Inferior glottic ridges that prevent vocal fold closure. (Laryngoscopic Clinic).

In this month's installment of LARYNGOSCOPIC CLINIC, we discuss two cases of inferior glottic ridges that prevented closure of the vocal fold and led to hoarseness.

Case reports

Patient 1. A 51-year-old woman, a recovery-room nurse, came to us with a 1-year history of voice changes. These changes had begun suddenly one morning upon awakening. Over the course of the year prior to our evaluation, the hoarseness worsened progressively. Initially, the degree of her symptoms fluctuated, and they never cleared completely. An otolaryngologist saw her 1 month after the onset of symptoms and diagnosed reflux laryngitis. Guaifenesin and omeprazole were prescribed. The otolaryngologist also ordered computed tomography (CT) of the neck and gadolinium-enhanced magnetic resonance imaging (MRI) of the head. Findings on both were negative. Her complete blood count and her blood levels of thyroid-stimulating hormone (TSH), thyroperoxidase antibody, antinuclear antibody, rheumatoid factor, Lyme titer, and anti-acetylcholine receptor antibody were within normal limits.

During the year prior to our evaluation, the patient experienced increasing vocal fatigue, but she denied a globus sensation, halitosis, throat clearing, and choking sensations. Her medical history was significant for a hysterectomy. The only medication she was currently taking was omeprazole at 20 mg once daily.

Our general head and neck examination detected a slight fullness of the thyroid gland. The patient's voice was moderately hoarse, slightly breathy, pressed, and abnormally low in pitch. Strobovideolaryngoscopy revealed a moderate degree of supraglottic hyperfunction, which improved only slightly with voluntary increases in pitch. The arytenoids were severely erythematous and moderately edematous; the interarytenoid region exhibited a severe degree of posterior cobblestoning, suggestive of reflux laryngitis (figure 1). Both vocal folds were mildly erythematous, and there was mild Reinke's edema. At the inferior margin of the vocal folds, two firm ridges ran parallel to the folds throughout their entire lengths. The ridges made contact anteriorly and led to the failure of glottic closure in the anterior, middle, and posterior segments of the musculomembranous vocal folds.

The patient's fluorescent treponemal antibody titer and antistriatal antibody titer were normal, as was her erythrocyte sedimentation rate (ESR). CT and gadolinium-enhanced MRI of the neck detected a minimal glottic narrowing and no evidence of a discrete mass. Findings on thyroid ultrasound were normal. The patient's dose of omeprazole was increased to 20 mg twice daily, and nizatidine at 300 mg at night was started. The patient also underwent speech and voice therapy.

Although her voice improved somewhat with therapy, she continued to have problems with laryngopharyngeal reflux. Her reflux appeared to worsen over the course of the next 9 months, despite reflux precautions and several changes and increases in her antireflux medications. A 24-hour pH probe study revealed a significant upright reflux, and the patient underwent laparoscopic Nissen fundoplication. Five months later, her reflux was better controlled and her voice had significantly improved. The inferior glottic ridges remained stable 18 months after the initial examination and 5 months after the fundoplication. Resection of these ridges will be considered only if the patient becomes sufficiently dissatisfied with her voice or if the ridges begin to change.

Patient 2. A 59-year-old man, a computer technologist, reported a lifelong history of difficulty with voice projection. He also complained of chronic throat clearing and cough. He had a history of heartburn but had never been treated for laryngopharyngeal reflux. His medical history was also significant for chronic otitis media, chronic sinusitis, idiopathic cardiomyopathy, and a motor vehicle accident, that had resulted in head trauma and multiple internal injuries. His surgical history included a splenectomy and gastric repair at the time of the motor vehicle accident in addition to an appendectomy and a tonsillectomy. He had also undergone functional endoscopic sinus surgery by another otolaryngologist 2 months prior to our assessment. His current medication regimen included quinapril, digoxin, fluvastatin, atorvastatin, amoxicillin, and prednisone. He had no known drug allergies.

The patient's voice was mildly to moderately hoarse, mildly breathy, and soft. Strobovideolaryngoscopy detected several laryngeal abnormalities. He had a moderate degree of supraglottic hyperfunction that improved slightly with a voluntary increase in pitch. There were fluctuating neurologic asymmetries in abduction, adduction, and longitudinal tension bilaterally. His arytenoids were mildly erythematous and mildly to moderately edematous, and there was a mild degree of pachydermia laryngis in the interarytenoid region, suggestive of reflux laryngitis. The vocal folds had a normal color and mucosal wave, but there was bilateral fullness involving the medial aspect of the vibratory margins, beginning just below the upper edge of the contact surface of the vocal folds anteriorly and extending subglottically (figure 2). This fullness appeared to be more consistent with hypertrophy than with true masses. The fullness resulted in a separation of the vocal folds, which caused glottic insufficiency through-out the m idportion of the musculomembranous segments of the vocal folds.

Laryngeal electromyography detected a 20% decrease in recruitment in the right cricothyroid muscle. The results of repetitive stimulation and Tensilon testing were normal. The patient's fasting blood glucose level was slightly elevated at 125 mg/d1 (reference range: 70 to 105). His ESR was also slightly high at 19 mm/hr (reference range: 0 to 15). An assay for rheumatoid factor was positive at a dilution of 1:160. The patient's cholesterol, triglyceride, [T.sub.3], [T.sub.4], TSH, antinuclear antibody, fluorescent treponemal antibody, and Lyme titer levels were all normal.

The reflux laryngitis was treated with lansoprazole at 30 mg twice daily, as well as with lifestyle and diet modifications. The cough abated with this antireflux regimen. As a result, the patient was satisfied with his voice and declined voice therapy. Follow-up laryngeal examinations were conducted regularly. Six months after our initial examination, the inferior glottic ridges and the voice remained stable, and the pachydermia laryngis and posterior laryngeal edema and erythema had diminished significantly.

Discussion

Both of these patients had signs and symptoms of reflux laryngitis that improved with appropriate antireflux regimens. It is unclear whether these inferior glottic ridges were sequelae to laryngopharyngeal reflux or separate, unrelated findings. Since their reflux has been controlled with medications and diet and lifestyle modifications, both patients have been satisfied with their voices, even though the ridges and the associated glottic-closure problems have persisted. Serial examination is warranted in such cases to monitor for the possible growth of these hypertrophic lesions. Biopsy will be performed if the lesions show signs of change.

From the Department of Otolaryngology, University of Illinois at Chicago (Dr. Heman-Ackah) and the Department of Otolaryngology-Head and Neck Surgery, Thomas Jefferson University, Philadelphia (Dr. Sataloff and Ms. Kelleher).