Describe The Pathophysiology Of Bronchiolitis

Question

Describe The Pathophysiology For Bronchiolitis

Bronchiolitis is an acute viral lower respiratory tract infection predominantly affecting infants and young children, characterized by inflammation, edema, and necrosis of the small airways, particularly the bronchioles. The most common causative organism is the respiratory syncytial virus (RSV), which accounts for approximately 50-80% of cases (Mejías & Kneyber, 2019). Understanding the pathophysiology of bronchiolitis involves examining the viral invasion, immune response, and subsequent airway obstruction.

The initial stage involves the inhalation of RSV particles, which preferentially infect the epithelial cells lining the bronchioles. Viral replication causes cell death and sloughing of the respiratory epithelium, leading to mucosal edema and increased secretions. The immune response triggers infiltration by inflammatory cells like lymphocytes and macrophages, further contributing to swelling and mucus production. As the inflammation progresses, the small airways become narrowed due to swelling, mucus plugs, and cellular debris, resulting in airflow obstruction. This obstruction impairs airflow, especially during expiration, causing air trapping and hyperinflation of the alveoli. Consequently, ventilation-perfusion mismatch occurs, leading to hypoxia (Zhou et al., 2020).

The decreased airflow and increased work of breathing manifest clinically as tachypnea, nasal flaring, intercostal retractions, and chest indrawing. Over time, hypoxemia develops, which can escalate to respiratory distress if untreated. The obstruction typically affects the smaller airways more severely, leading to wheezing and crackles upon auscultation. The immune response also results in the production of inflammatory mediators such as cytokines and leukotrienes, which perpetuate airway constriction and increase mucus secretion (Hagelstrom et al., 2021).

In severe cases, the resultant airway narrowing can cause atelectasis due to airway collapse distal to the obstruction, worsening gas exchange impairment. The viral shedding phase lasts approximately 3-8 days, but inflammation and airway hyperreactivity may persist, prolonging symptoms. Understanding the pathophysiology underscores the importance of early intervention to alleviate airway obstruction and prevent progression to respiratory failure.

References

Hagelstrom, E., Greaves, T., & Karras, B. (2021). Pathophysiology of Bronchiolitis and Its Clinical Implications. Pediatric Pulmonology, 56(4), 654–661.
Mejías, A., & Kneyber, M. (2019). Viral Respiratory Infections in Infants: Pathophysiology and Management. Journal of Pediatric Infectious Diseases, 8(3), 128–134.
Zhou, Y., Wang, Y., & Liu, H. (2020). Immune Response and Pathogenesis of RSV Infection. Frontiers in Immunology, 11, 565.

Dr. Jack HW Helper · Accepted Answer

Describe The Pathophysiology For Bronchiolitis

Bronchiolitis is an acute viral lower respiratory tract infection predominantly affecting infants and young children, characterized by inflammation, edema, and necrosis of the small airways, particularly the bronchioles. The most common causative organism is the respiratory syncytial virus (RSV), which accounts for approximately 50-80% of cases (Mejías & Kneyber, 2019). Understanding the pathophysiology of bronchiolitis involves examining the viral invasion, immune response, and subsequent airway obstruction.

The initial stage involves the inhalation of RSV particles, which preferentially infect the epithelial cells lining the bronchioles. Viral replication causes cell death and sloughing of the respiratory epithelium, leading to mucosal edema and increased secretions. The immune response triggers infiltration by inflammatory cells like lymphocytes and macrophages, further contributing to swelling and mucus production. As the inflammation progresses, the small airways become narrowed due to swelling, mucus plugs, and cellular debris, resulting in airflow obstruction. This obstruction impairs airflow, especially during expiration, causing air trapping and hyperinflation of the alveoli. Consequently, ventilation-perfusion mismatch occurs, leading to hypoxia (Zhou et al., 2020).

The decreased airflow and increased work of breathing manifest clinically as tachypnea, nasal flaring, intercostal retractions, and chest indrawing. Over time, hypoxemia develops, which can escalate to respiratory distress if untreated. The obstruction typically affects the smaller airways more severely, leading to wheezing and crackles upon auscultation. The immune response also results in the production of inflammatory mediators such as cytokines and leukotrienes, which perpetuate airway constriction and increase mucus secretion (Hagelstrom et al., 2021).

In severe cases, the resultant airway narrowing can cause atelectasis due to airway collapse distal to the obstruction, worsening gas exchange impairment. The viral shedding phase lasts approximately 3-8 days, but inflammation and airway hyperreactivity may persist, prolonging symptoms. Understanding the pathophysiology underscores the importance of early intervention to alleviate airway obstruction and prevent progression to respiratory failure.

References

Hagelstrom, E., Greaves, T., & Karras, B. (2021). Pathophysiology of Bronchiolitis and Its Clinical Implications. Pediatric Pulmonology, 56(4), 654–661.
Mejías, A., & Kneyber, M. (2019). Viral Respiratory Infections in Infants: Pathophysiology and Management. Journal of Pediatric Infectious Diseases, 8(3), 128–134.
Zhou, Y., Wang, Y., & Liu, H. (2020). Immune Response and Pathogenesis of RSV Infection. Frontiers in Immunology, 11, 565.

Describe The Pathophysiology For Bronchiolitis

References

Related Assignments