Abstract:ObjectivesThe purpose of the present study is to emphasize the efficacy of the myocardial performance index and tricuspid annular plane systolic excursion (TAPSE) in the determination of impaired cardiac functions and recovery period following the treatment in children with adenoid and/or tonsillar hypertrophy.MethodsFifty-three healthy children after routine laboratory, imaging and clinical examinations, with adenoid and/or tonsillar hypertrophy were evaluated before and 3 months after adenotonsillectomy for … Show more
“…According to the study by Acar et al [17] the TAPSE value was lower than normal, and elevated 3 months after T&A in children with ATH. TAPSE, which is easy and fast to perform, provides information about the right ven¬tricular systolic functions.…”
Purpose Adenotonsillar hypertrophy (ATH) that causes upper airway obstruction might lead to chronic hypoxemic pulmonary vasoconstriction and right ventricular (RV) dysfunction. We aimed to evaluate whether adenotonsillectomy (T&A) in children suffering from obstructive sleep apnea (OSA) due to severe ATH could improve RV function.Methods Thirty-seven children (boy:girl=21:16; mean age, 9.52±2.20 years), who underwent T&A forsleep apnea due to ATH, were included. We analyzedthe mean pulmonary artery pressure (mPAP), the presence and the maximal velocity of tricuspid regurgitation (TR), the tricuspid annular plane systolic excursion (TAPSE), and the right ventricular myocardial performance index (RVMPI) with tissue Doppler echocardiography (TDE) by transthoracic echocardiography pre- and post-T&A. The follow-up period was 1.78±0.27 years.Results Only the RVMPI using TDE improved after T&A (42.18±2.03 vs. 40±1.86, P=0.001). The absolute value of TAPSE increased (21.45±0.90 mm vs. 22.30±1.10 mm, P=0.001) but there was no change in the z score of TAPSE pre- and post-T&A (1.19±0.34 vs. 1.24±0.30, P=0.194). The mPAP was within normal range in children with ATH, and there was no significant difference between pre- and post-T&A (19.6±3.40 vs. 18.7±2.68, P=0.052). There was no difference in the presence and the maximal velocity of TR (P=0.058).Conclusion RVMPI using TDE could be an early parameter of RV function in children with OSA due to ATH.
“…According to the study by Acar et al [17] the TAPSE value was lower than normal, and elevated 3 months after T&A in children with ATH. TAPSE, which is easy and fast to perform, provides information about the right ven¬tricular systolic functions.…”
Purpose Adenotonsillar hypertrophy (ATH) that causes upper airway obstruction might lead to chronic hypoxemic pulmonary vasoconstriction and right ventricular (RV) dysfunction. We aimed to evaluate whether adenotonsillectomy (T&A) in children suffering from obstructive sleep apnea (OSA) due to severe ATH could improve RV function.Methods Thirty-seven children (boy:girl=21:16; mean age, 9.52±2.20 years), who underwent T&A forsleep apnea due to ATH, were included. We analyzedthe mean pulmonary artery pressure (mPAP), the presence and the maximal velocity of tricuspid regurgitation (TR), the tricuspid annular plane systolic excursion (TAPSE), and the right ventricular myocardial performance index (RVMPI) with tissue Doppler echocardiography (TDE) by transthoracic echocardiography pre- and post-T&A. The follow-up period was 1.78±0.27 years.Results Only the RVMPI using TDE improved after T&A (42.18±2.03 vs. 40±1.86, P=0.001). The absolute value of TAPSE increased (21.45±0.90 mm vs. 22.30±1.10 mm, P=0.001) but there was no change in the z score of TAPSE pre- and post-T&A (1.19±0.34 vs. 1.24±0.30, P=0.194). The mPAP was within normal range in children with ATH, and there was no significant difference between pre- and post-T&A (19.6±3.40 vs. 18.7±2.68, P=0.052). There was no difference in the presence and the maximal velocity of TR (P=0.058).Conclusion RVMPI using TDE could be an early parameter of RV function in children with OSA due to ATH.
“…Children with DS and OSA who underwent adenotonsillectomy showed significant improvement of obstructive and central apneic indices [42][43][44][45]. Additionally, OSA likely plays a long-term role in the development of PH, and adenotonsillectomy may help halt or reverse the progression of PH and right heart disease [46,47].…”
Approximately 50% of newborns with Down syndrome have congenital heart disease. Non-cardiac comorbidities may also be present. Many of the principles and strategies of perioperative evaluation and management for patients with congenital heart disease apply to those with Down syndrome. Nevertheless, careful planning for cardiac surgery is required, evaluating for both cardiac and noncardiac disease, with careful consideration of the risk for pulmonary hypertension. In this manuscript, for children with Down syndrome and hemodynamically significant congenital heart disease, we will summarize the epidemiology of heart defects that warrant intervention. We will review perioperative planning for this unique population, including anesthetic considerations, common postoperative issues, nutritional strategies, and discharge planning. Special considerations for single ventricle palliation and heart transplantation evaluation will also be discussed. Overall, the risk of mortality with cardiac surgery in pediatric patients with Down syndrome is no more than the general population, except for those with functional single ventricle heart defects. Underlying comorbidities may contribute to postoperative complications and increased length of stay. A strong understanding of cardiac and non-cardiac considerations in children with Down syndrome will help clinicians optimize perioperative care and long-term outcomes.
“…Subsequent research consolidated this finding [43][44][45][46][47] and has led to FDA approval of inhaled NO as a treatment modality for neonatal pulmonary hypertension in 1999 [48,49]. It is well documented in the literature that chronic oral breathing secondary to adeno-tonsillar hypertrophy induces pulmonary hypertension, right ventricular strain, and eventually right heart failure [50][51][52][53][54][55]. This entity has been termed "hypoxic corpulmonale" and has been erroneously attributed to alveolar hypoventilation [56].…”
Background: The physiological functions of the paranasal sinuses are as yet unclear, and it is often assumed that these empty air-filled spaces have no vital function in our body. Recently, nitric oxide has been reported to be synthetized in high concentration by the paranasal sinuses which seems to be the main function of these air-filled empty spaces. Body of abstract: The functional role of the paranasal sinuses is still ambiguous despite the several hypotheses that have been put forward to justify their existence. Although it has been recently demonstrated that the paranasal sinuses produce large amounts of nitric oxide (NO), otolaryngologists overwhelmed by attempting to unravel the enigmatic etiology underlying chronic rhinosinusitis have interpreted the high NO output in this context. Nevertheless, NO prime function is vasodilation and has long been recognized to be produced by the endothelial cells. In this review, evidence in the literature is piled and pieces of the puzzle are put together to show that NO synthesized in the paranasal sinuses functions as an airborne messenger that induces pulmonary vasodilation and thereby decreases the workload on the heart. Recognition that the paranasal sinuses are in fact an organ with known function is likely to foster further research and has an impact on our current surgical philosophy. Conclusion: The paranasal sinuses seem to play a vital physiological role in our body rather than being evolutionary remnants as initially thought. They are likely responsible for regulating the pulmonary blood pressure thereby preventing pulmonary hypertension.
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