While working with your family medicine preceptor you are scheduled to see Mr. John Barley, a 58-year-old male who has sought medical attention only rarely in the past 10 years. He comes to the office today because of a progressively worsening cough and shortness of breath during the previous month.
Before you and your preceptor, Dr. Wilson, enter the room to meet Mr. Barley, you think about the definition of dyspnea.
Dr. Wilson greets Mr. Barley, introduces you, and then excuses himself to go see another patient. He states he will be back for you to present Mr. Barley’s case to him.
You sit down across from Mr. Barley and say, “Hi, Mr. Barley. Thanks for letting me work with you.” Mr. Barley says, “Sure, anyone working with Dr. Wilson is OK by me.”
You begin eliciting the history:
“I understand you have a cough and shortness of breath. Can you tell me more about it?”
“OK. Have you noticed anything else that seems to be related to the cough? Things like weight loss, chest pain, and fever?”
“Have you had any nausea, vomiting, or diarrhea?”
“Do you have shortness of breath when you are active and when you are at rest?”
“Have you had in the past, or currently have exposures to things that can cause cough, like chemicals, and smoking?”
“Do you have any trouble lying flat when you sleep?”
You learn that he has not traveled recently, which could have exposed him to an unusual form of pneumonia. He also has not been exposed to tuberculosis. From other questions, you learn that Mr. Barley has no leg swelling or paroxysmal nocturnal dyspnea (PND). You know that he has had no orthopnea.
As a farmer, he is active during the day. Deconditioning is not likely.
Wondering if his shortness of breath is due to a panic disorder, you ask him a series of questions and note that his symptoms are not associated with paresthesia, choking, nausea, chest pain, derealization feeling, trembling or shaking, dizziness, palpitations, sweating, chills, or flushes.
Orthopnea Definition, Etiology, Symptoms
Dyspnea which occurs when lying flat.
It is associated with congestive heart failure through accumulation of excess fluid in the lungs as a result of left-sided heart failure. In a prone position, blood volume from the feet and legs redistributes to the lungs.
Patients with orthopnea typically have to sleep propped up in bed or sitting in a chair. It is commonly measured according to the number of pillows needed to prop the patient up to enable breathing (Example: “three pillow orthopnea”).
Paroxysmal nocturnal dyspnea (PND) – Definition, Etiology, Symptoms
Sudden, severe shortness of breath at night that awakens a person from sleep, often with coughing and wheezing.
It is most closely associated with congestive heart failure.
PND commonly occurs several hours after a person with heart failure has fallen asleep. PND is often relieved by sitting upright, but not as quickly as simple orthopnea. Also unlike orthopnea, it does not develop immediately upon lying down.
PATIENT HISTORY 2
Now that you have a good understanding of the history of the present illness, you continue the interview by turning to past medical, social, and family histories.
You say, “I think I have a clear idea about what brought you in today. Let me ask you now about your health in general.”
“Any serious illnesses in the past?”
“I’d like to ask about your personal life. Tell me about your home life.”
“Tell me about your immediate family health history.”
You say, “So I understand that you have had a cough with white phlegm for the past two winters and that you have been experiencing shortness of breath with exertion. You may have been exposed to some chemical irritants at your farm, but you have been careful about this. You also smoke cigarettes, and have been cutting down.”
“Let’s go in and do the physical together,” says Dr. Wilson. “But, first, what are you thinking so far, in terms of a differential?”
After pausing to think, you reply to Dr. Wilson, “He could have bronchitis.”
“Good thought.” Dr. Wilson added, “What in the history supports bronchitis?”
You reply that the cough and shortness of breath of two to three weeks duration could support acute bronchitis.
Dr. Wilson tells you, “While the duration of illness provides a clinical distinction between acute and chronic bronchitis, the actual mechanisms and pathophysiology also probably differ between the two. Chronic bronchitis causes long-term inflammation that can lead to irreversible structural changes. He might qualify for this diagnosis because he describes cough with phlegm production during the past two winters. But let’s assume for the moment that he doesn’t have chronic bronchitis.”
He then prompts you, “What else are you thinking for the differential diagnosis?”
Acute Versus Chronic Bronchitis
Clinical distinction between acute bronchitis & chronic bronchitis: duration of illness.
|Acute Bronchitis||Chronic Bronchitis|
|Cough with excess sputum with a course lasting 1 to 3 weeks||Cough with excess sputum production for equal or greater than 3 months per year in each of 2 consecutive years|
PHYSICAL EXAM FINDINGS
Dr. Wilson says, “Why don’t you review the physical examination findings consistent with COPD while I return a phone call to a patient?”
While Dr. Wilson is gone, you go online to learn more about what physical findings you should look for in a patient with COPD.
When you are finished, you rejoin Dr. Wilson and approach the exam room where Mr. Barley is waiting.
Classic Findings on Physical Exam for COPD
· Increased anteroposterior (AP) diameter of the chest
· Decreased diaphragmatic excursion
· Wheezing (often end-expiratory)
· Prolonged expiratory phase
How to measure laryngeal height
You perform a physical exam on Mr. Barley.
After knocking on the door to make sure Mr. Barley is ready you and Dr. Wilson enter the room.
You say to Mr. Barley, “I’m going to do the physical exam, and then Dr. Wilson will repeat it.” He nods assent.
Your exam reveals:
· Temperature is 37.2 °C (98.9 °F)
· Pulse is 94 beats/minute
· Respiratory rate is 22 breaths/minute
· Blood pressure is 128/78 mmHg
General: Appears mildly short of breath
Head, eyes, ears, nose and throat (HEENT):Normocephalic / atraumatic, conjunctivae and sclerae are normal, PERRL, oropharynx is normal.
Neck: Supple without masses, lymphadenopathy, or thyromegaly. Laryngeal height measures 2 cm from sternal notch to the top of the thyroid cartilage upon full expiration.
Lungs: Increased AP diameter. Percussion is normal. Inspiratory crackles at the bases, and end-expiratory wheezing diffusely.
Heart: Regular rate and rhythm. 2/6 systolic murmur loudest at the right upper sternal border (RUSB) with radiation to the left lower sternal border (LLSB).
Abdomen: Bowel sounds normal, no hepatomegaly, no tenderness.
Extremities: 1+ pitting pretibial edema.
DIAGNOSTIC TESTING 1
First confirming your findings with his own exam, Mr. Wilson then agrees that Mr. Barley has three signs of COPD:
· Increased AP diameter
· Laryngeal height 2 cm above the sternal notch
· Expiratory wheezing
DIAGNOSTIC TESTING 2
Here are examples of chest-x-rays with abnormal findings (not from Mr. Barley). This x-ray of pneumonia shows a wedge-shaped area of consolidation.
This x-ray shows advanced pulmonary tuberculosis, with bilateral infiltrates (white triangles) and caving formation (black arrows) in the right apical region.
Note the hyperinflated lungs in this patient with emphysema.
“However,” you ask, “if we got a chest x-ray, wouldn’t it also support the diagnosis?”
When Chest X-ray is Appropriate in Setting of Dyspnea
The current literature doesn’t support the use of chest x-ray to rule in or out COPD, but some studies suggest that a chest x-ray might be helpful for finding other causes of dyspnea.
The Global Initiative for Chronic Obstructive Lung Disease (GOLD) recommends getting a chest x-ray at first presentation to exclude causes or problems other than COPD.
Another study examined chest x-ray results in a screening program and found that 14% of all the radiographs detected potentially treatable causes of dyspnea other than lung cancer and COPD, including:
· Pulmonary fibrosis
· Pleural effusion
· Left ventricular failure
· Possible active tuberculosis
· Kyphoscoliosis (causes loss of lung volume & often caused by neuromuscular disease)
In addition, the chest radiograph found lung cancer in a significant number of patients.
In summary, it makes sense to get a chest x-ray when a patient presents with shortness of breath, not to rule in or out COPD, but to look for other diagnoses.
DIAGNOSTIC TESTING 3
While Mr. Barley gets dressed, Dr. Wilson takes the opportunity to teach you about pulmonary function tests. He shows you a graph, and explains how spirometry is helpful in diagnosing COPD:
Spirometry for Diagnosis/Monitoring COPD
Spirometry is the most commonly used office-based device for lung function testing. A spirometer is a hand-held device that can easily be used in the clinician’s office by a patient with the assistance of a technician.
How it works:
1. The patient is asked first to exhale completely, then to inhale deeply.
2. Next, the patient is told to exhale rapidly into the device until all the air is exhausted from the lungs.
These two steps measure the inspiratory and expiratory flow of air. A number of calculations can then be derived from these measurements. An individual’s spirometry results are based on comparison to predicted values of a standardized, healthy population.
· Forced Vital Capacity (FVC) = total amount of air the patient can expel from the lungs after a full inspiration
· Forced Expiratory Volume -1 second (FEV1) = amount of air the patient can expel after a full breath in one second
COPD causes the air in the lungs to be exhaled at a slower rate and in a smaller amount compared to a normal, healthy person (obstructive defect). The amount of air in the lungs will not be readily exhaled due to either a physical obstruction (such as with mucus production) or airway narrowing caused by chronic inflammation.
Post-bronchodilator FEV1-to-FVC ratio (FEV1/FVC) less than 70% (or less than the fifth percentile) with compatible symptoms and history, is diagnostic of COPD according to GOLD 2020 guidelines. There is evidence that this cut off over- and under- diagnoses older and younger patients respectively, with uncertain clinical significance.
Further, the FEV1 impairment defines the level of COPD severity:
|Measured post-bronchodilator FEV1 Impairment (Compared to Predicted)||Severity|
|> 80%||Mild – GOLD 1|
|50-79%||Moderate – GOLD 2|
|30-49%||Severe – GOLD 3|
|< 30%||Very severe – GOLD 4|
NARROWING THE DIFFERENTIAL DIAGNOSIS 1
Before taking another phone call, Dr. Wilson hands you some information on COPD. You read:
Chronic Obstructive Pulmonary Disease (COPD) – Definition, Epidemiology, Diagnosis
COPD encompasses both chronic bronchitis and emphysema and is characterized by airflow limitation that is progressive and not fully reversible with bronchodilators.
· Chronic bronchitis: chronic inflammation in the airways leading to destruction of the cilia and narrowing of the air passages in the lungs.
· Emphysema: chronic destruction of the lung architecture, particularly the alveoli, leading to reduced air exchange.
COPD is currently reported by the Global Initiative for Chronic Obstructive Lung Disease to be the 3rd leading cause of morbidity and mortality worldwide. Almost 30 million Americans have COPD.
A clinical diagnosis of COPD should be considered in any middle-aged or older adult who has:
· Chronic cough or sputum production, or
· A history of tobacco use
The diagnosis should be confirmed by spirometry.
COPD Versus Asthma
Since a major clinical distinction between these two diagnoses is that COPD is not reversible via bronchodilator therapy, and asthma is, spirometry data is collected twice: pre- and post-bronchodilator therapy.
Other major differences between COPD and asthma are outlined below:
|Onset in mid-life||Onset early in life|
|Symptoms slowly progress||Symptoms vary day to day|
|Symptoms during exertion||Symptoms more common at night or early morning|
|Long history of smoking||Not dependent on smoking|
|Not related to rhinitis, allergy, or eczema||Often related to rhinitis, allergy, or eczema|
|Largely irreversible||Air-flow limitation is largely reversible|
Differences between the mechanisms underlying COPD and asthma include:
· Cigarette smoke is more of a causal agent in COPD,
· Mast cells, T helper cells, and eosinophils play more of a role in what appears to be an allergic bronchoconstrictive response in asthma, and
· Macrophages, T killer cells, and neutrophils play a role in an inflammatory and destructive process in COPD.
· As noted on the previous card, a post-bronchodilator FEV1/FVC ratio < 70% confirms the presence of airflow limitation that is not fully reversible (hence a diagnosis of COPD).
· Significant reversibility is defined as an increase in FEV1 ≥ 12% after bronchodilator.
NARROWING THE DIFFERENTIAL DIAGNOSIS 2
“So let’s compare asthma to COPD,” suggests Dr. Wilson. “Why does it matter? Why worry about any differences between asthma and COPD?” You and Dr. Wilson discuss the differences in prognosis and treatment modalities for COPD versus asthma.
“Cigarette use makes either of the conditions worse, of course,” adds Dr. Wilson. “We will have to address that issue with him no matter what.”
Dr. Wilson finishes up the discussion of asthma by referring you to the 2020 Global Initiative for Chronic Obstructive Lung Disease (GOLD) guideline, which clarifies that it is not always possible to differentiate between asthma and COPD, and it makes sense to treat patients who have features of both as if they had asthma.
STAGES OF SEVERITY
Dr. Wilson notes, “The first step – often combined with confirming the diagnosis of COPD – is to determine the stage of severity. Different organizations use slightly different categories. Here are the GOLD criteria. All you have to remember is the FEV1 to FVC ratio is less than 0.7 for all stages of COPD, and then the cutoffs for FEV1 are 80, 50, and 30% of predicted.”
GOLD Spirometric Criteria for COPD Severity
|GOLD Grade||Severity||Spirometry Results||Clinical Presentation|
|1||Mild||· FEV1/FVC < 0.7· FEV1 ≥ 80% predicted||At this stage, the patient is probably unaware that lung function is starting to decline. Keep in mind that there is some evidence that using this fixed ratio may contribute to the overdiagnosis of obstruction in older (> 60 year old) individuals and, to a lesser degree, underdiagnosis in younger individuals.|
|2||Moderate||· FEV1/FVC < 0.7· 50% ≤ FEV1 < 80% predicted||Symptoms during this stage progress, with shortness of breath developing upon exertion.|
|3||Severe||· FEV1/FVC < 0.7· 30% ≤ FEV1 < 50% predicted||Shortness of breath becomes worse at this stage, and COPD exacerbations are common.|
|4||Very Severe||· FEV1/FVC < 0.7· FEV1 < 30% predicted||Quality of life at this stage is gravely impaired. COPD exacerbations can be life threatening.|
Therapy for Mild Symptomatic COPD
Prescribe an albuterol metered-dose inhaler on an as needed basis.
Albuterol is a member of a class of medications called bronchodilators that improve lung function by altering airway smooth muscle tone and reducing dynamic hyperinflation. Bronchodilators include:
· Inhaled short-acting and long-acting beta-2-agonists
· Inhaled long-acting anticholinergics, and
· Oral methylxanthines
Inhaled bronchodilators are essential for symptom management in COPD. According to the Global Initiative for Chronic Obstructive Lung disease:
· All symptomatic patients with COPD should be prescribed a short-acting bronchodilator (e.g., albuterol) on an as-needed basis.
· If symptoms are still inadequately controlled, a daily dose of long-acting bronchodilator should be added.
· The choice between beta-2-agonist, anticholinergic, theophylline, or combination therapy depends on availability and individual response in terms of symptom relief and side effects.
· Consider combining bronchodilators of different pharmacological classes, which may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator.
· Theophylline should be reserved for patients who can not tolerate, use, or afford other medications.
Risks of overuse of beta-agonists include:
· Long-acting beta-agonists may increase asthma exacerbations in patients with co-morbid asthma-COPD
· Exaggerated somatic tremor
· Hypokalemia (especially with concurrent use of thiazide diuretics)
Smoking cessation is the single-most-important treatment strategy for COPD. Assess your patient’s readiness to quit smoking, recommend smoking cessation, and provide information on available smoking-cessation programs.
Although COPD is usually caused by damage inflicted from long-term cigarette smoke or air pollution, it is occasionally caused by an alpha-1 antitrypsin deficiency. A clue that this may be present is when a patient younger than 45 years old is diagnosed with COPD, as they are not old enough to have developed the long-term effects from smoking. In such a case, especially if the patient has a family history of the disease, you may want to check alpha-1 antitrypsin levels—but you do not have to check this level in all adults who have COPD.
Systemic glucocorticoids, such as prednisone, may be useful during an acute COPD exacerbation. And systemic glucocorticoids may improve lung function for about 20 percent of patients with stable COPD. However, the risks of chronic systemic steroid use outweigh the benefits—prednisone, even at a low dose, can cause serious side effects, such as osteoporosis, suppression of the hypothalamus-pituitary-adrenal axis, diabetes, cataracts, and necrosis of the femoral head. Perhaps the most relevant side effect of long-term treatment with systemic glucocorticoids is steroid myopathy—contributing to muscle weakness, decreased functionality, and respiratory failure in advanced COPD.
Hospitalization is indicated only for a patient who needs observation and more intensive treatment than can be provided at home. Supplemental oxygen and continuous nebulizer therapy can be given in the hospital. In addition, the patient can be monitored closely for respiratory failure and the need for intubation and artificial ventilation.
This week, complete the Aquifer case titled “Family Medicine 28: 58-year-old man with shortness of breath”
Apply information from the Aquifer Case Study to answer the following discussion questions:
· Discuss the Mr. Barley’s history that would be pertinent to his respiratory problem. Include chief complaint, HPI, Social, Family and Past medical history that would be important to know.
· Describe the physical exam and diagnostic tools to be used for Mr. Barley. Are there any additional you would have liked to be included that were not?
· What plan of care will Mr. Barley be given at this visit, include drug therapy and treatments; what is the patient education and follow-up?