COPD in Pakistan: the TB history changes what a bronchodilator test means

Two facts from the Pakistan Chest Society's 2026 COPD guideline should change how you read a spirometry report in this country.

The first: Pakistan has the highest COPD prevalence in the WHO Eastern Mediterranean Region, at 13.8%.

The second: in COPD that follows tuberculosis, only 27% of patients have a positive bronchodilator response — against 82% in COPD alone.

Put those together and a familiar clinic scene looks different. A patient with a TB history, breathless, obstructed on spirometry, no meaningful reversibility. The instinct is to conclude that this is fixed scarring and there is nothing to give. The guideline's position is the opposite: that is exactly what post-TB obstruction looks like, and treatment for chronic airflow disease due to tuberculosis is the same as that of COPD.

The chapter GOLD does not have

Chapter 17 of the guideline is devoted to post-TB COPD. There is no equivalent in GOLD, and there is no reason there would be — it is a problem of high-burden countries. Pakistan ranks fifth among high-burden TB countries globally and accounts for 61% of the TB burden in the Eastern Mediterranean Region.

A Pakistani study found that 55.3% of treated pulmonary TB patients with breathlessness had an obstructive ventilatory defect. Obstruction can appear during the active phase or after treatment ends. Beyond the poor bronchodilator response, these patients have significantly lower FEV₁, higher airway resistance, and more frequent exacerbations than patients with COPD alone.

The mechanisms proposed are bronchiectasis, bronchiolar narrowing, bronchiolitis obliterans and accelerated emphysematous change — with small airway obstruction and destruction of extracellular matrix by matrix metalloproteinases feeding into chronic airflow limitation. The exact mechanism is not settled.

The prevention argument runs backwards, and it is worth saying to trainees: early diagnosis and proper treatment of tuberculosis is COPD prevention.

"Does she smoke?" is not a screening question here

The BOLD study looked at 4,291 never-smokers aged 40 and over. It found 6.6% met criteria for mild COPD and 5.6% for moderate-to-very-severe disease. Never-smokers accounted for 23.3% of all GOLD stage II+ cases — 20.5% even using the stricter lower-limit-of-normal threshold.

The risk factors behind that are age, lower educational attainment particularly in women, occupational exposure, childhood respiratory disease and abnormal body mass index. In Pakistan, household smoke belongs on that list, and the guideline gives advice that is unusually concrete about it:

Indoor pollution due to burning of wood and coal to keep houses warm in winter and use of biomass fuel in stoves should be minimized and measures should be taken to reduce exposure as by cooking in open air rather than a closed kitchen, having separate cooking area, making chimneys etc.

Cook outdoors. Separate the cooking area. Build a chimney. That is not a paragraph international guidance writes, and it is the kind of advice that can actually be followed.

On smoking itself: where time and resources are genuinely dedicated to cessation, long-term quit rates of 14–27% are reported, and counselling plus pharmacotherapy is the most effective combination. High nicotine dependence shows as smoking within 30 minutes of waking, smoking at night, 20 or more cigarettes a day, or a Fagerström score of 7–10.

Grading and treating

The guideline uses the ABE tool, the 2023 GOLD evolution that merged the old C and D groups into a single E to recognise that an exacerbation matters regardless of how symptomatic someone is between attacks:

• A — mMRC 0–1 or CAT under 10, no moderate or severe exacerbation in the past year. Start a bronchodilator.
• B — mMRC 2 or more or CAT 10 or more, no exacerbation in the past year. Start LABA + LAMA.
• E — one or more moderate or severe exacerbations in the past year, at any symptom level. Start LABA + LAMA, and consider adding ICS if blood eosinophils are 300 cells/µL or above.

Follow-up then splits by which trait persists, and the two tracks are genuinely different.

If breathlessness persists on LABA + LAMA: consider switching the device or the molecule, escalate the non-pharmacological side, consider adding ensifentrine — and go looking for another cause of the breathlessness.

If exacerbations persist: eosinophils decide. At 100 or above on dual therapy, add ICS. Below 100, consider roflumilast where FEV₁ is under 50% with chronic bronchitis, or azithromycin, or dupilumab in chronic bronchitis. And note the asymmetry when stepping down — de-escalating ICS is reasonable if pneumonia occurs, but with eosinophils at 300 or above, de-escalation is more likely to be followed by an exacerbation.

The exacerbation, and whether to admit

Severe means the blood gases have turned: PaCO₂ above 45 mmHg with pH below 7.35. Moderate is a heart rate of 90 or more, SaO₂ below 92% or a 3% drop from a known baseline, and CRP 10 mg/L or above. Peak expiratory flow is not useful for deciding on admission.

The admission table is a straight comparison across fourteen factors, and several of them are social rather than physiological — whether the patient can cope at home, whether there is anyone with them. Admit for severe breathlessness, poor or worsening general condition, cyanosis, worsening peripheral oedema, impaired consciousness or acute confusion, already being on oxygen, poor social support or living alone, chest X-ray changes, rapid onset, pH below 7.35, or PaO₂ below 52 mmHg.

In hospital: controlled oxygen by Venturi mask or nasal cannula to a target of SpO₂ 88–92%, with blood gases in the first hour and within an hour of any FiO₂ change. Nebulised salbutamol 5 mg with or without ipratropium 500 micrograms; if there is no nebuliser, a metered-dose inhaler works — salbutamol up to 6–8 puffs every half hour. Hydrocortisone 250 mg IV stat then 100 mg eight-hourly, switching to oral 30–40 mg daily as a single morning dose, up to 14 days. Antibiotics: a respiratory quinolone, amoxicillin-clavulanate or a second- or third-generation cephalosporin — with ciprofloxacin or a third-generation cephalosporin in severe COPD, where gram-negative infection is more common.

The decision the guideline asks you to make on arrival

This is the most distinctly Pakistani instruction in the document:

Patients must be stratified into 5 treatment escalation groups on admission and managed accordingly particularly in resource constraint settings.

The five: needing immediate intubation and ventilation; suitable for non-invasive ventilation and for escalation to intubation; suitable for NIV but not for intubation; not suitable for NIV but for full active medical management; or palliative care as the most appropriate management.

International guidance tends to treat the escalation decision as something that emerges as a patient deteriorates. This guideline asks for it on arrival, and states the reason plainly — resource constraint. Where there are three NIV machines and no free ICU bed, that decision gets made either way. The only question is whether it is made deliberately, written down and discussed with the family, or made at three in the morning by whoever happens to be on.

The guideline is equally direct about the other end: ICU admission may not be appropriate for patients with poor functional status or end-stage lung disease.

Bottom line

Stop using smoking history as the entry criterion — a fifth of moderate-to-severe COPD is in people who never smoked, and in Pakistan the exposure is often the kitchen. Ask about wood, coal and biomass, and give the household advice, because it is followable. In anyone with a TB history, expect a poor bronchodilator response and treat anyway. Grade with ABE, let the eosinophil count decide the inhaled steroid, and target 88–92% in an exacerbation. And decide the ceiling of care when the patient arrives, not when they crash.

Our COPD pathway carries the full ABE table, both follow-up tracks, the fourteen-point admission comparison, the hospital protocol and the post-TB chapter. See also the asthma pathway and the tuberculosis pathway, which is where post-TB COPD starts.

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