DDx: Asthma Flashcards Preview

10 PULMONARY AND CRITICAL CARE MEDICINE > DDx: Asthma > Flashcards

Flashcards in DDx: Asthma Deck (11):
1

Diffrerential Diagnosis of Asthma:

Asthma

COPD 

Vocal cord dysfunction

Heart failure

Medication side effect

Bronchiectasis

Pulmonary infiltrates with eosinophilia (ABPA, eosinophilic granulonatosis with angiitis

(Churg-Strauss),Loeffler syndrome, chronic eosinophilic pneumonia)

Obstructive sleep apnea

Mechanical airway obstruction

Cystic fibrosis

2

Asthma

Hx: Episodic cough triggered by cold air and hyperventilation. The symptoms are suggestive of cough-variant asthma. 

Mild persistent asthma: Symptoms more than 2 days per week but not daily, and wakes up once a week but not nightly. 

Dx: Spirometry: Abnormal spirometry results (reversible obstruction) can help to confirm an asthma diagnosis, but normal results do not exclude asthma.  A reduced FEV1 or a reduced FEV1/FVC ratio documents airflow obstruction. An increase in FEV1 of >12% with a minimum increase of 200 mL in FEV1 after bronchodilator use establishes the presence of airflow reversibility and the diagnosis of asthma. 

Peak flow variability: A patient with normal spirometry results but marked diurnal variability (based on a peak-flow diary kept for >2 wk) may have asthma, which may warrant an empiric trial of asthma medications or bronchoprovocation testing.

Bronchoprovocation testingIn a patient with a history highly suggestive of asthma and normal baseline spirometry results, a low PC20 (concentration of inhaled methacholine needed to cause a 20% drop in FEV1) on methacholine challenge testing supports a diagnosis of asthma. A normal bronchoprovocation test essentially excludes asthma.

Chest radiography: Chest radiography may be needed to exclude other diagnoses but is not recommended as a routine test in the initial evaluation of asthma.

Allergy skin testing: There is a strong association between allergen sensitization, exposure, and asthma. Allergy testing is the only reliable way to detect the presence of specific IgE to allergens. Skin testing (or in vitro testing) may be indicated to guide the management of asthma in selected patients, but results are not useful in establishing the diagnosis of asthma.

Tx: Regardless of disease severity, all patients are prescribed a short-acting, inhaled β-agonist medication.  Intermittent asthma

If short-acting bronchodilators are needed for symptom relief more than twice a week for daytime symptoms or twice a month for nighttime awakenings, a long-acting controller medication is indicated. Use of more than one canister of short-acting β-agonist per month may be a clue to poor control of asthma and warrants further investigation.

SABA: ALBUTEROL PRN

Mild persistent asthma: is treated with a single long-term controller medication.  A low-dose inhaled glucocorticoid is the preferred long-term controller medication; alternatives include a mast cell stabilizer, leukotriene modifier, or sustained-release methylxanthine.

LOW DOSE INHALED CORTICOSTEROID: PRED, METHYLPRED, BUDESONIDE

ALTERNATIVE:

MAST CELL STABILIZER: NEDOCROMIL, CROMOLYN

LEUKOTRIENE MODIFIER: MONTELEUKAST 10, ZAFIRLUKAST, ZILEUTON

MONOCLONAL (IgE) ANTIBODY: OMALIZUMAB, BENRALIZUMAB (FASENRA®)

 

DUONEB®/COMBIVENT®: IPATROPIUM AND ALBUTEROL

SPIRIVA®: TIOTROPIUM

Moderate persistent asthma: is treated with one or two long-term controller medications. Use either low doses of inhaled glucocorticoid and a long-acting β-agonist (preferred) or medium doses of a single inhaled glucocorticoid. In patients who remain symptomatic while taking medium doses of inhaled glucocorticoids, the addition of a long-acting bronchodilator (eg, salmeterol) results in improved lung physiology, decreased use of short-acting β-agonists, and reduced symptoms when compared with doubling the dose of inhaled glucocorticoid.

LOW DOSE INHALED CORTICOSTEROID: PRED, METHYLPRED, BUDESONIDE +

LABA: SALMETEROL (SEREVENT), FORMETEROL OR

MEDIUM DOSE INHALED CORTICOSTEROID: PRED, METHYLPRED, BUDESONIDE

ALTERNATIVE: 

LOW DOSE INHALED CORTICOSTEROID: PRED, METHYLPRED, BUDESONIDE  +

LEUKOTRIENE MODIFIER: MONTELEUKAST 10, ZAFIRLUKAST, ZILEUTON

 

SYMBICORT®: BUDESONIDE AND FORMETEROL

Severe persistent asthma: may require at least three daily medications to manage their disease (ie, high doses of an inhaled glucocorticoid plus a long-acting bronchodilator and possibly oral glucocorticoids). 

MEDIUM DOSE INHALED CORTICOSTEROID: PRED, METHYLPRED, BUDESONIDE + LABA: SALMETEROL (SEREVENT), FORMETEROL AND MONOCLONAL (IgE) ANTIBODY: OMALIZUMAB, BENRALIZUMAB (FASENRA®) IN THOSE WITH ALLERGIES

HIGH DOSE INHALED CORTICOSTEROID: PRED, METHYLPRED, BUDESONIDE + LABA: SALMETEROL (SEREVENT), FORMETEROL + ORAL CORTICOSTEROID AND MONOCLONAL (IgE) ANTIBODY: OMALIZUMAB, BENRALIZUMAB (FASENRA®) IN THOSE WITH ALLERGIES

3

COPD

Dx: GOLD CRITERIA:

Major Criteria: 

Increase in sputum volume

Increase in sputum purulence (generally yellow or green)

Worsening of baseline dyspnea

Additional Criteria:

Upper respiratory infection in the past 5 days

Fever of no apparent cause

Increase in wheezing and cough

Increase in respiration rate or heart rate 20% above baseline

Various nonspecific signs and symptoms may accompany these findings, such as fatigue, insomnia, depression, and confusion

Short-acting β-agonists (eg, albuterol, levalbuterol)—also known as “rescue” medications—act within a few minutes of administration, and their effect lasts approximately 4 to 6 hours. 

Long-acting β-agonists (eg, salmeterol, formoterol, arformoterol) achieve sustained and more predictable improvement in lung function than the short-acting agents. 

Vagal stimulation in the lung is mediated via muscarinic receptors. Anticholinergic drugs used to treat COPD include short-acting inhaled agents (eg, ipratropium) and tiotropium, a long-acting inhaled bronchodilator used in stable outpatients. Tiotropium selectively blocks the M3 muscarinic receptor. Short-acting anticholinergic agents are less potent than long-acting β-agonist or long-acting anticholinergic agents. 

Tx: 

I: Mild; FEV1/FVC <70%; FEV1 ≥80% of predicted (GOLD criteria); With or without chronic symptoms (cough, sputum production); Add short-acting bronchodilator when needed

II: Moderate; FEV1/FVC <70%; 50% ≤FEV1 <80% of predicted; With or without chronic symptoms (cough, sputum production); Add regular treatment with one or more long-acting bronchodilators; add pulmonary rehabilitation

III: Severe; FEV1/FVC <70%; 30% ≤FEV1 <50% of predicted; With or without chronic symptoms (cough, sputum production); Add inhaled corticosteroids if repeated exacerbations

IV: Very severe; FEV1/FVC <70%; FEV1 <30% of predicted or FEV1 <50% of predicted plus chronic respiratory failure; Add long-term oxygen therapy if chronic respiratory failure; consider surgical treatments

Resting hypoxemia, defined as arterial PO2 of 55 mm Hg or less or arterial oxygen saturation of 88% or less. In patients who qualify for continuous therapy because of resting hypoxemia, oxygen treatment should be administered for at least 15 h/day.

Oxygen therapy is a major component of therapy for very severe (stage IV) COPD and usually is prescribed for patients with arterial PO2 ≤55 mm Hg or oxygen saturation ≤88% with or without hypercapnia.

Mild to moderate exacerbations can be managed at home. Mild exacerbations require treatment with short-acting bronchodilators; moderate exacerbations require short-acting bronchodilators and systemic glucocorticoids and/or antibiotics.

Severe exacerbations are characterized by loss of alertness or a combination of two or more of the following parameters: dyspnea at rest, respiration rate ≥25/min, pulse rate ≥110/min, or use of accessory respiratory muscles.  Severe exacerbations are treated in the hospital

Oxygen therapy is the cornerstone of hospital management of COPD exacerbations, with a goal of adequate levels of oxygenation (arterial PO 2 >60 mm Hg [8.0 pKa] or oxygen saturation >90%). Arterial blood gas levels should be measured 30 to 60 minutes after oxygen therapy is started to ensure that oxygenation is adequate without carbon dioxide retention or acidosis.

There is a significant benefit to using antibiotics in patients who have moderate or severe COPD exacerbations. The predominant bacteria recovered are Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis. Generally, antibiotic regimens for community-acquired infection include coverage with a third-generation cephalosporin in combination with a macrolide or monotherapy with a fluoroquinolone.

Noninvasive intermittent ventilation alleviates respiratory acidosis and decreases respiration rate, severity of dyspnea, and length of hospital stay; importantly, mortality also is reduced. Indications for noninvasive ventilation include moderate to severe dyspnea with the use of accessory muscles of breathing and paradoxical abdominal motion, moderate to severe acidosis (pH <7.35) and/or hypercapnia (arterial PCO2 >45 mm Hg), and respiration rate >25/min.  Exclusion criteria include respiratory arrest, cardiovascular instability (hypotension, arrhythmias, myocardial infarction), change in mental status (lack of cooperation), high aspiration risk, viscous or copious secretions, recent facial or gastroesophageal surgery, craniofacial trauma, fixed nasopharyngeal abnormalities, burns, and extreme obesity.

Invasive mechanical ventilation is indicated for patients who cannot tolerate noninvasive ventilation and patients with severe dyspnea with a respiration rate >35/min, life-threatening hypoxia, severe acidosis (pH <7.25) and/or hypercapnia (arterial PCO 2 >60 mm Hg [8.0 kPa]), respiratory arrest, somnolence or impaired mental status, cardiovascular complications (hypotension, shock), or other complications (eg, metabolic abnormalities, sepsis, pneumonia, pulmonary embolism, barotrauma, massive pleural effusion).

4

Vocal cord dysfunction

Abrupt onset of severe symptoms, often with rapid improvement. Monophonic wheeze heard loudest during either inspiration or expiration. The preferred diagnostic test is direct visualization of the vocal cords during symptoms. May closely mimic asthma, particularly in young adults.

5

Heart failure (see Heart Failure)

Spirometry results may or may not be normal; wheezing may be a sentinel manifestation. Consider when there is not prompt improvement with asthma therapy. Heart failure always is a consideration for persons with underlying cardiac disease.

6

Medication side effect

Chronic cough may occur with certain medications (eg, ACE inhibitors).

7

Bronchiectasis

Bronchiectasis is the permanent and abnormal dilatation and destruction of bronchi and bronchiolar walls associated with impaired drainage and recurrent infection that leads to chronic inflammation. Voluminous sputum production, often purulent and sometimes blood tinged. Suspect if physical examination reveals crackles with wheezing or clubbing or if chest radiograph shows peribronchial thickening.

8

Pulmonary infiltrates with eosinophilia (ABPA, eosinophilic granulonatosis with angiitis

(Churg-Strauss),Loeffler syndrome, chronic eosinophilic pneumonia)

Wheezing may be seen in ABPA, chronic eosinophilic pneumonia, and eosinophilic granulonatosis with angiitis (Churg-Strauss). Note that in uncomplicated asthma, chest radiographs are normal. Findings of infiltrates, striking peripheral blood eosinophilia, and constitutional symptoms (eg, fever, weight loss) suggest chronic eosinophilic pneumonia. Asthma with eosinophilia, markedly high serum IgE levels, and intermittent pulmonary infiltrates is characteristic of ABPA. Difficult-to-treat asthma, upper airway and sinus disease, and multisystem organ dysfunction suggest eosinophilic granulonatosis with angiitis (Churg-Strauss).

9

Obstructive sleep apnea (see Obstructive Sleep Apnea)

OSA is defined by upper airway narrowing or collapse that results in cessation (apnea) or reduction (hypopnea) in airflow despite ongoing efforts to breathe. 

Hx: Loud snoring, gasping, and pauses in breathing are commonly observed by a bed partner.  Subjective symptoms include frequent awakenings, snorting, and nonrestorative sleep. The most important risk factor for OSA is obesity, particularly in patients with prominent distribution of adipose tissue in the trunk and neck. Less important risk factors include male sex, postmenopausal state, family history of OSA, and race. Some possible mechanisms by which obesity can cause OSA include increased upper airway fat deposition, leading to a decrease in airway size and muscle tone as well as reduced lung volume. Central obesity (larger waist-hip ratio) is more important than general obesity. Other risk factors for OSA are larger neck circumference (>17 inches in men; >16 inches in women), nasal narrowing or congestion, large tongue, low-lying soft palate, enlarged tonsils and adenoids, abnormalities of the face or jaw that contribute to airway narrowing, use of muscle relaxants, smoking and alcohol use, and primary medical disorders (acromegaly, androgen therapy, neuromuscular disorders, and stroke).

Dx: Polysomnography (PSG) is the gold standard for diagnosis of OSA. During PSG monitoring, upper airway events are classified as apneas (characterized by complete cessation of airflow) or hypopneas (reductions in airflow), collectively known as disordered breathing events. The apnea-hypopnea index (AHI) is the number of disordered breathing events per hour of sleep and is the standard for measuring the severity of OSA. An AHI of 5 to 15 indicates mild OSA; an AHI of 16 to 30 indicates moderate OSA, and an AHI of more than 30 indicates severe OSA.

Tx: CPAP should be considered first-line therapy in any patient who has OSA and associated symptoms, particularly excessive daytime sleepiness.  Optimal positive airway pressure therapy may have salutary effects on cardiovascular diseases that are associated with OSA.

10

Mechanical airway obstruction

Respiratory noises may be more pronounced in the inspiratory or expiratory phase of respiration, depending on location of obstruction. Diagnosed via flow-volume loop.

11

Cystic fibrosis

Associated with thick, purulent sputum containing bacteria and with GI symptoms due to pancreatic insufficiency. Recurrent respiratory infections may be present without GI or other system involvement.