Chronic Cough in Adults

Clinical Snapshot

Chronic cough is defined as a cough lasting more than 8 weeks. It sits at the end of a duration-based classification that also includes acute cough (under 3 weeks, usually infectious and self-limited) and subacute or postinfectious cough (persisting after an upper respiratory infection but usually resolving before 8 weeks). Cough receptors are distributed throughout the upper and lower respiratory tract and beyond, which gives chronic cough an unusually broad differential diagnosis — but in a nonsmoker with a normal chest x-ray who is not taking an angiotensin-converting enzyme (ACE) inhibitor, the cause is upper airway cough syndrome, cough-variant asthma, GERD-related cough, or nonasthmatic eosinophilic bronchitis in the large majority of cases.^[1]^[2] The core management principle is diagnostic, not symptomatic: chronic cough responds best to therapy directed at its underlying cause, and reaching for a nonspecific antitussive before that cause is identified risks masking or delaying the diagnosis of something that needs its own treatment — occasionally something serious.^[3]

Recognize the Condition

How chronic cough actually presents

Chronic cough itself is a single symptom with few distinguishing features on its own — dry or productive, its pattern (worse at night, with meals, with exertion, with position change), and its associated symptoms are what point toward a specific cause rather than the cough itself. A careful history aimed at eliciting those associated symptoms is the single most useful diagnostic tool.

Clues that point toward a specific cause

Postnasal drainage, throat clearing, nasal congestion or discharge, and a cobblestone appearance of the oropharyngeal mucosa point toward upper airway cough syndrome (UACS, formerly called postnasal drip syndrome).
Wheeze, chest tightness, or a personal/family history of atopy point toward cough-variant asthma — though classic asthma features are often absent, and cough may be the only symptom.
Heartburn, regurgitation, or a cough that is worse after meals or when lying flat suggests GERD-related cough — though up to half of GERD-related chronic cough occurs without typical reflux symptoms, so its absence does not rule this out.
A dry, nonproductive cough beginning anywhere from hours to months after starting an ACE inhibitor, with no other predisposing factor, suggests drug-induced cough — this is a class effect of every ACE inhibitor.
Minimal or no wheeze with a normal spirometry and negative bronchial challenge test, often in a postinfectious setting, suggests nonasthmatic eosinophilic bronchitis (NAEB).

Cough hypersensitivity

Many patients with chronic cough — whether an underlying cause has been found or not — describe a pattern of exaggerated sensitivity to low-level triggers that would not provoke cough in most people: cold air, perfume, smoke, talking, or laughing. This clinical pattern, termed cough hypersensitivity syndrome, reflects hypersensitivity of the airway's afferent (sensory) nerves combined with central augmentation of the cough reflex, and is the physiologic basis for the neuromodulator therapies used in refractory and unexplained chronic cough.^[1]

Risk Factors

Current or past tobacco or e-cigarette (vaping) use, including cannabis smoking.
Use of an ACE inhibitor — a class effect, not specific to any one agent.
Occupational or environmental exposure to irritants or allergens.
Personal or family history of atopy, allergic rhinitis, or asthma.
Known or suspected GERD, or risk factors for it (obesity, hiatal hernia).
Use of a statin or a beta-blocker — both are recognized, less common medication-related causes of chronic cough; a beta-blocker can also aggravate underlying asthma.
Obstructive sleep apnea — an increasingly recognized association, with some patients responding to continuous positive airway pressure therapy.

Red Flags & Refer

Any of the following findings should prompt urgent investigation (chest CT, referral) rather than an empiric cause-directed treatment trial:

Hemoptysis.
A smoking history of more than 15-20 pack-years.
Age over 45 years with a new or changed cough, or a cough accompanied by voice change, in a patient with a smoking history.
Age 55-80 years with a smoking history of more than 30 pack-years, who is either a current smoker or quit smoking within the past 15 years.
Prominent sputum production or dyspnea, especially at rest or at night.
Other local symptoms: hoarseness, dysphagia, odynophagia, vomiting, hematemesis, or chest pain.
Systemic symptoms: fever, unexplained weight loss, or peripheral edema with weight gain.
Recurrent respiratory tract infections (e.g., recurrent pneumonia).
Abnormal findings on respiratory examination or chest radiograph.

Assessment & Diagnosis

History and physical examination

A structured history should specifically cover: cough duration and its variation over the day; onset, severity, and character (wet versus dry); triggers; nocturnal symptoms and impact on quality of life; smoking/vaping history (tobacco and cannabis); current medication use, especially ACE inhibitors and, less commonly, statins or beta-blockers; symptoms of asthma, upper airway disease, and GERD; occupational and environmental exposures; and personal or family history of atopy or asthma. Examination should include the nasal cavities, oropharynx, and ear canals in addition to the respiratory and cardiac systems.^[1]

Objective testing

Chest x-ray and complete blood count in essentially every patient with chronic cough.
Spirometry, pre- and post-bronchodilator, to evaluate for asthma and COPD.
Methacholine (or other bronchial) challenge testing to detect airway hyperresponsiveness when asthma is suspected but spirometry is nondiagnostic — a positive test supports but does not by itself confirm cough-variant asthma, since false-positive challenge tests occur.
For suspected GERD: ambulatory pH monitoring is the most sensitive available test but still predicts acid-related cough imperfectly; impedance monitoring can detect nonacid reflux but is not widely available; upper GI series and endoscopy are frequently normal and are not first-line for this indication. A positive response to a therapeutic trial of acid suppression (an H2-receptor antagonist or a PPI) is a practical, widely used way to support the diagnosis when reflux-related cough is suspected.
For suspected NAEB: induced sputum eosinophilia, exhaled nitric oxide (where available), and a response to inhaled corticosteroids, in a patient with normal spirometry, a normal chest x-ray, and negative bronchial challenge testing.
Sputum for acid-fast staining and culture, sputum cytology, and CT chest for any patient with hemoptysis — refer to respirology for fibre-optic bronchoscopy.
Reserve CT chest and bronchoscopy for patients with no identified cause after initial evaluation and after cough remains refractory to empiric therapeutic trials for the common causes, or when a red flag or a specific clinical suspicion (malignancy, chronic infection such as tuberculosis, interstitial lung disease, bronchiectasis, foreign body aspiration, occult left heart failure, irritable larynx syndrome) points toward a less common cause.

Table 1 — Common causes of chronic cough: clinical features and investigations

Common cause	Clinical features	Potential investigations
Upper airway cough syndrome	Postnasal drainage; cobblestoning and mucus visible in the oropharynx; nasal discharge; throat clearing.	Nasal endoscopy; CT of the paranasal sinuses if chronic rhinosinusitis is suspected (plain sinus x-rays are generally unhelpful).
Cough-variant asthma	Other typical asthma features (e.g., wheeze) are often absent.	Spirometry pre-/post-bronchodilator; methacholine challenge; induced sputum eosinophilia; exhaled nitric oxide.
GERD-related cough	Considered after exclusion of other causes; often occurs without typical reflux symptoms.	No true gold-standard test. Options: upper GI series (limited sensitivity); pH monitoring/impedance (better sensitivity, moderate-to-poor specificity); endoscopy if pH monitoring is unavailable (less sensitive).
ACE inhibitor-induced cough	Dry, nonproductive cough; onset from hours to months after starting the drug; no predisposing factors; a class effect of every ACE inhibitor.	Diagnostic drug withdrawal — resolution or marked improvement within 1-4 weeks confirms the diagnosis.
Nonasthmatic eosinophilic bronchitis (NAEB)	Mainly dry, occasionally productive cough with minimal wheeze; often prolonged in a postinfectious setting.	Normal spirometry and chest x-ray; negative bronchial challenge testing; induced sputum eosinophilia; exhaled nitric oxide (where available).

Reserve the "potential investigations" column for patients with no overt cause identified on initial evaluation, or cough that is refractory to an adequately conducted empiric trial for the most likely common cause.

Treatment Targets

Identify the specific underlying cause (or causes — more than one can coexist) and select therapy directed at that cause, rather than defaulting to nonspecific cough suppression.
Minimize adverse effects of therapy, particularly of empiric trials that may ultimately prove unnecessary.
Avoid nonspecific cough-suppression therapy that could delay diagnosis of a curable underlying cause.
Prevent complications of persistent coughing itself — rib fracture, syncope, sleep disruption, aggravation of stress urinary incontinence, exercise intolerance, vomiting, epistaxis, and ocular injury or hemorrhage.
Ensure that uncommon but serious causes, particularly lung cancer, are not missed by premature closure on a benign diagnosis.

Choose Initial Treatment

Direct treatment rule

Any red flag (see Red Flags & Refer) overrides the standard cause-directed pathway — obtain urgent imaging or a specialist referral rather than starting an empiric trial.

Before beginning any empiric cause-directed trial, review the medication list specifically for an ACE inhibitor — this is a fully reversible, drug-induced cause and should be excluded or confirmed with a withdrawal trial before other causes are pursued.

Once red flags and ACE inhibitor use have been addressed, treat the most clinically likely cause first, based on the history and examination findings — upper airway symptoms point to UACS, wheeze or an atopic history points to cough-variant asthma, and reflux symptoms (or their absence, after other causes are excluded) point to GERD-related cough. More than one cause can coexist; if a trial produces partial but incomplete improvement, continue that therapy while investigating for an additional contributing cause rather than stopping it.

Reserve nonspecific antitussive or mucolytic therapy for adjunctive, short-term symptom relief once a diagnostic workup is underway or complete — never as a substitute for it.

Cause-directed treatment tracks

Upper airway cough syndrome (UACS)

Direct therapy at the specific cause of UACS where it can be identified. For allergic rhinitis, use an oral or intranasal antihistamine, an intranasal corticosteroid, or a leukotriene receptor antagonist (e.g., montelukast) — see the Pharmacologic Treatment Options table; nonsedating antihistamines such as loratadine can be effective for allergic-rhinitis-driven cough specifically.

For nonallergic rhinitis, use an intranasal corticosteroid, or an intranasal antihistamine (in Canada, available only in fixed-dose combination with an intranasal corticosteroid).

For chronic rhinosinusitis, first-line therapy is an intranasal corticosteroid or nasal saline irrigation/spray, with referral to an ear, nose, and throat specialist if this does not control symptoms.

If the specific cause of UACS cannot be identified, treat empirically with the combination of a first-generation antihistamine plus a decongestant — this combination is more effective than a newer, non-sedating antihistamine alone for cough related to idiopathic postnasal drip, but first-generation antihistamines are best avoided in older adults given their anticholinergic burden.^[4]

Cough-variant asthma

Manage per the stepwise inhaled-corticosteroid-based treatment framework described in the Asthma in Adults and Adolescents chapter — this chapter does not re-derive asthma dosing. Cough-variant asthma is treated the same as classic asthma; a positive response supports the diagnosis.

GERD-related cough

Begin with the lifestyle and dietary measures described in the Gastroesophageal Reflux Disease chapter (weight loss, dietary triggers, avoiding late meals, head-of-bed elevation) — this chapter does not re-derive PPI dosing.

If nonpharmacologic measures fail and the patient has heartburn or regurgitation, add a PPI trial for a minimum of 8 weeks per the Gastroesophageal Reflux Disease chapter's dosing.

Do not start empiric acid suppression in a patient with genuinely negative GERD investigations — current guidance does not support empiric PPI therapy once reflux has been reasonably excluded, since the overall evidence for PPI benefit in nonspecific chronic cough is weak outside patients with confirmed pathologic acid exposure.^[5]

Nonasthmatic eosinophilic bronchitis (NAEB)

Start a 2-4 week trial of an inhaled corticosteroid — see the Pharmacologic Treatment Options table for a specific starting dose.^[6]

If the response is incomplete, increase the inhaled corticosteroid dose, or add montelukast.

ACE inhibitor-induced cough

Confirmed or suspected — stop the ACE inhibitor as a diagnostic and therapeutic trial, regardless of how long the patient has been taking it or how long ago the cough started; this is a class effect that recurs with rechallenge with any agent in the class.

Substitute an angiotensin receptor blocker (ARB) — ARBs are not associated with this cough mechanism and are the preferred substitution when the original indication (hypertension, heart failure, post-MI, diabetic nephropathy) still requires renin-angiotensin system blockade. See Drug Tables for substitution options and starting doses.

Expect resolution or marked improvement within 1-4 weeks of stopping the ACE inhibitor (median around 1 week); if the cough has not improved by 4 weeks off the drug, the ACE inhibitor was probably not the cause and the standard workup for the other common causes should proceed.^[7]

Refractory or unexplained chronic cough

Use this category once red flags have been excluded, the common causes above have been adequately investigated and treated (or excluded), and cough either persists despite treatment of an identified cause (refractory chronic cough) or no cause is found after a complete evaluation and supervised therapeutic trials (unexplained chronic cough, UCC).

1st-line neuromodulator gabapentin — see Pharmacologic Treatment Options and Drug Tables for dosing; reassess efficacy at 6 months and taper if effective and stable.^[8]^[9]

Alternative — when gabapentin is not tolerated or not effective pregabalin or low-dose sustained-release morphine; both carry a higher adverse-effect burden than gabapentin, and morphine additionally carries misuse/dependence potential requiring close monitoring.

Not available in Canada gefapixant, a P2X3 receptor antagonist that reduces cough frequency in refractory and unexplained chronic cough in trial data, is approved in some other jurisdictions but is not available in Canada — the manufacturer cancelled its Health Canada New Drug Submission before a final decision was reached, following an unresolved Notice of Deficiency regarding cough-count methodology and efficacy-data robustness. Do not offer it as a current option.^[10]

Multimodality speech-language pathology therapy (laryngeal retraining, cough-suppression techniques) is an effective adjunct for cough hypersensitivity and for laryngeal dysfunction contributing to cough, and can be used alongside or instead of pharmacotherapy.

Non-Pharmacologic Treatment

Advise cessation of all tobacco products and e-cigarettes/vaping in every current user — a temporary worsening of cough can occur after quitting and may persist for several months; counsel patients about this in advance so it is not mistaken for treatment failure.
Advise avoidance of known allergens and environmental/occupational irritants.
For GERD-related cough: weight loss if overweight, avoidance of specific trigger foods/beverages, avoiding meals late in the evening, and nocturnal elevation of the head of the bed.
For UACS from chronic rhinosinusitis or nonallergic rhinitis: regular nasal saline irrigation or spray is a genuine first-line measure, not just an adjunct, and is safe for ongoing use.
Consider multimodality speech-language pathology therapy for laryngeal dysfunction and for unexplained chronic cough generally.
Consider suggestion therapy (hypnosis) or behavioural therapy for psychogenic (habit) cough — an uncommon presentation and a diagnosis of exclusion, not a first-line assumption.
Evaluate for obstructive sleep apnea in patients with suggestive symptoms; continuous positive airway pressure therapy has been associated with cough improvement in this subgroup.

Pharmacologic Treatment Options

Drug / intervention	Role	Dose / use	Important adverse effects	Teaching points
Fluticasone propionate, intranasal Preferred	UACS — allergic or nonallergic rhinitis, chronic rhinosinusitis	2 sprays (100 mcg) per nostril once daily, reduce to 1 spray per nostril once daily for maintenance	Nasal irritation, epistaxis, headache	First-line intranasal corticosteroid for UACS regardless of allergic/nonallergic cause.
Loratadine Preferred	UACS — allergic-rhinitis-driven cough	10 mg PO once daily	Headache; minimal sedation	Nonsedating; preferred over a first-generation antihistamine, especially in older adults.
Diphenhydramine + pseudoephedrine (combination) Alternative	UACS — empiric therapy when the specific cause cannot be identified	Combo: diphenhydramine 25-50 mg PO + pseudoephedrine 60 mg PO, both dosed up to every 4-6 hours	Sedation, anticholinergic effects (diphenhydramine); insomnia, hypertension (pseudoephedrine)	More effective than a nonsedating antihistamine alone for idiopathic postnasal-drip cough. Avoid the first-generation antihistamine component in older adults.
Montelukast Alternative	UACS (allergic rhinitis) or NAEB step-up	10 mg PO once daily	Headache; rare neuropsychiatric effects	Add for allergic-rhinitis-driven UACS not fully controlled with an antihistamine/INCS, or add for NAEB with incomplete ICS response.
Fluticasone propionate, inhaled Preferred	NAEB — 2-4 week diagnostic/therapeutic trial	250 mcg PO inhaled twice daily; increase to 500 mcg twice daily if response is incomplete	Oral candidiasis, dysphonia, hoarseness	Rinse mouth after each use. Discontinue if no response after an adequate trial; response supports the NAEB diagnosis.
Losartan (ARB substitution) Preferred	Confirmed ACE inhibitor-induced cough	50 mg PO once daily, titrate to 100 mg once daily as needed for the original indication	Hyperkalemia, hypotension, dizziness	ARBs are not associated with this cough mechanism. Select the specific agent and target dose based on the original ACE inhibitor indication.
Gabapentin Preferred	1st-line neuromodulator for refractory/unexplained chronic cough (cough hypersensitivity)	Start 100 mg PO TID (or 300 mg once daily), titrate to the maximum tolerated dose up to 900 mg PO BID	Sedation, ataxia, tremor, peripheral edema	Reassess efficacy at 6 months; discontinue if no benefit. Renal dose adjustment required.
Morphine, sustained-release Alternative	Refractory/unexplained chronic cough — when gabapentin/pregabalin are not tolerated or ineffective	5-10 mg PO BID (sustained-release formulation)	Constipation, sedation, respiratory depression, misuse/dependence potential	Response, if it occurs, is usually rapid — discontinue if no benefit within 1-2 weeks. Monitor closely for misuse.
Dextromethorphan Special situation	Short-term, adjunctive symptom relief only (e.g., to enable sleep) once a cause-directed workup is underway	15-30 mg PO every 6-8 hours, maximum 120 mg in 24 hours	Drowsiness, GI upset, blurred vision	Available without a prescription. Not a substitute for cause-directed therapy. Not useful for ACE inhibitor-induced cough.
Codeine Special situation	Short-term, adjunctive symptom relief only, adults 18 years of age and older	5-20 mg PO every 4-8 hours, maximum 120 mg in 24 hours	Constipation, sedation, respiratory depression with other CNS depressants	Health Canada restricts opioid-containing cough/cold products to patients 18 years of age and older. Use with caution in productive cough — may cause mucus retention.

Special Populations

Pregnancy

Data on the prevalence, causes, and treatment of chronic cough specifically in pregnancy are limited, and several of the common causes can be worsened by pregnancy — most notably GERD, given smooth-muscle relaxation and increased abdominal pressure. Start with lifestyle modification and antacids for GERD-related cough in pregnancy; H2-receptor antagonists have extensive reassuring safety experience in pregnancy, and PPI data, while less extensive, are also reassuring (see the Gastroesophageal Reflux Disease chapter for specific agent selection and dosing). The therapeutic approach to UACS and to cough-variant asthma is minimally changed by pregnancy — short-acting bronchodilators and inhaled corticosteroids are used per the Asthma in Adults and Adolescents chapter, and most intranasal corticosteroids are considered safe in pregnancy, though triamcinolone should be avoided given a possible association with congenital malformations; first-generation oral antihistamines are considered safe in pregnancy, and nasal saline is safe and effective throughout pregnancy and breastfeeding.^[11] Avoid an oral decongestant (pseudoephedrine) in the first trimester specifically — case-control data have linked first-trimester oral decongestant use to a small increase in specific birth defects, including gastroschisis; a short-acting intranasal decongestant is preferred if a decongestant is genuinely needed early in pregnancy. If an antitussive is needed, dextromethorphan is considered compatible with pregnancy and breastfeeding, while morphine and codeine carry recognized fetal and neonatal risks and should be avoided as a routine choice.

Breastfeeding

Antacids, H2-receptor antagonists, and PPIs (particularly omeprazole and pantoprazole) are considered safe during breastfeeding — see the Gastroesophageal Reflux Disease chapter. Most intranasal corticosteroids and nasal saline are safe in breastfeeding. Pseudoephedrine can reduce milk supply and should be used cautiously, favouring a short course or an intranasal alternative. Opioid antitussives (morphine, codeine) carry recognized infant toxicity risk during breastfeeding and should be avoided when an alternative is reasonable.

Older adults

Avoid routine use of first-generation antihistamines (e.g., diphenhydramine) for UACS in older adults — the 2023 AGS Beers Criteria specifically recommend against this class in this population given markedly increased anticholinergic toxicity, confusion, delirium, and fall risk.^[4] Use pseudoephedrine cautiously given increased cardiovascular sensitivity in this population. Gabapentin, pregabalin, and opioid antitussives all carry higher sedation and fall risk in older adults — start at the low end of the dose range and titrate more slowly.

Renal impairment

Gabapentin and pregabalin are both renally cleared and require dose reduction in renal impairment — consult product-specific renal dosing before starting or continuing either agent as chronic kidney disease progresses. Codeine and morphine active metabolites can accumulate in significant renal impairment, increasing the risk of oversedation and respiratory depression — use the lowest effective dose with close monitoring, or avoid.

Pediatrics

This chapter covers chronic cough in adults specifically; the diagnostic and treatment approach in children differs meaningfully and is not addressed here. First-generation antihistamines are not recommended in children under 6 years of age. Opioid-containing cough and cold products (codeine, hydrocodone) are restricted by Health Canada to patients 18 years of age and older and must not be used in children or younger adolescents.

Monitoring & Follow-Up

ACE inhibitor withdrawal trial: reassess at 1 week and again at 4 weeks — most patients improve within 1 week, but allow the full 4 weeks before concluding the ACE inhibitor was not the cause.
PPI trial for GERD-related cough: assess response no sooner than 8 weeks (see the Gastroesophageal Reflux Disease chapter).
Inhaled corticosteroid trial for NAEB: assess response at 2-4 weeks; escalate dose or add montelukast if incomplete.
Gabapentin for refractory/unexplained chronic cough: monitor closely for sedation, ataxia, and other adverse effects at each dose titration; formally reassess efficacy at 6 months, and taper toward the lowest effective dose or discontinuation if the cough has responded and remained stable.
Morphine trial: response, when present, is typically rapid — reassess at 1-2 weeks and discontinue if no benefit has occurred by then, rather than continuing to escalate the dose.
At every follow-up, confirm that the cough attributed to a given cause has genuinely resolved or substantially improved, not simply that a course of therapy was completed — an incompletely treated cause is a common reason for apparent treatment failure.

Treatment Failure / Next Step

Confirm the empiric trial that was tried was actually adequate — full recommended dose, for the full recommended duration (e.g., a genuine 4-week ACE inhibitor washout, a genuine 8-week PPI trial, a genuine 2-4 week inhaled corticosteroid trial) — before concluding it failed.
Reconsider whether more than one cause is present. Coexisting causes are common; continue any therapy that produced partial improvement while investigating for an additional contributing cause, rather than discontinuing it.
Move to the next most likely cause in the diagnostic sequence rather than declaring the cough unexplained after only one trial.
If the common causes have been adequately investigated and treated or excluded, and no red flag is present, proceed to less common causes (obstructive sleep apnea, chronic infection, structural/interstitial lung disease, occult heart failure, irritable larynx syndrome, foreign body) with CT chest and consideration of bronchoscopy referral.
If no cause is found after a complete evaluation (unexplained chronic cough) or an identified cause does not respond to appropriate cause-directed treatment (refractory chronic cough), refer to a cough specialty clinic and consider a neuromodulator approach targeting cough hypersensitivity — gabapentin first, then pregabalin or low-dose sustained-release morphine.
For a patient responding well to neuromodulator therapy, attempt a taper to the lowest effective dose, or a trial off therapy, at around 6 months.

Common Errors to Avoid

Starting an antitussive or mucolytic before completing a cause-directed workup — mucolytics in particular have no proven role in chronic cough, and premature symptom suppression can delay diagnosis of a treatable (or serious) cause.
Missing an ACE inhibitor as the cause because the cough started long after the drug was initiated — onset can occur anywhere from hours to months after starting the drug, so temporal distance alone does not rule it out.^[7]
Stopping an ACE inhibitor trial before 4 weeks and concluding it was not the cause, when resolution can take up to that long even though most patients improve within 1 week.
Starting empiric PPI therapy for chronic cough when GERD investigations are genuinely negative — current evidence does not support this, and it exposes the patient to unnecessary long-term acid suppression.^[5]
Treating a red flag (hemoptysis, significant smoking history with a new/changed cough pattern, systemic symptoms) with an empiric trial instead of urgent imaging or referral.
Routine use of a first-generation antihistamine in an older adult for UACS, rather than a nonsedating alternative or an intranasal corticosteroid.
Prescribing or recommending a codeine- or hydrocodone-containing product to a patient under 18 years of age.
Assuming a patient with unexplained chronic cough has no treatable option once initial testing is unrevealing — cough-hypersensitivity-targeted neuromodulator therapy (gabapentin first-line) is a real, evidence-based option, not a dead end.
Overestimating the efficacy of over-the-counter cough suppressants for chronic cough specifically — trial evidence for classic antitussives in this setting is limited, and they have, at most, a minor adjunctive role.

Clinical Decision Algorithm

Algorithm A — Initial evaluation and red-flag triage

Cough persisting more than 8 weeks

History and physical exam; chest x-ray; assess smoking history and red flags

Any red flag present (hemoptysis, significant smoking history with new/changed cough, systemic symptoms, abnormal exam/CXR)

Urgent CT chest and/or specialist referral — do not proceed to empiric cause-directed trials

No red flags

Review medication list specifically for an ACE inhibitor, proceed to Algorithm B

Algorithm B — ACE inhibitor exclusion and cause-directed empiric trials

No red flags; medication review complete

Taking an ACE inhibitor

Stop the ACE inhibitor as a diagnostic/therapeutic trial; substitute an ARB (e.g., losartan) if the original indication requires renin-angiotensin blockade

Cough resolves or markedly improves within 4 weeks

ACE inhibitor-induced cough confirmed — continue the ARB substitution

Cough unchanged after a full 4-week trial

ACE inhibitor unlikely to be the cause — proceed with the common-cause workup below

Not taking an ACE inhibitor

Assess for upper airway, asthma, and reflux symptoms; treat the most clinically likely cause first

Upper airway symptoms (postnasal drip, throat clearing, nasal congestion)

Treat as UACS: intranasal corticosteroid, oral/intranasal antihistamine, or empiric first-generation antihistamine + decongestant

Wheeze, atopic history, or high clinical suspicion

Spirometry +/- methacholine challenge; treat as cough-variant asthma per the Asthma in Adults and Adolescents chapter if positive

Reflux symptoms, or no UACS/asthma features

Lifestyle measures for GERD; add a PPI trial (8 weeks minimum) per the Gastroesophageal Reflux Disease chapter if symptoms persist

Algorithm C — Persistent cough after common-cause workup

Cough persists despite an adequate trial for the most likely common cause(s), ACE inhibitor excluded

Reassess for a second, coexisting cause; continue any therapy that produced partial improvement while investigating further

Evaluate for NAEB (induced sputum eosinophilia, exhaled nitric oxide) — trial inhaled corticosteroid 2-4 weeks if supported

A specific cause is identified at any point

Treat that cause directly using the corresponding track

No cause identified after complete evaluation (unexplained), or an identified cause does not respond to appropriate treatment (refractory)

Refer to a cough specialty clinic; start gabapentin (1st-line neuromodulator) targeting cough hypersensitivity, with pregabalin or low-dose sustained-release morphine as alternatives

Drug Tables

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Upper airway cough syndrome — intranasal corticosteroids

First-line for UACS regardless of allergic or nonallergic cause; also first-line for chronic-rhinosinusitis-driven UACS alongside nasal saline.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Fluticasone propionate, nasal spray	Initial: 2 sprays (100 mcg) per nostril once daily Maintenance: 1 spray per nostril once daily	Nasal irritation, epistaxis, headache, unpleasant taste/smell	None significant	Reduce to the lowest effective dose once symptoms are controlled.
Mometasone, nasal spray	Adults: 2 sprays (200 mcg total) per nostril once daily	Nasal irritation, epistaxis, headache	None significant	Alternative intranasal corticosteroid; comparable efficacy to fluticasone.
Budesonide, nasal spray	Initial: 2 sprays per nostril once daily Maintenance: 1 spray per nostril once daily	Nasal irritation, epistaxis, headache	None significant	Alternative intranasal corticosteroid.
Azelastine / fluticasone propionate, nasal spray	Adults: 1 spray per nostril twice daily	Bitter taste, nasal irritation, mild sedation (azelastine)	Additive sedation with other CNS depressants	Combination intranasal antihistamine/corticosteroid — in Canada, the intranasal antihistamine component is only available as this fixed-dose combination.
Olopatadine / mometasone furoate, nasal spray	Adults: 2 sprays per nostril twice daily	Bitter taste, nasal irritation, mild sedation (olopatadine)	Additive sedation with other CNS depressants	Alternative fixed-dose intranasal antihistamine/corticosteroid combination.

Upper airway cough syndrome — oral antihistamines and decongestant

Nonsedating antihistamines are preferred, particularly in older adults; the first-generation antihistamine plus decongestant combination is reserved for empiric therapy when the specific UACS cause cannot be identified.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Loratadine	Adults: 10 mg PO once daily	Headache; minimal sedation	None significant	Nonsedating; effective specifically for allergic-rhinitis-driven cough.
Desloratadine	Adults: 5 mg PO once daily	Headache; minimal sedation	None significant	Alternative nonsedating antihistamine.
Diphenhydramine (first-generation antihistamine, allergy/antihistamine use)	Adults: 25-50 mg PO every 4-6 hours as needed, maximum 300 mg in 24 hours	Sedation, dry mouth, blurred vision, urinary retention (anticholinergic)	Additive sedation with alcohol/CNS depressants; additive anticholinergic burden with other anticholinergic drugs; avoid with, or within 14 days of, an MAOI	Same oral tablet/capsule/liquid formulation as the sleep-aid-labelled Drug Database entry; this row reflects allergy/antihistamine dosing rather than the sleep-aid dose shown there. Avoid in older adults (Beers Criteria). Not recommended for children under 6 years of age.
Pseudoephedrine	Immediate-release: 60 mg PO every 4-6 hours 12-hour extended-release: 120 mg PO every 12 hours Maximum: 240 mg in 24 hours, any formulation	Insomnia, tremor, irritability, headache, palpitations, hypertension	Contraindicated with, or within 14 days of, an MAOI; may reduce beta-blocker antihypertensive effect; SNRIs may enhance tachycardic/vasopressor effects	Avoid dosing in the evening given the risk of insomnia. Use with caution in hypertension, coronary artery disease, and benign prostatic hyperplasia. Avoid in the first trimester of pregnancy.
Montelukast	Adults: 10 mg PO once daily	Headache; rare neuropsychiatric effects	None significant	For allergic-rhinitis-driven UACS not fully controlled with an antihistamine/intranasal corticosteroid.

Cough-variant asthma and GERD-related cough

Managed per the Asthma in Adults and Adolescents chapter and the Gastroesophageal Reflux Disease chapter respectively — dosing is not repeated here to avoid duplicating or drifting from that chapter's guidance.

Nonasthmatic eosinophilic bronchitis (NAEB)

A 2-4 week trial is both diagnostic and therapeutic; a positive response supports the diagnosis.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Fluticasone propionate, inhaled	Initial trial (2-4 weeks): 250 mcg PO inhaled twice daily If incomplete response: 500 mcg PO inhaled twice daily	Oral candidiasis, dysphonia, hoarseness	None significant	Rinse mouth after each use. Increase the dose, or add montelukast, if the response is incomplete after the initial trial.
Montelukast (add-on)	Adults: 10 mg PO once daily	Headache; rare neuropsychiatric effects	None significant	Add if the inhaled corticosteroid response is incomplete after dose escalation.

ACE inhibitor-induced cough — substitution agents (angiotensin receptor blockers)

Not associated with cough. Select the agent and target dose based on the original indication (hypertension, heart failure, post-MI, diabetic nephropathy) that required renin-angiotensin system blockade.

Drug	Dosage	Adverse effects	Drug interactions
Losartan	Initial: 50 mg PO once daily Target: up to 100 mg once daily	Hyperkalemia, hypotension, dizziness	Hyperkalemia risk with potassium-sparing diuretics/potassium supplements
Candesartan cilexetil	Initial: 8-16 mg PO once daily Target: per the original indication's target dose	Hyperkalemia, hypotension, dizziness	Hyperkalemia risk with potassium-sparing diuretics/potassium supplements
Telmisartan	Adults: 40 mg PO once daily, up to 80 mg once daily	Hyperkalemia, hypotension, dizziness	Hyperkalemia risk with potassium-sparing diuretics/potassium supplements
Irbesartan	Adults: 150 mg PO once daily, up to 300 mg once daily	Hyperkalemia, hypotension, dizziness	Hyperkalemia risk with potassium-sparing diuretics/potassium supplements
Valsartan	Adults: 80-160 mg PO once daily	Hyperkalemia, hypotension, dizziness	Hyperkalemia risk with potassium-sparing diuretics/potassium supplements

Refractory or unexplained chronic cough — neuromodulators

Reserved for confirmed refractory or unexplained chronic cough after red flags, ACE inhibitor use, and the common causes above have been addressed. Gabapentin is first-line; pregabalin and morphine are alternatives with a less favourable adverse-effect profile.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Gabapentin	Starting dose: 100 mg PO TID, or 300 mg PO once daily Titration: increase to the maximum tolerated dose Maximum: 900 mg PO BID (or 600 mg PO TID)	Sedation, ataxia, tremor, peripheral edema, rare respiratory depression	Increased hypotensive effect with antihypertensives; decreased clearance with oral contraceptives, tricyclic antidepressants, or CYP1A2 inhibitors (e.g., cimetidine, ciprofloxacin, fluvoxamine)	Discontinue after a 6-month trial if no benefit. Requires dose reduction in renal impairment.
Pregabalin	Starting dose: 75 mg PO BID Titration: increase as tolerated Maximum used in practice: 150 mg PO BID (300 mg/day)	Sedation, dizziness, peripheral edema, weight gain; higher misuse potential than gabapentin	Additive CNS depression with opioids, benzodiazepines, alcohol	Dosing here is extrapolated from neuropathic-pain regimens — no standardized chronic-cough-specific dose is established. More adverse effects and greater misuse potential than gabapentin, plausibly related to its faster onset of action. Requires dose reduction in renal impairment.
Morphine, sustained-release	Adults: 5-10 mg PO BID, sustained-release formulation Maximum used in practice: 20 mg in 24 hours	Constipation, sedation, nausea, respiratory depression, misuse/dependence potential	Additive sedation and respiratory depression with other CNS depressants	Response, when present, is usually rapid — discontinue if no benefit within 1-2 weeks rather than continuing to escalate. Monitor closely for signs of misuse.
Amitriptyline	Adults: 25-150 mg PO daily, starting low and titrating	Anticholinergic effects, sedation, weight gain, QT prolongation at higher doses	Avoid with, or within 14 days of, an MAOI; additive sedation with other CNS depressants	Evidence is insufficient for formal guideline inclusion — a lower-tier option when gabapentin, pregabalin, and morphine are not appropriate or not tolerated.

Nonspecific antitussives

Limited role in chronic cough overall; reserve for short-term, adjunctive symptom relief (e.g., to enable sleep) once a cause-directed workup is underway, never as a substitute for it. Use with caution in productive cough, since suppressing an effective cough can cause mucus retention. Not useful for ACE inhibitor-induced cough.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Dextromethorphan	Adults: 15-30 mg PO every 6-8 hours, maximum 120 mg in 24 hours	Drowsiness, GI upset, blurred vision, urinary hesitancy in slow metabolizers	Avoid with, or within 2 weeks of, an MAOI; SSRIs may enhance adverse effects; caution with other CNS depressants	Available without a prescription.
Codeine	Adults: 5-20 mg PO every 4-8 hours, maximum 120 mg in 24 hours	Constipation, sedation, nausea, respiratory depression with other CNS depressants	Additive sedation/respiratory depression with other CNS depressants	Restricted by Health Canada to patients 18 years of age and older. Variable CYP2D6 metabolism gives an unpredictable response and side-effect profile.
Hydrocodone bitartrate	Adults: 5 mg PO every 4-6 hours, maximum 30 mg in 24 hours	Constipation, sedation, nausea, respiratory depression with other CNS depressants	Additive sedation/respiratory depression with other CNS depressants	Restricted by Health Canada to patients 18 years of age and older.

References

ERS guidelines on the diagnosis and treatment of chronic cough in adults and children — European Respiratory Journal, European Respiratory Society (Morice AH, Millqvist E, Bieksiene K, et al.). Eur Respir J 2020;55(1):1901136
British Thoracic Society Clinical Statement on chronic cough in adults — Thorax, British Thoracic Society (Parker SM, Smith JA, Birring SS, et al.). Thorax 2023;78(Suppl 6):s3-s19
Classification of Cough as a Symptom in Adults and Management Algorithms: CHEST Guideline and Expert Panel Report — Chest, American College of Chest Physicians (Irwin RS, French CL, Chang AB, Altman KW; CHEST Expert Cough Panel). Chest 2018;153(1):196-209
American Geriatrics Society 2023 updated AGS Beers Criteria for potentially inappropriate medication use in older adults — Journal of the American Geriatrics Society, 2023 American Geriatrics Society Beers Criteria Update Expert Panel. J Am Geriatr Soc 2023;71(7):2052-2081
Chronic Cough Due to Gastroesophageal Reflux in Adults: CHEST Guideline and Expert Panel Report — Chest, American College of Chest Physicians (Kahrilas PJ, Altman KW, Chang AB, et al.). Chest 2016;150(6):1341-1360
Managing Chronic Cough Due to Asthma and Nonasthmatic Eosinophilic Bronchitis in Adults and Adolescents: CHEST Guideline and Expert Panel Report — Chest, American College of Chest Physicians (Cote A, Russell RJ, Boulet LP, et al.). Chest 2020;158(1):68-96
Cough and angioedema from angiotensin-converting enzyme inhibitors: new insights into mechanisms and management — Current Opinion in Allergy and Clinical Immunology (Dykewicz MS). Curr Opin Allergy Clin Immunol 2004;4(4):267-270
Treatment of Unexplained Chronic Cough: CHEST Guideline and Expert Panel Report — Chest, American College of Chest Physicians (Gibson P, Wang G, McGarvey L, et al.). Chest 2016;149(1):27-44
Gabapentin for refractory chronic cough: a randomised, double-blind, placebo-controlled trial — The Lancet (Ryan NM, Birring SS, Gibson PG). Lancet 2012;380(9853):1583-1589
Efficacy and safety of gefapixant, a P2X3 receptor antagonist, in refractory chronic cough and unexplained chronic cough (COUGH-1 and COUGH-2): results from two double-blind, randomised, parallel-group, placebo-controlled, phase 3 trials — The Lancet (McGarvey LP, Birring SS, Morice AH, et al.). Lancet 2022;399(10328):909-923
Rhinitis 2020: A practice parameter update — Journal of Allergy and Clinical Immunology, Joint Task Force on Practice Parameters (Dykewicz MS, Wallace DV, Amrol DK, et al.). J Allergy Clin Immunol 2020;146(4):721-767

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.