diseasemanagement\infectiousdisease\communitypneumonia.htm.

TABLE 26-3.

IDENTIFIED PATHOGENS IN COMMUNITY-ACQUIRED PNEUMONIA

Pathogen	Percentage of Cases	Usual Pattern Caused
Streptococcus pneumoniae	20–60	Typical
Haemophilus influenzae	3–10	Typical
Mycoplasma pneumoniae	1–6	Atypical
Staphylococcus aureus	3–5	Typical
Viral (various incl. influenza)*	2–16	Atypical
Legionella species	2–8	Typical
Chlamydia pneumoniae	4–6	Atypical
Aspiration	6–10	Variable
Gram-negative bacilli (Klebsiella, Pseudomonas, etc.)	3–10	Typical
Others	3–5	Variable

^*Percentage of viruses is highly variable and was as high as 36% in one study and may be higher in infants and young children than in adults.

Adapted from www.clevelandclinicmeded.com\diseasemanagement\infectiousdisease\communitypneumonia.htm.

TABLE 24-4.

RADIOGRAPHIC APPEARANCES OF COMMUNITY-ACQUIRED PNEUMONIA^*

Radiographic Pattern	Suggested Organisms
Lobar	Streptococcus pneumoniae, Klebsiella species, pneumonia due to bronchial obstruction
Diffuse patchy infiltrate involving multiple lobes	Staphylococcus aureus, Haemophilus influenzae or gram-negative organisms
Interstitial pattern	Mycoplasma pneumoniae, Legionella, viral, Pneumocystis (patients with HIV or HIV risks) Chlamydia psittaci
Cavitary lesions with air-fluid levels	S. aureus, Klebsiella, Pseudomonas aeruginosa, Mycobacterium tuberculosis†

^*The development and resolution of X-ray findings may lag clinical findings by hours to days.

^†Tuberculosis may take on almost any radiographic appearance with some predilection for the upper lobes.

Adapted from www.clevelandclinicmeded.com\diseasemangement\infectiousdisease\communitypneumonia.htm.

TABLE 26-5.

FACTORS IN PNEUMONIA DISPOSITION DECISION

PORT PSI Scoring
PORT Characteristics	Points Given for Presence of Characteristic
Demographics
Age—male patient	Age in years (one point per year)
Age—female patient	Age in years: −10
Lives in nursing home	+10
Coexisting illnesses
Neoplastic disease	+30
Liver disease	+20
CHF	+10
Cerebrovascular disease (TIA or CVA)	+10
Renal disease	+10
Physical examination findings
Acute disorientation, stupor or coma	+20
Respiratory rate 30 per minute	+20
Systolic blood pressure 90 mm Hg	+20
Temperature <35°C or 40°C	+15
Heart rate 125 beats per minute	+10
Laboratory and x-ray findings (if study performed)
Arterial pH <7.35	+30
Blood urea nitrogen 30 mg/dL	+20
Sodium <130 mmol/L	+20
Glucose 250 mg/dL	+10
Hematocrit <30%	+10
Partial pressure of arterial oxygen	+10
<60 mm Hg or oxygen saturation <90%
Pleural effusion	+10
Total points = age + (-10 if female) + sum of above comorbidities, examination findings, and testing

CHF, congestive heart failure; CVA, cerebrovascular accident; PORT, Patient Outcome Research Team; PSI, pneumonia-specific severity of illness; TIA, transient ischemic attack.

TABLE 26-6.

PSI CLASS BASED ON POINT TOTALS AND MORTALITY^*

Points Calculated from PSI	Class	Mortality
<51 points	I	0.1%
51–70	II	0.6%
71–90	III	0.9%
91–130	IV	9.5%
>130	V	26.7%

PSI, pneumonia-specific severity of illness.

^*Those patients who are younger than 50 years and without any comorbid illnesses or vital sign abnormalities fall into class I and may be safely treated as outpatients. Patients not falling into risk class I require additional laboratory testing so that they may be assigned to risk classes II to V. Patients in classes II and III may be appropriate for outpatient management or a brief observation stay. Patients in class IV or V require hospital admission with a subset requiring intensive care unit admission.

TABLE 26-7.

OTHER FACTORS (NOT PART OF PORT PSI) THAT IMPACT DISPOSITION DECISION

•Patient’s clinical appearance •Patient’s ability to tolerate oral intake •Patient reliability •Social factors such as home support •Clinical judgment of the physician (most important)

PORT PSI, Patient Outcome Research Team pneumonia-specific severity of illness score.

TABLE 26–8.

EMPIRICAL ANTIMICROBIAL THERAPY FOR COMMUNITY-ACQUIRED PNEUMONIA IN IMMUNOCOMPETENT ADULTS

Patient/Setting	Common Pathogens	IDSA/ATS Consensus 2007 Empiric Therapy
Outpatient <60 years old No comorbid diseases	Streptococcus pneumoniae Mycoplasma pneumoniae Chlamydia pneumoniae Haemophilus influenzae Viruses	A macrolide or doxycycline
Outpatient >65 years old or having comorbid disease or antibiotic therapy within past 3 months	S. pneumoniae (drug resistant)	Fluoroquinolone alone* or a macrolide plus a beta lactam
	M. pneumoniae C. pneumoniae H. influenzae Viruses
	Gram-negative bacilli*†
Inpatient Not severely Ill	M. pneumoniaeC. pneumoniaeH. influenzaeVirusesGram-negative bacilli*†InpatientNot severely IllStaphylococcus aureus*† S. pneumoniae
		A macrolide and beta lactam or a fluoroquinolone‡ alone
Inpatient Not severely ill	H. influenzae Polymicrobial Anaerobes S. aureus C. pneumoniae Viruses
Inpatient Severely ill	S. pneumoniae	Beta lactam/beta lactamase inhibitor and azithromycin, or a fluoroquinolone‡ Pseudomonas aeruginosa possible: (intravenous macrolide or fluoroquinolone and aminoglycoside intravenously) or (antipseudomonal quinolone) and antipseudomonal beta lactam For methicillin-resistant S. aureus Add vancomycin or linezolid
	Legionella Gram-negative bacilli M. pneumoniae Viruses S. aureus

ATS, American Thoracic Society; IDSA, Infectious Disease Society of America.

^*In the outpatient setting, many authorities prefer to reserve fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin, gemifloxacin) for patients with comorbid diseases/risk factors.

^†In most cases, patients with pneumonias due to these organisms should be hospitalized.

^‡Levofloxacin, gatifloxacin, moxifloxacin, or gemifloxacin

^§Critically ill patients in areas with significant rates of high-level pneumococcal resistance and a suggestive sputum gram-stain should receive vancomycin or a newer quinolone pending microbiologic diagnosis.