Dean Gianakos, MD

CASE Sam J. is a 56-year-old man with a 2-day history of severe pain in the front of his neck. He aches all over and says he had “a bad cold” a week ago, but no fever, chills, cough, or headache. He hasn’t had a toothache or difficulty swallowing, but he does complain of a sore throat and muscle aches. His temperature is 100.7°f. He has no respiratory distress or stridor. there are no tonsillar exudates. the pharynx is not red or inflamed.

When you palpate his thyroid gland, you find diffuse tenderness. What could be causing his pain?

The patient with a painful thyroid is uncommon in clinical practice. In most cases, the culprit is a viral infection, radiation, or a traumatic injury to the gland. Bacterial, fungal, parasitic, or mycobacterial infections also occur, but these are rare, making up only 0.1% to 0.7% of all thyroid disease.¹ Some thyroid infections can be devastating, necessitating quick interventions including airway protection, intravenous antibiotics, and surgical drainage in certain situations.

Subacute thyroiditis (ST), the most common source of thyroid pain, is less severe, but can be disabling if not recognized and appropriately treated.² Occasionally, thyroid cysts can rupture, mimicking a presentation of ST.

This article will focus on how to evaluate the painful thyroid, so as to differentiate among the various conditions that can produce this uncommon presentation.

Classifying thyroiditis: Pain or no pain

Thyroiditis can be classified in several ways, but the simplest classification is in terms of pain. Conditions that can cause painless thyroiditis include Hashimoto’s disease, postpartum thyroiditis, subacute lymphocytic thyroiditis, Reidel’s thyroiditis, and thyroiditis induced by drugs such as amiodarone, interleukin-2, lithium, and interferon-alfa.³ Conditions that can cause painful thyroiditis include acute suppurative thyroiditis (AST), radiation-induced thyroiditis, trauma, ST, and ruptured cysts.¹

Acute suppurative thyroiditis
AST is a rare condition most commonly caused by bacterial, mycobacterial, fungal, or parasitic infection. The thyroid is remarkably resistant to infection because the gland is encapsulated, rich in iodide content, and has an abundant blood supply and lymphatic drainage.^1,2 AST usually occurs in patients with underlying thyroid disease, such as thyroid cancer, Hashimoto’s thyroiditis, multinodular goiter, congenital thyroid abnormalities such as pyriform sinus fistulas in children, and in patients who are immunocompromised.^1,2

Patients with AST are acutely ill and will complain of fever, dysphagia, and severe anterior neck pain. Stridor and tracheal obstruction may occur, requiring intubation or tracheotomy. Thyroid hormone levels are sometimes increased secondary to the release of preformed hormone from the intensely inflamed gland. Computed tomography (CT) or magnetic resonance imaging (MRI) thyroid scans can identify abscesses and guide biopsies that clinch the diagnosis.

Management consists of airway support, broad-spectrum intravenous antibiotics until gram stains and cultures return (with particular attention to coverage against staphylococcal, streptococcal, and anaerobic organisms), and surgical drainage of abscesses.

Thyroiditis caused by radiation or trauma
One percent of patients develop thyroiditis after receiving radioactive iodine ablation for hyperthyroidism (Graves’ disease).⁴ This condition usually occurs 5 to 10 days after the treatment. Radiation triggers thyroid gland destruction, causing transient additional release of thyroid hormone. Similar damage occurs after external beam radiation for lymphomas and head and neck cancers. In such cases, use nonsteroidal anti-inflammatory drugs (NSAIDs) and prednisone to reduce inflammation and beta-blockers to control hyperthyroid symptoms.

Trauma to the thyroid—from motor vehicle accidents, falls, or physical assaults—can cause pain, tenderness, and abnormalities in thyroid hormone levels. Effects are usually self-limited, and management centers on airway protection and prevention of infection.

Subacute thyroiditis
The cause of ST is not clear. However, it typically follows an upper respiratory infection. Many viruses have been implicated in the disease, including Coxsackie, echo, adeno, and influenza viruses.⁵ It occurs more frequently during summer months, coinciding with the peak incidence of enterovirus.² ST is 4 times more common in women than men, and the median age for occurrence is 45.⁶

Patients with ST usually seek care for such symptoms as fever, myalgias, and malaise, which suggest a viral infection.^2,7-9 Neck pain is significant and may radiate to the jaw or ear.⁹ Patients may have pain on swallowing and a sore throat. It’s possible to confuse ST with severe pharyngitis or even epiglottitis if you fail to palpate the thyroid gland. When you examine the thyroid, the gland is exquisitely tender with ST. Patients with ST appear less ill than those with AST.

In 50% of ST patients, thyroid-stimulating hormone (TSH) is suppressed, and thyroid hormone levels are elevated.⁴ Patients with hyperthyroidism exhibit the usual signs and symptoms associated with high levels of the hormone: tremor, palpitations, heat intolerance, and diarrhea. After a few weeks, thyroid hormone levels normalize and then drop to below normal in the 4 to 6 months that follow. Levels return to normal in 95% of patients after 6 to 12 months. ST recurs in only 2% of patients.⁴

Sedimentation rates are almost always elevated in ST, reflecting the significant inflammation associated with the disease. Cytotoxic T lymphocytes damage thyroid follicles, causing release of preformed thyroid hormone, in turn suppressing TSH.⁴ Radioactive iodine scans show low uptake because TSH is needed for the uptake of iodine.¹⁰

Treatment of ST should focus on reducing inflammation and pain. NSAIDs may be sufficient, but patients with moderate to severe symptoms may require prednisone 40 mg daily, tapered over 4 to 6 weeks.² If the patient is hyperthyroid, you’ll need to control symptoms with beta-blockers.

Ruptured thyroid cyst: An ST look-alike
The clinical presentation of a ruptured cyst closely mimics that of ST: thyroid pain, history of a recent cold, sore throat, aches, and pains. Laboratory and nuclear medicine evaluations, however, reveal significant differences:

• TSH is not suppressed;
• ESR is not elevated;
• Radioactive iodine uptake is normal.

Palpation may reveal a thyroid nodule. You can confirm the diagnosis by ultrasound and a needle aspiration.

CASE The right diagnosis for Sam

Sam’s initial clinical presentation suggested St, and he was started on prednisone 40 mg daily to control his pain. but when laboratory and nuclear medicine evaluations became available the next day, the St diagnosis didn’t hold up: TSH, ESR, and radioactive iodine uptake were all normal.

When Sam came in for a follow-up visit 3 days later, his thyroid pain was gone and he was feeling much better. palpation of his thyroid revealed a slightly tender nodule that went undetected in the initial exam. Subsequent thyroid ultrasound showed a 2x2 cm nodule in the right lobe. a fine needle aspiration revealed a colloid cyst. the cyst had ruptured, causing acute pain from hemorrhage and inflammation.

CORRESPONDENCE Dean Gianakos, MD, 2323 Memorial Drive, #10, Lynchburg Family Medicine Residency, Lynchburg, VA 24501; [email protected]

CASE Sam J. is a 56-year-old man with a 2-day history of severe pain in the front of his neck. He aches all over and says he had “a bad cold” a week ago, but no fever, chills, cough, or headache. He hasn’t had a toothache or difficulty swallowing, but he does complain of a sore throat and muscle aches. His temperature is 100.7°f. He has no respiratory distress or stridor. there are no tonsillar exudates. the pharynx is not red or inflamed.

When you palpate his thyroid gland, you find diffuse tenderness. What could be causing his pain?

The patient with a painful thyroid is uncommon in clinical practice. In most cases, the culprit is a viral infection, radiation, or a traumatic injury to the gland. Bacterial, fungal, parasitic, or mycobacterial infections also occur, but these are rare, making up only 0.1% to 0.7% of all thyroid disease.¹ Some thyroid infections can be devastating, necessitating quick interventions including airway protection, intravenous antibiotics, and surgical drainage in certain situations.

Subacute thyroiditis (ST), the most common source of thyroid pain, is less severe, but can be disabling if not recognized and appropriately treated.² Occasionally, thyroid cysts can rupture, mimicking a presentation of ST.

This article will focus on how to evaluate the painful thyroid, so as to differentiate among the various conditions that can produce this uncommon presentation.

Classifying thyroiditis: Pain or no pain

Thyroiditis can be classified in several ways, but the simplest classification is in terms of pain. Conditions that can cause painless thyroiditis include Hashimoto’s disease, postpartum thyroiditis, subacute lymphocytic thyroiditis, Reidel’s thyroiditis, and thyroiditis induced by drugs such as amiodarone, interleukin-2, lithium, and interferon-alfa.³ Conditions that can cause painful thyroiditis include acute suppurative thyroiditis (AST), radiation-induced thyroiditis, trauma, ST, and ruptured cysts.¹

Acute suppurative thyroiditis
AST is a rare condition most commonly caused by bacterial, mycobacterial, fungal, or parasitic infection. The thyroid is remarkably resistant to infection because the gland is encapsulated, rich in iodide content, and has an abundant blood supply and lymphatic drainage.^1,2 AST usually occurs in patients with underlying thyroid disease, such as thyroid cancer, Hashimoto’s thyroiditis, multinodular goiter, congenital thyroid abnormalities such as pyriform sinus fistulas in children, and in patients who are immunocompromised.^1,2

Patients with AST are acutely ill and will complain of fever, dysphagia, and severe anterior neck pain. Stridor and tracheal obstruction may occur, requiring intubation or tracheotomy. Thyroid hormone levels are sometimes increased secondary to the release of preformed hormone from the intensely inflamed gland. Computed tomography (CT) or magnetic resonance imaging (MRI) thyroid scans can identify abscesses and guide biopsies that clinch the diagnosis.

Management consists of airway support, broad-spectrum intravenous antibiotics until gram stains and cultures return (with particular attention to coverage against staphylococcal, streptococcal, and anaerobic organisms), and surgical drainage of abscesses.

Thyroiditis caused by radiation or trauma
One percent of patients develop thyroiditis after receiving radioactive iodine ablation for hyperthyroidism (Graves’ disease).⁴ This condition usually occurs 5 to 10 days after the treatment. Radiation triggers thyroid gland destruction, causing transient additional release of thyroid hormone. Similar damage occurs after external beam radiation for lymphomas and head and neck cancers. In such cases, use nonsteroidal anti-inflammatory drugs (NSAIDs) and prednisone to reduce inflammation and beta-blockers to control hyperthyroid symptoms.

Trauma to the thyroid—from motor vehicle accidents, falls, or physical assaults—can cause pain, tenderness, and abnormalities in thyroid hormone levels. Effects are usually self-limited, and management centers on airway protection and prevention of infection.

Subacute thyroiditis
The cause of ST is not clear. However, it typically follows an upper respiratory infection. Many viruses have been implicated in the disease, including Coxsackie, echo, adeno, and influenza viruses.⁵ It occurs more frequently during summer months, coinciding with the peak incidence of enterovirus.² ST is 4 times more common in women than men, and the median age for occurrence is 45.⁶

Patients with ST usually seek care for such symptoms as fever, myalgias, and malaise, which suggest a viral infection.^2,7-9 Neck pain is significant and may radiate to the jaw or ear.⁹ Patients may have pain on swallowing and a sore throat. It’s possible to confuse ST with severe pharyngitis or even epiglottitis if you fail to palpate the thyroid gland. When you examine the thyroid, the gland is exquisitely tender with ST. Patients with ST appear less ill than those with AST.

In 50% of ST patients, thyroid-stimulating hormone (TSH) is suppressed, and thyroid hormone levels are elevated.⁴ Patients with hyperthyroidism exhibit the usual signs and symptoms associated with high levels of the hormone: tremor, palpitations, heat intolerance, and diarrhea. After a few weeks, thyroid hormone levels normalize and then drop to below normal in the 4 to 6 months that follow. Levels return to normal in 95% of patients after 6 to 12 months. ST recurs in only 2% of patients.⁴

Sedimentation rates are almost always elevated in ST, reflecting the significant inflammation associated with the disease. Cytotoxic T lymphocytes damage thyroid follicles, causing release of preformed thyroid hormone, in turn suppressing TSH.⁴ Radioactive iodine scans show low uptake because TSH is needed for the uptake of iodine.¹⁰

Treatment of ST should focus on reducing inflammation and pain. NSAIDs may be sufficient, but patients with moderate to severe symptoms may require prednisone 40 mg daily, tapered over 4 to 6 weeks.² If the patient is hyperthyroid, you’ll need to control symptoms with beta-blockers.

Ruptured thyroid cyst: An ST look-alike
The clinical presentation of a ruptured cyst closely mimics that of ST: thyroid pain, history of a recent cold, sore throat, aches, and pains. Laboratory and nuclear medicine evaluations, however, reveal significant differences:

• TSH is not suppressed;
• ESR is not elevated;
• Radioactive iodine uptake is normal.

Palpation may reveal a thyroid nodule. You can confirm the diagnosis by ultrasound and a needle aspiration.

CASE The right diagnosis for Sam

Sam’s initial clinical presentation suggested St, and he was started on prednisone 40 mg daily to control his pain. but when laboratory and nuclear medicine evaluations became available the next day, the St diagnosis didn’t hold up: TSH, ESR, and radioactive iodine uptake were all normal.

When Sam came in for a follow-up visit 3 days later, his thyroid pain was gone and he was feeling much better. palpation of his thyroid revealed a slightly tender nodule that went undetected in the initial exam. Subsequent thyroid ultrasound showed a 2x2 cm nodule in the right lobe. a fine needle aspiration revealed a colloid cyst. the cyst had ruptured, causing acute pain from hemorrhage and inflammation.

CORRESPONDENCE Dean Gianakos, MD, 2323 Memorial Drive, #10, Lynchburg Family Medicine Residency, Lynchburg, VA 24501; [email protected]

CASE Sam J. is a 56-year-old man with a 2-day history of severe pain in the front of his neck. He aches all over and says he had “a bad cold” a week ago, but no fever, chills, cough, or headache. He hasn’t had a toothache or difficulty swallowing, but he does complain of a sore throat and muscle aches. His temperature is 100.7°f. He has no respiratory distress or stridor. there are no tonsillar exudates. the pharynx is not red or inflamed.

When you palpate his thyroid gland, you find diffuse tenderness. What could be causing his pain?

The patient with a painful thyroid is uncommon in clinical practice. In most cases, the culprit is a viral infection, radiation, or a traumatic injury to the gland. Bacterial, fungal, parasitic, or mycobacterial infections also occur, but these are rare, making up only 0.1% to 0.7% of all thyroid disease.¹ Some thyroid infections can be devastating, necessitating quick interventions including airway protection, intravenous antibiotics, and surgical drainage in certain situations.

Subacute thyroiditis (ST), the most common source of thyroid pain, is less severe, but can be disabling if not recognized and appropriately treated.² Occasionally, thyroid cysts can rupture, mimicking a presentation of ST.

This article will focus on how to evaluate the painful thyroid, so as to differentiate among the various conditions that can produce this uncommon presentation.

Classifying thyroiditis: Pain or no pain

Thyroiditis can be classified in several ways, but the simplest classification is in terms of pain. Conditions that can cause painless thyroiditis include Hashimoto’s disease, postpartum thyroiditis, subacute lymphocytic thyroiditis, Reidel’s thyroiditis, and thyroiditis induced by drugs such as amiodarone, interleukin-2, lithium, and interferon-alfa.³ Conditions that can cause painful thyroiditis include acute suppurative thyroiditis (AST), radiation-induced thyroiditis, trauma, ST, and ruptured cysts.¹

Acute suppurative thyroiditis
AST is a rare condition most commonly caused by bacterial, mycobacterial, fungal, or parasitic infection. The thyroid is remarkably resistant to infection because the gland is encapsulated, rich in iodide content, and has an abundant blood supply and lymphatic drainage.^1,2 AST usually occurs in patients with underlying thyroid disease, such as thyroid cancer, Hashimoto’s thyroiditis, multinodular goiter, congenital thyroid abnormalities such as pyriform sinus fistulas in children, and in patients who are immunocompromised.^1,2

Patients with AST are acutely ill and will complain of fever, dysphagia, and severe anterior neck pain. Stridor and tracheal obstruction may occur, requiring intubation or tracheotomy. Thyroid hormone levels are sometimes increased secondary to the release of preformed hormone from the intensely inflamed gland. Computed tomography (CT) or magnetic resonance imaging (MRI) thyroid scans can identify abscesses and guide biopsies that clinch the diagnosis.

Management consists of airway support, broad-spectrum intravenous antibiotics until gram stains and cultures return (with particular attention to coverage against staphylococcal, streptococcal, and anaerobic organisms), and surgical drainage of abscesses.

Thyroiditis caused by radiation or trauma
One percent of patients develop thyroiditis after receiving radioactive iodine ablation for hyperthyroidism (Graves’ disease).⁴ This condition usually occurs 5 to 10 days after the treatment. Radiation triggers thyroid gland destruction, causing transient additional release of thyroid hormone. Similar damage occurs after external beam radiation for lymphomas and head and neck cancers. In such cases, use nonsteroidal anti-inflammatory drugs (NSAIDs) and prednisone to reduce inflammation and beta-blockers to control hyperthyroid symptoms.

Trauma to the thyroid—from motor vehicle accidents, falls, or physical assaults—can cause pain, tenderness, and abnormalities in thyroid hormone levels. Effects are usually self-limited, and management centers on airway protection and prevention of infection.

Subacute thyroiditis
The cause of ST is not clear. However, it typically follows an upper respiratory infection. Many viruses have been implicated in the disease, including Coxsackie, echo, adeno, and influenza viruses.⁵ It occurs more frequently during summer months, coinciding with the peak incidence of enterovirus.² ST is 4 times more common in women than men, and the median age for occurrence is 45.⁶

Patients with ST usually seek care for such symptoms as fever, myalgias, and malaise, which suggest a viral infection.^2,7-9 Neck pain is significant and may radiate to the jaw or ear.⁹ Patients may have pain on swallowing and a sore throat. It’s possible to confuse ST with severe pharyngitis or even epiglottitis if you fail to palpate the thyroid gland. When you examine the thyroid, the gland is exquisitely tender with ST. Patients with ST appear less ill than those with AST.

In 50% of ST patients, thyroid-stimulating hormone (TSH) is suppressed, and thyroid hormone levels are elevated.⁴ Patients with hyperthyroidism exhibit the usual signs and symptoms associated with high levels of the hormone: tremor, palpitations, heat intolerance, and diarrhea. After a few weeks, thyroid hormone levels normalize and then drop to below normal in the 4 to 6 months that follow. Levels return to normal in 95% of patients after 6 to 12 months. ST recurs in only 2% of patients.⁴

Sedimentation rates are almost always elevated in ST, reflecting the significant inflammation associated with the disease. Cytotoxic T lymphocytes damage thyroid follicles, causing release of preformed thyroid hormone, in turn suppressing TSH.⁴ Radioactive iodine scans show low uptake because TSH is needed for the uptake of iodine.¹⁰

Treatment of ST should focus on reducing inflammation and pain. NSAIDs may be sufficient, but patients with moderate to severe symptoms may require prednisone 40 mg daily, tapered over 4 to 6 weeks.² If the patient is hyperthyroid, you’ll need to control symptoms with beta-blockers.

Ruptured thyroid cyst: An ST look-alike
The clinical presentation of a ruptured cyst closely mimics that of ST: thyroid pain, history of a recent cold, sore throat, aches, and pains. Laboratory and nuclear medicine evaluations, however, reveal significant differences:

• TSH is not suppressed;
• ESR is not elevated;
• Radioactive iodine uptake is normal.

Palpation may reveal a thyroid nodule. You can confirm the diagnosis by ultrasound and a needle aspiration.

CASE The right diagnosis for Sam

Sam’s initial clinical presentation suggested St, and he was started on prednisone 40 mg daily to control his pain. but when laboratory and nuclear medicine evaluations became available the next day, the St diagnosis didn’t hold up: TSH, ESR, and radioactive iodine uptake were all normal.

When Sam came in for a follow-up visit 3 days later, his thyroid pain was gone and he was feeling much better. palpation of his thyroid revealed a slightly tender nodule that went undetected in the initial exam. Subsequent thyroid ultrasound showed a 2x2 cm nodule in the right lobe. a fine needle aspiration revealed a colloid cyst. the cyst had ruptured, causing acute pain from hemorrhage and inflammation.

CORRESPONDENCE Dean Gianakos, MD, 2323 Memorial Drive, #10, Lynchburg Family Medicine Residency, Lynchburg, VA 24501; [email protected]

A new patient comes into your office and tells you he experiences labored breathing on exertion, smokes a pack of cigarettes a day, and has a smoker’s cough.

• Would you perform spirometry to gauge airway obstruction?
• How do you think your decision would compare with those of your colleagues?

In this article, we put your answer into context by revealing just how underutilized spirometry is.

We also use a progressive case example to illustrate evidence-based recommendations and management tips for chronic obstructive pulmonary disease (COPD) and address often overlooked gaps in care.

Many of the recommendations in this article come from the Global Initiative for Chronic Obstructive Lung Disease (GOLD), published in the American Journal of Respiratory and Critical Care Medicine¹ and updated online at www.goldcopd.org. (This initiative, begun in 1998, provides specific, evidence-based guidelines on the prevention, assessment, and management of COPD patients.) We also refer to newly published American College of Physicians (ACP) evidence-based guidelines for managing chronic, stable COPD.^2,3

CASE: Shortness of breath, smoker’s cough

Mr. Jones, a 57-year-old patient in our practice, says that for the past 3 months he has increasingly experienced shortness of breath when walking up a flight of stairs. He has smoked cigarettes for many years and also acknowledges having a smoker’s cough. He brings up clear phlegm on most days.

Dyspnea is the most common symptom reported by patients with COPD. In a study of 2678 patients, the first and most troublesome symptom noted was dyspnea (71%), followed by cough (19%).⁴ Patients typically say their dyspnea has worsened over time. It tends to occur daily, particularly with exercise. Cough may be intermittent and nonproductive.

Consider the diagnosis whenever a patient with dyspnea has a risk factor for COPD, such as smoking (~80% of cases); extended second-hand smoke exposure; contact with occupational dust, home cooking and heating fuels, or other potentially toxic chemicals; or has a history of recurrent lung infections.⁵ With patients in their 30s or 40s exhibiting signs and symptoms suggestive of COPD, consider a work-up for alpha-1 antitrypsin deficiency. (See “Does your patient have alpha-1 antitrypsin deficiency?”.)

Physical examination has limited usefulness. It exhibits poor sensitivity for detecting mild-to-moderate COPD, unless wheezing is present. Wheezing in smokers (more than 40 pack-years) has a positive likelihood ratio of 8.3 for obstructive airway disease.⁶

Physical diagnosis is easier with more severe disease, especially if patients show classic signs of COPD, such as pursed-lip breathing, decreased breath sounds, and prolonged expiratory wheezes.

Spirometry is key, and underused. Demonstrating airflow obstruction on spirometry is essential to a COPD diagnosis. An FEV₁/FVC ratio <0.70 or FEV₁ <80% in patients who have received a test-bronchodilator confirms airflow obstruction.

Amazingly, a COPD diagnosis is assigned to less than half of the estimated 24 million patients with airflow obstruction in United States,⁷ despite the fact that COPD is the 4th leading cause of death, and the 12th leading cause of morbidity.¹ Most of those who are identified have advanced disease.⁸ This dramatic underdiagnosis is attributable to the underuse of office spirometry as a diagnostic tool.⁹

A Canadian study revealed that only 21% of physicians ordered spirometry when managing a middle-aged smoker with cough.^10,11 Another study showed that only 22% of North American physicians would order spirometry for a smoker with cough.^10,12 Only a third of patients had undergone spirometry within 2 years of a new diagnosis of COPD. The lowest frequency of testing was among elderly patients, especially among those older than 75 years.¹⁰ (Caveat: as patients age, FEV₁ naturally declines, making it easy to overdiagnose airflow obstruction in elderly patients.^8,13)

The above data regarding underuse of spirometry apply to symptomatic patients. A recent US Preventive Services Task Force analysis found that screening asymptomatic smokers does not improve health outcomes; the number needed to test with spirometry would be in the “hundreds” to defer a single exacerbation.⁹ (ACP grade: strong recommendation, moderate-quality evidence.)

Reserve chest radiographs and CT scans to rule out other disorders. Patients with COPD usually have elements of both chronic bronchitis (productive cough for 3 months in 2 consecutive years) and emphysema (defined anatomically as abnormal enlargement of airways distal to terminal bronchioles and destruction of alveolar walls). Radiographic tests may reveal the telltale signs of emphysema (flattened diaphragms, blebs, and bullous changes), but they are not necessary to make the diagnosis. They may be used, however, to exclude other causes of dyspnea, including congestive heart failure, pulmonary emboli, and interstitial lung disease (TABLE).

Managing stable COPD: ACP recommendations at a glance*

Recommendation 1 With patients who have respiratory symptoms, particularly dyspnea, perform spirometry to diagnose airflow obstruction. Spirometry should not be used to screen for airflow obstruction in asymptomatic individuals. (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 2 Reserve treatment for patients who have respiratory symptoms and an FEV₁ <60% predicted, as documented by spirometry. (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 3 Prescribe 1 of the following maintenance monotherapies for symptomatic patients with COPD and an FEV₁ <60% predicted: long-acting inhaled beta-agonists, long-acting inhaled anticholinergics, or inhaled corticosteroids. (Grade: strong recommendation, high-quality evidence.)

Recommendation 4 You may want to consider combination inhaled therapies for symptomatic patients with COPD and an FEV₁ <60% predicted. (Grade: weak recommendation, moderate-quality evidence.)

Recommendation 5 Prescribe oxygen therapy for patients with COPD and resting hypoxemia (PaO₂ ≤55 mm Hg). (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 6 Consider prescribing pulmonary rehabilitation for symptomatic individuals with COPD who have an FEV₁ <50% predicted. (Grade: weak recommendation, moderate-quality evidence.)

* Modified from Qaseem A et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2007;147:633-638.

TABLE
Suspect COPD? Rule out these disorders

CASE: Spirometry reveals airflow obstruction, FEV₁ <50%

Mr. Jones underwent spirometry, which revealed airflow obstruction and an FEV₁ <50%. We gave him a short-acting betaagonist to be used as needed. Two weeks later, he returned to the office with increasing cough and purulent sputum production, as well as worsening dyspnea.

The patient’s condition is consistent with an acute exacerbation of baseline COPD symptoms. Worsening dyspnea, cough, and sputum production—sometimes with purulence—are often accompanied by fever, fatigue, and anorexia.⁷

Match antibiotic therapy to sputum culture results or disease severity. Exacerbations are usually triggered by infection. Although an offending organism cannot be identified in one third of cases, common bacterial pathogens include Hemophilus influenza, Streptococcus pneumoniae, and Moraxella catarrhalis. Antibiotics have been shown to decrease mortality in patients with COPD exacerbations^1,5,7,14,15 (GOLD Evidence B). For mild-to-moderate exacerbations, older antibiotics such as trimethoprim/sulfamethoxazole or doxycycline are often appropriate. For more severe exacerbations, and for patients with chronic, comorbid conditions such as diabetes mellitus, a second- or third-generation cephalosporin or fluoroquinolone may be preferable.

Use steroids and beta-agonists. Oral steroids are also effective in treating exacerbations (GOLD Evidence A), although the dose of steroids required has not been adequately studied. Prednisone, 40 mg/d for 7 to 10 days, is reasonable and safe.¹ Also prescribe an inhaled short-acting beta-agonist for symptom control (GOLD Evidence A).¹

CASE: Doxycycline 100 mg bid, and prednisone 40 mg/d for 7 days

Mr. Jones returned to the office 2 weeks after the acute exacerbation, feeling much better after receiving doxycycline 100 mg bid and prednisone 40 mg/d for 7 days. He was no longer coughing up purulent sputum, but he still felt short of breath walking to his mailbox and while doing household chores. He wondered what else could be done to improve his quality of life.

The airflow obstruction associated with COPD, unlike that of asthma, is irreversible and varies little,¹⁶ and its progression is persistent. That is why prevention is an important goal for physicians and their patients. However, treatment can lessen the frequency of exacerbations and severity of symptoms, particularly dyspnea on exertion.

In our initial assessment of the patient, his FEV₁ was <50%. There was no need to repeat spirometry, as the evidence does not support ongoing spirometric evaluation.^2,3 Symptomatic patients with significant airflow obstruction (FEV₁ <60% predicted) are the ones most likely to benefit from therapy (ACP grade: strong recommendation, moderate-quality evidence).^2,3 Conversely, there is little evidence to justify treating asymptomatic patients who have airflow obstruction.

Monotherapy with long-acting inhaled beta-agonists, inhaled corticosteroids, or long-acting inhaled anticholinergics has been shown to reduce exacerbations and is preferable to short-acting, inhaled beta-agonists or short-acting anticholinergics (ACP grade: strong recommendation, high-quality evidence).^2,3 At this time, evidence is insufficient to support the use of combined therapies—eg, inhaled steroids plus long-acting beta-agonists.^2,3

For patients with a PaO₂ ≤55 mm Hg, survival is improved by using supplemental oxygen therapy for 15 or more hours a day. (ACP grade: strong recommendation, moderate quality evidence).^2,3

Finally, for symptomatic patients with an FEV₁ <50%, pulmonary rehabilitation may reduce hospitalizations and increase exercise capacity (ACP grade: weak recommendation, moderate-quality evidence).^2,3

For Mr. Jones, we prescribed 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium.

Smoking cessation critical

COPD progresses with aging and with continued smoking, and smoking cessation is critical to any management strategy.

CASE: Tiotropium, 1 inhalation daily, and a smoking cessation plan

We referred Mr. Jones to an outpatient smoking cessation program and gave him American Academy of Family Physicians patient education materials to review. His exercise tolerance improved with 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium, and he is making progress in his efforts to quit smoking.

Correspondence
Dean Gianakos, MD, Lynchburg Family Medicine Residency, 2097 Langhorne Road, Lynchburg, VA 24501; [email protected]

A new patient comes into your office and tells you he experiences labored breathing on exertion, smokes a pack of cigarettes a day, and has a smoker’s cough.

• Would you perform spirometry to gauge airway obstruction?
• How do you think your decision would compare with those of your colleagues?

In this article, we put your answer into context by revealing just how underutilized spirometry is.

We also use a progressive case example to illustrate evidence-based recommendations and management tips for chronic obstructive pulmonary disease (COPD) and address often overlooked gaps in care.

Many of the recommendations in this article come from the Global Initiative for Chronic Obstructive Lung Disease (GOLD), published in the American Journal of Respiratory and Critical Care Medicine¹ and updated online at www.goldcopd.org. (This initiative, begun in 1998, provides specific, evidence-based guidelines on the prevention, assessment, and management of COPD patients.) We also refer to newly published American College of Physicians (ACP) evidence-based guidelines for managing chronic, stable COPD.^2,3

CASE: Shortness of breath, smoker’s cough

Mr. Jones, a 57-year-old patient in our practice, says that for the past 3 months he has increasingly experienced shortness of breath when walking up a flight of stairs. He has smoked cigarettes for many years and also acknowledges having a smoker’s cough. He brings up clear phlegm on most days.

Dyspnea is the most common symptom reported by patients with COPD. In a study of 2678 patients, the first and most troublesome symptom noted was dyspnea (71%), followed by cough (19%).⁴ Patients typically say their dyspnea has worsened over time. It tends to occur daily, particularly with exercise. Cough may be intermittent and nonproductive.

Consider the diagnosis whenever a patient with dyspnea has a risk factor for COPD, such as smoking (~80% of cases); extended second-hand smoke exposure; contact with occupational dust, home cooking and heating fuels, or other potentially toxic chemicals; or has a history of recurrent lung infections.⁵ With patients in their 30s or 40s exhibiting signs and symptoms suggestive of COPD, consider a work-up for alpha-1 antitrypsin deficiency. (See “Does your patient have alpha-1 antitrypsin deficiency?”.)

Physical examination has limited usefulness. It exhibits poor sensitivity for detecting mild-to-moderate COPD, unless wheezing is present. Wheezing in smokers (more than 40 pack-years) has a positive likelihood ratio of 8.3 for obstructive airway disease.⁶

Physical diagnosis is easier with more severe disease, especially if patients show classic signs of COPD, such as pursed-lip breathing, decreased breath sounds, and prolonged expiratory wheezes.

Spirometry is key, and underused. Demonstrating airflow obstruction on spirometry is essential to a COPD diagnosis. An FEV₁/FVC ratio <0.70 or FEV₁ <80% in patients who have received a test-bronchodilator confirms airflow obstruction.

Amazingly, a COPD diagnosis is assigned to less than half of the estimated 24 million patients with airflow obstruction in United States,⁷ despite the fact that COPD is the 4th leading cause of death, and the 12th leading cause of morbidity.¹ Most of those who are identified have advanced disease.⁸ This dramatic underdiagnosis is attributable to the underuse of office spirometry as a diagnostic tool.⁹

A Canadian study revealed that only 21% of physicians ordered spirometry when managing a middle-aged smoker with cough.^10,11 Another study showed that only 22% of North American physicians would order spirometry for a smoker with cough.^10,12 Only a third of patients had undergone spirometry within 2 years of a new diagnosis of COPD. The lowest frequency of testing was among elderly patients, especially among those older than 75 years.¹⁰ (Caveat: as patients age, FEV₁ naturally declines, making it easy to overdiagnose airflow obstruction in elderly patients.^8,13)

The above data regarding underuse of spirometry apply to symptomatic patients. A recent US Preventive Services Task Force analysis found that screening asymptomatic smokers does not improve health outcomes; the number needed to test with spirometry would be in the “hundreds” to defer a single exacerbation.⁹ (ACP grade: strong recommendation, moderate-quality evidence.)

Reserve chest radiographs and CT scans to rule out other disorders. Patients with COPD usually have elements of both chronic bronchitis (productive cough for 3 months in 2 consecutive years) and emphysema (defined anatomically as abnormal enlargement of airways distal to terminal bronchioles and destruction of alveolar walls). Radiographic tests may reveal the telltale signs of emphysema (flattened diaphragms, blebs, and bullous changes), but they are not necessary to make the diagnosis. They may be used, however, to exclude other causes of dyspnea, including congestive heart failure, pulmonary emboli, and interstitial lung disease (TABLE).

Managing stable COPD: ACP recommendations at a glance*

Recommendation 1 With patients who have respiratory symptoms, particularly dyspnea, perform spirometry to diagnose airflow obstruction. Spirometry should not be used to screen for airflow obstruction in asymptomatic individuals. (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 2 Reserve treatment for patients who have respiratory symptoms and an FEV₁ <60% predicted, as documented by spirometry. (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 3 Prescribe 1 of the following maintenance monotherapies for symptomatic patients with COPD and an FEV₁ <60% predicted: long-acting inhaled beta-agonists, long-acting inhaled anticholinergics, or inhaled corticosteroids. (Grade: strong recommendation, high-quality evidence.)

Recommendation 4 You may want to consider combination inhaled therapies for symptomatic patients with COPD and an FEV₁ <60% predicted. (Grade: weak recommendation, moderate-quality evidence.)

Recommendation 5 Prescribe oxygen therapy for patients with COPD and resting hypoxemia (PaO₂ ≤55 mm Hg). (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 6 Consider prescribing pulmonary rehabilitation for symptomatic individuals with COPD who have an FEV₁ <50% predicted. (Grade: weak recommendation, moderate-quality evidence.)

* Modified from Qaseem A et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2007;147:633-638.

TABLE
Suspect COPD? Rule out these disorders

CASE: Spirometry reveals airflow obstruction, FEV₁ <50%

Mr. Jones underwent spirometry, which revealed airflow obstruction and an FEV₁ <50%. We gave him a short-acting betaagonist to be used as needed. Two weeks later, he returned to the office with increasing cough and purulent sputum production, as well as worsening dyspnea.

The patient’s condition is consistent with an acute exacerbation of baseline COPD symptoms. Worsening dyspnea, cough, and sputum production—sometimes with purulence—are often accompanied by fever, fatigue, and anorexia.⁷

Match antibiotic therapy to sputum culture results or disease severity. Exacerbations are usually triggered by infection. Although an offending organism cannot be identified in one third of cases, common bacterial pathogens include Hemophilus influenza, Streptococcus pneumoniae, and Moraxella catarrhalis. Antibiotics have been shown to decrease mortality in patients with COPD exacerbations^1,5,7,14,15 (GOLD Evidence B). For mild-to-moderate exacerbations, older antibiotics such as trimethoprim/sulfamethoxazole or doxycycline are often appropriate. For more severe exacerbations, and for patients with chronic, comorbid conditions such as diabetes mellitus, a second- or third-generation cephalosporin or fluoroquinolone may be preferable.

Use steroids and beta-agonists. Oral steroids are also effective in treating exacerbations (GOLD Evidence A), although the dose of steroids required has not been adequately studied. Prednisone, 40 mg/d for 7 to 10 days, is reasonable and safe.¹ Also prescribe an inhaled short-acting beta-agonist for symptom control (GOLD Evidence A).¹

CASE: Doxycycline 100 mg bid, and prednisone 40 mg/d for 7 days

Mr. Jones returned to the office 2 weeks after the acute exacerbation, feeling much better after receiving doxycycline 100 mg bid and prednisone 40 mg/d for 7 days. He was no longer coughing up purulent sputum, but he still felt short of breath walking to his mailbox and while doing household chores. He wondered what else could be done to improve his quality of life.

The airflow obstruction associated with COPD, unlike that of asthma, is irreversible and varies little,¹⁶ and its progression is persistent. That is why prevention is an important goal for physicians and their patients. However, treatment can lessen the frequency of exacerbations and severity of symptoms, particularly dyspnea on exertion.

In our initial assessment of the patient, his FEV₁ was <50%. There was no need to repeat spirometry, as the evidence does not support ongoing spirometric evaluation.^2,3 Symptomatic patients with significant airflow obstruction (FEV₁ <60% predicted) are the ones most likely to benefit from therapy (ACP grade: strong recommendation, moderate-quality evidence).^2,3 Conversely, there is little evidence to justify treating asymptomatic patients who have airflow obstruction.

Monotherapy with long-acting inhaled beta-agonists, inhaled corticosteroids, or long-acting inhaled anticholinergics has been shown to reduce exacerbations and is preferable to short-acting, inhaled beta-agonists or short-acting anticholinergics (ACP grade: strong recommendation, high-quality evidence).^2,3 At this time, evidence is insufficient to support the use of combined therapies—eg, inhaled steroids plus long-acting beta-agonists.^2,3

For patients with a PaO₂ ≤55 mm Hg, survival is improved by using supplemental oxygen therapy for 15 or more hours a day. (ACP grade: strong recommendation, moderate quality evidence).^2,3

Finally, for symptomatic patients with an FEV₁ <50%, pulmonary rehabilitation may reduce hospitalizations and increase exercise capacity (ACP grade: weak recommendation, moderate-quality evidence).^2,3

For Mr. Jones, we prescribed 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium.

Smoking cessation critical

COPD progresses with aging and with continued smoking, and smoking cessation is critical to any management strategy.

CASE: Tiotropium, 1 inhalation daily, and a smoking cessation plan

We referred Mr. Jones to an outpatient smoking cessation program and gave him American Academy of Family Physicians patient education materials to review. His exercise tolerance improved with 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium, and he is making progress in his efforts to quit smoking.

Correspondence
Dean Gianakos, MD, Lynchburg Family Medicine Residency, 2097 Langhorne Road, Lynchburg, VA 24501; [email protected]

A new patient comes into your office and tells you he experiences labored breathing on exertion, smokes a pack of cigarettes a day, and has a smoker’s cough.

• Would you perform spirometry to gauge airway obstruction?
• How do you think your decision would compare with those of your colleagues?

In this article, we put your answer into context by revealing just how underutilized spirometry is.

We also use a progressive case example to illustrate evidence-based recommendations and management tips for chronic obstructive pulmonary disease (COPD) and address often overlooked gaps in care.

Many of the recommendations in this article come from the Global Initiative for Chronic Obstructive Lung Disease (GOLD), published in the American Journal of Respiratory and Critical Care Medicine¹ and updated online at www.goldcopd.org. (This initiative, begun in 1998, provides specific, evidence-based guidelines on the prevention, assessment, and management of COPD patients.) We also refer to newly published American College of Physicians (ACP) evidence-based guidelines for managing chronic, stable COPD.^2,3

CASE: Shortness of breath, smoker’s cough

Mr. Jones, a 57-year-old patient in our practice, says that for the past 3 months he has increasingly experienced shortness of breath when walking up a flight of stairs. He has smoked cigarettes for many years and also acknowledges having a smoker’s cough. He brings up clear phlegm on most days.

Dyspnea is the most common symptom reported by patients with COPD. In a study of 2678 patients, the first and most troublesome symptom noted was dyspnea (71%), followed by cough (19%).⁴ Patients typically say their dyspnea has worsened over time. It tends to occur daily, particularly with exercise. Cough may be intermittent and nonproductive.

Consider the diagnosis whenever a patient with dyspnea has a risk factor for COPD, such as smoking (~80% of cases); extended second-hand smoke exposure; contact with occupational dust, home cooking and heating fuels, or other potentially toxic chemicals; or has a history of recurrent lung infections.⁵ With patients in their 30s or 40s exhibiting signs and symptoms suggestive of COPD, consider a work-up for alpha-1 antitrypsin deficiency. (See “Does your patient have alpha-1 antitrypsin deficiency?”.)

Physical examination has limited usefulness. It exhibits poor sensitivity for detecting mild-to-moderate COPD, unless wheezing is present. Wheezing in smokers (more than 40 pack-years) has a positive likelihood ratio of 8.3 for obstructive airway disease.⁶

Physical diagnosis is easier with more severe disease, especially if patients show classic signs of COPD, such as pursed-lip breathing, decreased breath sounds, and prolonged expiratory wheezes.

Spirometry is key, and underused. Demonstrating airflow obstruction on spirometry is essential to a COPD diagnosis. An FEV₁/FVC ratio <0.70 or FEV₁ <80% in patients who have received a test-bronchodilator confirms airflow obstruction.

Amazingly, a COPD diagnosis is assigned to less than half of the estimated 24 million patients with airflow obstruction in United States,⁷ despite the fact that COPD is the 4th leading cause of death, and the 12th leading cause of morbidity.¹ Most of those who are identified have advanced disease.⁸ This dramatic underdiagnosis is attributable to the underuse of office spirometry as a diagnostic tool.⁹

A Canadian study revealed that only 21% of physicians ordered spirometry when managing a middle-aged smoker with cough.^10,11 Another study showed that only 22% of North American physicians would order spirometry for a smoker with cough.^10,12 Only a third of patients had undergone spirometry within 2 years of a new diagnosis of COPD. The lowest frequency of testing was among elderly patients, especially among those older than 75 years.¹⁰ (Caveat: as patients age, FEV₁ naturally declines, making it easy to overdiagnose airflow obstruction in elderly patients.^8,13)

The above data regarding underuse of spirometry apply to symptomatic patients. A recent US Preventive Services Task Force analysis found that screening asymptomatic smokers does not improve health outcomes; the number needed to test with spirometry would be in the “hundreds” to defer a single exacerbation.⁹ (ACP grade: strong recommendation, moderate-quality evidence.)

Reserve chest radiographs and CT scans to rule out other disorders. Patients with COPD usually have elements of both chronic bronchitis (productive cough for 3 months in 2 consecutive years) and emphysema (defined anatomically as abnormal enlargement of airways distal to terminal bronchioles and destruction of alveolar walls). Radiographic tests may reveal the telltale signs of emphysema (flattened diaphragms, blebs, and bullous changes), but they are not necessary to make the diagnosis. They may be used, however, to exclude other causes of dyspnea, including congestive heart failure, pulmonary emboli, and interstitial lung disease (TABLE).

Managing stable COPD: ACP recommendations at a glance*

Recommendation 1 With patients who have respiratory symptoms, particularly dyspnea, perform spirometry to diagnose airflow obstruction. Spirometry should not be used to screen for airflow obstruction in asymptomatic individuals. (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 2 Reserve treatment for patients who have respiratory symptoms and an FEV₁ <60% predicted, as documented by spirometry. (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 3 Prescribe 1 of the following maintenance monotherapies for symptomatic patients with COPD and an FEV₁ <60% predicted: long-acting inhaled beta-agonists, long-acting inhaled anticholinergics, or inhaled corticosteroids. (Grade: strong recommendation, high-quality evidence.)

Recommendation 4 You may want to consider combination inhaled therapies for symptomatic patients with COPD and an FEV₁ <60% predicted. (Grade: weak recommendation, moderate-quality evidence.)

Recommendation 5 Prescribe oxygen therapy for patients with COPD and resting hypoxemia (PaO₂ ≤55 mm Hg). (Grade: strong recommendation, moderate-quality evidence.)

Recommendation 6 Consider prescribing pulmonary rehabilitation for symptomatic individuals with COPD who have an FEV₁ <50% predicted. (Grade: weak recommendation, moderate-quality evidence.)

* Modified from Qaseem A et al. Diagnosis and management of stable chronic obstructive pulmonary disease: a clinical practice guideline from the American College of Physicians. Ann Intern Med. 2007;147:633-638.

TABLE
Suspect COPD? Rule out these disorders

CASE: Spirometry reveals airflow obstruction, FEV₁ <50%

Mr. Jones underwent spirometry, which revealed airflow obstruction and an FEV₁ <50%. We gave him a short-acting betaagonist to be used as needed. Two weeks later, he returned to the office with increasing cough and purulent sputum production, as well as worsening dyspnea.

The patient’s condition is consistent with an acute exacerbation of baseline COPD symptoms. Worsening dyspnea, cough, and sputum production—sometimes with purulence—are often accompanied by fever, fatigue, and anorexia.⁷

Match antibiotic therapy to sputum culture results or disease severity. Exacerbations are usually triggered by infection. Although an offending organism cannot be identified in one third of cases, common bacterial pathogens include Hemophilus influenza, Streptococcus pneumoniae, and Moraxella catarrhalis. Antibiotics have been shown to decrease mortality in patients with COPD exacerbations^1,5,7,14,15 (GOLD Evidence B). For mild-to-moderate exacerbations, older antibiotics such as trimethoprim/sulfamethoxazole or doxycycline are often appropriate. For more severe exacerbations, and for patients with chronic, comorbid conditions such as diabetes mellitus, a second- or third-generation cephalosporin or fluoroquinolone may be preferable.

Use steroids and beta-agonists. Oral steroids are also effective in treating exacerbations (GOLD Evidence A), although the dose of steroids required has not been adequately studied. Prednisone, 40 mg/d for 7 to 10 days, is reasonable and safe.¹ Also prescribe an inhaled short-acting beta-agonist for symptom control (GOLD Evidence A).¹

CASE: Doxycycline 100 mg bid, and prednisone 40 mg/d for 7 days

Mr. Jones returned to the office 2 weeks after the acute exacerbation, feeling much better after receiving doxycycline 100 mg bid and prednisone 40 mg/d for 7 days. He was no longer coughing up purulent sputum, but he still felt short of breath walking to his mailbox and while doing household chores. He wondered what else could be done to improve his quality of life.

The airflow obstruction associated with COPD, unlike that of asthma, is irreversible and varies little,¹⁶ and its progression is persistent. That is why prevention is an important goal for physicians and their patients. However, treatment can lessen the frequency of exacerbations and severity of symptoms, particularly dyspnea on exertion.

In our initial assessment of the patient, his FEV₁ was <50%. There was no need to repeat spirometry, as the evidence does not support ongoing spirometric evaluation.^2,3 Symptomatic patients with significant airflow obstruction (FEV₁ <60% predicted) are the ones most likely to benefit from therapy (ACP grade: strong recommendation, moderate-quality evidence).^2,3 Conversely, there is little evidence to justify treating asymptomatic patients who have airflow obstruction.

Monotherapy with long-acting inhaled beta-agonists, inhaled corticosteroids, or long-acting inhaled anticholinergics has been shown to reduce exacerbations and is preferable to short-acting, inhaled beta-agonists or short-acting anticholinergics (ACP grade: strong recommendation, high-quality evidence).^2,3 At this time, evidence is insufficient to support the use of combined therapies—eg, inhaled steroids plus long-acting beta-agonists.^2,3

For patients with a PaO₂ ≤55 mm Hg, survival is improved by using supplemental oxygen therapy for 15 or more hours a day. (ACP grade: strong recommendation, moderate quality evidence).^2,3

Finally, for symptomatic patients with an FEV₁ <50%, pulmonary rehabilitation may reduce hospitalizations and increase exercise capacity (ACP grade: weak recommendation, moderate-quality evidence).^2,3

For Mr. Jones, we prescribed 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium.

Smoking cessation critical

COPD progresses with aging and with continued smoking, and smoking cessation is critical to any management strategy.

CASE: Tiotropium, 1 inhalation daily, and a smoking cessation plan

We referred Mr. Jones to an outpatient smoking cessation program and gave him American Academy of Family Physicians patient education materials to review. His exercise tolerance improved with 1 inhalation daily of the long-acting anticholinergic inhaler, tiotropium, and he is making progress in his efforts to quit smoking.

Correspondence
Dean Gianakos, MD, Lynchburg Family Medicine Residency, 2097 Langhorne Road, Lynchburg, VA 24501; [email protected]