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Does Pediatric Obstructive Sleep Apnea Syndrome Cause Systemic Microvascular Dysfunction?

Hasan Emre Koçak1, Ayşe Şermin Filiz Acipayam2, Harun Acipayam1

  • 1Department of Otorhinolaryngology-Head and Neck Surgery, Bakirköy Dr. Sadi Konuk Training and Research Hospital.

The Journal of Craniofacial Surgery
|March 3, 2018
PubMed

Insights

Pediatric obstructive sleep apnea syndrome (OSAS) from adenoid hypertrophy does not cause early microvascular dysfunction or cardiovascular risk. This study found no significant differences in capillary density or reactive hyperemia in children with OSAS.

Area of Science:

  • Pediatric Pulmonology
  • Cardiovascular Research
  • Sleep Medicine

Background:

  • Obstructive sleep apnea syndrome (OSAS) in children, often due to adenoid hypertrophy, is a growing concern.
  • The potential impact of pediatric OSAS on systemic microvascular function remains incompletely understood.
  • Early identification of cardiovascular risks associated with pediatric OSAS is crucial for timely intervention.

Purpose of the Study:

  • To investigate whether pediatric OSAS secondary to adenoid hypertrophy leads to systemic microvascular dysfunction.
  • To assess potential early cardiovascular risks in children diagnosed with OSAS.
  • To evaluate microvascular parameters in relation to the severity of OSAS.

Main Methods:

  • A prospective, single-blinded, case-control study involving 81 pediatric patients with OSAS and 26 healthy controls.
  • OSAS severity was categorized as mild, moderate, or severe based on lateral nasopharynx X-ray.
  • Videocapillaroscopy assessed nailfold capillary density (CD) and postocclusive reactive hyperemia (PORH) to evaluate microvascular function.

Main Results:

  • No statistically significant differences were observed in capillary density (CD) among the control group and the mild, moderate, and severe OSAS groups (P > 0.05).
  • Postocclusive reactive hyperemia (PORH) measurements also showed no significant variations across the different OSAS severity groups and the control group (P > 0.05).
  • The duration of symptoms in OSAS patients ranged from 6 months to less than 1 year.

Conclusions:

  • Pediatric OSAS secondary to adenoid hypertrophy does not appear to cause systemic microvascular dysfunction in the early stages.
  • The study suggests that early-stage pediatric OSAS, as evaluated by these microvascular parameters, does not carry an immediate cardiovascular risk.
  • Further research may be warranted to explore long-term effects or other potential indicators of cardiovascular risk in this population.

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