Pathogenesis and Hemodynamic Alterations
The development of a spasmodic coughing attack begins with the formation of a persistent excitation focus in the central nervous system. Impulses from the laryngeal receptors reach the brain, directly affecting the respiratory and autonomic centers. A sharp drop in the excitation threshold occurs: now any minor, nonspecific irritation can trigger a severe spasmodic cough attack.
A coughing fit triggers a cascade of hemodynamic disturbances:
- Pronounced spasm of the laryngeal muscles and bronchial tree occurs.
- Peripheral blood vessels undergo a reflex spasm.
- Blood congestion develops in the superior vena cava system.
- As a result, centrally mediated circulatory impairment progresses, leading to systemic hypoxia.
Clinical Manifestations
A classic paroxysmal coughing attack follows a strict pattern. First, a series of short, consecutive, staccato exhalations occurs, followed by a convulsive, deep inspiration (whoop). This distressing episode ends with the expulsion of very viscous sputum or reflex vomiting.
It is crucial to remember the specific presentation in infants. In early infancy, the typical spasmodic cough is entirely absent. Instead, the disease manifests with apnea (cessation of breathing), posing a direct threat of asphyxia.
Pathological Anatomy
Macroscopic Appearance The mucous membrane of the upper respiratory tract appears sharply hyperemic (engorged) and covered abundantly with viscous mucus. The lungs are in a state of emphysematous hyperinflation, which in severe cases can lead to spontaneous pneumothorax. A classic marker of the disease, visible during an oral examination, is the presence of characteristic tears and small ulcers on the lingual frenulum (resulting from trauma against the lower teeth during coughing).
Microscopic Appearance
- Respiratory tract: serous inflammation predominates in the larynx, trachea, and bronchial tree.
- Pulmonary parenchyma: tissue edema, vascular congestion, foci of atelectasis, and compensatory hyperplasia of peribronchial lymph nodes are detected.
- Central nervous system: edema and small perivascular hemorrhages are registered in the brain against the background of hypoxia.
Complications and Outcomes
The disease itself is protracted, lasting from 1.5 to 3 months. The main structural complications of pertussis are related less to the pathogen itself and more to secondary infections. The superposition of bacterial flora leads to severe panbronchitis and peribronchial pneumonia.
Currently, the outcome is predominantly favorable. The sole major exception is the risk of infant mortality from developing asphyxia during apnea episodes.