Objective, Chronic adenotonsillar hypertrophy (ATH) causing upper airway obstruction may lead to pulmonary hypertension and other cardiac abnormalities. This study aimed at the clinical and echocardiographic evaluation of cardiac abnormalities in children with chronic ATH and evaluation of these abnormalities after adenotonsillectomy.

Subjects and method, We studied 40 children with ATH indicated for adenotonsillectomy (group I) compared with another 35 sex and age matched normal children (Group II). Both groups were examined by otorhinolaryngologist and adenotonsillar hypertrophy was diagnosed with lateral neck x-ray. Clinical and echocardiographic examinations were compared in both groups. Adenotonsillectomy were performed in group I and reevaluation of clinical and echocardiographic findings were performed 6 months later in this group and results were compared with the preoperative findings in the same group.

Results, Compared with group II, group I has a significantly higher pulmonary artery pressure, right ventricular size, Interventricular septal wall thickness, left ventricular end-diastolic dimension, and longer E-wave deceleration time. Postoperative echocardiographic findings showed statistically significant decrease only in pulmonary artery pressure and E-wave deceleration time. Significant improvement in clinical symptoms and growth parameters were also noted postoperatively in group II.

Conclusion, Upper airway obstruction in children with ATH is associated with cardiac structural and functional abnormalities as demonstrated by echocardiography. Some of these abnormalities i.e. pulmonary hypertension and delayed LV diastolic relaxation are reversible after adenotonsillectomy.

Keywords, adenotonsillar hypertrophy, adenotonsillectomy, echocardiography, cardiac dysfunction

ATH, chronic adenotonsillar hypertrophy; SDB, sleep-disordered breathing; OSA, obstructive sleep apnea; LVESD, left ventricular end systolic diameter; LVEDD, left ventricular end diastolic diameter; FS, fractional shortening; EF, ejection fraction; IVSD, interventricular septum diastolic thickness; LA, left atrium; RVD, RV diastolic diameter; DT, deceleration time; TR, tricuspid regurgitation

Adenoids are located on the posterior nasopharyngeal wall posterior to the nasal cavity. They are a component of the Waldeyer ring of lymphoid tissue in the oropharynx and nasopharynx that consists mainly of the adenoids, the palatine tonsils, and the lingual tonsils.¹ Adenoids are present at birth and then begin to enlarge. They, along with the tonsils, continue to grow until individuals are aged 5-7 years.² Adenotonsillar enlargement is the most common cause of pharyngeal airway obstruction in infants and children.³ Frequent and loud snoring is a very frequent condition in prepubertal children affecting approximately 10% of all 2-8 year old children. Often this is mild and has no sequalae. However when constant and severe obstruction is present, a condition of sleep-disordered breathing (SDB) develops which leads to disturbed sleep, snoring, behavioral abnormalities, and sometimes growth failure. Long standing SDB is known to cause hypoxia, polycythemia, elevation of pulmonary artery pressure and cor-pulmonale.^4,5 Adult patients with obstructive sleep apnea (OSA) have higher morbidity and mortality due to cardiovascular disease compared with the general population.^6–12 Cardiac dysfunction, nocturnal hypertension, and myocardial and cerebral ischemia during obstructive apnea have been documented in adults.^13–16 In pediatric patients, severe adenotonsillar hypertrophy can lead to pulmonary arterial hypertension, cor-pulmonale, and congestive heart failure.¹³ However, neither the early stages of the pathophysiological changes that link adenotonsillar hypertrophy to cardiovascular disease nor the long-term impact of the disorder on the cardiovascular system are well understood. So, in the present study, we evaluated cardiac functions in children with chronic ATH mandating adenotonsillectomy, using echocardiographic and clinical evaluation before and after adenotonsillectomy.

Two groups were included in this study; group I included children who were admitted to ENT inpatient for adenotonsillectomy because of significant chronic ATH diagnosed by Otorhinolaryngeal examination and confirmed by lateral neck X-ray associated with marked sleep snoring for the last 6 months. Group II included age and sex matched normal healthy children attending the pediatric outpatient clinic in the same hospital during the same period of time.

Phase (I): pre-adenotonsillectomy phase

In this phase both groups underwent the following,

1. History taking (from parents) focusing on upper airway obstructive symptoms including snoring, mouth-breathing during sleep, restless sleeping, daytime somnolence, hyponasal voice and, nocturnal enuresis.
2. Complete clinical examination including, pulse, blood pressure, weight, height and complete cardiac examination.
3. Routine laboratory studies including complete blood count, Anti-streptolysine O titer, and erythrocyte sedimentation rate.
4. 12 leads surface electrocardiography.
5. Trans-thoracic echocardiography.

Phase (II): post-adenotonsillectomy phase

In this phase study group only was subjected to adenotonsillectomy in the same hospital within a week from the initial evaluation and re-evaluated by clinical and echocardiographic examination 6 months latter for comparison with the preoperative findings in the same group.

Echocardiography

Was performed in both groups pre-operatively and only in group I post-operatively. Two-dimensional, two-dimensionally directed M-mode, and color, pulsed and continuous-wave Doppler tracings were recorded using the Sonos 5,500 Ultrasound Imaging System (Agilent, Andover, MA) with 5 MHz phased-array transducer. We measured Left ventricular end systolic and end diastolic diameters (LVESD, LVEDD), fractional shortening (FS), ejection fraction (EF), Interventricular septum diastolic thickness (IVSD), Left atrium diastolic diameter (LA) and RV diastolic diameter (RVD). Doppler parameters included mitral E-wave (E), mitral A-wave (A) and mitral E-wave deceleration time (DT). Pulmonary artery systolic pressure was estimated using the tricuspid regurgitant velocity or the pulmonary acceleration time if no adequate tricuspid regurgitant Doppler signal could be obtained.^8,10 All measurements and estimations were made according to the recommendations of the American Society of Echocardiography.¹⁷ All studies were recorded on VHS videotapes and analyzed by a blinded experienced cardiologist. All measurements were made under standardized resting conditions with the child in the supine position after a minimum rest period of 5 minutes. Sedation was used only with non-cooperative children. Pre-operative and post-operative echocardiographic findings were compared within group I and pre-operative findings of group I were compared with group II.

Statistical analysis

Collected data was analyzed using the Statistical Package for Social Sciences 15 (SPSS Inc., Chicago, IL, USA).Chi square and the Fisher's exact test were used to test significance of the difference between qualitative data, Student's t test was used to test significance of the difference between quantitative data. Probability value (P) <0.05 was considered statistically significant.

We enrolled 40 (23 males, and 17 females) children in group I with a mean age 6.5+1.76 years. Group II included 35 (19 males, and 16 females) normal healthy children with a mean age 6.1+1.68 years, Growth parameters including weight, height, their percentiles, and body mass index showed statistically significant difference between control group (II) and preoperative state of study group (I) (p-value < 0.05). In post operative state of group (I) these parameters improved significantly and become statistically not different from control group (II) (P-value > 0.05) Table 1.

Table 2 demonstrates the improvement in obstructive symptoms postoperatively compared to the preoperative state (p-value <0.05). The highest improvement rates were noted in hyponasal voice and daytime somnolence (100%). All laboratory findings (red cell count, ESR, ASOT, and CRP) were significantly higher in the preoperative phase of group I compared with group II, and only ESR and CRP showed significant improvement postoperatively that reached normal levels of control group Table 3. Mild-moderate functional tricuspid regurgitation (TR) was reported by color Doppler in 32 (80%) children in group I, and in only 19 (54%) children in group II (P< 0.001). In cases with adequate continuous-wave TR Doppler signal, it was used for estimation of pulmonary artery pressure, while in the absence of this clear signal, pulmonary artery acceleration time (obtained by pulsed-wave Doppler) was used.¹⁷ Comparing pre-operative phase of group I with group II, pulmonary artery systolic pressure was significantly higher in group I (25.15±8.49 and 16.25±5.41 mmHg, P < 0.001). Similarly, RV size as measured by the diastolic diameter was significantly larger in group I (1.7±0.2 and 1.3±0.3 cm, P<0.02). LV size as measured by LVEDD was larger in the group I (3.7±0.6 and 3.2±0.5 cm, P<0.01) and similarly the ventricular septal thickness was higher in this group (7.1±1.2 and 6.2±1.4 cm, p< 0.02). Mitral E-wave deceleration time was longer in group I (175±46 and 128±26 ms, P< 0.001) indicating improper LV diastolic relaxation Table 4.

In the post-operative state of group I the only improved echocardiographic indices were the pulmonary artery systolic pressure (16.25±5.41j versus 25.15±8.49 mmHg in preoperative state, P< 0.001) Figure 1 and the mitral E-wave deceleration time (130±28 versus 175±46 ms in the preoperative state, P< 0. 0001) Figure 2 indicating better LV diastolic relaxation. Most upper airway obstruction in an otherwise healthy child is caused by adenotonsillar hypertrophy. And obstructive sleep apnea caused by this abnormality is a definite indication for surgery.^18–21 Prolonged partial airway obstruction during sleep may result in significant hypercapnia and hypoxemia, as well as daytime somnolence, night sweats, irritability, hyperactivity, behavioral problems, personality changes, poor school performance, morning headache, failure to thrive, obesity, and enuresis.^19–27 Children with ATH may also develop cardiopulmonary complications associated with hypercarbia and hypoxemia.^26,27 In the present study, Pre-operative clinical findings showed high prevalence of symptoms of adenotonsillar hypertrophy including snoring (100%), mouth breathing during sleep (95%), mouth breathing during daytime (75%), hyponasal voice (77.5%), restless sleeping (67.5%), daytime somnolence (52.5%) and nocturnal enuresis (42.5%). There were dramatic improvement of these clinical findings postoperatively with complete disappearance of both daytime somnolence and hyponasal voice and overall improvement in symptoms ranging from 77% to 100%.

Figure 1 Mean pulmonary artery pressure in both pre and post operative states of study group.

Figure 2 Mean deceleration time in both pre and post operative states of study group.

These findings are consistent with those reported by Miman et al.²⁸ who studied the improvement in symptom score of 17 children (mean age 41+37 months) with adenotonsillar hypertrophy after adenotonsillectomy. There was a significant improvement in symptoms after adenotonsillectomy as symptoms score dropped from 4.88±1.17 preoperatively to 0.53±0.72 postoperatively (p < 0.05). The significant improvement in growth parameters postoperatively reported in our study population is consistent with what has been reported by Selimoğlu et al.,²⁹ who studied 29 prepubertal children with obstructive adenotonsillar hypertrophy and recorded significant improvement in weight and height scores post-adenotonsillectomy. Results of echocardiographic examinations in our study revealed structural and functional abnormalities of both sides of the heart in patients with ATH. Mild-moderate functional TR was more prevalent in the case group than in the control group. PAP, RV size and Interventricular septal thickness were significantly higher in patients than in the control group and this observation has been reported in many other studies.^30,31 The etiological factors that lead to rise in pulmonary artery pressure from chronic upper airway obstruction are not completely understood. Hypoxemia and hypercarbia associated with chronic upper airway obstruction are potent mediators of pulmonary vasoconstriction, resulting in rise in PAP, and right ventricular after load, finally causing right ventricular hypertrophy and right ventricular heart failure.^32–35 Postoperative improvement was observed only in the level of pulmonary artery pressure but not in RV size. This could be explained in the light of the early assessment of cardiac function (6 months postoperatively) that may be enough for drop in pulmonary arterial pressure but not for regression of RV size which may occur later on.^32–35

Left sided echocardiographic abnormalities were also noted in the case group in the form of significantly larger LVEDD and longer E-wave deceleration time. These changes reflect the inherent Interventricular interaction in both systole and diastole. The detected changes in the E-wave deceleration time may be the earliest finding among the measured left ventricular diastolic indices. There is slower drop in the rate of decrease of left ventricular pressure, and the duration of relaxation is prolonged into mid- or even late-diastole. So that, relaxation may continue into mid- or late-diastole, which means less filling of the left ventricle in mid-diastole and prolongation of the deceleration time on the transmitral flow velocity curve. Left ventricular diastolic relaxation as measured by E-wave deceleration time showed significant postoperative improvement. A similar observation has been reported by Görür et al.³⁶

Study limitations

The small number of patients included in this study represents a methodological limitation and studying a larger patient population is recommended. Including patients with severe ATH indicated for adenotonsillectomy in this study may hinder the extrapolation of its results to milder forms of ATH. Indirect echocardiographic estimation of PAP using two different methods in this study is another limitation and a more objective and direct measurement of the pressure using invasive catheterization should be studied.

Upper airway obstruction in children with ATH is associated with cardiac structural and functional abnormalities as demonstrated by echocardiography. Some of these cardiac abnormalities i.e. pulmonary hypertension and delayed LV diastolic relaxation are reversible after adenotonsillectomy.

None.

The authors declare that there are conflicts of interest.

None.

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