Gastro-oesophageal reflux disease — diagnosis, classification and management viva

Stem

The examiner presents a 50-year-old man with several months of post-prandial retrosternal burning and asks: "What is the likely diagnosis, how would you classify and investigate this condition, and what is your stepwise management?"

Interpretation

• Likely diagnosis: GORD. Retrosternal burning after meals, relieved by antacid, with regurgitation, is the cardinal clinical picture. The diagnosis is clinical in the patient without alarm features, supported by an empirical PPI trial.^[1]
• Always screen for alarm features — dysphagia, weight loss, anaemia, GI bleeding, vomiting, onset over age 55, PPI non-response — which mandate urgent OGD rather than empirical therapy.

Key points

The examiner will probe each of these; be ready to defend them at viva depth:

1. Definition (Montreal) — GORD develops when reflux of stomach contents causes troublesome symptoms and/or complications (mild symptoms two or more days/week, or moderate-severe one or more days/week).^[1]
2. Classification — two phenotypes: erosive (ERD, 30 to 40 percent) vs non-erosive (NERD, 60 to 70 percent); Los Angeles grades A to D reproduced verbatim (A under 5 mm; B over 5 mm; C bridging folds; D circumferential). LA C/D + symptoms is conclusive GORD.^[1]
3. Lyon Consensus 2.0 (objective diagnosis) — AET over 6 percent conclusive; under 4 percent excluded; 4 to 6 percent inconclusive; over 40 reflux episodes/day supports pathological reflux.^[2]
4. Pathophysiology (five mechanisms) — TLESRs (dominant, ~50 to 80 percent in NERD; targeted by baclofen), hypotensive LES (under 10 mmHg; scleroderma), hiatus hernia (over 60 percent of severe ERD), impaired clearance (poor peristalsis, low saliva), delayed gastric emptying.^[2]
5. Investigation hierarchy — empirical PPI trial first; OGD for alarm features; pH-impedance for refractory/uncertain cases; manometry mandatory before surgery (exclude achalasia).
6. Management stepwise — lifestyle, antacid/alginate, H2RA (famotidine 20 mg bd), then PPI first-line: omeprazole 20 mg od, 30 min pre-meal, 4 to 8 weeks (8 weeks for erosive); refractory → double-dose PPI ± nocturnal H2RA ± baclofen; surgery (Nissen fundoplication) needs objective GORD + normal manometry.^[1]
7. Barrett oesophagus — intestinal metaplasia; ~0.5 percent/year adenocarcinoma risk; surveillance non-dysplastic at 1 year then every 2 to 3 years; high-grade dysplasia → RFA/EMR.^[3]
8. Long-term PPI risks — osteoporotic fracture, hypomagnesaemia, B12 deficiency, enteric infection (C. difficile, pneumonia), acute interstitial nephritis, rebound on abrupt cessation — taper, don't stop.

References

1. Katz PO, et al. ACG 2022 GERD guideline. Am J Gastroenterol 2022.^[1]
2. Gyawali CP, et al. Lyon Consensus 2.0. Gut 2018.^[2]
3. Spechler SJ, Souza RF. Barrett's esophagus. N Engl J Med 2014.^[3]

References3ShowHide

1. [1]Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol, 2022.PMID 34807007
2. [2]Gyawali CP, Kahrilas PJ, Savarino E, et al. Modern diagnosis of GERD: the Lyon Consensus. Gut, 2018.PMID 29437910
3. [3]Spechler SJ, Souza RF. Barrett's esophagus. New England Journal of Medicine, 2014.PMID 25162890