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Reversible cardio-pulmonary changes due to adeno-tonsilar hypertrophy
International Journal of Pediatric Otorhinolaryngology 55 (2000) 203 – 206 www.elsevier.com/locate/ijporl
Case report
Reversible cardio-pulmonary changes due to adeno-tonsilar hypertrophy S. Ramakrishna a, V.S. Ingle b, Santosh Patel c, Prasanna Bhat b, J.E. Dada b, Fahim Ahmed Shah a, P.S.N. Murty a,* a Department of ENT, Ibri Regional Referral Hospital, P.B. No. 46, P.C. 516, Sultanate of Oman, Oman Department of Paediatrics, Ibri Regional Referral Hospital, P.B. No. 46, P.C. 516, Sultanate of Oman, Oman c Department of Anaesthesia, Ibri Regional Referral Hospital, P.B. No. 46, P.C. 516, Sultanate of Oman, Oman b
Received 31 March 2000; received in revised form 13 July 2000; accepted 14 July 2000
Abstract Adeno-tonsillar hypertrophy, with signs of upper airway obstruction is a common presentation in ENT clinics. Recently it is identified as a major cause of sleep apnea syndrome. Several isolated case reports of pulmonary hypertension and corpulmonale appeared in the literature. The authors report two such children aged less than 2 years with cardio-pulmonary changes occurring secondary to chronic adeno-tonsillar hypertrophy that were successfully treated with the surgical removal. © 2000 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Adeno-tonsillar hypertrophy; Pulmonary hypertension; Corpulmonale
1. Introduction Adeno-tonsillar hypertrophy affecting swallowing, breathing and Eustachian tubal function in children is a common presentation in paediatric practice. Corpulmonale and pulmonary hypertension can occur due to CO2 retention. Periodic cyanosis and apnoeic attacks can occur due to * Corresponding author. Fax: +968-491915. E-mail address: [email protected] (P.S.N. Murty).
chronic adenotonsillar hypertrophy. Sdralis and Berkovitz [1] clinically and radiologically evaluated the cardiopulmonary changes in asymptomatic adenotonsillar hypertrophy and found significant number of children showing alveolar hypoventilation. Despite the current climate of increasing reluctance to subject the children for removal of tonsils and adenoids, this unusual presentation of seemingly innocuous adenotonsillar hypertrophy leading to chronic hypoxia, opens a new set of indications for surgical removal. The role of
0165-5876/00/$ - see front matter © 2000 Elsevier Science Ireland Ltd. All rights reserved. PII: S 0 1 6 5 - 5 8 7 6 ( 0 0 ) 0 0 3 8 9 - X
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S. Ramakrishna et al. / Int. J. Pediatr. Otorhinolaryngol. 55 (2000) 203–206
paediatric otolaryngologist in evaluating and managing such affected children needs to be stressed.
2. Case 1 A male child aged 1.5 years was referred to ENT Department for noisy breathing, breathlessness and recurrent lower respiratory tract infections to exclude upper respiratory tract contribution for the present problems. On examination, a sick looking child, moderately nourished with tonsillary hypertrophy was noted. X-ray nasopharynx revealed gross adenoid hypertrophy, O2 desaturation of up to 75% on breathing air was observed episodically during sleep. ABG analysis showed hypercarbia. X-Ray chest showed cardiomegaly. ECG revealed p-pulmonale and right ventricular hypertrophy. ECHO studies showed right ventricular and right atrial hypertrophy with raised pulmonary arterial pressure (70 mm Hg). ABG showed pH 7.24; PaO235.6 mm of Hg; PaCO2-80.1 mm of Hg; HCO3-33.1 m mole/H; BE-2.9 n mole; SaO256.1%. Patient was receiving O2 at 6l/min. with nasal catheter. The child was intubated, sedated and paralyzed and kept on ventilator in intensive care unit.Adenoidectomy was carried out 2 days later and was kept on ventilator and monitoring. Child extubated himself in weaning period. Post extubation ABG was normal and O2 saturation was 95%. Child was sent home after an uneventful stay. A total of 5 months later, the child developed similar complaints and ABG showed PaO2-51.2 mm of Hg; PaCO2-45.6 mm of Hg; SaO2-85.9%. He underwent elective tonsillectomy and scraping of hypertrophied adenoid remnants. Postoperative period was uneventful and was symptom free at the time of discharge. Child remained free from symptoms in later follow up period up to 1yr. Child gained weight. ABG showed PaO2-80 mm of Hg; SaO2-97% as measured with pulse oximetry. ECHO (carried our after 3 months) revealed normal pulmonary systolic pressure dimensions of cardiac chambers were normal.
3. Case 2 A 10 month Omani male child was admitted for recurrent respiratory tract infections and noisy breathing and nasal obstruction under paediatricians care. He was being treated with antibiotics, decongestants and bronchodilator nebulizations. He was referred to ENT department for ruling out upper airway obstruction. On examination, the child was looking sick with obstruction and minimal inspiratory stridor. Nasal catheter could be passed. Direct laryngoscopy showed normal looking epiglottis with adequate glottic chink and normal vocal cord movements. X-Ray neck lateral view showed moderate adenoid hypertrophy. CT-scan was carried out and revealed enlarged adenoid mass in nasopharynx. ECG showed moderate right atrial hypertrophy. Echocardiography revealed moderate tricuspid regurgitation and mildly dilated right atrium. ABG showed pH-7.370; PCO2-48.3 mm of Hg; PO2-56.3 mm of Hg; HCO2-27.3 mm of Hg; BE-1.7 m mol/H; SaO2-87.9%-suggestive of respiratory acidosis. Child was treated for respiratory tract infection and after improving the condition. Adenoidectomy was carried out and followed in ICU for postoperative apnoea. He was discharged after 2 days. Child was followed for 6 months without recurrence of symptoms and ECG and ECHO reverted to normal findings. ABG showed the parameters to be within normal limits. 4. Discussion In addition to infective and obstructive symptomatology, lymphoid tissue enlargement in the Pharynx can lead to episodes of apnoeic attacks, hypoxia, and hypercarbia. Significant number of cardio-pulmonary complications due to obstruction of the upper airway are reported in English literature, thus opening up the discussion on the newer indications and early intervention in case of surgical removal of tonsils and adenoids. With increasing reluctance by parents regarding the removal of tonsils and adenoids, it is probable that paediatricians and the otolaryngologists see more and more number of affected children.
S. Ramakrishna et al. / Int. J. Pediatr. Otorhinolaryngol. 55 (2000) 203–206
Adenotonsillar hypertrophy leading to partial upper airway obstruction due to decrease in the cross sectional area of pharynx is more pronounced during sleep when the pharyngeal musculature is relaxed. Subtle differences in the dimensions of Oro-nasopharynx in relation to lymphoid hypertrophy can tilt the existing balance and lead to obstructive symptoms [2]. The effect can be transient, increasing with attacks of acute and recurrent infections acquired during the childhood. The cumulative effect might result in increased airway resistance, hypoventilation, hypoxemia and hypercarbia. Extreme variant of this entity is now called as obstructive sleep apnoea [3]. Hypoxemic pulmonary hypertension [4], cor pulmonale [5], Pulmonary edema [6] and failure to thrive [7] are the known and documented sequelae of chronic upper airway obstruction requiring multiple admissions, antibiotic therapy, intubation and assisted ventilation in intensive care units. Maurizi et al. [8] described that 65.7% of clinically normal children with adenoid hypertrophy showed pulmonary function abnormalities. Hence, it becomes mandatory that the children undergoing tonsillectomy and adenoidectomy should be screened for corpulmonale and the investigations should include electrocardiography, echocardiography, pulse oximetry and chest radiography. Early surgical intervention by Tonsillectomy, adenoidectomy or both might reverse the cardiopulmonary changes. Sdralis and Berkowitz [1] and Shechtman et al. [9] advocated urgent adenotonsillectomy for life threatening upper airway obstruction in children. Case No. 1 illustrates the point. The child had to be intubated, ventilated and then proceeded with emergency adenoidectomy after cardiopulmonary stabilization. Chronic obstruction can cause a stormy postoperative period because of the removal of the hypoxic drive by adenotonsillectomy and can lead to possible respiratory arrest [5]. These children might require post-operative re-intubation, ventilation and management in intensive care units. The other cause can be the hyper-reactive pulmonary vascular bed leading to medullary or
205
hypothalamic dysfunction responsible for persistent hypercarbia. Increase in similar reports in literature should alert the treating paediatrician and the otolaryngologist the possibility of the increased morbidity and mortality. The patients should be evaluated for clinical, radiographic, electrocardiographic and echocardiographic evidence of cardiopulmonary involvement and surgical removal of tonsils and adenoids should be contemplated at the earliest to reverse the pathologic changes.
Acknowledgements The authors wish to acknowledge Ali Khalfan Al Mandari, Director General of Health Services, Al Dhahira Region, Fahad Masoud Al Jassasi, Actg. Administrative Director, Ibri Regional Referral Hospital and John Idikula, Medical Superintendent, Ibri Regional Referral Hospital for their valuable encouragement and Abraham Thomas, Medical Secretary for secretarial assistance.
References [1] T. Sdralis, R.G. Berkowitz, Early adenotonsillectomy for relief of acute upper airway obstruction due to acute tonsillitis in children, Int. J. Otorhinolaryngol. 35 (1996) 25 – 29. [2] L. Brodsky, E. Adler, J.F. Stanievich, Naso and oropharyngeal dimensions in children with obstructive sleep apnea, Int. J. Pediatr. Otorhinolaryngol 17 (1989) 1 – 11. [3] D. Gryczynska, Jb O.K. Powa, A. Zakizewska, The influence of tonsillectomy on obstructive sleep apnoea with malocclusion, Int. J. Pediatr. Otorhinolaryngol, suppl. 32 (1995) 5225 – 5228. [4] J.W. Bland, F.K. Edwards, D. Brinsfield, Pulmonary hypertension and Chronic heart failure in children with chronic upper airway obstruction, new concepts and etiologic factors, Am. J. Cardiol. 223 (1969) 830 – 837. [5] O.E. Brown, S.C. Manning, B. Ridenour, Corpulmonale secondary to tonsillar and adenoidal hypertrophy: Management considerations, Int. J. Pediatr. Otorhinolaryngol. 16 (1988) 131 – 139. [6] M.J. Luke, A. Mehrizi, G.M. Folger, E.D. Rove, Chronic nasopharyngeal obstruction as cause of cardiomegaly, cor-
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S. Ramakrishna et al. / Int. J. Pediatr. Otorhinolaryngol. 55 (2000) 203–206
pulmonale and pulmonary edema, Pediatrics 37 (1966) 762 – 768. [7] R. Schiffmann, J. Faber, A.C. Edelman, Obstructive hypertrophic adenoids and tonsils reversed by tonsillectomy and adenoidectomy, Int. J. Pediatr. Otorhinolaryngol. 9 (1985) 183 – 187.
[8] M. Maurizi, G. Paludetti, T. Todisco, V. Dottoniri Maud Grassi, Pulmonary function studies in adenoid hypertrophy, Int. J. Pediatr. Otorhinolaryngol 2 (1980) 243 – 250. [9] F.G. Shechtman, P.T. Lin, R.L. Piuncus, Urgent adenotonsillectomy for upper airway obstruction, Int. J. Pediatr. Otorhinolaryngol. 24 (1992) 83 – 89.
.
Case report
Reversible cardio-pulmonary changes due to adeno-tonsilar hypertrophy S. Ramakrishna a, V.S. Ingle b, Santosh Patel c, Prasanna Bhat b, J.E. Dada b, Fahim Ahmed Shah a, P.S.N. Murty a,* a Department of ENT, Ibri Regional Referral Hospital, P.B. No. 46, P.C. 516, Sultanate of Oman, Oman Department of Paediatrics, Ibri Regional Referral Hospital, P.B. No. 46, P.C. 516, Sultanate of Oman, Oman c Department of Anaesthesia, Ibri Regional Referral Hospital, P.B. No. 46, P.C. 516, Sultanate of Oman, Oman b
Received 31 March 2000; received in revised form 13 July 2000; accepted 14 July 2000
Abstract Adeno-tonsillar hypertrophy, with signs of upper airway obstruction is a common presentation in ENT clinics. Recently it is identified as a major cause of sleep apnea syndrome. Several isolated case reports of pulmonary hypertension and corpulmonale appeared in the literature. The authors report two such children aged less than 2 years with cardio-pulmonary changes occurring secondary to chronic adeno-tonsillar hypertrophy that were successfully treated with the surgical removal. © 2000 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Adeno-tonsillar hypertrophy; Pulmonary hypertension; Corpulmonale
1. Introduction Adeno-tonsillar hypertrophy affecting swallowing, breathing and Eustachian tubal function in children is a common presentation in paediatric practice. Corpulmonale and pulmonary hypertension can occur due to CO2 retention. Periodic cyanosis and apnoeic attacks can occur due to * Corresponding author. Fax: +968-491915. E-mail address: [email protected] (P.S.N. Murty).
chronic adenotonsillar hypertrophy. Sdralis and Berkovitz [1] clinically and radiologically evaluated the cardiopulmonary changes in asymptomatic adenotonsillar hypertrophy and found significant number of children showing alveolar hypoventilation. Despite the current climate of increasing reluctance to subject the children for removal of tonsils and adenoids, this unusual presentation of seemingly innocuous adenotonsillar hypertrophy leading to chronic hypoxia, opens a new set of indications for surgical removal. The role of
0165-5876/00/$ - see front matter © 2000 Elsevier Science Ireland Ltd. All rights reserved. PII: S 0 1 6 5 - 5 8 7 6 ( 0 0 ) 0 0 3 8 9 - X
204
S. Ramakrishna et al. / Int. J. Pediatr. Otorhinolaryngol. 55 (2000) 203–206
paediatric otolaryngologist in evaluating and managing such affected children needs to be stressed.
2. Case 1 A male child aged 1.5 years was referred to ENT Department for noisy breathing, breathlessness and recurrent lower respiratory tract infections to exclude upper respiratory tract contribution for the present problems. On examination, a sick looking child, moderately nourished with tonsillary hypertrophy was noted. X-ray nasopharynx revealed gross adenoid hypertrophy, O2 desaturation of up to 75% on breathing air was observed episodically during sleep. ABG analysis showed hypercarbia. X-Ray chest showed cardiomegaly. ECG revealed p-pulmonale and right ventricular hypertrophy. ECHO studies showed right ventricular and right atrial hypertrophy with raised pulmonary arterial pressure (70 mm Hg). ABG showed pH 7.24; PaO235.6 mm of Hg; PaCO2-80.1 mm of Hg; HCO3-33.1 m mole/H; BE-2.9 n mole; SaO256.1%. Patient was receiving O2 at 6l/min. with nasal catheter. The child was intubated, sedated and paralyzed and kept on ventilator in intensive care unit.Adenoidectomy was carried out 2 days later and was kept on ventilator and monitoring. Child extubated himself in weaning period. Post extubation ABG was normal and O2 saturation was 95%. Child was sent home after an uneventful stay. A total of 5 months later, the child developed similar complaints and ABG showed PaO2-51.2 mm of Hg; PaCO2-45.6 mm of Hg; SaO2-85.9%. He underwent elective tonsillectomy and scraping of hypertrophied adenoid remnants. Postoperative period was uneventful and was symptom free at the time of discharge. Child remained free from symptoms in later follow up period up to 1yr. Child gained weight. ABG showed PaO2-80 mm of Hg; SaO2-97% as measured with pulse oximetry. ECHO (carried our after 3 months) revealed normal pulmonary systolic pressure dimensions of cardiac chambers were normal.
3. Case 2 A 10 month Omani male child was admitted for recurrent respiratory tract infections and noisy breathing and nasal obstruction under paediatricians care. He was being treated with antibiotics, decongestants and bronchodilator nebulizations. He was referred to ENT department for ruling out upper airway obstruction. On examination, the child was looking sick with obstruction and minimal inspiratory stridor. Nasal catheter could be passed. Direct laryngoscopy showed normal looking epiglottis with adequate glottic chink and normal vocal cord movements. X-Ray neck lateral view showed moderate adenoid hypertrophy. CT-scan was carried out and revealed enlarged adenoid mass in nasopharynx. ECG showed moderate right atrial hypertrophy. Echocardiography revealed moderate tricuspid regurgitation and mildly dilated right atrium. ABG showed pH-7.370; PCO2-48.3 mm of Hg; PO2-56.3 mm of Hg; HCO2-27.3 mm of Hg; BE-1.7 m mol/H; SaO2-87.9%-suggestive of respiratory acidosis. Child was treated for respiratory tract infection and after improving the condition. Adenoidectomy was carried out and followed in ICU for postoperative apnoea. He was discharged after 2 days. Child was followed for 6 months without recurrence of symptoms and ECG and ECHO reverted to normal findings. ABG showed the parameters to be within normal limits. 4. Discussion In addition to infective and obstructive symptomatology, lymphoid tissue enlargement in the Pharynx can lead to episodes of apnoeic attacks, hypoxia, and hypercarbia. Significant number of cardio-pulmonary complications due to obstruction of the upper airway are reported in English literature, thus opening up the discussion on the newer indications and early intervention in case of surgical removal of tonsils and adenoids. With increasing reluctance by parents regarding the removal of tonsils and adenoids, it is probable that paediatricians and the otolaryngologists see more and more number of affected children.
S. Ramakrishna et al. / Int. J. Pediatr. Otorhinolaryngol. 55 (2000) 203–206
Adenotonsillar hypertrophy leading to partial upper airway obstruction due to decrease in the cross sectional area of pharynx is more pronounced during sleep when the pharyngeal musculature is relaxed. Subtle differences in the dimensions of Oro-nasopharynx in relation to lymphoid hypertrophy can tilt the existing balance and lead to obstructive symptoms [2]. The effect can be transient, increasing with attacks of acute and recurrent infections acquired during the childhood. The cumulative effect might result in increased airway resistance, hypoventilation, hypoxemia and hypercarbia. Extreme variant of this entity is now called as obstructive sleep apnoea [3]. Hypoxemic pulmonary hypertension [4], cor pulmonale [5], Pulmonary edema [6] and failure to thrive [7] are the known and documented sequelae of chronic upper airway obstruction requiring multiple admissions, antibiotic therapy, intubation and assisted ventilation in intensive care units. Maurizi et al. [8] described that 65.7% of clinically normal children with adenoid hypertrophy showed pulmonary function abnormalities. Hence, it becomes mandatory that the children undergoing tonsillectomy and adenoidectomy should be screened for corpulmonale and the investigations should include electrocardiography, echocardiography, pulse oximetry and chest radiography. Early surgical intervention by Tonsillectomy, adenoidectomy or both might reverse the cardiopulmonary changes. Sdralis and Berkowitz [1] and Shechtman et al. [9] advocated urgent adenotonsillectomy for life threatening upper airway obstruction in children. Case No. 1 illustrates the point. The child had to be intubated, ventilated and then proceeded with emergency adenoidectomy after cardiopulmonary stabilization. Chronic obstruction can cause a stormy postoperative period because of the removal of the hypoxic drive by adenotonsillectomy and can lead to possible respiratory arrest [5]. These children might require post-operative re-intubation, ventilation and management in intensive care units. The other cause can be the hyper-reactive pulmonary vascular bed leading to medullary or
205
hypothalamic dysfunction responsible for persistent hypercarbia. Increase in similar reports in literature should alert the treating paediatrician and the otolaryngologist the possibility of the increased morbidity and mortality. The patients should be evaluated for clinical, radiographic, electrocardiographic and echocardiographic evidence of cardiopulmonary involvement and surgical removal of tonsils and adenoids should be contemplated at the earliest to reverse the pathologic changes.
Acknowledgements The authors wish to acknowledge Ali Khalfan Al Mandari, Director General of Health Services, Al Dhahira Region, Fahad Masoud Al Jassasi, Actg. Administrative Director, Ibri Regional Referral Hospital and John Idikula, Medical Superintendent, Ibri Regional Referral Hospital for their valuable encouragement and Abraham Thomas, Medical Secretary for secretarial assistance.
References [1] T. Sdralis, R.G. Berkowitz, Early adenotonsillectomy for relief of acute upper airway obstruction due to acute tonsillitis in children, Int. J. Otorhinolaryngol. 35 (1996) 25 – 29. [2] L. Brodsky, E. Adler, J.F. Stanievich, Naso and oropharyngeal dimensions in children with obstructive sleep apnea, Int. J. Pediatr. Otorhinolaryngol 17 (1989) 1 – 11. [3] D. Gryczynska, Jb O.K. Powa, A. Zakizewska, The influence of tonsillectomy on obstructive sleep apnoea with malocclusion, Int. J. Pediatr. Otorhinolaryngol, suppl. 32 (1995) 5225 – 5228. [4] J.W. Bland, F.K. Edwards, D. Brinsfield, Pulmonary hypertension and Chronic heart failure in children with chronic upper airway obstruction, new concepts and etiologic factors, Am. J. Cardiol. 223 (1969) 830 – 837. [5] O.E. Brown, S.C. Manning, B. Ridenour, Corpulmonale secondary to tonsillar and adenoidal hypertrophy: Management considerations, Int. J. Pediatr. Otorhinolaryngol. 16 (1988) 131 – 139. [6] M.J. Luke, A. Mehrizi, G.M. Folger, E.D. Rove, Chronic nasopharyngeal obstruction as cause of cardiomegaly, cor-
206
S. Ramakrishna et al. / Int. J. Pediatr. Otorhinolaryngol. 55 (2000) 203–206
pulmonale and pulmonary edema, Pediatrics 37 (1966) 762 – 768. [7] R. Schiffmann, J. Faber, A.C. Edelman, Obstructive hypertrophic adenoids and tonsils reversed by tonsillectomy and adenoidectomy, Int. J. Pediatr. Otorhinolaryngol. 9 (1985) 183 – 187.
[8] M. Maurizi, G. Paludetti, T. Todisco, V. Dottoniri Maud Grassi, Pulmonary function studies in adenoid hypertrophy, Int. J. Pediatr. Otorhinolaryngol 2 (1980) 243 – 250. [9] F.G. Shechtman, P.T. Lin, R.L. Piuncus, Urgent adenotonsillectomy for upper airway obstruction, Int. J. Pediatr. Otorhinolaryngol. 24 (1992) 83 – 89.
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