Bethany Rettberg, NPC

Although patients over age 65 years are most at risk for severe complications related to COVID-19, data show that about 20% of deaths were within the 20-to-64 age group, which is higher than originally expected, and smoking and vaping can worsen the disease.

Person-to-person spread of COVID-19 has occurred throughout the world.

Coughing, fever, and shortness of breath are the hallmark symptoms noted in the majority of patients.

COVID-19 affects the lower respiratory tract, so those patients with chronic cardiovascular and lung disease are at high risk for complications of the disease.

Smoking and vaping have been shown to lead to chronic lung disease, such as chronic obstructive pulmonary disease.

In 2018, 7.6% of adults aged 18 to 24 and 4.2% of adults aged 25 to 44 used e-cigarettes daily.

This past fall and summer saw an outbreak of respiratory disease in the United States associated with e-cigarette or vaping product use. Vitamin E acetate was found to be one of the offending additives that cause alveoli thickening and exudate production in these patients’ lungs.

Vaporized e-cigarette fluid and smoke from conventional cigarettes are cytotoxic, pro-inflammatory, and inhibit phagocytosis in alveolar macrophages. Detection and phagocytosis of pathogens is a primary function of alveolar macrophages. It is usually these cells that initiate an immune response to infection in the airways. Therefore, any reduction in phagocytosis from cigarette smoke or e-cigarette vapor can decrease individuals’ innate immune response.

That means that it is not much of a stretch to hypothesize that patients who smoke and/or vape may have more serious consequences from COVID-19 than patients who do not smoke and/or vape.

With more fatalities in the 20-to-64-year-old age group from COVID-19 than originally expected, more studies are needed to look at a connection between smoking and/or vaping and the risk of severe illness from COVID-19. One study has been released from China analyzing the factors associated with COVID-19 disease outcomes. The study results showed that the proportion of patients with a history of smoking was significantly higher in the “progression” group (patients that advanced with more serious complications of the disease) than the “improvement/stabilization” group (patients with mild to moderate symptoms of the disease). This suggests that smoking is associated with disease progression.

As the world grapples with this disease and attempts to contain it, all health care providers should discuss smoking cessation with patients who smoke or vape and the additional threat that COVID-19 poses for them.

Bethany Rettberg, NPC, is a family nurse practitioner at CVS MinuteClinic in Mokena, Illinois.

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Articles

These poor health choices can lead to disease progression, even among younger people, for those who have the coronavirus.

Smoking or Vaping Increases COVID-19 Risks

Cigarette smoking is the leading cause of preventable death and disease in the United States, accounting for about 1 in every 5 deaths per year.

Conventional cigarette smoking has decreased in recent years, with nearly 21% of the US population reporting cigarette use in 2005 and 14% in 2017.

When a patient or provider makes the decision to quit smoking, it is critical to address not only the benefits of smoking cessation but the challenges that lie ahead. The better prepared the individual, the more likely he or she is to succeed at quitting.

The first consideration is how quitting smoking affects the body and its functions. Here is a rundown:

Blood pressure (BP) and pulse decrease back to a normal range.

The risk of myocardial infarction begins to decrease. Smoking lowers high-density lipoprotein cholesterol, raising the risk of coronary artery disease. BP also continues to drop to a normal level.

The sense of smell and taste begin to return, as the nerve endings damaged by smoking begin to heal. The lung’s cilia are also healing and starting to resume their function of sweeping debris and mucous out of the alveolar spaces.

After 3 days of not smoking, the nicotine levels in the body are completely depleted. Breathing is easier, and energy levels have increased, because of the return of normal blood flow.

Lung function continues to improve. Former smokers will notice less coughing and shortness of breath. Athletic endurance increases, and circulation continues to improve.

The cilia have completely recovered from the paralyzing toxins found in cigarette smoke, and the lungs have significantly healed themselves. Former smokers may, therefore, notice a decrease in the frequency of lung infections.

The risk for coronary artery disease has decreased by half and will continue to decrease past the 1-year mark.

The chances of a stroke are now the same as a nonsmoker. Toxins in cigarettes cause blood vessels to constrict and increase the likelihood of developing blood clots. At this point, the former smoker’s blood vessels have dilated back within a normal range that reduces the risk for stroke. Cervical cancer risk has also decreased to the level of a nonsmoker. Risk for cancer of the bladder, esophagus, mouth, and throat have been cut in half.

Lung cancer risk decreases by half, while the risk of laryngeal and pancreatic cancers also significantly decline.

After 15 years of not smoking the chances of coronary artery disease are the same as someone who has never smoked. Similarly, the risk of developing pancreatic cancer has reduced to the same level as a non-smoker.

The second consideration when reviewing what to expect when a smoker quits is the pathophysiological and psychological addiction to nicotine. Nicotine addiction changes the brain landscape.

Smokers inhale nicotine from a cigarette, where it is quickly absorbed in the lungs and travels to the brain. Once in the brain, it binds to nicotinic cholinergic receptors. Stimulation of these receptors releases a variety of neurotransmitters, including dopamine, which signals a pleasurable experience and is critical for reinforcing the effects of nicotine. Receptor activation also results in the development of new neural circuits, also known as neural plasticity, and, in association with environmental cues, behavioral conditioning.

When a person who is addicted to nicotine stops smoking, the urge to relapse is persistent and far outlasts physiological withdrawal symptoms. With regular smoking, the smoker comes to associate specific environmental factors, moods, or situations with the rewarding effects of nicotine.

Too often, these cues can lead to a relapse. Educating the smoker on these conditioned pitfalls can help prepare them for successfully quitting. Print out the

for patients who want are trying to kick the habit.

Call or text someone. Lean on trusted people. You do not have to do this alone.

Download a free application that can help track cravings and provide understanding of smoking patterns (smokefree.gov).

Talk to an expert, such as a primary-care provider or a retail health provider.

Remember the reasons for quitting, such as family and health.

Calculate the savings. Add up the money saved by not smoking, and think of something rewarding to do with it. This is a great way to stay motivated while a craving passes (smokefree.gov/quit-smoking/why-you-should-quit/how-much-will-you-save).

Chew gum, sip from a water bottle, or suck on a cinnamon stick, hard candy, or a straw to keep your mouth busy and mimic smoking.

Go for a jog or walk. Go up and down the stairs a few times. Physical activity, even in short bursts, can help beat a craving.

Meditate. Take 10 deep, slow breaths to calm anxiety and center yourself. Repeat 10 times or until the craving passes. Most cravings last 5 to 10 minutes. Remember this to push through.

Switch to doing something else as soon as a craving hits. Simply changing a routine can help eliminate the craving.

Visit a public place. Most public places do not allow smoking. Go to a movie, store, or other place where smoking is not allowed.

There are many forms, such as gum, lozenges, and patches. These can help with frequent cravings, but try to use them as a last resort. The goal is to change the behavior, so try to focus on interventions that do not use nicotine dependence as a crutch.

Help out a co-worker, family member, or friend. This shifts the focus to someone else and their needs instead of the craving.

is a family nurse practitioner at a CVS Minute Clinic in Mokena, Illinois.

The health consequences of smoking—50 years of progress: a report of the surgeon general. National Center for Chronic Disease Prevention and Health Promotion (US) Office on Smoking and Health. Atlanta (GA): Centers for Disease Control and Prevention (US); 2014.

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National Institutes of Health. How to manage cravings. Smokefree.gov website.

smokefree.gov/challenges-when-quitting/cravings-triggers/how-manage-cravings

When a patient or provider makes the decision to quit smoking, it is critical to address not only the benefits of smoking cessation but the challenges that lie ahead. 

What Should Smokers Expect When Quitting?

Chronic obstructive pulmonary disease (COPD) is a common respiratory condition that affects more than 5% of the population.

Associated with high morbidity and mortality, it is the third-ranked cause of death in the United States.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines the condition as follows:

“COPD is a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.”

Because of the chronic nature and high prevalence of COPD, patients suffering from this disease use a lot of resources, including chronic therapies, such as inhalers and oxygen; frequent clinician office visits; and recurrent hospitalizations, because of acute exacerbations.

These patients can present toclinics in an acute exacerbation or with stable disease or undiagnosed symptoms. As front-line providers it is imperative that clinicians  triage these patients efficiently so that care is neither delayed nor misguided.

The majority of pathological changes that occur as a result of COPD include airway collapse, because of the loss of tethering caused by alveolar wall destruction in emphysema; chronic inflammation; fibrosis; increased number of goblet cells; mucus gland hyperplasia; and narrowing and reduction in the number of small airways.

As a result, the 3 cardinal symptoms of COPD are chronic cough, dyspnea, and sputum production, with the most common early symptom being exertional dyspnea.

Patients who lead sedentary lifestyles require careful history questioning. Some patients unknowingly avoid exertional dyspnea by shifting their expectations and limiting their activity.

Evaluating a patient for COPD includes not only assessing for these main symptoms but also risk factors. Risk factors for COPD include biomass fuel exposure, cigarette smoking, and exposure to secondhand smoke.

Eighty percent of patients diagnosed with COPD have a history of smoking, and identifying the number of pack years smoked (packs of cigarettes per day multiplied by the number of years) is significant for the patient’s evaluation. The amount and duration of smoking usually dictates the severity of the disease.

The physical exam findings vary with the severity of the COPD. In early disease, the respiratory exam may only show prolonged expiration or wheezes with forced exhalation, if anything abnormal at all. As the disease progresses and airway obstruction becomes more significant, a physical exam may show crackles at the lung bases, decreased breath sounds, distant heart sounds, hyperinflation, and/or wheezing.

End-stage COPD will force the patient to adopt positions that relieve dyspnea, such as the tripod position (patient leans forward and supports weight on outstretched arms/palms). Other physical exam findings at this stage include breathing through pursed lips and using accessory respiratory muscles of the neck and shoulders.

Practitioners who suspect that a patient may have COPD should usepulmonary function tests, specifically spirometry, as the cornerstone of a diagnostic evaluation. Screening spirometry is not recommended and should only be performed on those patients who demonstrate COPD symptoms.

Spirometry is performed pre- and post-bronchodilator to determine whether airflow limitation is present and whether it is fully or partially reversible. Airflow limitation that is either irreversible or partially reversible is considered diagnostic for COPD.

Patients who present with a history of COPD but no acute symptoms should be asked about their medications, smoking cessation, and vaccination status(see

). Touching on these topics with a stable COPD patient can help prevent exacerbations and unnecessary medication changes.

An exacerbation of COPD is an acute event characterized by a worsening of the patient’s respiratory symptoms that is beyond typical daily variations. This includes an acute change to 1 of the 3 cardinal symptoms: changes in sputum character and/or changes in sputum character; an increase in cough frequency and severity; and an increase in dyspnea.

About 70% of COPD exacerbations are triggered by respiratory infections. The remaining 30% are to the results of environmental pollution, pulmonary embolism, or an unknown etiology.

The decision to triage the patient with a COPD exacerbation to home or the hospital is an important step in the initial evaluation. More than 80% of COPD exacerbations can be managed on an outpatient basis. However, the following criteria should prompt the provider to initiate emergency care for the patient: decreased mental status, suggestive of hypercapnia or hypoxemia; difficulty speaking because of respiratory effort; paradoxical abdominal or chest wall movements; resting dyspnea or respiratory distress; and use of accessory respiratory muscles.

Other criteria that can lead to a decision to hospitalize proposed by the GOLD guidelines are:

a history of frequent exacerbations or prior hospitalizations for exacerbations;

inadequate response to outpatient therapy (patients treated for a COPD exacerbation in a retail health setting should follow up with their primary care provider within 48 to72 hours); insufficient home support;

onset of new symptoms following initiation of outpatient treatment such as altered mental status or cyanosis; and

serious comorbidities, such ascardiac arrhythmia, diabetes, heart failure, kidney or liver failure, or pneumonia.

If a patient is deemed appropriate to be treated on an outpatient basis for a COPD exacerbation, management typically includes intensification of bronchodilator therapy and initiation of oral glucocorticoids. Oral antibiotics are also used in a select group of patients.

Inhaled short-acting beta adrenergic agonists (SABAs), such asalbuterol, are the cornerstone of therapy for COPD exacerbations. Evidence also shows that the concurrent use of a SABA and a short-acting anticholinergic agent, such as Ipratropium Bromide,, during COPD exacerbations produces bronchodilation in excess of either agent individually.

Current guidelines for systemic glucocorticoid therapy suggest a dose equivalent to prednisone 40 mg per day for 5 days.

Many clinical practice guidelines recommend antibiotic therapy only for those patients who are most ill or most likely to have a bacterial infection. A mild exacerbation (1 of the 3 cardinal symptoms present and no hospitalization) does not warrant antibiotic treatment.

GOLD guidelines specifically recommend antibiotics for moderately or severely ill patients with COPD exacerbation who have increased cough and sputum purulence.

Some additional clinical pearls specific to the retail health/urgent care setting regarding whether to refer include:

Follow-up plays an important role for many reasons. Even if a patient is scheduled to follow up with the primary care physician within 48 to 72 hours, call them 24 to 48 hours after the visit to check in. This will not only allow a quick assessment of how symptoms are progressing but it will also increase reliability and trust with the patient.

If a patient has a primary care physician, attempt to contact him or her to collaborate on the case. The physician may not be able to fit the patient in for a visit but most likely would be appreciative of a clinical consult. This collaboration can only improve the patient’s treatment plan.

Listen to patients to learn about them and their health journeys.

Table. Chronic Care Topics to Review for COPD

Avoid triggers of exacerbations (ie, biomass fuel, cigarette smoke, cooking fires, and wood-burning fires.

Recognize exacerbations, such as an increase in dyspnea, sputum production, and sputum purulence.

Influenza and pneumococcal vaccinations can help reduce infections and exacerbations.

Address e-cigarette use. E-cigarettes have been linked to the same inflammatory response in the lungs as smoking a conventional cigarette.

The best cessation rates are achieved when counseling is combined with medication therapy, such as bupropion, nicotine replacement therapy, or varenicline.

Reduces the rate of decline in lung function that occurs in smokers with COPD.

Obesity can contribute to dyspnea. Weight loss can help improve exercise tolerance and reduce dyspnea.

Vitamin D deficiency has been linked to reduced lung function and hospitalization for COPD exacerbations.

COPD indicates chronic obstructive pulmonary disease.

Wheaton AG, Liu Y, Croft JB, et al. Chronic obstructive pulmonary disease and smoking status — United States, 2017.

2019; 68(24):533—538. doi: 10.15585/mmwr.mm6824a1.

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McDonough, JE, Yuan R, Suzuki, M, et al. Small-airway obstruction and emphysema in chronic obstructive pulmonary disease.

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Han MK, Dransfield MT, Martinez FJ. Chronic obstructive pulmonary disease: definition, clinical manifestations, diagnosis and staging. UpToDate website.

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Barnes PJ, Celli BR. Systemic manifestations and comorbidities of COPD.

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Stoller JK. Management of exacerbations of chronic obstructive pulmonary disease. UpToDate website.

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Sethi S, Murphy TF. Infection in the pathogenesis and course of chronic obstructive pulmonary disease.

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Ferguson GT, Make B. Management of stable chronic obstructive pulmonary disease. UpToDate website.

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. Updated January 16, 2019. Accessed July 10, 2019.

9. Warnier MJ, van Reit EE, Rutten FH, De Bruin ML, Sachs AP. Smoking cessation strategies in patients with COPD.

2013;41(3):727-34. doi: 10.1183/09031936.00014012.

10. Higham A, Rattray NJ, Dewhurst JA, et al. Electronic cigarette exposure triggers neutrophil

2016;17(1):56. doi: 10.1186/s12931-016-0368x.

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines the condition as follows: â€œCOPD is a common, preventable, and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.â€ 

COPD: Should a Clinician Treat or Refer? 

E-cigarettes were introduced more than a decade ago, and their use in adults and youth has steadily increased since then. Some of the statistics related to e-cigarettes are sobering. Results of the FDA's 2014 Population Assessment of Tobacco and Health study showed that more than 2 million adults use e-cigarettes daily and more than 3 million (prevalence, 2.4%) use them occasionally.

Meanwhile, the surgeon general of the United States has described youth e-cigarette use as an "unprecedented epidemic." Between 2011 and 2015, use of e-cigarettes grew 900% among high school students.

Finally, 2018 National Youth Tobacco Survey results show astonishing increases in high school and middle school students' use of e-cigarettes. From 2017 to 2018, e-cigarette use increased 78% among high school students and 48% among middle school students.

Chances are, then, that a significant number of patients, especially within the teen group, are currently using, have previously used, or are exposed to e-cigarettes. Many will turn to health care professionals to answer questions about vaping. Counseling on smoking cessation, the harmful effects of both e-cigarette and conventional cigarette smoking, and dependable, trusted methods for quitting should all be a standard part of a pharmacist's visit with these patients. Teaching patients about what is happening to their bodies when they are exposed to e-cigarettes not only gives them powerful knowledge about the risks of smoking but also encourages a trusting relationship between patient and provider.

One common question from patients: If e-cigarettes are not as unhealthy as regular cigarettes, why do they cause a cough?

Many e-cigarette users think that the aerosol they are inhaling is not harmful. But as more studies are released on the pathophysiological effects of e-cigarette vapor, experts are discovering that that belief is untrue. A typical e-cigarette cartridge contains benzene, diacetyl, heavy metals (lead, nickel, and tin), propylene glycol, and often flavorings.

These components are responsible for cytotoxic, inflammatory responses in lung cells. Two of the products, diacetyl and propylene glycol, have been the focus of many recent studies, as these chemicals are found in much higher amounts in e-cigarettes than in conventional cigarettes.

Propylene glycol, or glycerol, is a synthetic chemical used to maintain moisture.

It is found in many skin care products, and as it exists in those products and in an e-cigarette cartridge, it is "generally recognized as safe" by the FDA.

Unfortunately, that changes when the product is heated. As an e-cigarette user inhales on the device, and an atomizer heats the liquid in the cartridge, changing it to an aerosol that users can then inhale (see figure). When heated, propylene glycol chemically converts to formaldehyde, a known carcinogen, and the FDA's "generally recognized as safe" designation no longer applies.

Many studies have noted that the change in composition of e-cigarette liquid once it is heated produces a variety of toxic chemicals, including free radicals, particulates, nitrosamines, and volatile organic compounds.

Further studies have found that exposure to e-cigarette vapor causes proinflammatory changes and increased activation of neutrophils. Neutrophil activation is a characteristic feature of chronic obstructive pulmonary disorder (COPD), raising concerns about long-term use of e-cigarettes and chronic disease.

In the same vein as inflammatory complications, e-cigarette vapor has been found to inhibit phagocytosis (cellular ingestion of bacteria) in alveolar macrophages (AMs). Detection and phagocytosis of pathogens is a primary function of AMs. Typically, AMs initiate an immune response to infection in the airways. Therefore, any reduction in phagocytosis from e-cigarette vapor can potentially decrease the body's innate immune response.

Historically, inhalation of food flavorings has been associated with acute respiratory distress and/or respiratory failure.

Diacetyl inhalation in a group of workers from a popcorn manufacturing plant is the most well-known case. The plant used diacetyl to flavor microwave popcorn until workers there started having breathing problems (dry cough, exhaustion, shortness of breath, and wheezing) after exposure to the airborne chemical. Those workers received a diagnosis of bronchiolitis obliterans, or popcorn lung.

Bronchiolitis obliterans is a type of obstructive lung disease of the small airways. It is rare, with characteristic features of fibrosis in terminal and distal bronchioles and spirometry showing airflow obstruction. It usually leads to a progressive decline in lung function with no cure.

Despite the widespread publicity surrounding popcorn lung, a recent study reported the presence of diacetyl in 70% of tested e-cigarettes.

Armed with research about the effects of e-cigarette vapor on lung tissue, how do pharmacists then convey this to patients? One of the most important tactics is to dispel the myth that e-cigarettes are safe. Using some basic biology terms and descriptions can engage patients and show them that the pharmacist wants to share knowledge, building on the patient-provider relationship. These educational moments go a long way in treatment adherence and patient/provider satisfaction. Here are some comments to help get the conversation going:

E-cigarettes have not been found to be less harmful than conventional cigarettes.

E-cigarette vapor contains chemicals that can irritate and inflame lung tissue, which can cause coughing. The body is rejecting the chemicals, and coughing to expel them from the lungs is a natural reflex.

Patients may be just as likely to develop serious lung conditions, such as COPD, using an e-cigarette versus a conventional cigarette.

Lungs have cells, called macrophages, that act as a defense system against bacteria. E-cigarette vapor is toxic to these cells. Without them, people are much more likely to get sick because their lungs are weaker and unable to defend themselves.

Rodu B, Plurphanswat N. E-cigarette use among US adults: Population Assessment of Tobacco and Health (PATH) study.

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US Department of Health & Human Services. E-cigarette use among youth and young adults: a report of the surgeon general—executive summary. e-cigarettes. surgeongeneral.gov/documents/2016_SGR_Exec_Summary_508.pdf. Published 2016. Accessed July 1, 2019.

Youth tobacco use: results from the National Youth Tobacco Survey. FDA website. www.fda.gov/TobaccoProducts/PublicHealthEducation/ProtectingKidsfromTobacco/ucm405173.htm. Updated May 29, 2019. Accessed July 1, 2019.

About electronic cigarettes (e-cigarettes). CDC website. cdc.gov/tobacco/basic_information/e-cigarettes/about-e-cigarettes.html. Updated November 15, 2018. Accessed March 25, 2019.

Chun LF, Moazed F, Calfee CS, Matthay MA, Gotts JE. Pulmonary toxicity of e-cigarettes.

2017;313(2):L193-L206. doi:10.1152/ajplung.00071.2017.

Scott A, Lugg ST, Aldridge K, et al. Pro-inflammatory effects of e-cigarette vapour condensate on human alveolar macrophages.

2018;73(12):1161-1169. doi:10.1136/thoraxjnl-2018-211663.

Higham A, Rattray NJ, Dewhurst JA, et al. Electronic cigarette exposure triggers neutrophil inflammatory responses.

2016;17(1):56. doi:10.1186/s12931-016-0368x.

Humectant. Merriam-Webster website. merriam-webster.com/dictionary/humectant. Accessed March 25, 2019.

McArthur S. Vaping: the good, the bad and the popcorn lung. MPH Online website. mphonline.org/vaping-public-health. Accessed July 2, 2019.

Farsalinos KE, Kistler KA, Gillman G, Voudris V. Evaluation of electronic cigarette liquids and aerosol for the presence of selected inhalation toxins.

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, is a famiy nurse practitioner at CVS MinuteClinic in Mokena, Illinois.

They may mistakenly believe that e-cigarettes are safe and wonder why they cause a cough.

Discuss Adverse Effects of Vaping With Patients

Acute bronchitis is one of the most common clinical conditions encountered in ambulatory care, accounting for about 10% of visits in the United States or 100 million visits per year.

It is characterized by an acute cough for more than 5 days in the absence of chronic obstructive pulmonary disease or pneumonia.

. The cough may be associated with either non-purulent or purulent sputum production.

In more than 90% of cases, acute bronchitis has a viral etiology with rhinovirus, enterovirus, influenza A and B, parainfluenza, coronavirus, and respiratory syncytial virus being the most commonly identified pathogens.

It is typically a self-limited disease, resolving within 1 to 4 weeks

Because of the high likelihood of viral etiology, antibiotics are not recommended for treatment of acute bronchitis.

The diagnoses that have the most overlap with acute bronchitis are upper respiratory infection (URI), acute rhinosinusitis (ARS) and pneumonia. The treatment plans for these differential diagnoses can vary widely. Therefore, an accurate history of present illness and physical exam are critical.

Acute bronchitis is often preceded by an ARS or URI. The first few days of illness can produce elevated temperature, headache, mild fever of less than 100.9F, nasal/sinus congestion, and pharyngitis.

With involvement of the lower respiratory tract, the cough becomes the dominant symptom. Rhonchi and wheezing may be auscultated upon exam. However, the rhonchi typically clear with a forceful cough. Mild dyspnea may be present, especially with physical activity.  Prolonged coughing can also create substernal musculoskeletal pain. Production of sputum, whether it is purulent or not, is common and does not correlate with a bacterial infection.

The cough associated with acute bronchitis can be very bothersome, stripping the patient of days at work or school, as well as sleep. Many patients and providers underestimate the time required to fully recover from acute bronchitis.

Ebell and colleagues (2013) conducted a population-based survey to determine patients’ expectations regarding the duration of a cough-related illness. Survey respondents reported a median duration of 5 to 7 days and a mean duration of 7 to 9 days. The mean duration of cough in evidence-based literature is 18 days.

It is essential to educate the patient about a realistic expected length of illness. This transparency can prevent inappropriate expectations of antibiotic use and possibly divert additional visits at a higher level of care.

An accurate medical history and a physical exam are critical to rule out more serious conditions.