Adenotonsillar Hypertrophy and Cardiopulmonary Status: A Correlative Study

Introduction Adenotonsillar hyperplasia in childhood is a common phenomenon. It has been reported in the literature that increased upper-airway resistance resulting from hypertrophied tonsils and adenoids can cause intermittent airway obstruction, chronic alveolar hypoventilation, and even lead to severe cardiopulmonary complications such as right ventricular (RV) failure and cor-pulmonale, a near-lethal culmination of pulmonary artery hypertension (PAH). This study was undertaken to explore and examine the association of adenotonsillar hypertrophy and cardiopulmonary status in patients with complaints of upper airway obstruction below the age of 20 years and to analyze the effect of adenotonsillar enlargement on pulmonary function tests and cardiac aberration reflected in the electrocardiography (ECG) changes.  Methods This study included patients visiting or admitted to the Otolaryngology/Ear, Nose, and Throat (ENT) and Paediatrics department of Acharya Vinoba Bhave Hospital, Sawangi (Meghe), Wardha, Maharashtra, India. It is an Observational Prospective Study conducted on 75 Patients (50 cases and 25 controls) below the age of 20 years. Inclusion criteria for cases included all patients of adenoid hypertrophy (AH) and adenotonsillar hypertrophy (ATH). Inclusion criteria for controls comprised all patients with a history and clinical examination not suggestive of any upper airway and pulmonary disease. All the patients were subjected to pulmonary function tests (PFT) and electrocardiography (ECG), and the values were compared. Results It was found that there was a decrease in the value of the parameters of the pulmonary function tests (PFT), which includes forced expiratory volume in the first second (FEV1), forced vital capacity (FVC), the ratio of the forced expiratory volume in the first one second to the forced vital capacity of the lungs (FEV1/FVC) and peak expiratory flow rate (PEFR) with increasing severity of the endoscopic grades of adenoid hypertrophy. This was found to be statistically significant. All the PFT parameters were significantly lower in the subset of patients with ATH compared to those with AH only, emphasizing the compounding effect of tonsillar volume. Between case and control subjects also, these differences were statistically significant. Seventeen (34%) out of the 50 patients studied in the present work were found to have abnormalities in their ECG, while no subject in the control group had any departure from normal. Nine of these 17 patients had AH, and eight had the adenotonsillar disease. In the 9 patients (18%) with AH, sinus arrhythmia was seen in 5 (10%), sinus tachycardia in 3 (6%), and Mobitz type 1 block in 1 (2%) patients. In 8 patients (16%) with AH, sinus arrhythmia was seen in 4 (8%), sinus tachycardia in 3 (6%), and Mobitz type 1 block in 1 (2%) patients. Overall, sinus arrhythmia was the commonest finding seen in 9 patients (18%). Conclusion Chronic obstructive adenotonsillar hypertrophy causes significant cardiovascular and pulmonary changes, which is often overlooked in the clinical setting. Symptoms of progressive pulmonary hypertension are minimal until the rapid onset of severe cardiac decompensation occurs. These entire cascades of events are reversible in the early stages and thus mandate early detection and treatment. Performing PFT and ECG in children with adenotonsillar disease is not mandatory but profitable even in the absence of obvious symptoms of upper airway obstruction.