Percutaneous Bone-Anchored Hearing Implant Surgery: Do Syndromic Children Have More Adverse Perioperative Outcomes?

OBJECTIVE: To evaluate and compare perioperative outcomes of percutaneous bone-anchored hearing implant (BAHI) surgery in syndromic and nonsyndromic pediatric patients. STUDY DESIGN: Retrospective cohort study. SETTING: McGill University Health Centre in Montreal, Quebec, Canada. PATIENTS: Forty-one pediatric patients (22 syndromic, 19 nonsyndromic) who underwent percutaneous BAHI surgery between March 2008 and April 2021. INTERVENTION: Percutaneous BAHI surgery. MAIN OUTCOME MEASURES: Patient demographics (age at surgery, gender, implant laterality), operative information (American Society of Anesthesia [ASA] score, anesthesia type, surgical technique, implant/abutment characteristics), and postoperative outcomes (implant stability, soft tissue integrity, surgical revisions, implant failure). RESULTS: The most frequent syndromes among implanted patients were Treacher Collins (27.3%), Goldenhar (13.6%), Trisomy 21 (13.6%), and Nager (9.1%). Syndromic patients were more frequently given higher ASA scores: 2 ( p = 0.003) and 3 ( p = 0.014). All cases of implant extrusion were in syndromic patients: two posttraumatic and two failures to osseointegrate. Nine (40.9%) syndromic patients experienced a Holgers Grade 4 skin reaction at one of their postoperative follow-up visits as compared to 0% of nonsyndromic patients ( p < 0.001). Implant stability was similar between cohorts at all postoperative time-points, except for significantly greater nonsyndromic implant stability quotient scores at 16 weeks ( p = 0.027) and 31+ weeks ( p = 0.016). CONCLUSIONS: Percutaneous BAHI surgery is a successful rehabilitation option in syndromic patients. However, it presents a relatively higher incidence of implant extrusion and severe postoperative skin reactions as compared to nonsyndromic patients. In light of these findings, syndromic patients may be great candidates for novel transcutaneous bone conduction implants.

The Biology of Vasopressin.

Vasopressins are evolutionarily conserved peptide hormones. Mammalian vasopressin functions systemically as an antidiuretic and regulator of blood and cardiac flow essential for adapting to terrestrial environments. Moreover, vasopressin acts centrally as a neurohormone involved in social and parental behavior and stress response. Vasopressin synthesis in several cell types, storage in intracellular vesicles, and release in response to physiological stimuli are highly regulated and mediated by three distinct G protein coupled receptors. Other receptors may bind or cross-bind vasopressin. Vasopressin is regulated spatially and temporally through transcriptional and post-transcriptional mechanisms, sex, tissue, and cell-specific receptor expression. Anomalies of vasopressin signaling have been observed in polycystic kidney disease, chronic heart failure, and neuropsychiatric conditions. Growing knowledge of the central biological roles of vasopressin has enabled pharmacological advances to treat these conditions by targeting defective systemic or central pathways utilizing specific agonists and antagonists.