Ann Thorac Surg 2000;70:2142-2143
© 2000 The Society of Thoracic Surgeons
Case report
Tuberculous lymphadenopathy of superior mediastinum causing vocal cord paralysis
Mohammed A. Rafay, FRCSEda
a Thoracic Unit, King Khaled University Hospital, Riyadh, Saudi Arabia
Accepted for publication September 30, 1999.
Address reprint requests to Dr Rafay, 25/15, 3rd Main, 1st stage BTM Layout, opposite Mácuti Layout Bangalore, Kaenataka State 560029, India
e-mail: rafay{at}bgl.vsnl.net.in
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Abstract
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Vocal cord paralysis because of involvement of recurrent laryngeal nerve by benign and acute inflammatory lymphadenopathy is a rare condition. Presented here is a case of tuberculous lymphadenopathy of superior mediastinum causing left recurrent laryngeal nerve paralysis, which was successfully treated by antituberculosis treatment, with complete recovery of vocal cord function.
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Introduction
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Tuberculous lymphadenopathy of superior mediastinum is a common condition in underdeveloped countries [1], but presentation with paralysis of recurrent laryngeal nerve (RLN) and hoarseness of the voice is rare [2]. An extensive search of the literature published since 1966 revealed seven reports on the subject, and only three were reported in the English literature.
A 32-year-old Indian man presented to the Thoracic Unit, Department of Surgery, at King Khaled University Hospital, Riyadh, in December 1998, with severe hoarseness of voice of 3 weeks duration and a history of vague symptoms such as malaise, night sweats, and anorexia. He also had a 3-month history of contact with a tuberculosis (TB) patient who was his mother. Clinical examination was normal except for hoarseness of the voice. Indirect laryngoscopy showed left vocal cord paralysis.
Investigation showed lymphocytosis, raised erythrocyte sedimentation rate, and reversed albumin/globulin ratio. Sputum culture for acid-fast bacilli was negative on three occasions. A chest roentgenogram did not reveal any obvious pathologic condition. Computed axial tomograms of the chest with contrast medium showed matted aortopulmonary and subaortic lymph nodes that were approximately 1.5 cm in the coronal section, with central low attenuation and rim enhancement, a characteristic finding suggestive of TB lymphadenopathy [3] (Fig 1). Flexible bronchoscopy revealed no endobronchial lesion. The bronchioalveolar lavage was negative for pathognomic organisms, and acid-fast bacilli and cytology were negative for malignancy. The Mountoux test was strongly positive for TB.
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Fig 1. Computed tomogram of pretreatment aortopulmonary and subaortic matted lymph nodes, with central low attenuation and rim enhancement.
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The diagnosis of TB was made from the history and complementary findings on investigation [1]. The possibility of differential diagnosis of primary and secondary malignant lymphadenopathy was thought to be equally important, in view of lack of tissue and microbiological confirmation.
The patient was offered either a trial of anti-TB treatment and follow-up, or a surgical procedure under general anesthesia and biopsy of lymph nodes, for histologic and microbiological confirmation of the diagnosis. He opted for the former strategy and was started on four drugs: namely, isoniazide, ethambutol, rifampicin, and pyrizinamide, along with pyridoxine prophylaxis for anticipated neuritis.
Follow-up after 6 weeks showed subjective improvement of about 50% of symptoms, including phonation. The bronchioalveolar lavage was positive for Mycobacterium TB after 4 weeks. Follow-up after 3 months showed complete return of vocal cord movement and function. A repeat computed tomographic scan of the chest 6 months later showed complete resolution of mediastinal lymphadenopathy (Fig 2).
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Fig 2. Computed tomogram of posttreatment aortopulmonary and subaortic area, showing resolution of lymphadenopathy.
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Comment
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Chronic pulmonary tuberculosis with pleuropulmonary fibrosis particularly affecting the upper lobes has been well documented as a cause of vocal cord paralysis. The pathology could result from entrapment of RLN in the scar [4], traction neuropathy, or compression by enlarged TB nodes [5]. Thus, a late sequel of TB with neuropathy can be anticipated.
In the present case, minimal mass lesion with TB lymphadenitis affecting the RLN symbolize the singularity. I believe that it is the unique location of the nodes in the aorto-pulmonary window and arch of aorta, with confined space, where enlarged TB nodes and inflammatory swelling predispose to compression and dysfunction of RLN.
Mycobacterium TB induces T cell–mediated immune response and leads to caseous necrosis of tissue, and healing by fibrosis is the rule. "Direct spread of infection from perforated lymph node abscess damage the RLN rather than mechanical factors alone," as suggested by Fowler and Hetzel [6], is unlikely. Direct spread of infection will cause permanent damage of the nerve because of caseous necrosis, and even after treatment with anti-TB drugs, healing will induce fibrosis but not regeneration, and in both circumstances proceed to irreversible damage of the nerve. Complete recovery of RLN palsy occurs because of resolution of TB lymphadenitis and the ensuing decompression of the nerve after anti-TB treatment, and supports the compression dysfunction hypothesis as the cause of nerve palsy.
In developed countries superior mediastinal lymphadenopathy with vocal cord paralysis strongly suggests primary or secondary malignant lymphadenopathy [6]. Wayne and colleagues [2] reported a case of mass lesion of the left upper lobe of the lung with enlarged hilar nodes and vocal cord paralysis, which was treated with a therapeutic dose of radiation on the basis of high clinical and radiologic suspicion of malignancy. However, radiotherapy caused the TB to flare up in both the lungs, with a fatal result [2]. In underdeveloped countries TB is rampant and is common among immigrants from such countries [1]. Thus, TB lymphadenopathy of the superior mediastinum should be considered as a possible cause of vocal cord palsy [2, 6].
Finally, as judiciously advised by Fowler and Hetzel [6] and by Wayne and colleagues [2], the biopsy specimens must be cultured and examined histologically, as vocal cord paralysis may rarely be caused by tuberculous mediastinal lymphadenopathy and a delay in making the correct diagnosis will prevent an effective cure.
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References
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Bloomberg T.J., Dow C.J. Contemporary mediastinal tuberculosis. Thorax 1980;35:392-396.[Abstract/Free Full Text]
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Wayne C., Fulkerson L.L., Stein E. Vocal cord paralysis due to pulmonary tuberculosis. Am Rev Respir Dis 1975;112:565-569.[Medline]
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Moon W.K., Im J.G., Yeon K.M., et al. Mediastinal tuberculous lymphadenitis: CT findings of active and inactive disease. Am J Roentgenol 1998;170:715-718.[Abstract/Free Full Text]
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Gupta S.K. The syndrome of spontaneous laryngeal palsy in pulmonary tuberculosis. J Laryngol Otol 1960;74:106-113.
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Radner D.B., Snider G.L. Recurrent laryngeal nerve paralysis as a complication of pulmonary tuberculosis. Am Rev Tuberc 1952;65:93-99.
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Fowler R.W., Hetzel M.R. Tuberculous mediastinal lymphadenopathy can cause left vocal cord paralysis. BMJ 1983;286:1562.
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Abstract
Introduction
