Cardiopulmonary Changes Secondary to Chronic Adenotonsillitis

Abstract

\s=b\Thirty children with lower respiratory tract infection of varying degrees secondary to chronic tonsillitis and/or enlarged adenoids were studied clinically and roentgenographically. Symptoms and signs of alveolar hypoventilation and signs of cor pulmonale were present in two of them. These symptoms and signs improved markedly after adenoidectomy and tonsillectomy. The relationship of the lung changes to the incidence of cor pulmonale is discussed. The development of recurrent attacks of severe lower respiratory tract infection secondary to diseased tonsils and adenoids is believed to play an important role in the pathogenesis of cor pulmonale in children with upper respiratory tract obstruction due to chronically enlarged tonsils and adenoids.

Release of NT-pro brain natriuretic peptide in children before and after adenotonsillectomy

“…This airway obstruction may result in alveolar hypoventilation, hypoxia and hypercarbia while asleep [12][13][14]. This may lead to hypoxic pulmonary vasoconstriction and also increased pulmonary artery pressures with high pulmonary vascular resistance, if the disease persists for a long time [12].…”

“…This may lead to hypoxic pulmonary vasoconstriction and also increased pulmonary artery pressures with high pulmonary vascular resistance, if the disease persists for a long time [12]. In addition, secreted vasoactive substances, such as endothelin-1, from endothelial cells and increased permeability to Ca ++ due to chronic hypoxia and hypercarbia in alveolar capillary ends are possibly responsible of hypoxic pulmonary vasoconstriction [14,15]. In children with adenotonsillar hypertrophy, chronic nocturnal hypoxia and hypercarbia decrease sensitivity of respiratory center in central nervous system to peripheral stimuli and existing upper airway resistance syndrome result in obstructive sleep apnea syndrome [16].…”

Pulmonary hypertension due to recurrent juvenile laryngeal papillomatosis

“…The relationship between upper airway obstruction and pulmonary hypertension is well established, with the most common cause of upper airway obstruction leading to pulmonary hypertension being adenotonsillar hyperplasia [2][3][4][5][6].…”

“…We admit a number of patients with severe airway obstruction due to laryngeal papillomatosis, but only three of these patients have had pulmonary hypertension. There is a poorly understood individual variability in the reactivity of the pulmonary vasculature to the hypoxic stimulus and it appears that the inherent reactivity of the pulmonary vascular bed to hypoxic stimuli may be a significant factor in the development of pulmonary hypertension [6].…”

“…Although the association between upper airway obstruction due to adenotonsillar hyperplasia and pulmonary hypertension has been well described [2][3][4][5][6], the association between laryngeal papillomatosis and pulmonary hypertension has not previously been documented. We report three patients with recurrent juvenile laryngeal papillomatosis that presented with varying degrees of pulmonary hypertension.…”