Bamboo nodes associated with mixed connective tissue disease as a cause of hoarseness
In June 2004, a 43-year-old female primary school teacher had a sudden onset of hoarseness. She consulted an otolaryngologist and received antibiotics, which did not improve her voice quality. In November 2004, she was first examined in our Department of Pedaudiology and Phoniatrics at the Medical School Hannover. A mixed connective tissue disease (MCTD) had been diagnosed in 1998. Raynaud’s phenomenon has been present until today. The blood examination had revealed antinuclear (ANA) and ribonuclease-sensitive (RNP) antibodies. Recent X-ray of the thorax showed subpleural emphysematous signs in the upper lung and basal interstitial reticular changing. As recommended by her immunologist, she did not receive prednisolone as a maintenance dose. The most prominent perceptual feature was an unstable voice with intermittent roughness. She also complained that an increased effort was required to produce voice.\nThe rigid laryngeal endoscopy revealed bilateral whitish transverse band stripes in the submucosa, which lent a slightly protruded aspect to the vocal folds. One lesion was found at the junction of the middle and posterior thirds of the right vocal fold, and another one was observed in the middle of the left vocal fold (Fig. ). The site of the bilateral lesion became more evident during the stroboscopic examination. Moreover, the stroboscopic view during chest voice phonation showed a decreased amplitude vibration throughout the vocal folds except for the lesion, where no vibratory pattern between the portions anterior and posterior to the transverse lesion in the vocal fold was visible in the continuous image of the videostroboscopy.\nMaximum phonation time was 12.9 s (mean 21 s, normal ≥ 7 s). Real-time analysis of connected speech during reading a short text (“Der Nordwind und die Sonne”; a German equivalent to the Rainbow passage) showed a mean fundamental frequency of 167 Hz (adult women range 190–240 Hz) and an interperiodic irregularity [] of 26.57% (normal < 11%).\nOn the basis of other case reports in the literature, we suggested an intralesional steroid injection. This was applied four times using prednisolone (5 mg) in both vocal folds. Inter-injection interval was 1 week. After the second injection, the voice improved. Since the patient still wished further improvement, we injected steroids for the third time, but unfortunately the voice became hoarse again. We decided to apply a fourth injection, but the voice quality did not change after that.\nFinally, we decided to perform an excision of the lesions. Microlaryngoscopic surgery was done under general anesthesia in January 2005. The surgical technique consisted of an incision lateral to the lesion on the superior surface of the vocal fold, followed by exploration of the mucosal layer along and under the lesion. A hard and crumbly whitish substance without an encapsulating structure was found under the mucosal layer, which joint the vocal ligament transversally. Because of the infiltration depth, the substance could not be removed completely on both sides without endangering the m. vocalis.\nThe histopathologic examination of vocal cord biopsies (hematoxylin–eosin staining) revealed an extensive fibrinoid necrosis surrounded by a rim of histiocytes in a palisading fashion. The histiocyte-rich granulomatous infiltrate with a necrotic core closely resembled rheumatoid nodules. On morphologic grounds, a connective tissue disease was suspected in the histopathology report (Fig. ).\nIn March 2005, 2 months after surgery, the patient’s voice was better than before surgery and acceptable for normal and professional voice use. She returned to her teaching activities. Following surgery, the patient received speech training for several months (20 times) in order to stabilize voice quality. One month after surgery, a laryngoscopic examination showed reduced bilateral whitish transverse band stripes in the submucosa (Fig. ). The stroboscopic view during chest voice phonation demonstrated the already-known decreased amplitude vibration throughout the vocal folds with the exception of the lesion on the left side. On the right side, a small vibratory pattern between the portions anterior and posterior to the transverse lesion in the vocal fold was visible again in the continuous image of the videostroboscopy. Maximum phonation time was 14.5 s. Real-time analysis of speech showed a mean fundamental frequency of 195 Hz and an interperiodic irregularity [] of 10.9% (normal < 10%). In comparison with data from before the first conservative treatment, there is an improvement in all aspects of voice quality as measured by objective means.\nIn August 2010, the stroboscopic view during chest voice phonation demonstrated the already-known decreased amplitude vibration throughout the vocal folds with the exception of the lesion on the left side. On the right side, a small vibratory pattern between the portions anterior and posterior to the transverse lesion in the vocal fold was visible again in the continuous image of the videostroboscopy. Maximum phonation time was 15.0 s. Real-time analysis of speech showed a mean fundamental frequency of 205 Hz and an interperiodic irregularity [] of 11.84% (normal < 11%). With an average follow-up period of 6 years, we noted a long-term stabilization of her voice quality. Short intervals of speech therapy for a year now have been helping to keep good laryngeal function. At the moment, she is working full-time as a teacher.