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Pathophysiology of Intrapulmonary Right-to-Left Shunt in Infants With Obstructive ApneaIntrapulmonary Shunt in Infants With Apnea FREE TO VIEW

Denis A. Cozzi, MD; Silvia Ceccanti, MD
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From the Pediatric Surgery Unit, Sapienza University of Rome, Azienda Policlinico Umberto I.

Correspondence to: Denis A. Cozzi, MD, Pediatric Surgery Unit, Sapienza University of Rome, Viale Regina Elena, 324, 00161 Rome, Italy; e-mail: da.cozzi@uniroma1.it


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(1):360-361. doi:10.1378/chest.13-0566
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To the Editor:

We read with great interest the article by Shaikh et al1 in CHEST (January 2013). The authors concluded that in adults with severe sleep apnea syndrome, closure of the patent foramen ovale is not followed by a reduction in nocturnal desaturation, suggesting the coexistence of an alternative mechanism of residual right-to-left shunt (RLS). Here we propose a potential source of residual RLS.

In infants with Pierre Robin syndrome, with choanal atresia/stenosis, or with esophageal atresia, the pathogenic mechanism of glossoptosis apnea is similar to that of sleep apnea.2 The main difference is that in infancy, sleeping is not an essential prerequisite for the development of glossoptosis apnea.3

The study of breathing patterns during respiratory distress shows that these infants present recurrent obstructed inspiratory efforts (an equivalent of Müller maneuver). The obstructed inspiration is followed by a prolonged and interrupted expiratory flow, despite a positive expiratory intrathoracic pressure (an equivalent of Valsalva maneuver), and then by a retarded expiratory flow (grunting expiration).4,5 The association between obstructive apnea and expiratory grunt suggests that the functional upper airway obstruction may cause a lower airway instability.3-5 Grunting expiration is a breathing strategy to defend lung volume and lower airway patency by forcing gas into the peripheral airways.

Infants with glossoptosis apnea/hypopnea rarely experience severe complications, including hypoxemia and hypercapnia, pulmonary hypertension, anoxic brain damage, cor pulmonale, and sudden death.3 They frequently experience a blood gas derangement characterized by a degree of hypoxemia greater than the degree of hypercapnia and a hypoxemia relatively resistant to oxygen administration.3 Increasing Fio2, required to maintain Po2 between 60 and 80 mm Hg, results in a considerable increase in alveolar-arterial oxygen difference (Fig 1). No lung opacities or only small areas of collapse or consolidation are usually found on chest radiographs.3 Oxygen compared with other gases is more rapidly absorbed from the alveolus. Therefore, the most likely explanation for such large alveolar-arterial oxygen differences is that the high oxygen concentration in the inspired air converts in microatelectasis those segments of the lung with lower airways instability. The development of atelectasis may well explain the intrapulmonary RLS.3-5 From the results of our research group studies, we speculate that an intrapulmonary RLS may be the source of residual RLS in some adults with sleep apnea undergoing closure of patent foramen ovale.

Figure Jump LinkFigure 1. In 32 infants with esophageal atresia, 14 with Pierre Robin syndrome, and 11 with congenital nasal obstruction, increasing Fio2 to relieve hypoxemia results in a large A-aO2 difference. A-aO2 = alveolar-arterial oxygen.Grahic Jump Location

References

Shaikh ZF, Jaye J, Ward N, et al. Patent foramen ovale in severe obstructive sleep apnea: clinical features and effects of closure. Chest. 2013;143(1):56-63. [CrossRef] [PubMed]
 
Cozzi F. Glossoptosis as cause of apnoeic spells in infants with choanal atresia. Lancet. 1977;310(8042):830-831. [CrossRef]
 
Cozzi F, Pierro A. Glossoptosis-apnea syndrome in infancy. Pediatrics. 1985;75(5):836-843. [PubMed]
 
Cozzi F, Myers NA, Madonna L, et al. Esophageal atresia, choanal atresia, and dysautonomia. J Pediatr Surg. 1991;26(5):548-552. [CrossRef] [PubMed]
 
Cozzi F, Bonanni M, Cozzi DA, Orfei P, Piacenti S. Assessment of pulmonary mechanics and breathing patterns during posturally induced glossoptosis in infants. Arch Dis Child. 1996;74(6):512-516.
 

Figures

Figure Jump LinkFigure 1. In 32 infants with esophageal atresia, 14 with Pierre Robin syndrome, and 11 with congenital nasal obstruction, increasing Fio2 to relieve hypoxemia results in a large A-aO2 difference. A-aO2 = alveolar-arterial oxygen.Grahic Jump Location

Tables

References

Shaikh ZF, Jaye J, Ward N, et al. Patent foramen ovale in severe obstructive sleep apnea: clinical features and effects of closure. Chest. 2013;143(1):56-63. [CrossRef] [PubMed]
 
Cozzi F. Glossoptosis as cause of apnoeic spells in infants with choanal atresia. Lancet. 1977;310(8042):830-831. [CrossRef]
 
Cozzi F, Pierro A. Glossoptosis-apnea syndrome in infancy. Pediatrics. 1985;75(5):836-843. [PubMed]
 
Cozzi F, Myers NA, Madonna L, et al. Esophageal atresia, choanal atresia, and dysautonomia. J Pediatr Surg. 1991;26(5):548-552. [CrossRef] [PubMed]
 
Cozzi F, Bonanni M, Cozzi DA, Orfei P, Piacenti S. Assessment of pulmonary mechanics and breathing patterns during posturally induced glossoptosis in infants. Arch Dis Child. 1996;74(6):512-516.
 
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