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Laryngopharyngeal tuberculosis: a rare entity in the era of antibiotics
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  1. Vasco Sousa Abreu1,
  2. Filipa Lima Coelho2,
  3. Joana Cardoso3 and
  4. Joana Ferreira Pinto2
  1. 1Department of Neuroradiology, Centro Hospitalar Universitário do Porto, Porto, Portugal
  2. 2Department of Radiology, Centro Hospitalar Universitário do Porto, Porto, Portugal
  3. 3Department of Infectious Diseases, Centro Hospitalar Universitário do Porto, Porto, Portugal
  1. Correspondence to Dr Joana Ferreira Pinto; joanapintodx{at}gmail.com; Dr Vasco Sousa Abreu; vrlsa1993{at}gmail.com

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Description

A man in his 30s with active consumption of cocaine, heroin and alcohol presented with progressive half-year evolution of hoarseness, dysphonia, dysphagia (initially for solids, later for liquids), dyspnoea and cough, associated with fever, night sweats and significant weight loss (30–40 kg); he was in poor general condition, very thin and dehydrated.

Laboratory tests revealed a lymphocytic leucocytosis with a marked increase in C reactive protein; arterial blood gas analysis showed type I respiratory failure; HIV test was negative.

Nasopharyngolaryngoscopy revealed hypertrophy/hyperaemia of the pharyngolaryngeal mucosa from the epiglottis to the ventricular bands, making it impossible to assess the vocal cords.

Chest CT demonstrated multiple cavitated lesions on the pulmonary parenchymal, the main lesion located in the right lung apex; it also revealed countless small, well-defined, centrilobular nodules connected to linear branching opacities, the so-called tree-in-bud appearance: typical findings of postprimary tuberculosis (TB) (figure 1). CT scan of the neck also showed a diffuse thickening and enhancement from the epiglottis to the hypopharynx and vocal cords, symmetrically, with no exophytic lesions (figure 2).

Figure 1

Chest CT, lung window: axial (A,B,D,E) and sagittal (C,F) sections before and after treatment (top and bottom rows, respectively). Presence of multiple cavitated lesions disperse on the pulmonary parenchymal, with the main lesion located in the right lung apex (A,D), and countless small, centrilobular nodules connected to linear branching opacities: tree-in-bud appearance (main imaging finding in B). After treatment, there is marked regression of the size of the cavitated lesions and disappearance of the tree-in-bud sign.

Figure 2

Contrast CT scan of the neck: sagittal (A,E) and axial sections in the plane of the epiglottis (B,F), hypopharynx (C,G) and glottis (D,H), before and after treatment (top and bottom rows, respectively). Pretreatment images show marked mucosal thickening and contrast enhancement of the epiglottis, aryepiglottic folds, hypopharynx and vocal cords, symmetrically, with no evident focal exophytic lesions; the airway remains patent, although slight stenosis. After treatment there is marked regression, without any significant pathological findings in the previously affected pharyngolaryngeal structures, except for a slight thickening on the right vocal cord.

Sputum smear microscopy–Ziehl-Neelsen and auramine stains–revealed acid-fast bacilli. Nucleic acid amplification tests were positive for Mycobacterium tuberculosis. Standard induction treatment was initiated with isoniazid (INH), rifampicin (RIF), pyrazinamide (PAZ) and ethambutol (EMB) and maintained for 2 months with favourable clinical response. Drug susceptibility was later confirmed, and subsequently there was a transition to the maintenance regimen with INH and RIF, continued for another 7 months.

Once the therapeutic regimen was completed, there was an overall clinical improvement with minor residual hoarseness. Post-treatment nasopharyngolaryngoscopy showed no residual pathological changes. Radiological resolution was documented in cross-sectional imaging, with few and small persistent lung cavities and very discreet right vocal cord thickening (figures 1 and 2).

Pharyngolaryngeal tuberculosis (PLTB) was one of the most common extrapulmonary forms of the disease before the era of antibiotics.1 2 Although the literature reports an annual incidence of 1%, its prevalence is increasing in some countries, mainly fuelled by HIV epidemics and immunosuppressive therapeutics.1–4

PLTB generally accompanies a pulmonary involvement, mostly from pooling of highly infectious sputum or even by haematogenous spread.1 2 It affects men more commonly and it is often associated with heavy smoking and alcohol consumption.4 Clinical presentation includes hoarseness/dysphonia, odynophagia, dysphagia, which may accompany pneumological symptoms like cough or haemoptysis.

Although definitive diagnosis may require confirmation by direct sputum microscopy, molecular biology techniques and/or histological analysis, cross-sectional imaging is a valuable tool in early evaluation of head and neck TB, accurately demonstrating the sites of involvement, pattern and extension of the disease, being able to truthfully demonstrate the diffuse nature of the disease when compared with nasopharyngolaryngoscopy.5 Despite the integrity of the pharyngolaryngeal architecture may be preserved (destruction of adjacent cartilages and para-mucosal extension are rarely seen), severe stenosis of the airway may be a serious complication.5

Although no potential target was available to be biopsied, we believe laryngopharyngeal TB is the most likely diagnosis, considering patient’s social/epidemiological context, personal history, concomitant pulmonary TB with a diffuse pharyngolaryngeal infectious process, and the excellent favourable response to the instituted treatment.

Recommended first-line regimen consists of an intensive phase of HRZE (isoniazid, rifampicin, pyrazinamide and ethambutol) for 2 months followed by HR (isoniazid and rifampicin) for 4 months with particular attention to drug-resistant bacilli who may need additional drugs.

Acknowledgement of PLTB is markedly important because early diagnosis and therapy may prevent a permanent pharyngolaryngeal damage, loss of function and/or unnecessary surgery, as well as improving public health.

Learning points

  • Despite mycobacterium tuberculosis infection being a worldwide problem, laryngeal tuberculosis (TB) is relatively rare, with an annual incidence of 1%, occurring due to haematogenous spread or directly from pooling of highly infectious sputum.

  • Laryngeal TB should be suspected in all patients in an unfavourable epidemiological context presenting with chronic cough, hoarseness, dysphonia and/or significant dysphagia (pneumological symptoms may also be present if lung disease coexists).

  • Cross-sectional imaging may help in achieving a diagnosis, evaluating the infectious pattern and the extension of the pharynx and larynx infection, particularly when nasopharyngolaryngoscopy gives such a few information, specially about the vocal cords’ involvement.

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References

Footnotes

  • Contributors VSA compiled the information, performed the literature review for the case, and drafted the article. FLC compiled the information and critically revised the case report. JP, a radiologist, was involved in the diagnosis of this patient. JC was involved in the management (treatment and follow-up) of this patient.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.