Laryngeal Tuberculosis: A Case Report Christine E. Jones, MD, and Beulah D. Jones, MD Yonkers, New York
A case of laryngeal tuberculosis, in a 21-year-old female, is presented. The pathophysiology and natural course of the disease are discussed. The incidence of apical tuberculosis and associated laryngeal spread is noted.
In the preantibiotic era, endolaryngeal seeding was a frequent complication of far advanced or disseminated tuberculosis. This phenomenon was seen in 10 to 20 percent of cases showing bronchial involvement.' In rare cases, it was the presenting complaint which resulted from mucosal exposure to highly infected secretions. Endobronchial involvement was the usual etiology and apical disease was associated in only one percent of cases.2 Hematogenous dissemination was more common in extrinsic involvement of the laryngeal structure but was preceded in five percent of cases by chronic tuberculous laryngitis.3 In terminal cases, laryngeal involvement approaches 100 percent. The typical patient is a middle-aged male with long-standing disease. Of 37 patients in a series reviewed at the Institute Of Laryngology and Otology, less than six percent were under age 30.4 The following case is one in which apical tuberculosis is complicated by laryngeal lesions in a young female.
Requests for reprints should be addressed to Dr. C. E. Jones, 353 Hawthorne Avenue, Yonkers, NY 10705.
Case Report A 21-year-old Oriental female presented with a three-month history of intermittent hoarseness. She had spent all of her life, except the last two years, in the Orient. Since arriving in the United States, she denied any complaints except her voice change. After several trials of unsuccessful medical therapy, she presented at the hospital in November 1976. She had generalized fatigue and a 15 lb weight loss. Indirect mirror laryngoscopy revealed edema of the right arytenoid and true cord. Chest roentgenography showed a dense network of punctate structures filling the upper one-third of both hemithoraces. The upper lung fields were contracted and compensatory emphysematous changes were noted in the lower lung segments. Calcifications were not seen. The roentgenologist's diagnosis was severe bilateral pulmonary granulomatous disease. Miliary tuberculosis limited to the upper lobes (rather unl6sual) and the possibilities of fungus infection and atypical sarcoidosis were considered. The patient was scheduled for admission in December 1976 for a more complete workup. Her hospital course was unremarkable except for odynphagia which increased with intake of
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 1, 1979
orange juice. A comprehensive study for acid fast disease was undertaken. Significant findings showed (1) chest PA and lateral x-ray changes similar to those noted on previous examination; (2) apical lordotics with cavitation in the left subapex; (3) gastric washings positive for acid bacilli on two occasions; and (4) a strongly positive firststrengh purified protein derivative (PPD) in 48 hours. With a presumptive diagnosis of tuberculosis, she was started on isoniazid and ethambutal after an ophthalmology consult. She was discharged in mid-December 1976 to be followed up with pulmonary evaluations. In January 1977 she returned to the clinic with dysphagia. Indirect mirror laryngoscopy revealed edema of the right true vocal cord and a fungating grayish white mass on the laryngeal surface of the epiglottis and left aryepiglotic fold. Small lesions were also noted subglottically. Direct laryngoscopy showed that the mass was confined to the laryngeal surface of the epiglottis. There was hypertrophy of the right ventricular folds. The true vocal cords were not invovled. Pathologic examination confirmed the diagnosis of active caseous granulomatous disease of the larynx and epiglottitis (Figure 1). Fungal-like colonies were noted in the necrotic specimens, but cultures were negative. Cultures of gastric washings were positive for Mycobacterium tuberculosis. Followup examination in the clinic showed healing and beginning resolution of the laryngeal lesions. 37
Figure 1. Photomicrograph showing granuloma of the larynx. Note necrotic area in lower field and epithelioid cells and scattered mononuclear exudate in the upper field.
Discussion In the past, tuberculosis of the larynx was thought to be a disease of younger people, but in the past 20 years, there has been an increased incidence in patients over 60 years of age. In general, the lesions are four times more common in the male than in the female. Laryngeal disease is distinctly more common in middle-aged men who are debilitated, alcoholic, or tobacco smokers. Socioeconomic factors, race, respiratory tract pathology, and pregnancy cause people to show a particular predilection for laryngeal spread. The usual lesion is a tubercle involving the posterior commissure, interarytenoid space ventricles, vocal folds, and epiglottis. The process can continue to ulceration and involve the underlying cartilage. Granulation tissue mimicking keratosis, epithelial hyperplasia, and confluent granulomas with skip areas have been seen.' It is not known why lesions are rare in the tracheobronchial tree, or why there can be extensive laryngeal disease in the absence of sputum production. Likewise the etiology is obscure when there is copious sputum production without laryngeal involvement. The occurrence of tuberculous laryngitis, in the absence of sputum, is thought to be due to the organism's being carried in the submucous lymphatics or vascular network of the primary site and transported to the submucosa of the larynx. Certain tuberculous lesions are allergic and are known to progress rapidly dur38
ing puberty, pregnancy and the puerperium, in diabetes, and in patients with endocrine changes. The lesions are progressive and liquefaction necrosis of tissue occurs. Two types of lesions are clincially recognizable: (1) exudative, which shows diffuse inflammation with hyperemia, edema and infiltration of the subepithelial space with a nonspecific exudate; (2) productive, which is characterized by granulation tissue located in the subepithelal stroma. Tubercles may form and progress to yellowish grey nodules. The overlying epithelium may be lost and ulceration, secondary to chronic infection, can cause cartilaginous destruction2'5 and involve the joint, most frequently the cricoarytenoid. Tuberculomas, reparative in nature, result in hyperplastic epithelium and subepithelial fibrosis. Edema of the epiglottis and arytenoids is a sign of late disease. Healing is accompanied by fibrosis encapsulation and tubercle replacement. Advanced lesions can cause complete stenosis and fixation of the cricoarytenoid joint. The characteristic heart-shaped epiglottis and club-shaped arytenoid are results of chronic edematous changes.6 Hoarseness is among thd first symptoms the patient will notice.7 This can progress to aphonia or dysphonia without visible cord lesions. Dry throat with odynphagia is common, particularly if there is cartilaginous involvement. Dysphagia and dyspnea are common when the disease is manifested princi-
pally by edematous changes. Laryngeal tuberculosis must be distinguished from verrucose carcinoma and other granulomatous diseases.5'8'9 Since these two entities occur with great frequency, they must be differentiated and appropriate therapy instituted promptly.
Comment Since tuberculous involvement of the larynx occurs with sufficient frequency, physicians must be aware of its potential, particularly when encountered in advanced disease. Apical tuberculosis, complicated by laryngeal involvement, is rare and is seen in only one percent of cases. Literature Cited 1. Weinstein L, Brown R: Otolaryngologic manifestations of extrinsic infectious diseases. Otolaryngol Clin North Am 9(3):647-648, 1976 2. Beeson PB, McDermott W (eds): CecilLoeb Textbook of Medicine, ed 12. Philadelphia, WB Saunders, 1967, p 683 3. Travis LW, Work WP, Whitehouse WM: A radiologic advance in the diagnosis of disorders of the larynx. Laryngoscope 86(6):780-784, 1976 4. Paparella M, Shrumrick D: Otolaryngology, Head and Neck. Philadelphia, WB Saunders, 1973, vol 3, pp 620-624 5. Travis LW, Hybels RL, Newman MH: Tuberculosis of the larynx. Laryngoscope 86(4):549-558, 1976 6. Robbins SL: Pathology, ed 3. Philadelphia, WB Saunders, 1969, pp 738-739 7. Diagnostic Standards and Classification of Tuberculosis. New York. National Tuberculosis and Respiratory Disease Association, 1969, pp 79-80 8. Batsakis J: Tumors of the Head and Neck, Clinical and Pathological Considerations. Baltimore, Williams and Wilkins, 1974, p 139 9. Ballenger JJ: Diseases of the Ear, Nose, and Throat, ed 11. Philadelphia, Lea and Febiger, 1969, pp 366-369
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 1, 1979
A case of laryngeal tuberculosis, in a 21-year-old female, is presented. The pathophysiology and natural course of the disease are discussed. The incidence of apical tuberculosis and associated laryngeal spread is noted.
In the preantibiotic era, endolaryngeal seeding was a frequent complication of far advanced or disseminated tuberculosis. This phenomenon was seen in 10 to 20 percent of cases showing bronchial involvement.' In rare cases, it was the presenting complaint which resulted from mucosal exposure to highly infected secretions. Endobronchial involvement was the usual etiology and apical disease was associated in only one percent of cases.2 Hematogenous dissemination was more common in extrinsic involvement of the laryngeal structure but was preceded in five percent of cases by chronic tuberculous laryngitis.3 In terminal cases, laryngeal involvement approaches 100 percent. The typical patient is a middle-aged male with long-standing disease. Of 37 patients in a series reviewed at the Institute Of Laryngology and Otology, less than six percent were under age 30.4 The following case is one in which apical tuberculosis is complicated by laryngeal lesions in a young female.
Requests for reprints should be addressed to Dr. C. E. Jones, 353 Hawthorne Avenue, Yonkers, NY 10705.
Case Report A 21-year-old Oriental female presented with a three-month history of intermittent hoarseness. She had spent all of her life, except the last two years, in the Orient. Since arriving in the United States, she denied any complaints except her voice change. After several trials of unsuccessful medical therapy, she presented at the hospital in November 1976. She had generalized fatigue and a 15 lb weight loss. Indirect mirror laryngoscopy revealed edema of the right arytenoid and true cord. Chest roentgenography showed a dense network of punctate structures filling the upper one-third of both hemithoraces. The upper lung fields were contracted and compensatory emphysematous changes were noted in the lower lung segments. Calcifications were not seen. The roentgenologist's diagnosis was severe bilateral pulmonary granulomatous disease. Miliary tuberculosis limited to the upper lobes (rather unl6sual) and the possibilities of fungus infection and atypical sarcoidosis were considered. The patient was scheduled for admission in December 1976 for a more complete workup. Her hospital course was unremarkable except for odynphagia which increased with intake of
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 1, 1979
orange juice. A comprehensive study for acid fast disease was undertaken. Significant findings showed (1) chest PA and lateral x-ray changes similar to those noted on previous examination; (2) apical lordotics with cavitation in the left subapex; (3) gastric washings positive for acid bacilli on two occasions; and (4) a strongly positive firststrengh purified protein derivative (PPD) in 48 hours. With a presumptive diagnosis of tuberculosis, she was started on isoniazid and ethambutal after an ophthalmology consult. She was discharged in mid-December 1976 to be followed up with pulmonary evaluations. In January 1977 she returned to the clinic with dysphagia. Indirect mirror laryngoscopy revealed edema of the right true vocal cord and a fungating grayish white mass on the laryngeal surface of the epiglottis and left aryepiglotic fold. Small lesions were also noted subglottically. Direct laryngoscopy showed that the mass was confined to the laryngeal surface of the epiglottis. There was hypertrophy of the right ventricular folds. The true vocal cords were not invovled. Pathologic examination confirmed the diagnosis of active caseous granulomatous disease of the larynx and epiglottitis (Figure 1). Fungal-like colonies were noted in the necrotic specimens, but cultures were negative. Cultures of gastric washings were positive for Mycobacterium tuberculosis. Followup examination in the clinic showed healing and beginning resolution of the laryngeal lesions. 37
Figure 1. Photomicrograph showing granuloma of the larynx. Note necrotic area in lower field and epithelioid cells and scattered mononuclear exudate in the upper field.
Discussion In the past, tuberculosis of the larynx was thought to be a disease of younger people, but in the past 20 years, there has been an increased incidence in patients over 60 years of age. In general, the lesions are four times more common in the male than in the female. Laryngeal disease is distinctly more common in middle-aged men who are debilitated, alcoholic, or tobacco smokers. Socioeconomic factors, race, respiratory tract pathology, and pregnancy cause people to show a particular predilection for laryngeal spread. The usual lesion is a tubercle involving the posterior commissure, interarytenoid space ventricles, vocal folds, and epiglottis. The process can continue to ulceration and involve the underlying cartilage. Granulation tissue mimicking keratosis, epithelial hyperplasia, and confluent granulomas with skip areas have been seen.' It is not known why lesions are rare in the tracheobronchial tree, or why there can be extensive laryngeal disease in the absence of sputum production. Likewise the etiology is obscure when there is copious sputum production without laryngeal involvement. The occurrence of tuberculous laryngitis, in the absence of sputum, is thought to be due to the organism's being carried in the submucous lymphatics or vascular network of the primary site and transported to the submucosa of the larynx. Certain tuberculous lesions are allergic and are known to progress rapidly dur38
ing puberty, pregnancy and the puerperium, in diabetes, and in patients with endocrine changes. The lesions are progressive and liquefaction necrosis of tissue occurs. Two types of lesions are clincially recognizable: (1) exudative, which shows diffuse inflammation with hyperemia, edema and infiltration of the subepithelial space with a nonspecific exudate; (2) productive, which is characterized by granulation tissue located in the subepithelal stroma. Tubercles may form and progress to yellowish grey nodules. The overlying epithelium may be lost and ulceration, secondary to chronic infection, can cause cartilaginous destruction2'5 and involve the joint, most frequently the cricoarytenoid. Tuberculomas, reparative in nature, result in hyperplastic epithelium and subepithelial fibrosis. Edema of the epiglottis and arytenoids is a sign of late disease. Healing is accompanied by fibrosis encapsulation and tubercle replacement. Advanced lesions can cause complete stenosis and fixation of the cricoarytenoid joint. The characteristic heart-shaped epiglottis and club-shaped arytenoid are results of chronic edematous changes.6 Hoarseness is among thd first symptoms the patient will notice.7 This can progress to aphonia or dysphonia without visible cord lesions. Dry throat with odynphagia is common, particularly if there is cartilaginous involvement. Dysphagia and dyspnea are common when the disease is manifested princi-
pally by edematous changes. Laryngeal tuberculosis must be distinguished from verrucose carcinoma and other granulomatous diseases.5'8'9 Since these two entities occur with great frequency, they must be differentiated and appropriate therapy instituted promptly.
Comment Since tuberculous involvement of the larynx occurs with sufficient frequency, physicians must be aware of its potential, particularly when encountered in advanced disease. Apical tuberculosis, complicated by laryngeal involvement, is rare and is seen in only one percent of cases. Literature Cited 1. Weinstein L, Brown R: Otolaryngologic manifestations of extrinsic infectious diseases. Otolaryngol Clin North Am 9(3):647-648, 1976 2. Beeson PB, McDermott W (eds): CecilLoeb Textbook of Medicine, ed 12. Philadelphia, WB Saunders, 1967, p 683 3. Travis LW, Work WP, Whitehouse WM: A radiologic advance in the diagnosis of disorders of the larynx. Laryngoscope 86(6):780-784, 1976 4. Paparella M, Shrumrick D: Otolaryngology, Head and Neck. Philadelphia, WB Saunders, 1973, vol 3, pp 620-624 5. Travis LW, Hybels RL, Newman MH: Tuberculosis of the larynx. Laryngoscope 86(4):549-558, 1976 6. Robbins SL: Pathology, ed 3. Philadelphia, WB Saunders, 1969, pp 738-739 7. Diagnostic Standards and Classification of Tuberculosis. New York. National Tuberculosis and Respiratory Disease Association, 1969, pp 79-80 8. Batsakis J: Tumors of the Head and Neck, Clinical and Pathological Considerations. Baltimore, Williams and Wilkins, 1974, p 139 9. Ballenger JJ: Diseases of the Ear, Nose, and Throat, ed 11. Philadelphia, Lea and Febiger, 1969, pp 366-369
JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION, VOL. 71, NO. 1, 1979
