Laryngeal Tuberculosis

Myron W. Yencha, MD, * Ronald Linfesty, MD, and Ana Blackmon, MD~

Since the introduction of antituberculous medications, the incidence of laryngeal tuberculosis

(TB) has decreased and remains stable. However, with the incidence of TB increasing, mainly
caused by the acquired immunodeficiency syndrome epidemic, the incidence of laryngeal
involvement may be on the rise. The main presenting symptom of laryngeal TB is dysphonia.
The diagnosis is confirmed with the identification of granulomatous inflammation, caseating
granulomas, and acid-fast bacilli on histopathologic examination of biopsied laryngeal tissue.
However, making the diagnosis difficult can be the presence of psuedoepitheliomatous
hyperpiasia, which mimics squamous cell carcinoma. Treatment is primarily with antitubercu-
Ious medications with surgery reserved for those cases of airway compromise. Laryngeal
complications can occur; thus, long-term follow-up is recommended. We report a case of
laryngeal TB in a human immunodeficiency virus-negative patient and review the literature.
(Am J Otolaryngo12000;21:122-126. Copyright 2000 by W.B. Saunders Company)

(Editorial Comment: Laryngeal tuberculosis is
decidedly unusual in North America. The authors
speculate, however, that the incidence of laryngeal
tuberculosis is on the rise; therefore, it behooves
otolaryngologists to consider this in the differential
diagnosis of laryngeal lesions.)
Tuberculosis is an infectious disease caused
by Mycobacterium tuberculosis. Typically, pa-
tients present with fever, chills, night sweats,
weight loss, and cough. This disease mainly
affects the pulmonary system but can also
involve extrapulmonary sites such as the
larynx.
In the preantibiotic era, laryngeal TB was
considered the most common disease of the
larynx, affecting 35% to 83% of patients with
TB, and the mortality rate was 45% to 90%.1,2
Involvement of the larynx was considered a
preterminal event. With the development of
antituberculous medications, isolation proto-
cols, and early detection methods, laryngeal
involvement decreased to less than 1% of
From the *Department of Otolaryngology--Head and
Neck Medicine, US Naval Hospital, Pensacola, FL, and
the Departments of tPathology and :~lnternal Medicine,
US Naval Hospital, Yokosuka, Japan.
The opinions or assertions expressed herein are those
of the authors and are not to be construed as official or as
reflecting the views of the Department of the Navy or the
Department of Defense.
Address reprint requests to Myron W. Yencha, MD,
Department of Otolaryngology-Head and Neck Surgery,
US Naval Hospital-Pensacola, 6000 West Highway 98,
Pensacola, FL 32512.
This is a US government work. There are no restric-
tions on its use.
0196-0709/00/2102-001050.00/0
122 American Journal of Otolaryngology, Vo121, No 2 (March-April), 2000: pp 122-126
patients infected with TB, and the mortality
rate decreased to less than 2%. 1,2 However,
because the incidence of TB is on the rise
worldwide (mainly caused by the emergence
of the acquired immunodeficiency syndrome
[AIDS] epidemic) the incidence of laryngeal
involvement may also be increasing. We re-
port a case of laryngeal TB in a human immu-
nodeficiency virus (HIV)-negative patient and
review the literature.
CASE REPORT
A 58-year-old white male presented to the
internal medicine clinic with a 1-month his-
tory of cough, dysphonia, dysphagia, and
odynophagia. This patient was the health care
provider on a sea-going vessel and had self-
treated with amoxicillin without resolution of
his symptoms. He denied weight loss, fever,
chills, hemoptysis, or decrease in appetite. He
also denied any allergies and was not on any
medications. His past medical history was
significant for a positive purified protein de-
rivative (PPD) test, for which he received
treatment, and an abnormal chest radiograph
(CXR). Neither old films or radiological re-
ports were available for review. His social
history included one pack of cigarettes per day
for 50 years and a history of alcohol abuse.
This patient lives in the Philippines and re-
cently traveled to Thailand and Singapore.
Physical examination showed an ill-appearing
male in no apparent distress. Head and neck
examination revealed a 2.5-cm, soft, mobile
LARYNGEAL TUBERCULOSIS 123

adenopathy of the left anterior neck. The voice

was described as being hoarse, and pulmonary
examination was normal. The rest of the exami-
nation was normal. A CXR was obtained and
showed bilateral upper lobe infiltrates, right
pleural effusion, and left superior mediastinal
and bilateral hilar adenopathy. The CXR find-
ings were consistent with a diagnosis of TB.
The patient was admitted, placed in isolation,
and sputum samples for acid-fast bacilli (AFB)
were ordered. The results of the sputum
samples were positive for AFB, cultures were
sent, and the patient was started on the follow-
ing antituberculous medications: isoniazid 300
mg per day, ethambutol 2 g per day, rifampin
600 mg per day, and pyrazinamide 2 g per day. Fig 2. IntraoperaUve photograph shows edematous
HIV testing was negative. An otolaryngology TVC (large arrow) and subglottic stenosis (small arrow).
consult was obtained after the patient had
been on antituberculous medications for 3 was edematous (turban-shaped) with superfi-
weeks. The history showed resolution of the cial ulcerations and a fine nodular appearance
odynophagia and a significant decrease in the (Fig 1). The supra-arytenoid tissues were
dysphagia; however, the dysphonia persisted edematous and nodular appearing. The TVC
and remained unchanged. Physical examina- were edematous (Reinke's edema) and poly-
tion showed a decrease in the left neck ad- poid in appearance with a fine fibrinous exu-
enopathy to 1.5 cm at level IV. Flexible fiberop- date, the false vocal cords (FVC) were edema-
tic examination revealed a grossly abnormal tous with a nodular appearance, and a
endolarynx with bilateral mobile true vocal subglottic stenosis was noted on the left (Fig
cords (TVC). The voice was strained, rough, 2). Biopsies were taken from multiple sites,
and without stridor. The rest of the head and and histopathologic examination showed a
neck examination was normal. A fine-needle granulomatons inflammation with caseating
aspiration was "performed on the lymph node; granulomas, numerous AFB, and psuedoepi-
however, the pathologist could not rule out a theliomatous hyperplasia (Figs 3,4). Cultures
malignancy. Informed consent was obtained, of the biopsied tissue returned a diagnosis of
and the patient was taken to the operating pansensitive Mycobacterium tuberculosis. The
room for a direct microlaryngoscopy and bi- patient was discharged on the above antituber-
opsy. Under direct visualization, the epiglottis culous medications and returned for a fol-
low-up appointment one month later. The

Fig 1. Intraoperative photograph shows an edema- Fig 3. Photomicrograph shows numerous acid-fast
tous (turban-shaped) epiglottis with nodularity and ulcer- bacilli (arrows). (Kinyoun acid-fast stain; original magni-
ations. fication x 1000).
124
Fig 4. Photomicrograph shows psuedoepithelioma-
tous hyperplasia. Note how the well differentiated squa-
mous epithelium extends deep into the dermis. There
are also islands of squamous epithelium in the dermis,
(Hematoxylin & eosin; original magnification x250).
patient's dysphonia was resolving, and he
denied stridor or dyspnea. Fiberoptic examina-
tion showed slowly resolving edema and nod-
ularity of the endolarynx with persistance of
the subglottic stenosis. A computed axial to-
mography scan of the larynx and trachea with
sagittal reconstruction showed a noncircumfer-
ential stenosis of the subglottis measuring 2
cm in length. The patient was scheduled for a
direct laryngoscopy and brochoscopy for a
more accurate evaluation of the stenotic seg-
ment but .failed to keep this appointment.
Unfortunately, the patient has been lost to
follow-up.
DISCUSSION
The incidence of laryngeal TB continues to
remain stable; however, since the advent of
the AIDS epidemic, there has been a world-
wide increase in the incidence of TB. TB is
more common and tends to be more aggressive
with poor localization, early dissemination,
and up to 80% extrapulmonary involvement
in the HIV-infected population. 3,4 In fact, in
HIV-infected patients, extrapulmonary TB is
considered an AIDS-defining illness. With this
increase in incidence of TB, there may be an
overall increase in the incidence of laryngeal
involvement.
Currently, there are 2 theories that attempt
to explain the etiology of laryngeal TB. The
first is called the bronchogenic theory and
states that the larynx is infected by direct
spread from the endobronchial tree. 5 This
YENCHA, LINFESTY,AND BLACKMON
accounts for the ma)ority of cases. The other
theory is called the hematogenous theory, and
it states that the larynx is infected by hemato-
genous spread from sites other than the lungs. 5
These patients do not show pulmonary in-
volvement as demonstrated by a normal CXR.
The etiology in our patient was consistent
with the bronchogenic theory.
The most common presenting symptom is
dysphonia, which was present in 100% of
patients in several studies. 5,6,7 Other symp-
toms relating to the upper aerodigestive tract
include dysphagia, odynophagia, stridor,
cough, and hemoptysis. Laryngeal pathology
should be suspected in any patient with dys-
phonia. The only symptom in our patient that
persisted, unchanged despite medical therapy,
was dysphonia. The physical examination
findings associated with laryngeal TB can
consist of any or all the following: edema,
hyperemia, nodularity, ulcerations, exophytic
mass, and obliteration of anatomic land-
marks. 2,5,8 Specifically, the epiglottis can be
markedly edematous (turban-shaped), and the
TVC edema can resemble polypoid corditis.
Subglottic edema may result in airway compro-
mise, thereby necessitating the need for a
tracheostomy. Although classically described
as involving only the posterior larynx, TB can
involve any laryngeal structure with the order
of frequency of sites involved from most to
least common as follows: TVC, epiglottis, FVC
and ventricle, arytenoid/interarytenoid area,
and subglottis. 7,9,1
The patient with laryngeal TB is referred to
the otolaryngologist for evaluation of dyspho-
nia, often without the diagnosis of TB. The
work-up is initiated with a complete history
and physical including laryngoscopy, which
often reveals an abnormal endolarynx and an
initial impression of SCCA. Next, a CXR is
obtained and reviewed with a radiologist. If
TB is suspected, the patient should be placed
in isolation, a PPD test placed, sputums col-
lected for AFB, and infectious disease consul-
tation obtained. Unfortunately, in HIV-in-
fected patients, a negative PPD test does not
rule out TB. When TB is confirmed, treatment
is initiated with antituberculous medications.
However, if symptoms and/or physical find-
ings persist during the course of treatment,
further evaluation is required. The surgical
procedure of choice is direct microlaryngos-
LARYNGEAL TUBERCULOSIS
copy because it allows direct visualization of
the endolarynx and a means of obtaining
tissue for diagnosis. The diagnosis of laryngeal
TB is established with the identification of
granulomatous inflammation, caseating granu-
lomas, and AFB on histopathologic examina-
tion. However, the presence of psuedoepithe-
liomatous hyperplasia, which mimics SCCA,
can make the diagnosis difficult; thus, the
pathologist should be informed that TB is part
of the differential diagnosis. Also, laryngeal
TB and laryngeal SCCA can coexist in the
same patient, and laryngoscopy findings are
often indistinguishable; thus, biopsies should
be taken from all suspicious lesions and at
multiple sites. 9,1~Furthermore, the typical pa-
tient with laryngeal TB has similar risk factors
(tobacco and alcohol abuse) as those for laryn-
geal SCCA.
In one study of HIV-infected patients with
laryngeal TB, SCCA was the initial impression
on laryngoscopy (even though systemic symp-
toms were present but attributed to their HIV
status). 12 This resulted in a delay of diagnosis
in all of these patients, thereby putting the
examining physician at risk for aquiring TB.
Thus, HIV-infected patients with laryngeal
lesions should be considered infectious, and
appropriate precautions should be taken until
proven otherwise.
The differential diagnosis of laryngeal TB
includes neoplasms (mainly SCCA), sarcoid-
osis, Wegener's granulomatosis, mycotic infec-
tions, syphilis, and chronic nonspecific laryn-
gitis.7,13,14
Treatment consists of culture-sensitive anti-
tuberculous medications and respiratory isola-
tion. Surgical intervention (tracheostomy) is
reserved for those cases of airway compro-
mise.
After therapy, the patient's symptoms should
resolve. However, in those cases of persistent
dysphonia, further investigation is warranted.
As the larynx heals, fibrosis of laryngeal tis-
sues can occur resulting in the following se-
quelae: cricoarytenoid joint fixation, posterior
glottic stenosis, subglottic stenosis, or persis-
tent dysphonia. 6nLls
From an epidemiological standpoint, our
patient was a health care provider who was
actively seeing patients despite being symp-
tomatic (for 2 months) and infected with TB,
although undiagnosed. After the patient was
125
diagnosed with TB, PPD testing was per-
formed on all members of that ship. The
results showed that 12 members, who were
known to have had a recent negative PPD test,
tested positive although none had active pul-
monary TB. Subsequently, all were treated
with isoniazid for 6 months.
Finally, dysphonia is a complaint heard
frequently by the otolaryngologist and has
many etiologies. In the HIV-infected popula-
tion, where TB is on the rise, dysphonia could
be the presenting symptom of laryngeal TB;
thus, precautions should be taken to ensure
safety of the otolaryngologist and their staff.
SUMMARY
Since the introduction of antituberculous
medications, the incidence of laryngeal TB
has declined and remains stable. As a result,
many physicians do not consider TB in the
differential diagnosis of laryngeal lesions.
However, with the incidence of TB increasing,
the overall incidence of laryngeal involvement
may be on the rise. The main presenting
symptom is dysphonia, and the diagnosis is
confirmed by histopathologic examination of
biopsied tissue showing granulomatous inflam-
mation, caseating granulomas, and AFB. Possi-
bilities that may make the diagnosis difficult
include the presence of psuedoepithelioma-
tous hyperplasia, which mimics SCCA. Treat-
ment primarily consists of antituberculous
medications with surgery reserved for those
cases of airway compromise. Finally, laryn-
geal complications can occur; thus, long-term
follow-up is recommended.
REFERENCES
1. Lindell MM, Jing BS, Wallace S: Laryngeal tuberculo-
sis. Am J Roentgenol 129:677-680, 1 9 7 7
2. Brodovsky DM: Laryngeal tuberculosis in an age of
chemotherapy. Can J Otolaryngol 4:161-176, 1975
3. Ellner JJ: Tuberculosis in the time of AIDS: The
factors and the message. Chest 98:1051-1052, 1990
4. Beck K: Mycobacterial disease associated with HIV
infection. J Gen Intern Med 6:$19-$23, 1991 (suppl)
5. Ramadan HH, Tarazi AE, Baroudy FM: Laryngeal
tuberculosis: Presentation of 16 cases and review of the
literature. J Otolaryngo122:39-41, 1993
6. Soda A, Rubio H, Salazar M, et al: Tuberculosis of the
larynx: Clinical aspects in 19 patients. Laryngoscope
99:1147-1150, 1989
7. Smallman LA, Clark DR, Raine CH, et al: The presen-
tation of laryngeal tuberculosis. Clin Otolaryngol 12:221-
225, 1987
126
8. Chodosh PL, Willis W: Tuberculosis of the upper
respiratory tract. Laryngoscope 80:679-696, 1970
9. Leveson MJ, Ingerman M, Grimes C, et al: Laryngeal
Tuberculosis: Review of twenty cases. Laryngoscope 94:
1094-1097, 1984
10. Galietti F, Giorgis GE, Gandol FG, et al: Examina-
tion of 41 cases of laryngeal tuberculosis observed be-
tween 1975-1985. Eur Respir J 2:731-732, 1989
11. Rupa V, Bhanu TS: Laryngeal tuberculosis in the
eighties--an Indian experience. J Laryngo] Otol 103:864-
868, 1989
YENCHA, LINFESTY, AND BLACKMON
12. Singh B, Balwally AN, Nash M, et al: Laryngeal
tuberculosis in HIV-infected patients: a difficult diagno-
sis. Laryngoscope 106:1238-1240, 1996
13. Couldery AD: Tuberculosis of the upper respiratory
tract misdiagnosed as Wegener's granulomatosis--an im-
portant distinction. J Laryngol Otol 104:255-258, 1990
14. Riley EC, A m u n d s o n DE: Laryngeal Tuberculosis
revisited. A m Fam Physician 49:759-762, 1992
15. Park SS, Streitz JM, Rebeiz EE, et ah Idiopathic
Subglottic Stenosis. Arch Otolaryngol Head Neck Surg
121:894-897, 1995