To describe surgical management of calcium hydroxylapatite (CaHA) inappropriately located within the superficial lamina propria (SLP) in patients undergoing injection laryngoplasty (IL) for unilateral vocal fold paralysis (UVFP).
Retrospective chart review.
Three patients with persistent or worsening dysphonia after previous CaHA IL underwent attempted endolaryngeal excision of superficially located CaHA. In the patient with the least CaHA duration, a subepithelial CaHA mass was partially debulked via microlaryngoscopic cordotomy. However, in two patients with extended CaHA dwell time, residual CaHA took of the form of microspheres, which were either easily removed (if encapsulated) or diffusely scattered throughout the SLP, making extirpation impossible.
CaHA can persist in the SLP for years following IL. Microlaryngoscopic explantation can improve voice in patients with malpositioned superficial injections; however, this may not be achievable, depending on the CaHA distribution, which may be a function of time elapsed since the initial IL.
Injection laryngoplasty (IL) is a longstanding treatment for augmenting the paraglottic space in phonatory glottic insufficiency due to unilateral vocal fold paralysis (UVFP) [ ]. A number of techniques for office-based IL and types of injectables are used depending on physician preference or patient factors [ ]. Current injectables include calcium hydroxylapatite (CaHA), carboxymethylcellulose (CMC), hyaluronic acid, collagen, dermis, and fat [ ]. CaHA is chemically similar to the main structural component of human bone and has been approved for IL by the Food and Drug Administration. Many authors have reported successful, long-term clinical use of CaHA-based injectables [ ]. Others have documented complications from use of this product requiring microlaryngoscopic removal of the injectable from the vocal fold at timeframes ranging from 4 weeks to 2 years post-injection [ ]. This series describes intra-operative findings in a group of patients who underwent microlaryngeal CaHA extirpation at times ranging from 8 months to over 5 years following their initial CaHA IL’s.
We performed a single institution retrospective chart review of patients seen in a laryngology practice at NorthShore University HealthSystem between August 2012 and May 2019. Inclusion criteria were patients with a chief complaint of hoarseness who had undergone previous IL with CaHA and were subsequently found to have glottic subepithelial CaHA deposits on stroboscopic evaluation as a suspected contribution to persistent dysphonia. All patients underwent suspension microlaryngoscopy with attempted removal of the injectable. The study was classified as exempt by the Institutional Review Board under the purview of quality.
Three patients were identified who underwent attempted microlaryngoscopic extirpation of subepithelial true vocal fold CaHA deposits. Details of the three cases are presented below and summarized in Table 1 .
|Case||Number of Prior CaHA IL’s||CaHA Injection Volumes (per outside operative report)||Number of Vocal Fold Injection Sites (per outside operative report)||Time from CaHA Injection Laryngoplasty to Microlaryngoscopic Extirpation||Intraoperative Findings of SLP CaHA Distribution at Extirpation|
|1||2||0.7 ml; 0.7 ml||2, 2||5 years 5 months; 4 years 10 months||Microsphere deposits that were encapsulated and able to be suctioned once capsule was entered|
|2||2||N/A||N/A||4 years 2 months||Microsphere deposits that were not encapsulated and could not be removed|
|3||2||0.35 ml; 0.3 ml||4, 5||10 months; 8 months||Deposit was a three dimensional mass; debulked piecemeal|
A 60-year-old female with a history of multiple sclerosis presented to clinic with a seven-year history of idiopathic UVFP. She had previously undergone two CaHA IL’s by another otolaryngologist over 5 years prior to her initial evaluation in our clinic but had persistent hoarseness. She worked in customer service with significant occupational voice demands.
On examination, her voice was high pitched, mild to moderately breathy, and moderately strained. Stroboscopy demonstrated known right UVFP with a moderate phonatory glottic gap and two ipsilateral subepithelial true vocal fold opacifications, consistent with residual CaHA. The anterior lesion was near the striking zone, ~1 mm from the free vocal edge and focally reduced the mucosal wave propagation ( Fig. 1 A and B). Suspension microlaryngoscopy with phonosurgical extirpation was performed. This anteromedial lesion was found to be encapsulated, and after breaching the capsule, a semi-liquid slurry of CaHA microspheres were relatively easily removed with suction and irrigation; a similar technique was applied to the second posterolateral vocal fold deposit ( Table 1 , Fig. 1 C–F).
At 3-week post-operative follow up, the patient reported improved voicing but stroboscopic exam revealed stably reduced ipsilateral vocal fold pliability. She continued to follow up for another 2.5 years, during which the pliability of her ipsilateral vocal fold improved compared to her pre-operative stroboscopy, and the initial glottic intra-SLP CaHA deposits were now absent. Laryngeal framework surgery was offered to further rehabilitate her voice, but the degree of vocal improvement after CaHA removal alone was sufficient enough for her to decline the procedure.
A 40-year-old female presented with left UVFP following a thyroid lobectomy. Other otolaryngologists had subsequently performed two CaHA IL’s (more than four years ago) as well as two ipsilateral type I (silastic implant) thyroplasties prior to her seeking another opinion at our clinic. Formally a competitive singer, she was now working in marketing, with high daily vocal demands. Her voice was moderately to severely strained. Stroboscopy demonstrated known left vocal fold immobility with a mild to moderate posterior phonatory glottic gap and an absent mucosal wave along the anterior half of the paralyzed vocal fold. There were multiple submucosal white deposits consistent with residual CaHA, the largest of which was ~1 mm away from of the free edge of the vocal fold, near the striking zone, as well as a malpositioned silastic implant ( Fig. 2 A).