Vocal Polyps and Nodules Workup

Updated: May 22, 2019
  • Author: Robert A Buckmire, MD; Chief Editor: Arlen D Meyers, MD, MBA  more...
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Workup

Imaging Studies

Gomaa et al studied the value of high-resolution ultrasonography in the diagnosis of laryngeal lesions that had already been detected with rigid endoscopy. They concluded that it is an alternative technique for diagnosing some lesions, particularly small subglottic lesions. [16]

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Other Tests

No specific laboratory studies are singularly diagnostic of these conditions. Measurements within a voice laboratory, including aerodynamic, acoustic, and videostroboscopic baselines (as well as a high-quality audio recording of the patient's voice) are all helpful for appropriate pretreatment and posttreatment documentation. Lastly, clinician and patient perceptual measures are commonly performed to more subjectively gauge the impact of the vocal disability and improvement.

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Diagnostic Procedures

Videostrobolaryngoscopy is far more sensitive for detecting laryngeal lesions when compared with other indirect laryngoscopy techniques because of its ability to demonstrate subtle differences in the appearance, pliability, and mucosal wave characteristics (ie, symmetry, periodicity, amplitude, vertical phase difference) of the TVF cover.

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Histologic Findings

On a structural level, a significant body of work has been performed to identify pathologic structural characteristics of benign vocal cord lesions and from this to infer pathogenesis. Immunohistochemical characterization of the extracellular matrix of excised, clinically diagnosed, benign laryngeal lesions revealed nodules to more commonly have a thickened basement membrane zone (BMZ) and dense fibronectin arrangement within the superficial lamina propria (LP), as compared with those diagnosed as polyps. These polypoid lesions tended to exhibit an unaltered BMZ thickness and to have fibronectin depositions clustered around neovasculature.

These patterns of structural deviation from the normal layered microanatomy of the TVF have been reported previously. In 1995, Gray et al formulated a theory of causation and pathologic response, hypothesizing as follows: "The vocal folds sustain enough injury to lead to BMZ disruption and injury to the superficial layer of the lamina propria. The injury, if repetitive, leads to aberrant healing and a fibroblastic response involving increased fibronectin deposition." [17]

On an ultrastructural level, nodules tend to demonstrate epithelial changes in the form of increased thickness, gaping of the intracellular junctions, and absence of the basal lamina. These changes were much less prominent in the polyps examined. Conversely, polyps tended to show variable pathologic patterns; some demonstrated marked vascularity, and others had hyaline stromal changes. The authors interpreted differences as perhaps indicative of a more long-standing exposure to injurious agents in the case of VFNs; they interpreted "microstromal hemorrhages" as potentially playing a role in the formation of VFPs. Gray et al speculated that the heterogeneous findings might be due to the stage in the life cycle of the polyp examined. [8]

A prospective, histopathologic study by Effat and Milad indicated that in comparison with vocal polyps in nonsmokers, those in people who do smoke tend to be larger and to display increased keratinization, dysplasia, basement membrane thinning, and hyaline degeneration. The study examined polyps from 29 patients, including smokers and nonsmokers. [18]

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