Tuberculosis — DCE Clinical Case

The approach to this station

This is the classic "old TB" respiratory short case: the examiner wants a systematic examination, honest description of apical signs, and then — the actual test — your discrimination between inactive scarring and active disease, plus the differential of apical pathology [1].

Focused history — what you would establish

• The prior episode: when, where, what treatment and for how long, whether completed, any drug resistance, and any relapses since [2].
• Current symptoms: duration and character of the cough, sputum, haemoptysis, fevers, drenching night sweats, weight loss — the reactivation tetrad sought actively, not passively [3].
• Reactivation risk now: new immunosuppression (steroids, biologics, chemotherapy), diabetes, chronic kidney disease, significant weight change, alcohol [3].
• Exposure: unwell household or workplace contacts, recent travel to endemic regions.
• Function: exercise tolerance and occupational impact — old apical fibrosis can be asymptomatic or limiting.

Examination — the findings and their meaning

From the end of the bed: cachexia or normal habitus; respiratory rate; any thoracic surgery scars (older patients may have thoracoplasty or plombage scars). Hands: clubbing is unusual in TB and should push you toward suppurative or malignant differentials. Trachea: deviation toward an apex signals upper-lobe volume loss from fibrosis. Chest: reduced expansion at the affected apex; dull percussion over fibrosis or a cavity rim; apical crackles; bronchial breath sounds over consolidated or cavitated upper-lobe segments; post-tussive crackles are a traditional clue to apical disease [1].

Present the findings structurally, then stop and let the examiner take you to interpretation [1].

Presentation template (deliver this to the examiner)

"Mrs Tran is a comfortable 62-year-old woman with no signs of respiratory distress. There is reduced expansion, dullness to percussion, bronchial breath sounds and fine crackles at the right apex, with mild tracheal deviation to the right, consistent with upper-lobe volume loss and fibrosis. In the context of treated pulmonary tuberculosis 20 years ago, these findings are most consistent with chronic post-tuberculous apical change. The key clinical question is whether there is current activity — reactivation of TB, or a new process in scarred lung. I would establish this from her symptom history, comparison with old imaging, and sputum testing for smear, nucleic acid amplification and culture." [1] [4]

The active-versus-inactive discrimination

Inactive post-TB change is a radiological and clinical stability diagnosis: no constitutional symptoms, imaging unchanged over time, and no microbiological yield. Activity is declared by symptoms (the tetrad), new or changing infiltrates or cavitation on imaging, and organisms — smear, NAAT or culture — remembering that roughly half of culture-positive pulmonary TB is smear-negative, so a negative smear settles nothing [1] [4]. In a patient treated before, always request rifampicin-resistance testing on any positive NAAT and full phenotypic susceptibility on culture, because re-treatment without susceptibility results risks months of functional monotherapy [2] [4].

Differentials of apical disease to offer

Post-tuberculous fibrosis; reactivation TB; non-tuberculous mycobacterial disease (classically M. avium complex in middle-aged women, or cavitary disease in damaged lung); cavitating squamous lung cancer; fungal infection including aspergilloma colonising an old cavity (which is also the explanation for recurrent haemoptysis in a scarred apex); and apical vasculitic or rheumatoid disease [1].

Probing questions

"Her chest X-ray shows a rounded opacity inside an old apical cavity. What is it and what do you do?" — "An aspergilloma until proven otherwise — a fungal ball colonising the residual cavity. Most need only observation; recurrent or massive haemoptysis changes the answer to bronchial artery embolisation, with surgical resection for selected fit patients because medical therapy penetrates the cavity poorly." [1]

"Her sputum Xpert is positive but she was fully treated 20 years ago. Does that prove active TB?" — "It strongly suggests viable or recently viable bacilli and must be acted on, but molecular tests can detect DNA from dead organisms, so I confirm with smear and culture and full susceptibility — and the rifampicin-resistance result on the Xpert decides the initial regimen the same day." [4] [2]

"She asks why she got TB in the first place and whether it can come back." — "Most adult TB is reactivation of infection acquired years earlier and held dormant in granulomas; lifetime reactivation risk in a healthy person is about 5–10 per cent, concentrated in the first two years after infection, and it rises with immunosuppression, diabetes, kidney disease and age. Completing her treatment 20 years ago is the strongest protection she has — and the reason she must report new constitutional symptoms early." [3]