Prominent or enlarged blood vessels that exist on the vibratory surface of the vocal fold may eventually cause problems from hemorrhage or mass effect within the lamina propria and may cause dysphonia by disrupting the vibratory pattern and closure of the true vocal folds.
Vascular lesions found within the true vocal fold may threaten the career of a professional vocalist because of recurrent inopportune hemorrhage or scar formation. In the asymptomatic patient, they may create a management dilemma due to the risk of future hemorrhage versus the immediate risks of intervention.
In a retrospective study of 499 vocal performers, Tang et al found that the hemorrhage rate in those with vocal fold varices was 2.68% at 12 months, versus 0.8% in performers without varices. Based on a Cox proportional hazard regression analysis, performers with varices were reported to have a hazard ratio of 10.1 for hemorrhage development compared with the other performers.[1]
An image depicting vascular lesions of the vocal fold can be seen below.
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Vocal cords in a performing artist with minor difficulty singing. Videostroboscopy revealed fullness of the entire fold as well as slightly decreased ....
No widely accepted system of nomenclature is available for vascular lesions. Microvascular lesions of the true vocal folds are known as varices, capillary ectasias, papillary ectasias, capillary and venous lakes, and spider telangiectasias. The anatomic variations based on these terms are subtle, and treatment approaches are similar regardless of the type. A varix is a prominent, dilated, and commonly tortuous vein found on the surface of the vocal fold. Ectasias are distinguished by a coalescent hemangiomatous appearance.
Vocal fold varices occur most commonly in female professional vocalists, although they are not rare in males. Postma et al found a prevalence of 3.5% among their patient population, with 14.5% of those cases occurring in female professional voice users.[2] Prevalence in the general population is unknown.
Formation of varices is related to vocal use, abuse, and trauma.[3] Most patients presenting with symptoms stemming from these lesions are professional voice users. Repeated trauma may lead to new blood vessel formation and weakening of the vessel walls.
The immediate cause of vocal fold varices is unknown, although they may originate from shearing stress along the lateral fold near the termination and reversal point of the mucosal wave. A hormonal cause has been postulated because of the prevalence in female singers, but this has not been proven. In addition, physiologic and histologic changes associated with menses may increase the risk of variceal hemorrhage. However, hormonally directed therapy has not been successful in treatment of these lesions. The predilection may be attributable to the unique anatomy and associated mechanics of voice production in female vocalists.
The clinical presentation of vocal vascular lesions is highly variable. Vocal fold varices may be entirely asymptomatic, or they may result in dysphonia through hemorrhage and edema, scarring, or mass effect with resultant disruption of mucosal wave. Dysphonia may be severe with an acute, dramatic onset. This presentation typically appears after episodic vocal abuse or straining. Other presentations can be subtle, with patients having an apparently normal voice while being easily fatigued or incurring loss of normal vocal range. Patients with recurrent hemorrhage may relate a history of episodes of hoarseness followed by resolution.
Patients may have completely normal sounding voices with a pronounced varix on the surface of the true vocal fold. Patients presenting immediately after an acute bleed may have extensive ecchymosis and hemosiderosis of the involved true vocal fold. Acute hemorrhage may resolve without event, or it may transform into a hemorrhagic polyp, cyst, or scar, which then causes dysphonia through a mass effect or vibratory margin effects.
In women, the appearance of the lesion may depend on the stage of the menstrual cycle; therefore, periodic examinations may be required to accurately establish severity.
Indications for surgical intervention in a patient with a vascular lesion of the vocal fold include enlargement of the lesion, recurrent hemorrhage, development of a mass in conjunction with the varix, unacceptable dysphonia, and uncertainty as to the diagnosis.
Vascular lesions appear on the superior surface of the vocal fold or, less commonly, along the vibratory margin. Because of the large numbers of vascular arcades found in the vocal fold, they are not critical to the blood supply of the tissue. Varices may manifest as abnormally dilated capillary arcades running in the anterior-to-posterior direction or as clusters of capillaries. Another formation is a dot, which represents the tip of a vascular loop rising superficially from the underlying mucosa. Finally, venous lakes may form that are so large as to appear as a chronic area of hemorrhage. Hochman et al postulated that vascular lesions are more likely to form on the superior lateral surface of the vocal fold because of the shearing forces generated by the termination of the mucosal wave at that point.[4]
Evaluate patients presenting with dysphonia by indirect laryngoscopy and videostroboscopy, with particular attention paid to vocal fold mobility, glottic closure, and presence, amplitude, and symmetry of the mucosal wave.
Use of medications with anticoagulant properties should cease if they are not medically necessary. Treat any conditions predisposing to trauma and irritation (eg, cough, reflux disease) with the appropriate therapy. Hormonal therapy has not been proven effective in either prevention or treatment of varices. Voice use should be modified, limiting the frequency, intensity, and duration of voice use and maximizing vocal rest. Hard glottal attacks should be avoided and easy-onset patterns used. Applicable speech therapy techniques include direct, indirect, and confidential voice therapy (see the Medscape Reference article Voice Therapy).
Surgery is recommended for recurrent hemorrhage, enlargement of the lesion, development of an associated mass, or intolerable dysphonia. In addition, in some instances, an acute hemorrhage may require evacuation to prevent formation of a hemorrhagic polyp. Surgical candidates must be willing to postpone speaking and singing engagements for at least 3 months postoperatively. Intervention in an asymptomatic patient should be approached with caution, as the potential always exists for a worse voice postoperatively.
Office-based pulse dye laser is an alternative for patients with small microvascular lesions. Ivey noted a 70% improvement in 11 if 29 lesions after 1 or 2 treatments.[5]
Evaluate patients presenting with dysphonia by indirect laryngoscopy and videostroboscopy, with particular attention paid to vocal fold mobility, glottic closure, and presence, amplitude, and symmetry of the mucosal wave. Ensure that any concurrent medical conditions affecting the voice (eg, reflux laryngitis, allergic rhinitis) are evaluated and treated. In addition, the stage of the menstrual cycle in women can be important for accurate gauging of clinical severity and timing of intervention. Often the size and nature of the blood vessels of the vocal folds increase and become more fragile in the premenstrual period (approximately 5 days prior to menses).
Maximally reduce all known sources of mechanical trauma prior to considering surgical therapy to determine reversibility and to hopefully prevent a postoperative recurrence. This is accomplished in part by medical and speech therapy directed at reducing vocal trauma through improved technique and vocal hygiene. Surgery is reserved for lesions that show no reversibility with exhaustive medical and speech therapy.
Surgical technique begins by identifying the feeding and emptying vessels, which are then photocoagulated sequentially with a carbon dioxide laser or specific photoangiolytic lasers such as the KTP (potassium titanyl phosphate) or 585 nm pulsed dye laser. The primary lesion may then be excised via a microflap approach or photocoagulated, depending upon its size. The goal of surgical excision is preservation of the mucosal cover with minimal disruption of the underlying tissue. Scar formation should not be a factor if the power is kept at 1-2 W, pulse width at 0.1 second, and spot size at 300-400 µm. Use of iced saline and/or topical 1:10,000 epinephrine solution can be beneficial in hemostatic control and possibly in limiting spread of the zone of thermal injury.[6] Direct surgical excision of the vascular abnormalities is another treatment option. This technique uses cold steel phonomicrosurgical techniques and instruments.
Place patients on strict voice rest for 2 weeks after microflap surgery. Patients with more extensive dissections may be placed on a short course of corticosteroids. All patients receive antibiotics and a mild narcotic for pain relief. Patients with symptoms or findings of laryngopharyngeal reflux are treated medically. Encourage patients to avoid aspirin and nonsteroidal anti-inflammatory agents in the first 2 weeks postoperatively.
Reexamine patients at 2, 4, 8, and 12 weeks postoperatively. Perform videostroboscopy at the 2-week postoperative visit. The patient resumes therapy with a speech pathologist at this point. A gradual return to voice use occurs over the first few weeks. Singers may begin to work with a vocal pedagogue (ie, singing teacher) after 1 month. Most patients can expect 90% of their functional surgical result after approximately 3 months.
Complications are related either to laryngoscopy or to vocal fold mucosal injury. Pressure effects from suspension laryngoscopy may cause tongue numbness, altered taste, and oropharyngeal, mucosal, and dental injuries. Deep plane dissection or exposure of the vocal ligament can result in scarring and fibrosis of the mucosa with loss of mucosal wave and glottal insufficiency. Injudicious use of the laser can result in a wide zone of thermal damage with mucosal scarring and fibrosis and in unintended burn injuries and endotracheal tube fires.
In their study of 11 lesions, Postma et al reported no recurrences with follow-up periods as long as 4.5 years.[2] Patients who adhere to principles of healthy voice production and avoid vocal overuse and trauma have an excellent prognosis. However, no long-term studies of the recurrence rates of variceal lesions are available.
A retrospective study by Lennon et al indicated that in patients who have experienced vocal fold hemorrhage, the presence of varices is a risk factor for recurrence. The study included 47 patients with vocal fold hemorrhage who were found to have varices, mucosal lesions, and/or vocal fold paresis. Twelve patients (26%) suffered repeat hemorrhage, including 48% of patients with a varix. Multivariate logistic regression analysis indicated that varix was the only condition significantly associated with recurrence.[7]
The exact cause of vascular lesions of the vocal fold is still largely unknown; therefore, identifying patients at risk is difficult. The issue of hormonal therapy also remains unresolved. Some surgeons differ on the use of the laser as opposed to cold dissection in surgical treatment of these lesions.
John Schweinfurth, MD, Professor, Department of Otolaryngology, University of Mississippi Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Robert H Ossoff, DMD, MD, Maness Professor of Laryngology and Voice, Department of Otolaryngology, Executive Medical Director, Vanderbilt Voice Center, Vanderbilt Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Robert M Kellman, MD, Professor and Chair, Department of Otolaryngology and Communication Sciences, State University of New York Upstate Medical University
Disclosure: Nothing to disclose.
Chief Editor
Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .
Additional Contributors
Clark A Rosen, MD, Director, University of Pittsburgh Voice Center; Professor, Department of Otolaryngology and Communication Science and Disorders, University of Pittsburgh School of Medicine
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Merz North America Inc<br/>Received consulting fee from Merz North America Inc for consulting; Received consulting fee from Merz North America Inc for speaking and teaching.
Lin P, Stern JC, Gould WJ. Risk factors and management of vocal fold hemorrhages. J Voice. 1991. 5:74-7.
Vocal cords in a performing artist with minor difficulty singing. Videostroboscopy revealed fullness of the entire fold as well as slightly decreased mucosal wave.
Vocal cords in a performing artist with minor difficulty singing. Videostroboscopy revealed fullness of the entire fold as well as slightly decreased mucosal wave.
Hemorrhagic polyp on the surface of the true vocal fold in a professional singer. Note the fullness along the medial edge of the true vocal fold in the area of the lesion.
Untreated or recurrent hemorrhage can evolve into a large hemorrhagic polyp. Conservative therapy has little chance of success at this point, and these lesions can lead to scarring if untreated.
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