Lung Pathology |

Laryngeal Tuberculosis: A Forgotten Cause of Dysphagia? FREE TO VIEW

Frank Genese, DO; Pius Ochieng, MD; Raymonde Jean, MD
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St.Lukes-Roosevelt Hospital Center, New York, NY

Chest. 2015;148(4_MeetingAbstracts):626A. doi:10.1378/chest.2268350
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SESSION TITLE: Lung Pathology Student/Resident Case Report Posters

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Tuberculosis is a plausible DDx for many clinical presentations since it may have protean manifestations. We present a case of a gravid patient with severe dysphagia who was found to have active tuberculosis.

CASE PRESENTATION: Thirty five year old G1P0 woman at 25 weeks gestation presented for endoscopic evaluation of dysphagia. She reported 3 months of progressive dysphagia with some heartburn and throat discomfort that culminated in almost total inability to swallow. She had lost 14 lbs and was started on partial parenteral nutrition. She had been treated with antacids and omeprazole without any response. Laryngoscopy by ENT revealing severe edema of arytenoids without visualization of vocal cords led to the diagnosis of laryngopharyngeal reflux and thus the omeprazole dose was increased. Owing to persistent symptoms, EGD was attempted. The procedure was aborted due to poor ventilation after sedation and requirement for Laryngeal Mask ventilation, as she could not be intubated owing to severe cord edema. After recovery from sedation she had chest imaging that revealed left upper lobe cavitary lesion leading to suspicion of tuberculosis in spite of negative PPD during her pregnancy and no reported exposure to tuberculosis or chronic cough. Induced sputum smear was heavily positive for acid-fast bacilli speciated as mycobacterium tuberculosis. The diagnosis of pulmonary and likely laryngeal tuberculosis was made and the patient was started on antituberculosis therapy with resolution of dysphagia.

DISCUSSION: High prevalence of acid reflux in pregnancy and negative PPD may have displaced tuberculosis as a differential diagnosis in this patient. Laryngeal tuberculosis accounts for less than 1 percent of tuberculosis cases. It has a male predominance and presents in fourth to sixth decades. It may present as hoarseness, cough and odynophagia. It is typically from hematogenous spread, lymphatic seeding or more commonly through bronchogenic spread, which may be applicable in our case. Interestingly, the gross appearance of laryngeal tuberculosis is highly variable ranging from nonspecific inflammation or edema to ulcerative, granulomatous or polypoid lesions. Case series suggest that lesions mostly affect true vocal cords and posterior commissure followed by the false cords and epiglottis. Laryngeal tuberculosis generally responds well to standard treatment regimens; however, delays in treatment initiation may lead to vocal cord paralysis, subglottic stenosis or laryngeal fibrosis sometimes necessitating tracheotomy.

CONCLUSIONS: Laryngeal TB generally does not present with the classic prodrome attributable to TB and should not be overlooked by clinicians.

Reference #1: Lim JY,Kim KM,Choi EC,Kim YH,Kim HS,Choi HS.Current clinical propensity of laryngeal tuberculosis:review of 60 cases.Eur Arch Otorhinolaryngol.2006 Sep;263(9):838-42

Reference #2: Wang CC,Lin CC,Wang CP,Liu SA,Jiang RS.Laryngeal tuberculosis:a review of 26 cases.Otolaryngol Head Neck Surg.2007 Oct;137(4):582-8

DISCLOSURE: The following authors have nothing to disclose: Frank Genese, Pius Ochieng, Raymonde Jean

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