Laryngopharyngeal Reflux
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Direct answer
Laryngopharyngeal reflux (LPR) is retrograde passage of gastric contents above the upper oesophageal sphincter onto mucosa not built to resist it — hoarseness worst in the morning, chronic throat clearing, globus, dry cough and sore throat, frequently without heartburn, which distinguishes it from gastro-oesophageal reflux disease. Laryngoscopy shows posterior laryngitis: erythema and oedema of the arytenoids and interarytenoid bar, ventricular obliteration and subglottic pseudosuecus oedema. Diagnosis is clinical, supported by the Reflux Symptom Index (a score of 13 or more) and Reflux Finding Score (7 or more); treatment is a twice-daily proton-pump inhibitor before meals for three to six months with lifestyle measures, which is slower and less certain than patients expect.
What you must remember
- LPR versus GERD in one pair: GERD is supine, post-prandial and burning behind the sternum with oesophagitis; LPR is upright, daytime, laryngeal and often silent — heartburn is present in only a minority of LPR patients, the fact most quoted in exams.
- Symptom set with Reflux Symptom Index: hoarseness, throat clearing, excess throat mucus or postnasal drip, difficulty swallowing, coughing after lying down, breathing difficulties, troublesome cough, throat lump sensation and heartburn — the RSI is abnormal at 13 or above.
- Laryngoscopic signs with Reflux Finding Score: subglottic oedema or pseudosuecus, ventricular obliteration, erythema and hyperaemia, vocal cord oedema, diffuse laryngeal oedema, posterior commissure hypertrophy and granuloma or thickening — an RFS of 7 or more supports LPR.
- Why the larynx suffers more than the oesophagus: the laryngeal epithelium lacks the protective defences of oesophageal mucosa, so fewer, briefer reflux episodes — including gaseous, weakly acidic or pepsin-bearing aerosol events — suffice to injure it.
- Pepsin, not acid alone: active pepsin adheres to laryngeal cells and reactivates when acid arrives; this underlies the rationale for acid suppression even though pepsin itself is not blocked.
- Treatment protocol: a proton-pump inhibitor twice daily 30-60 minutes before breakfast and dinner for three to six months, plus weight reduction, no meals within three hours of sleep, head-end elevation, and avoidance of late tea, coffee, alcohol and tobacco; alginates at night as adjunct; refractory cases need pH-impedance testing or fundoplication assessment.
- Complications and associations to quote: contact granulomas and Reinke's oedema that fail to settle, chronic cough, subglottic stenosis in intubated patients, laryngospasm, and suspected — though debated — contribution to laryngeal carcinoma risk in smokers.
From score sheet to follow-up
A 42-year-old bank officer reports a year of morning hoarseness clearing by noon, constant throat clearing and thick mucus no lozenge shifts; she has never had heartburn. Her Reflux Symptom Index totals 19, and laryngoscopy shows oedematous arytenoids with a hypertrophied interarytenoid bar — a Reflux Finding Score of 10 — with mobile cords and no lesion.
The plan: omeprazole 20 mg twice daily before breakfast and dinner for three months, with a lifestyle sheet — dinner three hours before lying down, head-end elevation, no late snacking. At review she is better but not fully, and the message examiners test is that LPR responds slowly: a further three-month course is standard, and incomplete response prompts pH-impedance testing rather than endless empiric therapy. Had laryngoscopy shown a unilateral lesion or granuloma, biopsy would precede any reflux label.
Where examiners dig
Two probes recur. First, why does a patient without heartburn have reflux disease? Because the larynx has no acid-protective mucosa, upright daytime gaseous reflux events that the oesophagus barely registers injure the larynx — hence "silent reflux". Second, why twice-daily and pre-meal proton-pump inhibitors? Because the drugs block only active pumps, which are meal-activated, and a single morning dose under-covers the day; the three-to-six-month duration tests the examiner's patience as much as the patient's, and candidates who prescribe "two weeks PPI" fail the pharmacology point. The final trap is overdiagnosis: erythema alone is subjective, and laryngeal findings are scored precisely because the RFS exists to discipline the diagnosis.
Frequently asked questions
How does laryngopharyngeal reflux differ from gastro-oesophageal reflux disease?
LPR involves upright, daytime reflux of gastric contents to the laryngopharynx with hoarseness and throat clearing, often without heartburn; GERD is supine acid reflux with heartburn and oesophagitis.
What are the Reflux Symptom Index and Reflux Finding Score thresholds?
An RSI of 13 or more and a Reflux Finding Score of 7 or more support the diagnosis of LPR and are used to monitor treatment response.
Why must proton-pump inhibitors be taken before meals in LPR?
They inhibit only actively secreting proton pumps; dosing 30-60 minutes before breakfast and dinner ensures drug presence when pumps are stimulated, and twice-daily dosing covers daytime reflux.
Which laryngoscopic findings suggest laryngopharyngeal reflux?
Posterior laryngitis — arytenoid and interarytenoid erythema with oedema, ventricular obliteration, diffuse laryngeal oedema and subglottic pseudosuecus — typically with mobile cords and no mass lesion.
What is done for LPR unresponsive to adequate medical therapy?
Twenty-four-hour dual-probe pH-impedance monitoring with symptom correlation to confirm the association, re-examination to exclude other laryngeal pathology, and consideration of fundoplication in proven, compliant, refractory cases.