sign in sign up
<<
Home , Epiglottitis, Shortness of breath, Tachypnea

Acute Dyspnea in the Office ROGER J. ZOOROB, M.D., M.P.H., and JAMES S. CAMPBELL, M.D. Louisiana State University School of , Kenner, Louisiana

Respiratory difficulty is a common presenting complaint in the outpatient primary care set- ting. Because patients may first seek care by calling their physician’s office, telephone triage plays a role in the early management of dyspnea. Once the patient is in the office, the initial goal of assessment is to determine the severity of the dyspnea with respect to the need for oxygenation and intubation. Unstable patients typically present with abnormal , altered mental status, , or unstable , and require supplemental , intravenous access and, possibly, intubation. Subsequent management depends on the dif- ferential diagnosis established by a proper history, , and ancillary stud- ies. Dyspnea is most commonly caused by respiratory and cardiac disorders. Other causes may be upper , , a psychogenic disorder, or a neuro- muscular condition. Differential diagnoses in children include , , epiglotti- tis, and . Pertinent history findings include , sore throat, , , and . The physical examination should focus on vital signs and the , , , and lower extremities. Significant physical signs are , rales, wheez- ing, , , or absent breath sounds. Diagnostic work-up includes pulse oximetry, , , and chest radiography. If the patient is admitted to the or hospital, blood gases, ventilation-perfusion scan, D-dimer tests, and spiral computed tomography can help clarify the diagnosis. In a stable patient, management depends on the underlying etiology of the dyspnea. (Am Fam Physician 2003; 68:1803-10. Copyright© 2003 American Academy of Family Physicians.)

hortness of breath, or dyspnea, is a tem, motor cortex, and peripheral receptors in common problem in the outpatient the upper airway, lungs, and chest wall.1 Vari- primary care setting. Establishing a ous states can produce dyspnea in diagnosis can be challenging slightly different manners, depending on the because dyspnea appears in multiple interaction of efferent signals with receptors Sdiagnostic categories. Underlying disorders of the central nervous system, autonomic sys- range from the relatively simple to the more tem, and peripheral nerves. The actual sensa- serious, which are best addressed in an emer- tion of muscular effort and breathlessness gency department. Timely assessment, diag- results from the simultaneous activation of nosis, and initiation of appropriate therapy the sensory cortex at the time the chest mus- play an important role in controlling the cles are signaled to contract.2 Good evidence commonly associated . Family physi- demonstrates that increased

cians should be prepared and equipped to partial pressure (PCO2) levels stimulate the triage, manage, and stabilize patients with feeling of breathlessness independent of the acute dyspnea. effects of ventilation or the oxygen partial 2 pressure (PO2) level. Pathophysiology Dyspnea is described as faster Clinical Presentation and Triage accompanied by the sensations of running out At presentation, an adult patient usually of air and of not being able to breathe fast or describes a sensation of difficult or uncom- deeply enough. The sensations are similar to fortable breathing. Triage begins with deter- that of thirst or hunger (i.e., an unignorable mining the degree of urgency by assessing the feeling of needing something). Dyspnea duration of the condition, whether it is acute results from multiple interactions of signals or chronic, and the severity of symptoms. and receptors in the autonomic nervous sys- Studies have shown that the type and severity

Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright© 2003 American Academy of Family Physicians. For the private, noncommercial use of one individual user of the Web site. All other rights reserved. Telephone Triage for Acute Dyspnea

Children Adults

<3 months of age Severe dyspnea or or sudden onset new dyspnea at rest or or sore throat sudden onset of chest pain or croupy cough or No No Yes lethargy or History of CHF History of COPD ED temperature above 38.8°C (102°F) or or progressive dyspnea history of and progress dyspnea

Yes No Inform physician • Increase diuretic Inform physician ED Same-day • Weigh daily • Adjust bronchodilator dosage office visit • Advise office visit or • Add ED visit as indicated • Consider • Home health visit • Advise office visit or ED visit as indicated • Home health visit

FIGURE 1. Telephone triage of acute dyspnea in the physician’s office. (CHF = congestive ; COPD = chronic obstructive pulmonary disease; ED = emergency department)

of an underlying or heart disease corre- Unstable patients typically present with one lates well with the way the patient describes or more symptom patterns: the dyspnea.3 The first communication with • , altered mental status, the physician’s office, especially for established hypoxia, or unstable arrhythmia. patients, may be by telephone. Telephone • Stridor and breathing effort without air triage is an important initial step in manage- movement (suspect upper airway obstruction). ment. Protocols and clearly written office pro- • Unilateral tracheal deviation, hypoten- cedures for staff are recommended to provide sion, and unilateral breath sounds (suspect proper care and minimize risk.4 A triage algo- tension ) rithm (Figure 1) can be used by office nurses. • above 40 breaths per minute, retractions, cyanosis, low oxygen Recognition and Management saturation. of Unstable Patients The same initial treatment process should Definitive care, which must follow stabi- be applied for any of these symptom patterns. lization, depends on the specific diagnosis. First, administer oxygen. Consider intubation An initial quick assessment will help the if the patient is working to breathe (gasping), physician determine if a patient is unstable apneic, or nonresponsive, following advanced (Table 1). cardiac life support (ACLS) guidelines.5 Next, establish intravenous line access and start administration of fluids. Perform needle Studies have shown that the type and severity of an under- in patients with tension pneu- mothorax. Administer a nebulized bron- lying lung or heart disease correlates well with the way the chodilator if obstructive pulmonary disease is patient describes the dyspnea. present.Administer intravenous or intramuscu- lar furosemide if is present.

1804 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 68, NUMBER 9 / NOVEMBER 1, 2003 Dyspnea

TABLE 1 Once an emergent situation has been excluded, the patient’s Initial Assessment of Patients airway, mental status, ability to speak, and breathing effort with Dyspnea should be reevaluated. A focused history should be obtained,

Assess airway patency and listen to the lungs. and a physical examination completed. Observe breathing pattern, including use of acces- sory muscles. Monitor cardiac rhythm. In children, the most common causes of Measure vital signs and pulse oximetry. Obtain any history of cardiac or pulmonary disease, acute dyspnea are acute asthma, pulmonary or trauma. , and upper airway obstruction. Evaluate mental status. Some conditions associated with dyspnea, such as epiglottitis, croup, , asthma, and , are serious and may be fatal. In children, always consider Disposition and transfer of the patient foreign body aspiration, croup, and bronchi- depends on the diagnosis or differential diag- olitis caused by respiratory syncytial virus.8,9 nosis. Unstable patients should be transported to the closest emergency department for fur- HISTORY ther evaluation and treatment. Trained health A complete history should emphasize any care personnel should accompany the patient coexisting cardiac and pulmonary symptoms. in the ambulance and continue management Cardiac and pulmonary problems are the until supervision is transferred to the emer- most common causes of dyspnea. Determine gency department team. onset, duration, and occurrence at rest or exertion. The presence of cough may imply Further Assessment of Stable Patients asthma or ; cough combined with Once an emergent situation has been a change in the character of may be excluded, obtain a history to determine the caused by exacerbation of chronic obstructive level of acuity. Reassess the patient’s airways, pulmonary disease (COPD). In adults, mental status, ability to speak, and breathing effort. Check vital signs, and question the patient (or a family member) about the dura- TABLE 2 tion of the dyspnea and any underlying car- Differential Diagnosis of Acute Dyspnea in Adults diac or pulmonary disease. Include a focused history of medication use, cough, fever, and Cardiac: congestive heart failure, , arrhythmia, chest pain. Ask about any history of trauma , acute , and continue the focused physical examina- Pulmonary: chronic obstructive pulmonary disease, asthma, pneumonia, tion by listening to breath sounds and observ- pneumothorax, , , metastatic disease, pulmonary edema, gastroesophageal reflux disease with aspiration, restrictive ing skin color. lung disease Psychogenic: panic attacks, , pain, anxiety DIFFERENTIAL DIAGNOSIS Upper airway obstruction: epiglottitis, foreign body, croup, Epstein-Barr virus Obtaining an expanded history and per- Endocrine: metabolic acidosis, medications forming a comprehensive physical examina- Central: neuromuscular disorders, pain, aspirin overdose tion and appropriate initial testing are neces- Pediatric: bronchiolitis, croup, epiglottitis, foreign body aspiration, myocarditis sary to reach a proper diagnosis. The differential diagnosis of acute dyspnea in the Information from references 1, 6, and 7. adult patient is presented in Table 2.1,6,7

NOVEMBER 1, 2003 / VOLUME 68, NUMBER 9 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 1805 Anxiety symptoms may imply psychogenic causes of dysp- TABLE 3 nea, but organic etiologies always should be considered first. Clues to the Diagnosis of Dyspnea

Symptoms or features in the history Possible diagnosis

epiglottitis should be ruled out when severe Cough Asthma, pneumonia sore throat is associated with acute dyspnea.10 Severe sore throat Epiglottitis In children, fever associated with dyspnea usually implies an infectious cause, such as Pleuritic chest pain Pericarditis, pulmonary 10 embolism, pneumothorax, pneumonia, croup, or bronchiolitis. pneumonia Chest pain during dyspnea may be caused Orthopnea, nocturnal Congestive heart failure by coronary or , depending on paroxysmal dyspnea, the quality and description of the pain. Pleu- edema ritic chest pain could be caused by pericardi- Tobacco use Chronic obstructive tis, pneumonia, pulmonary embolism, pneu- pulmonary disease, mothorax, or pleuritis. Dyspnea or congestive heart failure, with pleuritic chest pain occurs in 97 percent pulmonary embolism of patients who have clinically apparent pul- Indigestion, Gastroesophageal reflux monary embolism, although some researchers disease, aspiration have questioned reliance on clinical presenta- Barking cough Croup tion as an accurate indicator of pulmonary embolism.11 Sudden at rest is sugges- tive of pulmonary embolism or pneumotho- Chest pain is almost universal in sponta- rax. Severe respiratory distress continuing neous pneumothorax, while dyspnea is the over one to two hours suggests congestive second most common symptom.12 Anginal heart failure or asthma. Consider nonrespira- chest pain accompanied by shortness of tory causes of dyspnea (e.g., anemia, acidosis, breath may signify ischemia associated with drug poisoning). left ventricular dysfunction. Paroxysmal dysp- nea or pulmonary edema may be the only clinical presentation in 10 percent of patients with myocardial infarction.13 The Authors Consider spontaneous pneumothorax in ROGER J. ZOOROB, M.D., M.P.H., is associate chair of the Department of Family Med- patients with COPD, , or icine at Louisiana State University (LSU) Health Sciences Center, New Orleans, and 14 director of the LSU School of Medicine’s family practice residency program at the acquired immunodeficiency syndrome. Kenner Regional Medical Center, Kenner, La. He earned his medical degree and a Spontaneous recurrent or nonrecurrent master of public health degree from the American University of Beirut, Beirut, pneumothorax in young females in conjunc- Lebanon. He completed a residency in family medicine at Anderson Memorial Hospi- tal, Anderson, S.C., and a faculty development fellowship at the University of Ken- tion with menstruation is an uncommon tucky, Lexington. condition referred to as catamenial pneu- 15 JAMES S. CAMPBELL, M.D., is assistant professor at the Louisiana State University mothorax. A history of scuba diving may School of Medicine’s family practice residency program at the Kenner Regional Med- suggest barotrauma. Vehicle airbag trauma ical Center. He earned his medical degree from the University of Virginia School of has been reported to cause pneumothorax; Medicine, Charlottesville, and completed a residency in family medicine at Battle Creek Area Medical Education Corporation, Battle Creek, Mich. note any history of penetrating or nonpene- trating trauma.16 Address correspondence to Roger J. Zoorob, M.D., M.P.H., Department of Family Med- icine, LSU–HSC School of Medicine, 200 W. Esplanade, Ste. 409, Kenner, LA 70065 (e- Inquire about indigestion or dysphagia, mail: [email protected]). Reprints are not available from the authors. which may indicate gastroesophageal reflux or

1806 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 68, NUMBER 9 / NOVEMBER 1, 2003 Dyspnea

aspiration.17 Anxiety symptoms may imply embolism. Rales are present in pulmonary psychogenic causes of dyspnea, but organic edema and pneumonia.20 etiologies always should be considered first. A Rapid or irregular pulse may signify a dys- diagnosis of hyperventilation syndrome can- rhythmia. An S3 gallop suggests a left ventric- not be made before organic disease is ruled ular systolic dysfunction in congestive heart 18 out. When obtaining the history, note smok- failure. An S4 gallop suggests left ventricular ing habits, secondhand smoke exposure, and dysfunction or ischemia. A loud P2 may be pertinent medication use (give particular heard in patients with pulmonary hyperten- attention to agents that have potential adverse sion or cor pulmonale. Murmurs can be an cardiopulmonary effects, such as beta block- indirect sign of congestive heart failure, and ers, ophthalmologic drops). A history of distant heart sounds can point to cardiac orthopnea, pedal edema, or nocturnal parox- tamponade.21 ysmal dyspnea is suggestive of congestive Abdominal Examination. Look for hepato- heart failure.19 Table 3 summarizes clues in the megaly and . Assessing for hepatojugu- history that help in the diagnosis of dyspnea. lar reflux is a valid bedside maneuver in the diagnosis of congestive heart failure in PHYSICAL EXAMINATION patients with acute dyspnea. General Appearance and Vital Signs. To Extremities. Check the lower extremities for determine the severity of dyspnea, carefully edema and any signs suggestive of deep observe respiratory effort, use of accessory venous .22 Examine the digits for muscles, mental status, and ability to speak. clubbing or cyanosis. may exist in COPD, asthma, Table 4 summarizes physical findings in the or . Stridor is indicative of diagnosis of dyspnea. an upper airway obstruction.10 It may be nec- essary to obtain a rectal temperature to detect fever, since oral airflow may decrease the oral TABLE 4 temperature. Physical Examination Findings in the Diagnosis of Acute Dyspnea Neck Examination. Distention of the neck veins may imply cor pulmonale caused by Findings Possible diagnosis severe COPD, congestive heart failure, or car- Wheezing, pulsus paradoxus, accessory Acute asthma, COPD diac tamponade. Check the thyroid for muscle use exacerbation enlargement because congestive heart failure Wheezing, clubbing, barrel chest, decreased COPD exacerbation may result from or hypothy- breath sounds roidism. Ensure that the is in the mid- Fever, , increased Pneumonia line. Auscultate for stridor. Edema, neck vein distension, S3 or S4 hepatojugular Congestive heart failure, Cardiac and Pulmonary Examination. Pal- reflux, murmurs, rales, , wheezing pulmonary edema pate the chest for Wheezing, friction rub, lower extremity swelling Pulmonary embolism and crepitus, and percuss for dullness, an indi- Absent breath sounds, hyperresonance Pneumothorax cation of consolidations or effusions. Hyper- Inspiratory stridor, rhonchi, retractions Croup resonance on suggests pneumo- Stridor, drooling, fever Epiglottitis thorax or bullous emphysema. Auscultate the heart and lungs for murmurs Stridor, wheezing, persistent pneumonia Foreign body aspiration or extra heart sounds; absent breath sounds Wheezing, flaring, intercostal retractions, Bronchiolitis may be consistent with pneumothorax or Sighing Hyperventilation pleural effusion. Wheezing usually is consis- tent with but can be COPD = chronic obstructive pulmonary disease. caused by pulmonary edema or pulmonary

NOVEMBER 1, 2003 / VOLUME 68, NUMBER 9 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 1807 narrowed anteroposterior tracheal air column DIAGNOSTIC WORK-UP on radiograph) suggests croup, whereas radio- The office work-up depends on available graphic enlargement of the is patho- diagnostic modalities. Table 5 and Figure 2 gnomonic for epiglottitis.24 summarize a diagnostic approach to acute Electrocardiography detects ischemia, left dyspnea. ,20 and arrhythmia. Pulse oximetry determines a patient’s level of Perform bedside spirometry and obtain a oxygenation. In the evaluation of acute dyspnea, peak expiratory flow rate in patients with sus- obtain chest radiographs to rule out conditions pected exacerbation of asthma or COPD.6 A such as pneumothorax, pneumonia, COPD, complete blood count is useful for suspected pulmonary edema, or congestive heart failure.23 or anemia. Obtain lateral neck radiographs when stridor is D-Dimer testing, although not an office present or when upper airway obstruction, such procedure, can be useful in the hospital setting as foreign body aspiration, epiglottitis, or croup, to check for suspected pulmonary embolism. is suspected. Subglottic edema (appearing as a Negative rapid and standard enzyme-linked

TABLE 5 Diagnostic Evaluation in Acute Dyspnea

Testing

Possible diagnosis Radiography Pulse oximetry/spirometry Other tests

Acute asthma, chronic Hyperinflated lungs Decreased , — obstructive pulmonary decreased peak expiratory disease exacerbation flow rate and forced expiratory volume in 1 second Pneumonia Infiltrates, effusion, consolidation Decreased or normal oxygen Normal or high white saturation blood cell count Congestive heart failure Interstitial edema, effusion, Decreased oxygen saturation Left ventricular hypertrophy, cardiomegaly ischemia, or arrhythmia on ECG; low hemoglobin Pulmonary embolism Normal, , pleural Decreased oxygen saturation Right bundle branch block effusion, wedge-shaped density on ECG; Pneumothorax Collapsed lung, mediastinal shift Decreased oxygen saturation — Croup Subglottic narrowing by AP plain Decreased or normal oxygen — film or computed tomography saturation Epiglottitis Enlarged epiglottis Decreased or normal oxygen High white blood cell count saturation Foreign body aspiration Visualized foreign body, air Decreased or normal oxygen Normal or high white blood trapping, hyperinflation saturation cell count Bronchiolitis Hyperinflation, atelectasis Decreased or normal oxygen Normal white blood cell count; saturation RSV swab Hyperventilation Normal Normal —

ECG = electrocardiography; AP = anteroposterior; RSV = respiratory syncytial virus.

1808 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 68, NUMBER 9 / NOVEMBER 1, 2003 Diagnostic Approach to Dyspnea

Dyspnea

Check CXR

CXR abnormal CXR normal

Perform spirometry

Cardiac disease Primary pulmonary disease

Check echocardiogram Pleural effusion, pneumonia, Spirometry normal Spirometry abnormal pneumothorax, pulmonary edema, Check room interstitial lung disease, air ABG No valvular Valvular pulmonary vascular disease, Large airway Respiratory abnormality abnormality emphysema, chest wall deformity, obstruction, muscle carcinoma of the lung , weakness restrictive disease , , mitral stenosis CNS lesion Primary muscle weakness

PaO2 <70 mm Hg PaO2 >70 mm Hg

Perform ventilation-perfusion scan Measure O2 saturation

Scan normal Mismatched defect Normal Abnormal

Perform cardiac Pulmonary Check HCT Carbon monoxide catheterization embolus poisoning, methemoglobinemia, abnormal HCT >35% HCT <35% hemoglobin Catheterization Catheterization normal abnormal Perform exercise PFTs Anemia

Idiopathic , dyspnea right-to-left cardiac shunt, cardiac Normal PFTs Abnormal PFTs

Deconditioning, Fixed cardiac psychogenic dyspnea, output, exercise- hypermetabolic states induced asthma

FIGURE 2. A diagnostic approach to dyspnea. (CXR = chest x-ray film; ABG = arterial blood gases; CNS = central nervous system; PaO2 = partial pressure of oxygen; O2 = oxygen; HCT = hematocrit; PFTs = pulmonary function tests) Reprinted with permission from Healey PM, Jacobson EJ. Common medical diagnoses: an algorithmic approach. 3d ed. Philadelphia: Saun- ders, 2000:15.

NOVEMBER 1, 2003 / VOLUME 68, NUMBER 9 www.aafp.org/afp AMERICAN FAMILY PHYSICIAN 1809 Dyspnea

immunosorbent assay (ELISA) D-Dimer tests 10. Godden CW, Campbell MJ, Hussey M, Cogswell JJ. Double blind placebo controlled trial of nebulised can help exclude pulmonary embolism, budesonide for croup. Arch Dis Child 1997;76: whether performed alone or in conjunction 155-8. with normal alveolar dead-space fraction.7,25 11. Hoffman JM, Lee A, Grafton ST, Bellamy P, Hawkins RA, Webber M. Clinical in pul- Spiral computed tomography (CT) also has a monary embolism. A reassessment. Clin Nucl Med role in the diagnostic work-up of pulmonary 1994;19:803-8. embolism in a hospitalized patient, especially 12. Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000;342:868-74. when the ventilation-perfusion scan is nondi- 13. Lusiani L, Perrone A, Pesavento R, Conte G. Preva- agnostic. Spiral CT may eventually replace lence, clinical features, and acute course of atypical pulmonary angiography.26 Bilateral venous myocardial infarction. Angiology 1994;45:49-55. 14. Sassoon CS. The etiology and treatment of sponta- Doppler imaging should be ordered simulta- neous pneumothorax. Curr Opin Pulm Med 1995; neously with spiral CT and, if findings are 1:331-8. suggestive of deep venous thrombosis, treat- 15. Roe D, Brown K. herald- ing menarche in a 15-year-old adolescent. Pediatr ment for pulmonary embolism should be ini- Emerg Care 1997;13:390-1. tiated. A right-heart strain pattern on 16. Morgenstern K, Talucci R, Kaufman MS, Samuels echocardiogram may be one finding in a LE. Bilateral pneumothorax following air bag deployment. Chest 1998;114:624-6. patient with acute pulmonary embolism. 17. Siegel PD, Katz J. Respiratory complications of gastresophageal reflux disease. Prim Care 1996;23: The authors indicate that they do not have any con- 433-41. flicts of interest. Sources of funding: none reported. 18. Saisch SG, Wessely S, Gardner WN. Patients with acute hyperventilation presenting to an inner-city REFERENCES emergency department. Chest 1996;110:952-7. 19. Ciocon JO, Fernandez BB, Ciocon DG. Leg edema: 1. Mahler DA, Mejia R. Dyspnea. In: Davis GS, ed. clinical clues to the differential diagnosis. Geriatrics Medical management of pulmonary . New 1993;48:34-40,45. York: Marcel Dekker, 1999:221-32. 20. Gillespie ND, McNeill G, Pringle T, Ogston S, 2. Calverley PMA, Pride NB. Chronic obstructive pul- Struthers AD, Pringle SD. Cross sectional study of monary disease. London: Chapman & Hall, 1995: contribution of clinical assessment and simple car- 205-42. diac investigations to diagnosis of left ventricular 3. Kunitoh H, Watanabe K, Sajima Y. Clinical features systolic dysfunction in patients admitted with acute to predict hypoxia and/or in acute dyspnoea. BMJ 1997;314:936-40. asthma attacks. J Asthma 1994;31:401-7. 21. Rich MW. Epidemiology, pathophysiology, and eti- 4. Robinson DL, Anderson MM, Erpenbeck PM. Tele- ology of congestive heart failure in older adults. J phone advice: new solutions for old problems. Am Geriatr Soc 1997;45:968-74. Nurse Pract 1997;22:179-80,183-6,189 passim. 22. Worsley DF, Palevsky HI, Alavi A. A detailed evalua- 5. Hazinski MF, Cummins RO, Field JM. 2000 hand- tion of patients with acute pulmonary embolism book of emergency cardiovascular care for health- and low- or very-low-probability lung scan inter- care providers. Dallas, Tex.: American Heart Associ- pretations. Arch Intern Med 1994;154:2737-41. ation, 2000. 23. Butcher BL, Nichol KL, Parenti CM. High yield of 6. Brenner B, Kohn MS. The acute asthmatic patient chest radiography in walk-in clinic patients with in the ED: to admit or discharge. Am J Emerg Med chest symptoms. J Gen Intern Med 1993;8:115-9. 1998;16:69-75. 24. Frantz TD, Rasgon BM, Quesenberry CP Jr. Acute 7. Kline JA, Israel EG, Michelson EA, O’Neil BJ, Plewa epiglottitis in adults. Analysis of 129 cases. JAMA MC, Portelli DC. Diagnostic accuracy of a bedside 1994;272:1358-60. D-Dimer assay and alveolar dead-space measure- 25. Oger E, Leroyer C, Bressollette L, Nonent M, Le ment for rapid exclusion of pulmonary embolism: a Moigne E, Bizais Y, et al. Evaluation of a new, multicenter study. JAMA 2001;285:761-8. rapid, and quantitative D-Dimer test in patients 8. Fitzgerald D, Mellis C, Johnson M, Allen H, Cooper with suspected pulmonary embolism. Am J Respir P, Van Asperen P. Nebulized budesonide is as effec- Crit Care Med 1998;158:65-70. tive as nebulized in moderately severe 26. Paterson DI, Schwartzman K. Strategies incorporat- croup. Pediatrics 1996;97:722-5. ing spiral CT for the diagnosis of acute pulmonary 9. Levy BT, Graber MA. Respiratory syncytial virus embolism: a cost-effectiveness analysis. Chest infection in infants and young children. J Fam Pract 2001;119:1791-800. 1997;45:473-81.

1810 AMERICAN FAMILY PHYSICIAN www.aafp.org/afp VOLUME 68, NUMBER 9 / NOVEMBER 1, 2003