Breath Easy: Navigating Asthma and COPD Exacerbations
/Asthma
Background
Asthma is a chronic inflammatory disorder of the airways characterized by episodes of wheezing, coughing, shortness of breath, and chest tightness. While it can affect individuals of any age, it is often diagnosed in childhood. In an emergency context, asthma can quickly escalate from mild to life-threatening, necessitating prompt recognition and intervention. Asthma exacerbations are often precipitated by a variety of factors, including allergens, respiratory infections, exercise, cold air, and irritants like smoke or strong odors.
The Global Initiative for Aѕthma (GINA) has set forth a formal definition for asthma as "a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheеze, shortness of breath, chest tightness, and cough that vary over time and in intensity, together with variable expiratory airflow limitation.”[1]
Epidemiology
Worldwide, it is estimated that approximately 260 million individuals have aѕthma, with the estimated prevalence in the United States being 25 million individuals. [2,3] In 2020, the CDC estimates that asthma exacerbations accounted for almost 1,000,000 ED visits and almost 100,000 inpatient hospitalizations. [4]
Pathophysiology
Atopy, or the genetic predisposition to develop allergic conditions, is the strongest risk factor for the development of asthma. Currently, asthma is best thought of as a syndrome with multiple underlying mechanisms that contribute in varied amounts between individuals with differing phenotypes. [5]
Mast cell activation by allergens plays a predominant role in both the initial and late phase of the asthmatic reaction. In the early phase, provocative factors such as allergens or cold result in activation of mast cells with release of mediators such as histamine, prostaglandin D2, and cysteinyl leukotrienes, which all cause direct contraction of airway smooth muscle. During the late phase, recurrence of bronchoconstriction occurs several hours later due to an influx of inflammatory cells such as monocytes, dendritic cells, neutrophils, and T lymphocytes, eosinophils, and basophils. These cells release mediators that both cause smooth muscle contraction and result in direct airway epithelial damage, airway remodeling, and fibrosis.
The narrowing of the airway lumen is the primary mechanism behind the clinical presentation of acute asthma exacerbation. This narrowing is due to contraction of smooth muscle, thickening of the airway wall due to edema and cellular components described above, mucous plugging, and airway remodeling.
Presentation
Acute asthma exacerbation can present with:
Dyspnea
Wheezing
Cough +/- sputum production
Prolonged expiration
Accessory muscle use
Reduced peak expiratory flow rate
Respiratory fatigue/failure
Paradoxical respiration
Altered mental status
Silent chest on auscultation
Cyanosis
Evaluation/Management
See our full TamingtheSRU protocol here
COPD
Introduction
Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory disorder that leads to obstructed airflow from the lungs. This progressive disease includes conditions such as emphysema and chronic bronchitis, and it primarily affects older adults. COPD is characterized by episodes of exacerbations, which require prompt recognition and management due to their potential to escalate rapidly and cause significant morbidity and mortality. Exacerbations are often precipitated by various triggers, including respiratory infections, environmental pollutants, and allergens.
Epidemiology
Globally, more than 300 million people are affected by COPD, marking it as the third leading cause of death worldwide. [6,7] In the United States, COPD is estimated to affect about 16 million people, with many more likely undiagnosed. Annually, there are approximately 1.5 million emergency department (ED) visits and about 700,000 hospitalizations attributed to COPD exacerbations. [8] These exacerbations significantly contribute to healthcare costs and adversely affect the quality of life for patients with COPD.
Pathophysiology
COPD is predominantly associated with a significant chronic inflammatory response to harmful particles or gases, predominantly from tobacco smoke. The pathophysiology involves structural changes and narrowing of the airways due to this persistent inflammation. Exacerbations often result from increased airway inflammation, increased mucus production, and a heightened inflammatory response.
The chronic inflammation leads to structural changes such as loss of elasticity, enlargement of air spaces (emphysema), and obliteration of the small airways. During exacerbations, increased inflammation due to infections or irritants exacerbates airway obstruction and impairs gas exchange further. This results in a vicious cycle of hypoxia, hypercapnia, and increased respiratory drive, which may lead to respiratory failure if not promptly managed.
Presentation
Patients with COPD exacerbation typically present with:
Increase in cough, sputum, or dyspnea beyond the normal day-to-day variation
Hypoxemia
Tachypnea
Tachycardia
Hypertension
Cyanosis
Altered mental status
Hypercapnia
Accessory respiratory muscle use
Pursed-lip exhalation
Reduced exercise/activity tolerance
Evaluation/Management
Workup
ABC’s – Assess airway, respiratory, and mental status
Vitals – urgent intervention as indicated
Supplemental O2 to 88-92% O2 Sat
NIPPV for work of breathing
Intubation
CBC, BMP, VBG/ABG
CXR
ECG
Consider:
Sputum culture
BNP
Troponin
Lactate
PT-INR/PTT
D-dimer
Lung ultrasound / POCUS
Conclusion
Both asthma and COPD, while distinct in their pathophysiology and population demographics, share a common thread when it comes to their acute exacerbations: the need for rapid, accurate assessment and timely intervention. Armed with algorithms and with albuterol in hand, remember to take a deep breath and help your patients to do so as well!
Post by blaine oldham, MD
Dr. Vaughn is a PGY-1 in Emergency Medicine at the University of Cincinnati
Editing by Casey Glenn, MD and ryan LaFollette, MD
Dr. Glenn is a PGY-4 in Emergency Medicine. Dr. LaFollette is an Associate Professor in Emergency Medicine at the University of Cincinnati and co-editor of TamingtheSRU.com
References
2024 Global Initiative for Asthma (GINA) Report: Global Strategy for Asthma Management and Prevention. https://ginasthma.org/2024-report/
GBD 2019 Diseases and Injuries Collaborators. Global burden of 369 diseases and injuries in 204 countries and territories, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019. Lancet. 2020 Oct 17;396(10258):1204-1222. doi: 10.1016/S0140-6736(20)30925-9. Erratum in: Lancet. 2020 Nov 14;396(10262):1562. doi: 10.1016/S0140-6736(20)32226-1. PMID: 33069326; PMCID: PMC7567026
National Health Interview Survey. Current Asthma Population Estimates — in thousands by Age, United States, 2018. https://www.cdc.gov/asthma/nhis/2018/table3-1.htm
https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm
Moore WC, Meyers DA, Wenzel SE, Teague WG, Li H, Li X, D'Agostino R Jr, Castro M, Curran-Everett D, Fitzpatrick AM, Gaston B, Jarjour NN, Sorkness R, Calhoun WJ, Chung KF, Comhair SA, Dweik RA, Israel E, Peters SP, Busse WW, Erzurum SC, Bleecker ER; National Heart, Lung, and Blood Institute's Severe Asthma Research Program. Identification of asthma phenotypes using cluster analysis in the Severe Asthma Research Program. Am J Respir Crit Care Med. 2010 Feb 15;181(4):315-23. doi: 10.1164/rccm.200906-0896OC. Epub 2009 Nov 5. PMID: 19892860; PMCID: PMC2822971.
Ruvuna L, Sood A. Epidemiology of Chronic Obstructive Pulmonary Disease. Clin Chest Med. 2020 Sep;41(3):315-327. doi: 10.1016/j.ccm.2020.05.002. PMID: 32800187.
Saloni Dattani, Fiona Spooner, Hannah Ritchie and Max Roser (2023) - “Causes of Death” Published online at OurWorldinData.org. Retrieved from: 'https://ourworldindata.org/causes-of-death' [Online Resource]
Mannino DM, Homa DM, Akinbami LJ, Ford ES, Redd SC. Chronic obstructive pulmonary disease surveillance--United States, 1971-2000. MMWR Surveill Summ. 2002 Aug 2;51(6):1-16. PMID: 12198919.