Gastroesophageal reflux disease is a chronic condition in which retrograde flow of gastric contents into the esophagus causes troublesome symptoms such as heartburn and regurgitation, and/or mucosal complications.

Exam domain	One-glance essentials
Definition / diagnosis	*GERD is troublesome symptoms and/or complications caused by reflux of gastric contents* ^[2] GERD is broader than reflux oesophagitis: many patients have symptoms with normal endoscopy (NERD) ^[2] Typical cardinal symptoms are heartburn and acid regurgitation ^[2]
Epidemiology / risks	Obesity increases intra-abdominal pressure and promotes hiatus hernia ^[2] Sliding hiatus hernia disrupts the anti-reflux barrier and is the main hernia type associated with GERD ^[2] Smoking, alcohol, pregnancy, delayed gastric emptying and LES-relaxing drugs increase risk ^[2]
Core mechanism	*Excessive transient LES relaxations (tLESRs), rather than constant low LES pressure, are the dominant mechanism* ^[2] Hiatus hernia removes crural compression, shortens the intra-abdominal oesophagus and blunts the angle of His ^[2] Impaired oesophageal clearance prolongs acid exposure ^[2]
Clinical picture	Heartburn is retrosternal burning, typically post-prandial and worse supine, bending or lying down ^[2] Acid regurgitation suggests reflux reaching the mouth or hypopharynx; volume regurgitation may persist despite PPIs ^[2] Dysphagia, weight loss, anaemia, bleeding, odynophagia or persistent vomiting are alarm features ^[1]^[2]
Investigations	Perform urgent OGD for alarm features, new symptoms at age > 55, refractory symptoms or pre-operative assessment ^[1]^[2] Normal OGD does not exclude GERD; ambulatory pH monitoring confirms doubtful cases, with AET > 6% diagnostic ^[2] Pre-operative assessment requires OGD with biopsy, pH monitoring and manometry; manometry excludes achalasia and aperistalsis ^[2]
Management	Lifestyle measures for all: weight loss, head-of-bed elevation, avoid late meals, smoking and alcohol; identify dietary triggers ^[2] PPI is mainstay; administer most PPIs 30–60 min before meals, then step down to the lowest effective dose ^[2] Consider fundoplication for objectively proven reflux with severe regurgitation, large hiatus hernia or PPI dependence; aperistalsis contraindicates Nissen ^[2]
Complications	Chronic reflux may progress to oesophagitis, ulceration, peptic stricture, Barrett’s metaplasia, dysplasia and adenocarcinoma ^[2] Progressive solid-food dysphagia suggests peptic stricture, but malignancy must be excluded ^[1]^[2] Hiatus hernia complications include Cameron lesions, volvulus and strangulation; Borchardt triad signals emergency volvulus ^[2]
Prevention / follow-up	Reduce recurrence with weight control, smoking cessation, alcohol avoidance, head-of-bed elevation and no meals shortly before sleep ^[2] Severe LA C/D oesophagitis generally needs long-term maintenance PPI and repeat OGD to confirm healing ^[2] Barrett’s requires lifelong acid suppression and surveillance: non-dysplastic disease typically OGD every 3–5 years ^[2]
Exam traps	Exclude coronary artery disease before attributing retrosternal pain to GERD, especially with exertional symptoms or cardiac risk factors ^[2] Heartburn plus regurgitation can be achalasia: undigested food, dysphagia to solids and liquids, and manometry are key clues ^[2] PPIs reduce acidity but do not prevent reflux; persistent regurgitation is not automatically PPI failure ^[2] Barrett’s diagnosis needs endoscopic columnar lining plus biopsy-proven intestinal metaplasia with goblet cells ^[2]

References

^[1] Lecture slides: GC 189. I can't swallow oesophageal cancer.pdf ^[2] Senior notes: maxim.md (GERD surgical treatment, Hiatal hernia sections)

Gastroesophageal Reflux Disease (GERD)

Gastroesophageal Reflux Disease (GERD) is defined by the Montreal Consensus as a condition that develops when the reflux of stomach contents causes troublesome symptoms and/or complications ^[1]^[2].

Let's break this down carefully:

GERD ≠ reflux. Everyone refluxes — after a big meal, a small amount of gastric content may transiently enter the distal oesophagus. That is physiological reflux: post-prandial, short-lived, asymptomatic, and rarely occurs during sleep ^[2].
Pathological reflux = symptomatic, causes mucosal injury, often includes nocturnal episodes ^[2].
GERD is the clinical label applied to patients with symptoms suggestive of reflux or its complications — but not necessarily with visible oesophageal inflammation ^[2].
Reflux oesophagitis is a subset of GERD where endoscopy (and histology) confirms actual oesophageal mucosal inflammation ^[2].

Think of it this way: GERD is the umbrella diagnosis (symptom-based), and reflux oesophagitis is the endoscopy-confirmed subset. Most GERD patients actually have no visible mucosal damage on endoscopy.

Feature	Detail
Global prevalence	~8–33% of the adult population worldwide; increasing globally
Prevalence in Asia	Historically lower (~5–10%) but rising rapidly due to obesity, westernised diet
Hong Kong prevalence	~6–9% (rising trend, particularly in urban populations)
Age	Increases with age (peak in 40–60 years); can occur at any age
Sex	Slight male predominance for erosive disease and complications (Barrett's, adenocarcinoma); NERD is more equal
Socioeconomic trend	Higher prevalence with westernised lifestyle, increased BMI
Burden	Most common outpatient GI diagnosis; massive PPI consumption worldwide

Hong Kong Context

In Hong Kong, the prevalence of GERD has been steadily increasing over the last two decades, mirroring rising obesity rates and westernised dietary habits. While squamous cell carcinoma still dominates oesophageal cancer in HK, the incidence of adenocarcinoma (arising from Barrett's oesophagus, a GERD complication) is on the rise ^[2]^[3].

Understanding risk factors requires understanding the pathophysiology (covered in detail below). Every risk factor either (a) lowers LES pressure, (b) increases intra-abdominal pressure, (c) increases gastric acid/volume, or (d) impairs oesophageal clearance.

Category	Risk Factor	Mechanism
Obesity	Increased BMI	↑ Intra-abdominal pressure → overcomes LES; also promotes hiatus hernia; visceral adiposity releases pro-inflammatory cytokines
Age	Aging	Loss of LES tone; ↓ oesophageal peristaltic efficiency; ↓ saliva production (less bicarbonate for acid neutralisation)
Pregnancy	Progesterone + gravid uterus	Progesterone relaxes smooth muscle → ↓ LES tone; gravid uterus → ↑ intra-abdominal pressure ^[2]
Smoking	Tobacco	Directly ↓ LES pressure; ↓ saliva production; ↓ oesophageal mucosal defence
Alcohol	Ethanol	↓ LES tone; direct mucosal irritant; ↓ oesophageal motility
Dietary factors	Fat, chocolate, coffee, peppermint	All relax the LES. Fat also delays gastric emptying → more material available for reflux ^[2]
Drugs	NSAIDs, aspirin, contraceptives/HRT	NSAIDs/aspirin: direct mucosal injury + ↓ prostaglandins → impaired mucosal defence. OCP/HRT: progesterone component ↓ LES tone ^[2]
	Calcium channel blockers, nitrates, anticholinergics, benzodiazepines, theophylline	All ↓ LES tone via smooth muscle relaxation
Hiatus hernia	Sliding (Type I) hernia	Loss of the extrinsic compression of the diaphragmatic crura on the LES; loss of abdominal-thoracic pressure gradient; loss of angle of His (see Anatomy below) ^[2]^[3]
↑ Intra-abdominal pressure	Chronic cough, constipation, heavy lifting, ascites	Raises pressure gradient across a potentially incompetent LES ^[2]
Family history / Genetics	GI diseases in immediate family; genetically predetermined variations in upper GI physiology	Suggests heritable component to LES tone, oesophageal motility, and visceral pain sensitivity ^[2]
Gastroparesis / Delayed emptying	Diabetes, post-vagotomy	More gastric content → more opportunity for reflux

High Yield

The most important modifiable risk factors for GERD are obesity, smoking, alcohol, and dietary triggers. In Hong Kong clinical practice, weight loss is first-line lifestyle advice.

Anatomy & Function of the Anti-Reflux Barrier

To understand GERD, you must first understand why we don't all reflux all the time. The anti-reflux barrier is a multi-component system:

Located at the gastro-oesophageal junction (GOJ/GEJ), approximately 40 cm from the incisors.
Not a true anatomical sphincter (no distinct sphincter muscle), but a 3–4 cm high-pressure zone of tonically contracted smooth muscle in the distal oesophagus.
Resting LES pressure: ~10–30 mmHg above intragastric pressure.
Normal physiology: contracted at rest by intrinsic myogenic tone + cholinergic (vagal) excitatory input. Relaxes only during swallowing (mediated by inhibitory neurons releasing NO and VIP from the myenteric plexus) ^[2].

The right crus of the diaphragm forms a sling around the distal oesophagus as it passes through the oesophageal hiatus.
During inspiration, contraction of the crura squeezes the oesophagus — this is the extrinsic sphincter that augments the LES.
This is why hiatus hernia (where the GOJ slides above the diaphragm) disrupts the anti-reflux mechanism: the crural "pinch" is lost ^[3].

The acute angle at which the oesophagus enters the stomach (normally ~40–60°).
Creates a flap-valve mechanism: as the stomach distends, the fundus presses against the intra-abdominal oesophagus, occluding it.
In hiatus hernia, this angle becomes obtuse → flap valve lost ^[2]^[3].

Normally 2–4 cm of the distal oesophagus lies below the diaphragm, within the abdominal cavity.
Positive intra-abdominal pressure compresses this segment, helping to keep it closed.
In hiatus hernia, this segment retracts into the negative-pressure thorax → compression lost ^[3].

Folds of gastric mucosa at the GOJ help create a mucosal plug that seals the junction.

Primary peristalsis (swallow-triggered) and secondary peristalsis (distension-triggered) clear refluxed material.
Saliva (containing bicarbonate) neutralises residual acid.
Gravity assists clearance in the upright position (hence nocturnal reflux is worse).

Why does hiatus hernia cause GERD?

A sliding hiatus hernia disrupts three components simultaneously: (1) the diaphragmatic crural sling is no longer around the LES, (2) the intra-abdominal oesophageal segment is pulled into the thorax (negative pressure instead of positive pressure), and (3) the angle of His becomes obtuse, destroying the flap-valve effect. Almost all patients who develop oesophagitis, Barrett's oesophagus, and peptic strictures have a hiatus hernia ^[2]^[3].

Etiology & Pathophysiology

The fundamental problem in GERD is an imbalance between aggressive factors (refluxate) and defensive factors (anti-reflux barrier + oesophageal mucosal resistance). Let's dissect each mechanism.

A. Mechanisms of Increased Reflux

Abnormality	Explanation
↓ Basal LES tone	Resting pressure < 10 mmHg → tonically weak sphincter; seen in severe GERD with erosive disease
Transient LES relaxations (tLESRs)	The most common mechanism of reflux in GERD. These are relaxations of the LES that are NOT triggered by swallowing. They occur via a vagovagal reflex triggered by gastric distension (e.g., post-prandially). In GERD patients, tLESRs occur more frequently and are more likely to be accompanied by acid reflux.
Drug-induced LES relaxation	CCBs, nitrates, anticholinergics, theophylline, progesterone → pharmacological ↓ in LES tone

Key concept: In most GERD patients, the LES resting pressure is actually normal. The dominant mechanism is excessive tLESRs, not a permanently weak sphincter. This is why patients get intermittent symptoms rather than constant reflux.

As described above. The hiatus hernia acts as a reservoir — refluxed material trapped in the hernia sac can re-reflux into the oesophagus during swallow-induced LES relaxation (the "re-reflux" phenomenon).

Types of hiatus hernia (important for surgical discussion):

Type	Description
Type I (Sliding)	GOJ slides upward through the hiatus into the thorax. Most common (> 90%). The principal type associated with GERD ^[3].
Type II (Paraesophageal/Rolling)	Fundus herniates through the hiatus, but GOJ remains in normal position. GERD is less common because the GOJ is intact. Risk of gastric volvulus and strangulation ^[3].
Type III (Mixed)	Both GOJ and fundus herniate — combination of Types I and II ^[3].
Type IV	Herniation of organs other than stomach (e.g., colon, spleen, omentum) through a large hiatal defect ^[3].

Obesity, pregnancy, chronic cough, constipation, ascites.
Raises the pressure gradient across the LES → overcomes sphincter resistance → reflux.

Large meals, gastroparesis, gastric outlet obstruction → ↑ gastric volume → ↑ risk of reflux.
Zollinger-Ellison syndrome → massive acid hypersecretion.

B. Mechanisms of Impaired Clearance

Defective oesophageal and gastric peristaltic activity → increased time of exposure to acid ^[2].
Disorders like scleroderma (fibrosis of oesophageal smooth muscle) severely impair peristalsis → severe GERD.

Smoking, Sjögren syndrome, anticholinergic drugs → ↓ saliva → ↓ bicarbonate buffering of residual acid.

Gravity no longer assists clearance → prolonged acid contact time.
Swallowing frequency drops during sleep → less primary peristalsis.

The oesophageal mucosa (stratified squamous epithelium) is inherently vulnerable to acid because, unlike gastric mucosa, it lacks:

Mucus-bicarbonate barrier
Tight intercellular junctions (relative to gastric epithelium)
Rapid epithelial turnover

When refluxate (containing HCl, pepsin, and potentially bile acids and pancreatic enzymes in duodenogastric reflux) contacts the oesophageal mucosa, it causes:

Acid + pepsin → protein denaturation, mucosal erosion
Bile acids (particularly in alkaline/bile reflux) → disrupt cell membranes → inflammation
Inflammatory cascade → oesophagitis → ulceration → fibrosis (stricture) → metaplasia (Barrett's)

The progression is: GERD → Oesophagitis → Ulcer → Stricture → Barrett's oesophagus (10%) → Metaplasia → Adenocarcinoma (0.5%/year risk in Barrett's) ^[3]^[4].

Classification

Category	Description
Non-erosive reflux disease (NERD)	Major category (~60–70% of GERD patients). Typical reflux symptoms but normal oesophageal mucosa on upper endoscopy ^[2].
Erosive oesophagitis	Mucosal breaks/erosions visible on endoscopy. May have local complications: stricture, Barrett's, adenocarcinoma ^[2].
Extra-oesophageal disease	Extra-oesophageal manifestations: asthma, chronic cough, globus sensation, posterior laryngitis, sleep disorders, non-cardiac chest pain ^[2]. Symptoms may or may not be due to reflux.

Exam Pearl

A common mistake is thinking GERD always means visible oesophageal damage. In fact, the majority of GERD patients have NERD — completely normal endoscopy. The diagnosis is clinical (symptoms ± response to PPI trial) or by 24-hour pH monitoring.

This is the standard endoscopic grading system for erosive reflux oesophagitis. It grades the severity of mucosal breaks (erosions) seen at OGD.

Grade	Description	Key Feature
A	One or more mucosal breaks, each ≤ 5 mm in length, that do not extend between the tops of two mucosal folds	Small, isolated erosions
B	One or more mucosal breaks > 5 mm long that do not extend between the tops of two mucosal folds	Longer erosions but still confined
C	One or more mucosal breaks that are continuous between ≥ 2 mucosal folds but involve < 75% of the oesophageal circumference	Confluent erosions, < 75% circumference ^[2]
D	One or more mucosal breaks that involve ≥ 75% of the oesophageal circumference	Near-circumferential/circumferential erosions ^[2]

Clinical significance: LA Grades A/B = mild-to-moderate; LA Grades C/D = severe. Severe grades (C/D) are more likely to be associated with complications (stricture, Barrett's) and less likely to respond to lifestyle measures alone.

LA Classification — High Yield for Exams

Remember the LA classification by mucosal break characteristics:

A = ≤ 5 mm, single fold
B = > 5 mm, single fold
C = Crosses folds, < 75% circumference
D = ≥ 75% circumference

The 2022 Lyon Consensus update considers LA Grade A as potentially a normal variant (low specificity for pathological reflux), while LA Grade C/D is considered conclusive evidence of pathological GERD even without pH testing.

These three conditions are inter-related but can occur independently ^[3]:

You can have GERD without hiatus hernia
You can have hiatus hernia without GERD (especially paraesophageal types)
You can have oesophagitis from causes other than GERD (e.g., eosinophilic, pill, infectious)

Clinical Features

A. Symptoms

Symptom	Description	Pathophysiological Basis
Heartburn (pyrosis)	Retrosternal burning sensation, rising from the epigastrium towards the throat. Worse post-prandially, on lying down, bending forward. Relieved by antacids/PPIs.	Acid and pepsin contact the squamous epithelium of the distal oesophagus → stimulation of chemosensitive nociceptors (TRPV1 receptors) in the oesophageal mucosa → afferent signals via vagus nerve → perceived as burning chest pain. Worsened by supine position because gravity no longer assists clearance.
Acid regurgitation	Perception of flow of refluxed gastric content into the mouth or hypopharynx. Sour/bitter taste.	Large-volume reflux that reaches the proximal oesophagus/hypopharynx. Occurs when LES + upper oesophageal sphincter (UES) are both overcome. Bitter taste = bile (duodenogastric reflux); sour taste = acid.
Dysphagia	Difficulty swallowing; may be progressive for solids	Multiple mechanisms: (1) Oesophageal dysmotility from chronic inflammation disrupting peristalsis; (2) Peptic stricture — chronic oesophagitis → fibrosis → luminal narrowing; (3) Oesophageal oedema during acute inflammation; (4) Barrett's-related stricture; (5) Must exclude malignancy (adenocarcinoma arising in Barrett's). Dysphagia in GERD is an alarm symptom requiring endoscopy ^[1].
Odynophagia	Painful swallowing	Indicates severe oesophagitis with ulceration. Acid contacts raw ulcer base → direct stimulation of exposed nociceptors.
Water brash	Sudden filling of the mouth with clear, slightly salty fluid	A vagal reflex: oesophageal acid stimulation → vagal afferents → salivary nuclei → massive salivary hypersecretion. This is actually a protective reflex to neutralise acid with salivary bicarbonate, but patients find it distressing.
Epigastric pain	Burning/gnawing pain in the epigastrium	Overlap with peptic ulcer disease. Acid irritation of the distal oesophageal and gastric cardia mucosa.
Belching (eructation)	Excessive burping	Aerophagia (swallowing air due to frequent swallowing in response to reflux) + tLESRs that vent gas.
Nausea	Feeling of sickness	Vagal afferent stimulation from oesophageal/gastric mucosal irritation → nausea centre in the medulla.

These are critically important because they may be the presenting complaint with no typical heartburn:

Symptom	Pathophysiological Basis
Chronic cough	Two mechanisms: (1) Microaspiration — refluxate reaches the larynx/tracheobronchial tree → vagal-mediated cough reflex; (2) Oesophago-bronchial reflex — distal oesophageal acid → vagal afferents → reflex bronchospasm and cough without aspiration ^[2].
Asthma / Wheezing	Same mechanisms as chronic cough. Reflux-induced bronchospasm via vagal reflex arc. GERD is found in ~50–80% of asthmatics. Note: asthma medications (theophylline, β-agonists) can also worsen reflux by ↓ LES tone.
Posterior laryngitis (laryngopharyngeal reflux, LPR)	Acid and pepsin directly contact the laryngeal mucosa → inflammation of posterior larynx (interarytenoid region, vocal processes). Laryngeal epithelium is far more sensitive to acid than oesophageal epithelium (damage occurs at pH < 5 vs pH < 2 for oesophagus). Presents as hoarseness, voice fatigue, throat clearing ^[2].
Globus sensation	Persistent sensation of a "lump in the throat" without actual obstruction. Thought to be due to upper oesophageal sphincter (UES) hypertonia or cricopharyngeal spasm triggered by distal oesophageal acid exposure via vagal reflex ^[2].
Non-cardiac chest pain	Oesophageal nociceptors share spinal segments (T1–T6) with cardiac afferents → referred pain is indistinguishable from angina. GERD is the most common oesophageal cause of non-cardiac chest pain ^[2].
Dental erosions	Chronic acid exposure to dental enamel (particularly lingual surfaces of upper teeth) → erosion. Seen in severe reflux.
Sleep disturbance	Nocturnal reflux → repeated micro-arousals → poor sleep quality. Also, obstructive sleep apnoea generates large negative intrathoracic pressures → promotes reflux (bidirectional relationship) ^[2].
Recurrent otitis media / sinusitis	Nasopharyngeal reflux (especially in children) → eustachian tube inflammation.

Extra-Oesophageal GERD — Exam Trap

Do NOT diagnose extra-oesophageal GERD without concomitant typical symptoms (heartburn/regurgitation) or objective evidence of reflux (pH monitoring). Many of these symptoms (cough, asthma, hoarseness) have multiple other causes, and treating GERD empirically has low yield if typical symptoms are absent.

These suggest complications (stricture, Barrett's, malignancy) or alternative diagnoses:

Alarm Feature	Concern
Dysphagia	Stricture, malignancy
Odynophagia	Severe ulceration, malignancy
Weight loss	Malignancy
Anaemia / GI bleeding (haematemesis/melaena)	Erosive oesophagitis with ulceration, oesophageal/gastric malignancy
Recurrent vomiting	Stricture, gastric outlet obstruction
Epigastric mass	Gastric cancer
Age > 55 with new-onset symptoms	Higher risk of malignancy
Family history of upper GI cancer	Higher risk of malignancy

Any patient with alarm symptoms requires urgent OGD ^[1]^[4].

GERD is largely a symptom-based diagnosis. Physical examination is usually unremarkable. However, look for:

Sign	Pathophysiological Basis
Epigastric tenderness	Mucosal inflammation at the GOJ/gastric cardia
Dental erosions (lingual surface of upper incisors)	Chronic acid exposure
Laryngeal signs (on laryngoscopy): posterior laryngeal erythema, oedema, vocal cord granulomas	Acid/pepsin damage to laryngeal mucosa (LPR)
Pharyngeal erythema	Acid exposure
Signs of complications: pallor (anaemia from chronic blood loss), cachexia (malignancy), palpable supraclavicular lymph node (Virchow's node — left supraclavicular, suggests advanced oesophageal/gastric malignancy)	Late-stage complications
Wheezing on auscultation	Reflux-triggered bronchospasm (oesophago-bronchial reflex)
Signs of obesity (↑ BMI, central adiposity)	Identifies the key modifiable risk factor

Physical Exam in GERD — Mostly Normal

The main role of the physical exam in GERD is to exclude red flag signs (cachexia, lymphadenopathy, anaemia, epigastric mass) that point to malignancy or complications, rather than to confirm the diagnosis of GERD itself.

Since Barrett's oesophagus is the key pre-malignant complication of GERD, a focused summary is essential here:

Definition: Intestinal metaplasia of the oesophageal stratified squamous epithelium to columnar epithelium with mucus-secreting goblet cells, as an adaptation to long-term acid reflux ^[3]^[4].
Why does this happen? Chronic acid exposure damages the squamous epithelium → during regeneration, stem cells differentiate into columnar (intestinal-type) epithelium, which is more resistant to acid. This is an adaptive but pre-malignant change.
The metaplastic sequence: Normal squamous epithelium → Columnar metaplasia (Barrett's) → Low-grade dysplasia → High-grade dysplasia → Adenocarcinoma ^[3]^[4].
Risk of adenocarcinoma: ~0.5% per year in Barrett's ^[4].
H. pylori infection is a protective factor for Barrett's/oesophageal adenocarcinoma — because H. pylori causes parietal cell atrophy → ↓ acid production → less reflux damage ^[4].
Classification: Classic (≥ 3 cm) vs Short-segment (< 3 cm) ^[4]. Graded by the Prague C&M classification (C = circumferential extent, M = maximal extent) ^[4].

This is an important conceptual chain for exams:

Oesophageal adenocarcinoma mostly arises from a region of Barrett's metaplasia, which is due to GERD ^[1]^[2].

Feature	SCC (Upper 2/3)	Adenocarcinoma (Lower 1/3)
Location	Upper and middle oesophagus	Distal oesophagus / GOJ
Risk factors	Smoking, alcohol, hot drinks, nitrosamines; achalasia; Plummer-Vinson; corrosive injury	GERD, Barrett's oesophagus, obesity, smoking
Most common in HK	SCC is most common in HK (90%) ^[1]^[3]	More common in Western countries; rising in HK
Precursor	Squamous dysplasia	Barrett's metaplasia → dysplasia

From the neonatal surgery slides, a few relevant points:

Physiological GER is extremely common in neonates and infants (immature LES, liquid diet, supine position, short intra-abdominal oesophagus).
Most resolve by 12–18 months as the child grows and the LES matures.
Pathological GERD in neonates may present with: failure to thrive, feeding refusal, recurrent aspiration pneumonia, apparent life-threatening events (ALTE), Sandifer syndrome (dystonic posturing with reflux).
Relevant congenital conditions associated with GERD: oesophageal atresia (post-repair), diaphragmatic hernia.

Mechanism Category	Specific Abnormality	Result
↓ LES competence	↓ Basal LES tone, excessive tLESRs, drug-induced LES relaxation	Reflux of gastric contents into oesophagus
Anatomical disruption	Hiatus hernia (loss of crural sling, angle of His, intra-abdominal segment)	Loss of extrinsic anti-reflux mechanisms
↑ Intra-abdominal pressure	Obesity, pregnancy, ascites, chronic cough, constipation	Pressure overcomes LES resistance
↑ Gastric volume/acid	Large meals, gastroparesis, GOO, Zollinger-Ellison	More refluxate available
↓ Oesophageal clearance	Impaired peristalsis, ↓ saliva, supine position	Prolonged acid contact time
↓ Mucosal defence	Squamous epithelium vulnerability, NSAIDs	Greater mucosal damage per unit of acid exposure

High Yield Summary

Definition: GERD = troublesome symptoms and/or complications from reflux of gastric contents (Montreal definition). GERD ≠ oesophagitis (most have NERD — normal endoscopy).

Key Risk Factors: Obesity (most important modifiable), hiatus hernia, smoking, alcohol, dietary triggers (fat, chocolate, coffee), drugs (NSAIDs, CCBs, progesterone), pregnancy, ↑ intra-abdominal pressure.

Pathophysiology: The dominant mechanism is transient LES relaxations (tLESRs), NOT permanent LES weakness. Hiatus hernia disrupts multiple anti-reflux mechanisms simultaneously.

Classification: NERD (60–70%) > Erosive oesophagitis > Extra-oesophageal disease. LA classification (A–D) grades erosive disease.

Clinical Features:

Typical: Heartburn + acid regurgitation (cardinal symptoms)
Atypical: Chronic cough, asthma, laryngitis, globus, non-cardiac chest pain
Alarm features (dysphagia, weight loss, anaemia, GI bleeding, age > 55 new onset) → urgent OGD

Complication Chain: GERD → Oesophagitis → Stricture → Barrett's (intestinal metaplasia) → Dysplasia → Adenocarcinoma (0.5%/year risk in Barrett's).

Barrett's: Columnar metaplasia with goblet cells replacing squamous epithelium. Prague C&M classification. H. pylori is protective.

HK Focus: SCC still most common oesophageal cancer in HK (90%), but adenocarcinoma (from GERD/Barrett's) is rising.

Active Recall - GERD: Definition, Epidemiology, Pathophysiology & Clinical Features

^[1] Lecture slides: GC 189. I can't swallow oesophageal cancer.pdf ^[2] Senior notes: felixlai.md (GERD section, pp. 349–351) ^[3] Senior notes: maxim.md (GERD, Barrett's oesophagus, Hiatal hernia sections, pp. 57–60) ^[4] Senior notes: maxim.md (Barrett's oesophagus section, p. 57); felixlai.md (Barrett's oesophagus section, p. 365) ^[5] Lecture slides: Neonatal Surgery.pdf

Differential Diagnosis of GERD

When a patient presents with the classic GERD triad — retrosternal burning, acid regurgitation, and symptoms worsened by meals/supine position — the diagnosis may seem straightforward. But the reality is that many conditions mimic GERD, and conversely, GERD can mimic many other conditions (especially cardiac disease). A systematic approach to differential diagnosis is essential.

The key principle: GERD is a clinical diagnosis, but you must actively exclude dangerous mimics before settling on it, particularly coronary artery disease, oesophageal malignancy, and peptic ulcer disease.

GERD presents along several symptom axes, each with its own differential:

Heartburn / retrosternal burning — DDx of epigastric/retrosternal pain
Dysphagia — DDx of difficulty swallowing
Chronic cough / hoarseness / asthma — DDx of extra-oesophageal symptoms
Upper GI bleeding — DDx of haematemesis/melaena (when GERD causes erosive oesophagitis)

These are the conditions that present with epigastric or retrosternal pain/burning and may be confused with GERD:

Differential	Key Distinguishing Features	Why It Can Mimic GERD
Coronary artery disease (CAD)	Exertional chest pain, relieved by rest/GTN, associated with diaphoresis, dyspnoea. Risk factors: HTN, DM, smoking, hyperlipidaemia, FHx. ECG changes.	Cardiac and oesophageal pain share the same spinal afferent segments (T1–T6) → referred pain is nearly identical. A case study highlights a 50-year-old heavy smoker with retrosternal chest discomfort radiating to the throat, waking him at night — GERD was the diagnosis, but CAD must be actively excluded ^[6]. The key distinguishing feature: GERD pain has no relation to exertion and is relieved by antacids/water, not GTN ^[6].
Peptic ulcer disease (PUD)	Epigastric pain — gastric ulcer: precipitated by food; duodenal ulcer: 2–5 hours after meals, relieved by food/antacids, night-time awakening. 4 major risk factors: H. pylori, NSAIDs, stress, excess gastric acid ^[7].	Overlap in location (epigastric), timing (post-prandial), and partial relief by antacids. Differentiate by OGD. PUD pain is more "gnawing" and localized; GERD pain is more "burning" and retrosternal with upward radiation ^[7].
Functional (non-ulcer) dyspepsia	Rome IV criteria: postprandial fullness, early satiety, epigastric pain/burning for ≥ 3 months with onset ≥ 6 months prior. No structural disease on investigation. Accounts for ~60% of all dyspepsia ^[7].	Significant symptom overlap — epigastric burning can be identical. Heartburn is technically not a dyspeptic symptom but frequently coexists ^[7]. Functional dyspepsia is a diagnosis of exclusion after OGD is normal.
Infective oesophagitis	Odynophagia is prominent (more so than heartburn). Immunocompromised patients (HIV, transplant, chemotherapy). Caused by Candida (most common — white plaques), HSV (shallow ulcers), CMV (deep ulcers) ^[6].	Can cause retrosternal burning, but odynophagia dominates and there is usually an immunocompromised background. OGD with biopsy/culture differentiates.
Pill oesophagitis	Temporal relationship with oral medication (patient takes pill with insufficient water, or lies down immediately after). Common culprits: bisphosphonates (alendronate), tetracyclines (doxycycline), NSAIDs, KCl, iron supplements ^[6].	Causes localised oesophageal injury — burning, odynophagia. History of the offending pill + temporal relationship is diagnostic. OGD shows discrete ulcers, often mid-oesophagus (where the aortic arch or left atrium compresses the oesophagus, slowing tablet transit).
Eosinophilic oesophagitis (EoE)	Young males with atopic history (asthma, eczema, food allergy). Intermittent dysphagia, food bolus impaction. Characteristic OGD: rings ("trachealization"), furrows, white exudates. Biopsy: ≥ 15 eosinophils/HPF ^[6].	Can cause heartburn and dysphagia. Often misdiagnosed as GERD — the clue is failure to respond to PPIs (though ~50% of EoE patients show partial PPI response, now called PPI-responsive oesophageal eosinophilia).
Oesophageal motility disorders	Achalasia: progressive dysphagia for solids AND liquids, regurgitation of undigested food, chest pain. Diffuse oesophageal spasm (DES): intermittent chest pain + dysphagia; "corkscrew oesophagus" on barium. Jackhammer (nutcracker) oesophagus: intense chest pain ^[6]^[8].	Achalasia can cause heartburn (from food stasis → fermentation → lactic acid irritation, NOT acid reflux). Both GERD and achalasia present with heartburn and regurgitation — oesophageal manometry is diagnostic of achalasia ^[8].
Oesophageal / gastric malignancy	Painless progressive dysphagia (solids → liquids) over weeks. Weight loss, anorexia, anaemia. Risk factors: smoking, alcohol, Barrett's, achalasia ^[1]^[9].	Advanced oesophageal cancer can cause retrosternal pain. The key alarm features (progressive dysphagia, weight loss, anaemia) mandate urgent OGD ^[1].
Biliary colic / cholecystitis	RUQ/epigastric pain, worse after fatty meals, Murphy's sign positive.	Epigastric pain after fatty meals overlaps. Biliary colic is more colicky and localised to RUQ; GERD is burning and retrosternal. USS abdomen differentiates.
Acute pancreatitis	Severe epigastric pain radiating to back, relieved by leaning forward. ↑ Amylase/lipase.	Epigastric pain can mimic. Radiation to back, severity, and biochemistry differentiate.
Gastritis / Duodenitis	Epigastric pain, nausea. May be drug-induced (NSAIDs, alcohol), stress-induced, or H. pylori-related. Diagnosis by OGD ^[7]^[10].	Mucosal inflammation without discrete ulceration. Symptom overlap is extensive; OGD differentiates.

The Most Dangerous Mimic

Coronary artery disease is the most dangerous condition that mimics GERD. The case study in the notes describes a 50-year-old male heavy smoker with a father who had CAD at 55 — presenting with retrosternal discomfort radiating to the throat, sometimes waking him at night. Despite the classic GERD features (relief by water, no exertional component), cardiac disease MUST be excluded first given the risk factor profile ^[6]. Remember: always exclude the deadly differential before diagnosing the common one.

GERD-associated dysphagia may be due to peptic stricture, oedema, or Barrett's-related changes. But dysphagia has a broad differential that must be considered systematically ^[9]:

Category	Conditions	Distinguishing Features
Structural — Intramural	CA oesophagus	Painless progressive dysphagia (solids → liquids), weight loss. ≥ 75% luminal stenosis before dysphagia occurs ^[1]^[9].
	Peptic stricture (GERD complication)	Long history of GERD/heartburn → progressive solid-food dysphagia. Smooth, concentric narrowing on OGD/barium ^[2].
	Oesophageal rings/webs	Intermittent, non-progressive solid-food dysphagia. Schatzki ring (lower oesophagus at squamocolumnar junction); Plummer-Vinson web (upper oesophagus, associated with IDA) ^[9].
	Corrosive/caustic stricture	History of caustic ingestion. Progressive dysphagia developing weeks–months later ^[9].
	Eosinophilic oesophagitis	Young atopic male, food impaction, rings on OGD ^[6].
Structural — Extramural	Lung cancer, lymphoma, retrosternal goitre, thoracic aortic aneurysm	Extrinsic compression. The mnemonic "4T's of extramural compression": Tumour/LN, Thyroid, Thymus, Thoracic aortic aneurysm ^[9].
Functional (Motility)	Achalasia	Dysphagia for solids AND liquids simultaneously from onset. Regurgitation of undigested food. Bird's beak sign on barium. Manometry diagnostic ^[8]^[9].
	Diffuse oesophageal spasm	Intermittent dysphagia + chest pain. "Corkscrew" oesophagus. Normal LES relaxation on manometry (unlike achalasia) ^[8].
	Scleroderma (systemic sclerosis)	CREST syndrome. Fibrosis of oesophageal smooth muscle → absent peristalsis in distal 2/3 + incompetent LES → severe GERD + dysphagia ^[9].
	Neurological	Stroke, MND, Parkinson's, MS, MG, myopathies — cause oropharyngeal (transfer) dysphagia with coughing/choking on initiation of swallowing ^[9].

Key clinical distinction: Painless progressive dysphagia (over weeks) is malignancy until proven otherwise ^[9].

When GERD presents primarily with extra-oesophageal symptoms, the differential broadens considerably:

Symptom	GERD Mechanism	Other Differentials to Exclude
Chronic cough	Microaspiration or oesophago-bronchial vagal reflex ^[2]	Asthma, post-nasal drip (upper airway cough syndrome), ACE inhibitor cough, bronchiectasis, TB, lung cancer
Asthma / Wheezing	Vagal reflex bronchospasm ^[2]	True asthma (atopic), COPD, cardiac asthma (HF)
Hoarseness / Posterior laryngitis	Acid/pepsin damage to laryngeal mucosa ^[2]	Vocal cord nodules/polyps, laryngeal cancer, RLN palsy (lung apex tumour, thyroid surgery), functional dysphonia
Non-cardiac chest pain	Oesophageal nociceptors share spinal segments with cardiac afferents ^[2]	CAD (must exclude first), musculoskeletal (costochondritis), PE, pericarditis, anxiety/panic disorder
Globus sensation	UES hypertonia from distal oesophageal acid exposure ^[2]	Pharyngeal/oesophageal malignancy, thyroid enlargement, anxiety, cricopharyngeal bar

Erosive oesophagitis from GERD can cause UGIB. The differential of UGIB must be considered ^[10]:

Cause	Key Feature
Peptic/duodenal ulcers (most common cause of UGIB)	H. pylori, NSAIDs history. Visible vessel or adherent clot on OGD ^[7]^[10].
Oesophagogastric varices	Portal hypertension, liver cirrhosis. Massive haematemesis ^[10].
Erosive oesophagitis/oesophageal ulcers	History of GERD. Usually self-limiting bleed ^[10].
Gastritis/duodenitis	Drug-induced, alcohol, stress. Self-limiting ^[10].
Mallory-Weiss syndrome	Longitudinal mucosal laceration at GOJ following forceful retching/vomiting. ↑ intra-abdominal pressure → tear ^[10].
Upper GI malignancy	Constitutional symptoms (weight loss, anorexia). Usually slower bleed ^[10].
Dieulafoy's lesion	Dilated aberrant submucosal vessel, usually proximal stomach. Massive, intermittent bleed without surrounding ulcer ^[10].
Portal hypertensive gastropathy	Diffuse mucosal oozing in context of portal hypertension ^[10].

Feature	GERD	CAD	PUD	Achalasia	Oesophageal Cancer
Pain character	Burning, retrosternal	Crushing, tight	Gnawing, epigastric	Pressure, retrosternal	Dull ache, progressive
Relation to meals	Worse post-prandial	No relation	GU: worse with food; DU: relieved	After meals (food stasis)	No relation
Relation to exertion	None	Worsened	None	None	None
Relieved by	Antacids, PPI, water	GTN, rest	Food (DU), antacids	None reliably	Nothing
Dysphagia	If stricture/Barrett's	No	No	Solids + liquids from onset	Progressive solids → liquids
Weight loss	Uncommon	No	Possible	Yes (late)	Yes (prominent)
Key investigation	OGD, pH monitoring	ECG, troponin	OGD + H. pylori test	Oesophageal manometry ^[8]	OGD + biopsy ^[1]

Achalasia vs GERD — A Classic Exam Pitfall

Both GERD and achalasia can present with heartburn and regurgitation. In achalasia, "heartburn" is due to fermentation of retained food (lactic acid), NOT gastric acid reflux. The regurgitation in achalasia is of undigested food (no sour/bitter taste), while in GERD it is acidic/bitter. Oesophageal manometry is diagnostic of achalasia (elevated LES resting pressure, failure of LES relaxation, absent peristalsis) ^[8]. If you prescribe a PPI for achalasia, it won't work — and the patient's dysphagia will progress.

Pseudoachalasia — Don't Miss the Cancer

Malignancy at the GOJ can cause pseudoachalasia by invading the oesophageal neural plexus directly (adenocarcinoma at GOJ) or via paraneoplastic syndrome. Manometric findings are identical to true achalasia. Differentiate by OGD + endoscopic ultrasound (EUS) — look for a mass at the GOJ, "shouldering/heaping" on barium swallow, short duration of symptoms (< 6 months), age > 55, and significant weight loss ^[8].

High Yield Summary

Core differential of GERD symptoms:

Coronary artery disease — most dangerous mimic; shared spinal afferents T1–T6; exclude if cardiac risk factors present
Peptic ulcer disease — overlapping epigastric pain; differentiate by meal relationship and OGD
Functional dyspepsia — diagnosis of exclusion; accounts for 60% of dyspepsia; no structural disease
Infective oesophagitis — immunocompromised; odynophagia dominates; Candida (most common), HSV, CMV
Pill oesophagitis — temporal relationship with medication; mid-oesophageal ulcers
Eosinophilic oesophagitis — young atopic males; food impaction; PPI-refractory; ≥ 15 eos/HPF
Achalasia — dysphagia for solids AND liquids, undigested food regurgitation; manometry diagnostic
Oesophageal malignancy — painless progressive dysphagia is cancer until proven otherwise

When to worry: Alarm features (dysphagia, weight loss, anaemia, GI bleeding, age > 55 new onset) → urgent OGD.

Key differentiating test: OGD for structural pathology; oesophageal manometry for motility disorders; 24h pH-impedance monitoring for equivocal cases.

Active Recall - Differential Diagnosis of GERD

References

^[1] Lecture slides: GC 189. I can't swallow oesophageal cancer.pdf ^[2] Senior notes: felixlai.md (GERD section, pp. 349–351) ^[3] Senior notes: maxim.md (GERD, Hiatal hernia sections) ^[6] Senior notes: felixlai.md (GERD case study and differential diagnosis, pp. 351–358) ^[7] Senior notes: felixlai.md (Dyspepsia section, pp. 327–329; PUD section, pp. 388–389) ^[8] Senior notes: felixlai.md (Achalasia section, pp. 360–361); maxim.md (Achalasia section) ^[9] Senior notes: maxim.md (Dysphagia differential diagnosis table); Lecture slides: GC 189. I can't swallow oesophageal cancer.pdf ^[10] Senior notes: felixlai.md (Upper GI bleeding differential, pp. 334–335); maxim.md (UGIB section)

Diagnostic Criteria & Diagnostic Algorithm for GERD

Unlike many conditions where a single test gives you a definitive answer (e.g., troponin for MI, biopsy for cancer), GERD has no single gold-standard diagnostic criterion that applies to all patients. Here's why:

Most GERD patients have normal endoscopy (NERD = 60–70%) — so you can't rely on endoscopy alone to "rule in" GERD ^[2]^[6].
pH monitoring is the most objective test, but it's uncomfortable, not widely available, and still misses ~10–20% of true GERD ^[6].
Symptom-based diagnosis is ~80–90% accurate for typical presentations, but extra-oesophageal presentations are notoriously unreliable ^[6].

Therefore, GERD diagnosis relies on a combination of methods, applied in a stepwise fashion depending on the clinical scenario.

The Lyon Consensus provides the most widely accepted framework for defining objective evidence of GERD. Think of it as a traffic-light system:

Evidence Level	Criteria	Interpretation
Conclusive evidence FOR GERD	LA Grade C or D oesophagitis on OGD	Pathological reflux confirmed — no further testing needed
	Long-segment Barrett's oesophagus (≥ 1 cm with intestinal metaplasia on biopsy)	Pathological reflux confirmed
	Peptic stricture on OGD	Pathological reflux confirmed
	Acid exposure time (AET) > 6% on ambulatory pH monitoring	Pathological reflux confirmed ^[6]
Borderline / Inconclusive	LA Grade A or B oesophagitis	May be normal variant (Grade A especially); supportive but not conclusive alone
	AET 4–6%	Grey zone — needs adjunctive metrics (symptom correlation, number of reflux episodes)
Against GERD	Normal OGD + AET < 4% + normal reflux episode count	GERD excluded — consider functional heartburn or reflux hypersensitivity

Why LA Grade A Is No Longer Conclusive

The 2022 Lyon Consensus downgraded LA Grade A oesophagitis because studies showed that up to 5–7.5% of asymptomatic healthy volunteers have LA Grade A changes on endoscopy. It has low specificity for pathological GERD. LA Grade C/D, however, is conclusive evidence of GERD — you don't even need pH monitoring.

There are 4 main methods that can be used alone or in combination ^[6]:

Symptom questionnaires
Upper endoscopy (OGD)
Ambulatory 24-hour oesophageal pH monitoring
Proton pump inhibitor (PPI) testing

Let's dissect each.

Investigation Modalities — Detailed Breakdown

Feature	Detail
Principle	Typical symptoms (heartburn + acid regurgitation) in a classic pattern have ~80–90% accuracy for diagnosing GERD ^[6]
Validated tools	GERD-Q (GERD Questionnaire), RDQ (Reflux Disease Questionnaire), GERD-HRQL
Accuracy	~80–90% ^[6]
When sufficient alone	Young patient (< 55), typical symptoms, no alarm features → can proceed directly to empirical PPI trial without investigation
Limitations	Cannot detect complications (stricture, Barrett's, cancer); cannot distinguish NERD from functional heartburn; poor accuracy for extra-oesophageal symptoms

Key symptom characteristics to elicit ^[6]:

Site: Retrosternal area
Onset: After meals / leaning forward (bending) / lying flat in bed
Character: Burning pain
Radiation: Up towards the throat
Associated symptoms: Cough when lying down
Time course: More than once a week
Exacerbating factors: Alcohol, chocolate, caffeine, fatty meals, CCBs, anticholinergic drugs
Relieving factors: Antacids, acid-blocking drugs

Feature	Detail
Principle	If symptoms are caused by acid reflux, suppressing acid should relieve them. Constitutes a therapeutic trial conducted over 1–4 weeks ^[6].
Protocol	Standard-dose PPI (e.g., omeprazole 20 mg BD or esomeprazole 40 mg OD) for 4–8 weeks
Interpretation	Patients responding favourably are likely to have a reflux component to their symptoms ^[6]
Sensitivity	~78% for erosive oesophagitis; lower (~50%) for NERD
Specificity	Moderate (~54%) — other acid-related conditions (PUD, functional dyspepsia, eosinophilic oesophagitis) may also improve
Advantages	Non-invasive, inexpensive, widely available, doubles as treatment
Limitations	Positive response does not definitively confirm GERD (placebo response rate ~20–40%); negative response does not exclude GERD (may need higher dose, longer trial, or non-acid reflux is the problem)

PPI Trial — Practical Interpretation

Think of the PPI trial as a screening test, not a diagnostic test. A positive response makes GERD likely but doesn't prove it. A negative response should prompt further investigation (OGD ± pH monitoring) rather than abandoning the GERD diagnosis entirely. Also remember: some patients have non-acid reflux (bile, weakly acidic) that won't respond to PPIs — these need impedance-pH monitoring to detect.

This is the primary investigation (not first-line diagnostic tool) for GERD. It does NOT diagnose GERD per se — it detects complications and excludes mimics.

Feature	Detail
What it does	Detects erosive oesophagitis and other macroscopic complications ^[6]. Direct visualisation of the oesophageal mucosa; allows biopsy.
Key findings	Erosive oesophagitis (LA Grade A–D), peptic stricture, Barrett's oesophagus, hiatus hernia, malignancy
Sensitivity for GERD	Only accounts for 20–40% of symptomatic patients — meaning 60–80% have normal endoscopy (NERD) ^[6]
Interpretation	Presence of lesions supports the diagnosis, but absence is unhelpful ^[6] — a normal OGD does NOT exclude GERD
Biopsy indications	Barrett's (confirm intestinal metaplasia + assess dysplasia), suspected malignancy, suspected eosinophilic oesophagitis (≥ 15 eos/HPF), suspected infective oesophagitis

Indications for OGD in GERD ^[1]^[3]^[6]:

Alarm features: dysphagia, odynophagia, weight loss, anaemia, GI bleeding, persistent vomiting, epigastric mass
Age > 55 with new-onset symptoms
Symptoms refractory to PPI trial
Screening for Barrett's in high-risk patients (chronic GERD > 5 years, male, age > 50, obesity, smoking, family history of Barrett's/oesophageal adenocarcinoma)
Pre-operative assessment before anti-reflux surgery ^[3]

OGD findings and their significance:

Finding	Significance	Next Steps
Erosive oesophagitis (LA C/D)	Conclusive evidence of pathological GERD	Grade using LA classification; treat with PPI; repeat OGD in 8 weeks to confirm healing and exclude Barrett's
Erosive oesophagitis (LA A/B)	Supportive but borderline; consider confirmatory testing	If clinical picture fits → treat as GERD; if doubt → pH monitoring
Normal mucosa	NERD or functional heartburn or reflux hypersensitivity	pH-impedance monitoring to differentiate
Barrett's oesophagus	Salmon-pink velvety mucosa replacing pale glossy squamous epithelium; proximal migration of Z-line > 1 cm; biopsy shows intestinal metaplasia with goblet cells ^[4]^[11]	Grade with Prague C&M; biopsy using Seattle protocol (every 1–2 cm in 4 quadrants) ^[4]; ± chromoendoscopy (NBI, Lugol's iodine) for higher sensitivity ^[4]
Peptic stricture	Smooth, concentric narrowing in distal oesophagus; long GERD history	Biopsy to exclude malignancy; endoscopic dilatation
Hiatus hernia	Upward displacement of Z-line; Hill classification on OGD ^[3]	Document type and size; assess GOJ competence
Mass / irregular ulcer	Suspect malignancy	Multiple biopsies; staging workup

Barrett's Diagnostic Criteria on OGD

Two criteria must be fulfilled to diagnose Barrett's oesophagus ^[11]:

The endoscopist must document that columnar epithelium lines the distal oesophagus (salmon-pink velvety epithelium extending proximal to the GOJ)
Histological examination of the biopsy must reveal specialised intestinal metaplasia (characterised by goblet cells)

Without biopsy confirmation of goblet cells, you cannot call it Barrett's — you can only say "columnar-lined oesophagus."

Important OGD landmarks ^[11]^[12]:

Gastro-oesophageal junction (GOJ/GEJ): defined endoscopically as the level of the most proximal extent of gastric folds. This is an imaginary anatomical line.
Squamocolumnar junction (Z-line): the visible line where pale glossy squamous epithelium meets reddish velvety columnar epithelium.
Normal: Z-line coincides with GOJ.
Barrett's: Z-line is proximal to GOJ (i.e., columnar epithelium has replaced squamous epithelium in the distal oesophagus).

This is the most objective test for quantifying acid reflux.

Feature	Detail
Status	Gold standard for diagnosing pathological acid reflux ^[6]
Availability	Inconvenient, uncomfortable, and not widely available. Seldom used as first-line diagnostic tool ^[6]
Accuracy	Sensitivity ~80–90% ^[6]

Types of pH monitoring:

Type	Mechanism	Pros	Cons
Catheter-based pH monitoring	Slim catheter with pH-sensitive probe inserted through the nose, positioned 5 cm above the GOJ. Intraluminal pH is recorded over 24 hours while patient performs normal activities ^[6].	Well-validated; can correlate symptoms with reflux events	Uncomfortable; may alter behaviour (eat less, avoid triggers) → false negatives
Wireless pH monitoring (Bravo™ system)	Catheter-free system — a small pH capsule is endoscopically attached to the oesophageal mucosa 6 cm above the GOJ. Records pH wirelessly for 48–96 hours ^[6].	More comfortable; longer recording period; more physiological data	Requires endoscopy for placement; capsule may detach prematurely; more expensive
Combined pH-impedance monitoring	Measures both pH (acid) AND impedance (detects liquid/gas bolus movement regardless of pH). Detects acid, weakly acidic, and non-acid reflux events.	Detects non-acid reflux (bile, weakly acidic); most comprehensive; essential "on PPI" testing	More complex interpretation; availability limited

Key measurements and interpretation ^[6]:

Parameter	Normal	Abnormal (Diagnostic of GERD)
Acid exposure time (AET) — % of total study time with pH < 4	< 4%	> 6% is diagnostic of reflux disease ^[6]
		4–6% = borderline (inconclusive)
Number of reflux episodes	< 40 in 24h (catheter); < 80 in 24h (Bravo 48h)	> 80 in 24h supports pathological reflux (Lyon 2022)
DeMeester score (composite)	< 14.7	> 14.7 = abnormal (combines AET, number of episodes, longest episode, etc.)
Symptom association probability (SAP)	—	> 95% = positive symptom-reflux correlation
Symptom index (SI)	—	> 50% = positive

Indications for pH monitoring ^[6]:

Diagnosis of GERD is doubtful
Planning for endoscopic or surgical therapy (pre-operative confirmation of reflux is mandatory before anti-reflux surgery ^[3])
Persistent symptoms despite PPIs — to determine if there is continued acid exposure (PPI failure) or non-acid reflux
Persistent symptoms despite reflux surgery

"On PPI" vs "Off PPI" testing — which to choose?

Scenario	Test of Choice	Rationale
Never proven GERD, no prior endoscopic evidence	pH monitoring off PPI (stop PPI ≥ 7 days)	Need to establish baseline acid exposure without treatment
Proven GERD (prior LA C/D or Barrett's) but persistent symptoms on PPI	pH-impedance monitoring on PPI	Already know they have GERD; question is whether current symptoms are due to breakthrough acid, non-acid reflux, or something else

Feature	Detail
Principle	Measures pressure inside the oesophagus — evaluates location and function of LES and oesophageal body peristalsis ^[6]
What it detects	LES resting pressure, LES relaxation (integrated relaxation pressure/IRP), peristaltic pattern
Role in GERD	NOT recommended in patients with uncomplicated GERD ^[6]. Its role is to exclude motility disorders that mimic GERD and to assess peristalsis before anti-reflux surgery

Indications ^[6]:

Diagnosis of GERD is doubtful — to exclude achalasia, DES, scleroderma
Planning for endoscopic or surgical therapy — manometry before fundoplication is mandatory to:
- Confirm the LES is anatomically locatable (for pH probe placement)
- Assess oesophageal body peristalsis (aperistalsis is a contraindication to Nissen fundoplication because the tight 360° wrap + absent peristalsis = severe post-op dysphagia ^[3])
- Identify achalasia (which needs myotomy, not fundoplication)

Manometric findings of an abnormal LES ^[6]:

Resting pressure < 6 mmHg
Overall length < 2 cm or abdominal length < 1 cm

Key manometric patterns to differentiate:

Condition	LES Resting Pressure	LES Relaxation (IRP)	Peristalsis
GERD	Normal or low	Normal	Normal or mildly impaired
Achalasia	Elevated	Failed (IRP ≥ 15 mmHg)	Aperistalsis
DES	Normal	Normal	Premature contractions (> 20%)
Scleroderma	Very low	Normal	Absent in distal 2/3 (smooth muscle)

Feature	Detail
Role in GERD	Limited; largely superseded by OGD and pH monitoring
Useful for	Demonstrating hiatus hernia, peptic stricture morphology, anatomical assessment pre-surgery; suspected proximal oesophageal lesion, known complex tortuous stricture, or negative OGD but mechanical obstruction still suspected ^[12]
GERD findings	Free barium reflux into oesophagus (low sensitivity); hiatus hernia; stricture; mucosal irregularity
Achalasia findings	Bird's beak/rat-tail appearance (contracted LES + dilated proximal oesophagus) ^[8]^[12]
Contrast choice	Barium: avoid if risk of perforation (barium peritonitis). Gastrografin: avoid if risk of aspiration (chemical pneumonitis). If high aspiration risk, use Omnipaque (lower osmolarity, lower risk of pulmonary oedema) ^[9]

Investigation	When Used	Key Findings
CBC	All patients with alarm features	Anaemia (iron-deficiency from chronic blood loss in erosive oesophagitis/Barrett's ulcer)
H. pylori testing	As part of dyspepsia workup; note: H. pylori is protective against Barrett's ^[4]	Urea breath test (most accurate non-invasive), stool antigen, serology; or CLO test/histology at OGD
ECG / Cardiac workup	If chest pain is the dominant symptom	Exclude CAD before attributing to GERD
CXR	If hiatus hernia suspected or pre-operative	Gastric bubble in retrocardiac area (hiatus hernia) ^[3]; aspiration pneumonia
CT thorax with oral contrast	Hiatus hernia characterisation	Diagnostic for type and size of hiatus hernia ^[3]
Laryngoscopy	Extra-oesophageal symptoms (hoarseness, globus)	Posterior laryngeal erythema, vocal cord oedema/granulomas (LPR)

The Diagnostic Pathway in Practice

Step 1: History — typical vs atypical symptoms, alarm features, cardiac risk factors.

Step 2: If young + typical + no alarms → PPI trial (this is both diagnostic AND therapeutic).

Step 3: If alarms, atypical, PPI-refractory, or pre-surgical → OGD.

Step 4: If OGD normal + persistent symptoms → pH-impedance monitoring (the only way to differentiate NERD from functional heartburn from reflux hypersensitivity).

Step 5: If surgery considered → manometry + pH monitoring + OGD are all mandatory pre-operatively ^[3]^[6].

This is a conceptually important distinction that relies on pH-impedance monitoring:

Condition	Endoscopy	Acid Exposure Time	Symptom-Reflux Correlation	Pathophysiology
NERD	Normal	Abnormal (AET > 6%)	Positive	True pathological reflux, but no visible mucosal damage
Reflux hypersensitivity	Normal	Normal (AET < 4%)	Positive (symptoms correlate with physiological reflux episodes)	Normal amount of reflux, but heightened visceral perception
Functional heartburn	Normal	Normal (AET < 4%)	Negative	No reflux correlation at all; central pain processing disorder

This matters because NERD responds to PPIs, reflux hypersensitivity partially responds, and functional heartburn does NOT respond to PPIs — it needs neuromodulators (e.g., TCAs, SSRIs) and psychological therapy.

Pre-op workup includes: oesophageal manometry, 24h ambulatory pH monitoring, and OGD with biopsy ^[3]:

Investigation	Purpose	Critical Finding That Alters Management
Oesophageal manometry	Assess peristalsis; exclude achalasia	Aperistalsis = contraindication to Nissen (360°) fundoplication → use partial wrap (Toupet 270°) or consider other options ^[3]
24h pH monitoring	Objective confirmation of pathological reflux	If AET < 4% with no symptom correlation, surgery will NOT help — reconsider diagnosis
OGD + biopsy	Assess mucosal status; exclude Barrett's, malignancy, stricture	Barrett's with dysplasia needs surveillance/ablation plan; malignancy needs staging, not fundoplication

Investigation	First-Line?	What It Tells You	Key Diagnostic Threshold
Symptom questionnaire	Yes	Likelihood of GERD	~80–90% accuracy ^[6]
PPI trial	Yes (if no alarms)	Symptom response supports GERD	Relief within 1–4 weeks ^[6]
OGD	If alarms or PPI-refractory	Mucosal damage, complications, excludes mimics	LA Grade C/D = conclusive; normal = unhelpful alone ^[6]
24h pH monitoring	If OGD normal + persistent symptoms	Acid exposure, symptom correlation	AET > 6% = diagnostic ^[6]
pH-impedance	Gold standard for refractory/atypical	Acid + non-acid reflux	AET + impedance events + SAP/SI
Oesophageal manometry	Pre-surgical or if motility disorder suspected	LES function, peristalsis	IRP ≥ 15 mmHg = achalasia; aperistalsis = avoid Nissen ^[3]^[6]
Barium swallow	Limited role	Anatomy (hiatus hernia, stricture)	Bird's beak = achalasia ^[12]

High Yield Summary

Diagnostic criteria (Lyon Consensus 2022):

Conclusive GERD: LA Grade C/D oesophagitis, long-segment Barrett's, peptic stricture, or AET > 6%
LA Grade A is no longer conclusive (may be normal variant)
AET 4–6% is borderline

Four main diagnostic methods (can be used alone or in combination):

Symptom questionnaires (~80–90% accuracy)
PPI trial (1–4 weeks; therapeutic trial)
OGD (detects complications; normal in 60–80%)
24h pH monitoring (gold standard; AET > 6% diagnostic)

OGD indications: alarm features, age > 55 new onset, PPI-refractory, Barrett's screening, pre-operative

pH monitoring indications: doubtful diagnosis, pre-surgical planning, persistent symptoms despite PPI/surgery

Manometry indications: NOT for uncomplicated GERD; used to exclude motility disorders and pre-operatively (aperistalsis → contraindication to Nissen)

Pre-op triad: Manometry + pH monitoring + OGD (all mandatory before anti-reflux surgery)

Barrett's diagnosis requires TWO criteria: endoscopic documentation of columnar-lined oesophagus + histological confirmation of intestinal metaplasia with goblet cells

Active Recall - Diagnosis of GERD

References

^[1] Lecture slides: GC 189. I can't swallow oesophageal cancer.pdf ^[2] Senior notes: felixlai.md (GERD section, pp. 349–351) ^[3] Senior notes: maxim.md (GERD surgical treatment, Hiatal hernia sections) ^[4] Senior notes: maxim.md (Barrett's oesophagus section, p. 57) ^[6] Senior notes: felixlai.md (GERD diagnosis and case study, pp. 352–358) ^[8] Senior notes: felixlai.md (Achalasia diagnosis, pp. 361–362); maxim.md (Achalasia section) ^[9] Senior notes: maxim.md (Dysphagia investigations, contrast choice) ^[11] Senior notes: felixlai.md (Barrett's diagnostic criteria, p. 367) ^[12] Senior notes: felixlai.md (Dysphagia investigations — OGD, barium swallow, manometry, pp. 325–326)

Management of GERD

GERD management follows a stepwise, escalating approach. The logic is simple:

Reduce the aggressor (acid) — lifestyle, antacids, H2RAs, PPIs
Fix the barrier (anti-reflux mechanism) — surgery, endoscopic procedures
Treat the complications (stricture, Barrett's) — endoscopic/surgical

The critical concept to grasp is that PPIs only change acidic reflux into non-acidic reflux (change the pH) but do NOT prevent reflux itself ^[13]. They relieve heartburn and heal oesophagitis by reducing acidity, but regurgitation usually remains uncorrected since the reflux mechanism is not affected — this requires anti-reflux surgery ^[13]. This distinction is the key to understanding when to escalate from medical to surgical management.

Lifestyle measures should be recommended to every GERD patient, regardless of severity. They are the foundation — even if a patient needs PPIs, lifestyle changes improve outcomes.

Measure	Mechanism	Evidence Level
Weight loss	↓ Intra-abdominal pressure → ↓ pressure gradient across LES; ↓ visceral adiposity → ↓ pro-inflammatory mediators	Strongest evidence of all lifestyle measures; even modest weight loss (5–10%) improves symptoms significantly
Elevation of bed head (15–20 cm)	Gravity assists oesophageal clearance during sleep → improves nocturnal symptoms ^[6]	Head of bed elevation (not just extra pillows — the whole bed head must be raised, e.g., with blocks or a wedge pillow)
Avoidance of late meals (eating > 2–3 hours before bedtime) ^[6]^[13]	Allows gastric emptying before supine position → less nocturnal reflux	Moderate evidence
Dietary modifications	Specific foods relax LES or stimulate acid: low-fat diet, avoidance of chocolate, spicy food, coffee ^[6]	Variable evidence; patient-specific triggers should be identified
Smoking cessation ^[6]	Smoking ↓ LES pressure, ↓ saliva production, ↓ mucosal defence	Moderate evidence
Avoid alcohol ^[6]	Alcohol ↓ LES tone, direct mucosal irritant, ↓ oesophageal motility	Moderate evidence
Eat small, frequent meals ^[13]	Large meals → gastric distension → more tLESRs → more reflux	Moderate evidence
Avoidance of tight belts, corsets ^[6]	↑ External abdominal pressure → ↑ intra-abdominal pressure → reflux	Weak evidence but logical
Avoid lying down after meals	Same principle as bed elevation — gravity assists clearance	Moderate evidence

Lifestyle Measures — Important for Exams

Always mention lifestyle modification first in any GERD management answer. The three highest-yield measures are: weight loss, bed head elevation, and avoiding late meals. Examiners want to see that you don't jump straight to PPIs.

Step 2: Medical Treatment

Feature	Detail
Mechanism	Neutralisation of acid — direct chemical reaction (e.g., Mg(OH)₂ + 2HCl → MgCl₂ + 2H₂O) ^[6]
Examples	Aluminium hydroxide, magnesium hydroxide (often combined: Maalox, Gaviscon)
Role	Rapid but short-lived symptom relief (minutes to ~1 hour). No healing of oesophagitis.
Indications	Mild, intermittent symptoms; on-demand use for breakthrough symptoms alongside PPI
Side effects	Al(OH)₃ → constipation (aluminium "clogs"); Mg(OH)₂ → diarrhoea (magnesium = "moves")

Alginates (e.g., Gaviscon Advance): form a "raft" of alginate gel on top of the gastric pool, creating a physical barrier that prevents reflux. Particularly useful for post-prandial symptoms and nocturnal reflux (the "acid pocket" concept — a pool of unbuffered acid sits on top of the meal near the GOJ; alginate displaces this pocket).

"H₂" = histamine receptor subtype 2 (on parietal cells). "Antagonist" = blocker.

Feature	Detail
Mechanism	↓ Gastric acid secretion by competitive blockade of histamine H₂ receptors on parietal cells → ↓ basal and meal-stimulated acid output ^[6]
Examples	Cimetidine, famotidine ^[13] (ranitidine withdrawn globally in 2020 due to NDMA contamination)
Efficacy	Symptomatic benefits ^[6]; inferior to PPIs for healing erosive oesophagitis (healing rate ~50% vs 80–90% for PPIs)
Indications	Mild (LA Grade A–B) oesophagitis; Non-erosive GERD (NERD) ^[13]; nocturnal acid breakthrough (bedtime H2RA added to daytime PPI)
Key limitation	Regular use leads to tolerance and loss of therapeutic effects → should be used intermittently only ^[13]
Side effects	Generally well-tolerated. Cimetidine: anti-androgenic effects (gynaecomastia, impotence), CYP450 inhibitor (drug interactions). Famotidine is preferred.

Why do H2RAs cause tolerance but PPIs don't? H2RAs block only one of three stimulatory pathways to the parietal cell (histamine). When histamine is chronically blocked, the parietal cell upregulates the other two pathways (gastrin and acetylcholine) — leading to tachyphylaxis. PPIs, in contrast, irreversibly block the final common pathway (the H⁺/K⁺-ATPase proton pump itself), so compensatory upregulation cannot bypass the block.

PPIs are the most effective medical therapy for GERD. Let's understand them from the molecule up.

Name breakdown: "Proton pump" = the H⁺/K⁺-ATPase enzyme on the apical membrane of parietal cells; "inhibitor" = blocks it irreversibly.

Feature	Detail
Mechanism	Irreversibly bind and inhibit the H⁺/K⁺-ATPase proton pump — the final common pathway of gastric acid secretion. This is downstream of all three stimulatory inputs (histamine, gastrin, acetylcholine), making PPIs more effective than H2RAs.
Examples	Omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole, dexlansoprazole ^[6]^[13]
Activation	PPIs are prodrugs — they are inactive at neutral pH. They are absorbed in the small intestine, enter the bloodstream, concentrate in the acidic canaliculi of active parietal cells (pH ~1), and are protonated there → converted to the active sulfenamide form → covalently binds to the proton pump.
Dosing timing	ALL PPIs except dexlansoprazole should be administered 30 min–1 hour BEFORE meals to ensure maximal efficacy ^[13]. Why? Because the pump must be actively secreting acid to be exposed to the drug. Meals stimulate parietal cell activity → more pumps on the surface → more targets. Dexlansoprazole has a dual delayed-release formulation.
Efficacy	Healing rate of erosive oesophagitis: 80–90% at 8 weeks (vs ~50% for H2RAs). Superior for both symptom relief and mucosal healing. Especially for patients with erosive oesophagitis — provides optimal initial healing and long-term maintenance therapy ^[6].

PPI Indications in GERD ^[13]:

Indication	Regimen
Mild oesophagitis (LA Grade A–B)	Standard dose OD (e.g., omeprazole 20 mg OD or esomeprazole 40 mg OD) × 4–8 weeks
Severe oesophagitis (LA Grade C–D)	Standard or double dose × 8 weeks → repeat OGD to confirm healing → long-term maintenance (often indefinite)
NERD	Standard dose OD × 4–8 weeks; can step down to on-demand or lowest effective dose
Barrett's oesophagus	High-dose PPI for life ^[4] — to reduce ongoing acid injury and potentially slow dysplasia progression
Extra-oesophageal GERD	Double dose (BD) × 8–12 weeks trial (longer trial needed because extra-oesophageal symptoms respond more slowly than typical symptoms)
Pre-operative	Heal oesophagitis before anti-reflux surgery to reduce inflammation and improve surgical field

Step-down strategy after initial healing:

NERD / LA Grade A–B: Step down to lowest effective dose → on-demand therapy (take PPI only when symptomatic) → aim for eventual discontinuation if possible
LA Grade C–D: Usually need long-term maintenance (high relapse rate ~80% if PPI stopped)
Barrett's: Indefinite PPI regardless of symptom status

Long-term PPI adverse effects (important to know, but risk is generally low and should not deter use when indicated):

Adverse Effect	Mechanism	Clinical Significance
↓ Calcium absorption → osteoporosis/fractures	Acid aids calcium dissolution; chronic acid suppression → ↓ Ca²⁺ absorption	Modest increase in hip fracture risk with > 1 year use. Ensure adequate calcium/vitamin D intake.
↓ Magnesium absorption → hypomagnesaemia	Impaired active intestinal Mg transport	Can cause muscle cramps, arrhythmias. Monitor Mg in long-term users.
*↑ Risk of C. difficile* colitis**	Acid is a defence barrier against ingested bacteria; suppression allows colonisation	Particularly relevant in hospitalised/elderly patients
↑ Risk of community-acquired pneumonia	Gastric acid kills aspirated bacteria; suppression → ↑ bacterial burden in refluxate	Small absolute risk increase
↓ Iron/B12 absorption	Acid-dependent absorption of non-haem iron and B12	Monitor in long-term users; rarely clinically significant
Fundic gland polyps	Acid suppression → ↑ gastrin → parietal cell hyperplasia → benign fundic gland polyps	Benign and reversible on PPI cessation
Kidney disease (AIN)	Idiosyncratic acute interstitial nephritis	Rare; monitor renal function
Rebound acid hypersecretion	Chronic acid suppression → compensatory ↑ gastrin → when PPI stopped, hypergastrinaemia drives acid oversecretion → symptom rebound	Taper PPIs gradually (step down over 2–4 weeks) rather than abrupt cessation

Why Long-Term PPI Use Motivates Surgery

Young and fit PPI-dependent patients are ideal surgical candidates — so as to avoid long-term use of PPI ^[3]. A successful fundoplication means PPI independence, eliminating decades of potential adverse effects and drug costs. PPI independence rate after fundoplication is ~60% ^[3].

Agent	Mechanism	Role in GERD
Prokinetics (metoclopramide, domperidone)	D₂-receptor antagonists → ↑ gastric motility, accelerate gastric emptying, ↑ LES tone	Limited role; used as adjunct in patients with associated gastroparesis or significant regurgitation. Side effects limit use (metoclopramide: extrapyramidal effects, tardive dyskinesia; domperidone: QT prolongation).
Baclofen	GABA-B agonist → ↓ transient LES relaxations (tLESRs)	Useful in refractory GERD with confirmed non-acid reflux (tLESRs still occur on PPI). Side effects: drowsiness, dizziness limit use.
Sucralfate	Forms a protective barrier over ulcerated mucosa (binds to positively charged proteins in ulcer base)	Limited role; occasionally used in pregnancy (not absorbed systemically)
Neuromodulators (low-dose TCA, SSRI)	↓ Visceral hypersensitivity via central pain modulation	For functional heartburn and reflux hypersensitivity (normal pH monitoring, no structural disease) — these are NOT true GERD

Step 3: Surgical Treatment

When medical therapy is insufficient or undesirable long-term, surgery addresses the root cause of GERD — the incompetent anti-reflux barrier — rather than just suppressing acid.

Indication	Rationale
Young and fit PPI-dependent patients	To avoid long-term PPI use ^[3]
Failure to respond to long-term medical maintenance therapy ^[6]	Very rare; if truly refractory, first consider alternative diagnosis ^[3]
Presented with severe regurgitation ^[6]	PPIs do not correct the reflux mechanism — regurgitation persists ^[13]. Surgery mechanically restores the anti-reflux barrier.
Barrett's oesophagus ^[6]	Controversial — surgery may reduce reflux exposure, but whether it prevents cancer progression is debated. Current consensus: consider if young, fit, and PPI-dependent with Barrett's.
GERD/complications unresponsive to medical treatment ^[3]	Very rare; important to confirm GERD objectively before surgery
Large hiatus hernia with GERD	Anatomical repair + anti-reflux procedure addresses both problems
Volume regurgitation causing aspiration	PPIs don't reduce volume of refluxate; surgery does

Contraindication: Aperistalsis → risk of dysphagia ^[3]. If manometry shows absent oesophageal peristalsis (e.g., scleroderma, end-stage achalasia), a tight fundoplication will trap food above it since there is no peristalsis to push food through → severe dysphagia.

Pre-op: oesophageal manometry, 24h ambulatory pH monitoring, OGD × biopsy ^[3].

Test	Purpose
Oesophageal manometry	Exclude achalasia; assess peristalsis (determines type of wrap); locate LES for pH probe
24h pH monitoring	Objective confirmation of pathological reflux — do not operate without this
OGD + biopsy	Assess mucosal status; grade oesophagitis; detect Barrett's; exclude malignancy

Principle: Wrap the gastric fundus around the distal oesophagus to create a valve effect that augments LES pressure. The name "fundoplication" = fundus + plication (folding).

Goals of fundoplication ^[3]:

Close the hiatal defect (cruroplasty — suture the diaphragmatic crura back together)
Restore the pressure around the LES and angle of His
Lengthen the intra-abdominal part of the oesophagus (pull the GOJ back below the diaphragm)

Types of Fundoplication:

Type	Wrap	Characteristics	Indication
Nissen	360° (total)	More durable anti-reflux effect, but more dysphagia ^[3]	Standard choice when peristalsis is normal
Toupet	Posterior 270° (partial)	Less dysphagia than Nissen; preferred in Chinese patients — less dysphagia ^[3]	Impaired peristalsis (but not absent); patient preference; HK practice often favours partial wraps
Dor / Watson	Anterior 90° or 180° (partial)	Least anti-reflux effect but least dysphagia	Used in Heller's myotomy for achalasia ^[3] (Heller-Dor procedure) — provides mild anti-reflux protection without compressing the myotomy site

Why is the partial wrap preferred in Chinese patients? Chinese patients tend to have smaller body habitus and narrower hiatus. A full 360° wrap in a smaller frame is more likely to cause significant post-operative dysphagia. Practically, partial (Toupet) fundoplication is preferred in Chinese — less dysphagia ^[3].

Complication	Mechanism	Management
Gas bloat syndrome (90%, especially Nissen)	The improved anti-reflux mechanism prevents belching and vomiting → gas trapped in stomach → bloating, inability to burp or vomit, excessive flatulence. Self-limiting in 4 weeks ^[3].	Reassurance; dietary advice (eat slowly, avoid carbonated drinks); resolves spontaneously
Dysphagia (50% early post-op, 10% long-term)	Wrap is too tight → mechanical obstruction of the oesophageal lumen ^[3]	Ix: Water-soluble contrast swallow ^[3]. Tx: Endoscopic bougie/balloon dilatation; if persistent, revise fundoplication ^[3]
Recurrence of reflux	Wrap is too loose → inadequate augmentation of LES pressure ^[3]	Redo surgery or long-term PPI
Surgical emphysema	Gas absorbed in mediastinum during laparoscopic dissection around the hiatus ^[3]	Usually self-limiting; monitor
Perforation → mediastinitis	Iatrogenic oesophageal or gastric perforation during dissection ^[3]	Urgent surgical repair
Slipped Nissen	Wrap slides down, GOJ retracts into chest ^[3] → wrap is no longer around the GOJ → dysphagia + reflux	Redo surgery

Efficacy: PPI independence rate ~60% ^[3]. This means ~40% of patients may still need some PPI use post-operatively — patients should be counselled about this.

Surgical Complications — Exam Favourites

The three most commonly asked complications of fundoplication are: (1) Gas bloat syndrome (inability to burp/vomit — very common, self-limiting), (2) Post-op dysphagia (too tight — investigate with water-soluble contrast swallow), and (3) Slipped Nissen (wrap slides down — recurrent reflux + dysphagia). Know the investigation and management for each.

These are newer, less invasive alternatives to surgery. Currently considered emerging treatment options ^[3]:

Procedure	Mechanism	Status
Radiofrequency ablation (RFA) of LES (Stretta procedure)	Induces LES hypertrophy via thermal energy delivery to the LES muscle → thickened, stronger LES ^[3]	Moderate evidence; reduces PPI use but less durable than surgery
Transoral incisionless fundoplication (TIF)	Targets EGJ — creates a partial fundoplication endoscopically using a device (EsophyX) introduced through the mouth ^[3]	Avoids abdominal incisions; suitable for small hiatus hernia; less durable than laparoscopic fundoplication
Magnetic sphincter augmentation (LINX device)	A ring of magnetic titanium beads placed laparoscopically around the LES; resting magnetic attraction keeps the LES closed, but swallowing force opens it	Growing evidence; good for moderate GERD; contraindicated in patients needing MRI; not yet widely available in HK

Step 4: Management of Specific Complications

Aspect	Detail
Pathophysiology	Chronic oesophagitis → transmural inflammation → fibrosis → luminal narrowing (usually distal oesophagus)
Presentation	Progressive solid-food dysphagia in a patient with longstanding GERD
Management	OGD with endoscopic dilatation (bougie or balloon) + long-term PPI to prevent recurrence. Multiple sessions may be needed. Always biopsy to exclude malignancy.

Dysplasia Status	Management
No dysplasia	High-dose PPI for life + endoscopic surveillance: OGD + biopsy Q3–5y (Q3y if ≥ 3 cm, Q5y if < 3 cm) ^[4]
Low-grade dysplasia	OGD at 6 months × 2, then Q1y if negative; or endoscopic treatment ^[4]
High-grade dysplasia	Intense surveillance (Q3 months); or endoscopic treatment (e.g., EMR/ESD/RFA) — advised ^[4]
Intramucosal carcinoma (T1a)	Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD) — oesophageal preservation
Submucosal invasion (T1b) or beyond	Oesophagectomy with lymph node dissection

Barrett's Surveillance — Know the Intervals

The exam loves these numbers. No dysplasia: Q3–5 years depending on segment length. LGD: confirm, then Q6 months × 2, then Q1 year OR treat endoscopically. HGD: Q3 months OR (preferably) endoscopic ablation/resection. Seattle protocol: biopsy every 1–2 cm in 4 quadrants ^[4].

Usually self-limiting and responds to PPI therapy
Rarely requires endoscopic haemostasis (unlike peptic ulcer bleeding)
IV PPI infusion (pantoprazole/esomeprazole 80 mg stat, then 8 mg/h for 72 hours) is indicated when significant ulcer bleeding is identified at endoscopy — the higher pH stabilises the clot since platelet function depends on normal pH ^[14]^[15]
For massive bleeding unresponsive to PPI: OGD with dual therapy (adrenaline injection + heater probe or clips) ^[14]^[15]

Type	Management
Sliding hernia (Type I) — Conservative	Weight loss, smoking cessation, reduce alcohol intake. Treat GERD: PPI ^[3]
Rolling/Paraesophageal (Type II–IV) — Surgical	Hernia repair + Nissen fundoplication. Indicated if symptomatic despite max medical treatment OR rolling type (increased risk of gastric volvulus) ^[3]
Emergency presentation (volvulus, strangulation, perforation)	NG tube decompression + emergency open/laparoscopic surgery ^[3]

Special Situations

First-line: Lifestyle modification + antacids/alginates (safe)
Second-line: Sucralfate (not absorbed; safe)
Third-line: H2RAs (famotidine — category B; generally considered safe)
PPIs: Omeprazole is category C but widely used when needed (benefits generally outweigh risks). Lansoprazole and esomeprazole have less safety data.
Avoid: Misoprostol (prostaglandin analogue — causes uterine contractions → contraindicated)

When symptoms persist despite double-dose PPI:

Confirm compliance and timing (30–60 min before meals)
Confirm the diagnosis — OGD + pH-impedance monitoring on PPI
Consider: functional heartburn, eosinophilic oesophagitis, bile reflux, achalasia
If confirmed reflux: baclofen (↓ tLESRs) or surgical referral
If functional heartburn: neuromodulators (low-dose TCA e.g., amitriptyline 10–25 mg nocte; or SSRI)

Feature	Medical (PPI)	Surgical (Fundoplication)
Target	Reduces acid pH	Restores anti-reflux barrier
Effect on reflux	Does NOT prevent reflux — only changes acidic to non-acidic ^[13]	Physically prevents reflux
Heartburn relief	Excellent	Excellent
Regurgitation relief	Poor — usually remains uncorrected ^[13]	Excellent
Barrett's regression	Uncertain	Uncertain (may reduce progression)
Duration	Lifelong medication	One-time procedure (if successful)
PPI independence	N/A	~60% ^[3]
Key risk	Long-term adverse effects	Post-op dysphagia, gas bloat, recurrence

High Yield Summary

Stepwise management of GERD:

Lifestyle modification — all patients: weight loss, bed head elevation, avoid late meals, low-fat diet, stop smoking/alcohol, avoid chocolate/coffee/spicy food, avoid tight clothing
Medical therapy — PPI is the mainstay (most effective); H2RA for mild disease; antacids/alginates for breakthrough
Surgery — laparoscopic fundoplication for PPI-dependent young/fit patients, refractory GERD, severe regurgitation, Barrett's

PPI key points:

Irreversibly inhibit H⁺/K⁺-ATPase proton pump (final common pathway)
Give 30–60 min before meals (except dexlansoprazole)
Change acidic reflux to non-acidic BUT do not prevent reflux itself
Step-down to lowest effective dose when possible

Surgical key points:

Pre-op triad: manometry + pH monitoring + OGD (mandatory)
Contraindication: aperistalsis
Nissen (360°) = most durable but more dysphagia; Toupet (270°) preferred in Chinese
Complications: gas bloat syndrome (90%, self-limiting), dysphagia (investigate with water-soluble contrast swallow), slipped Nissen, recurrence
PPI independence rate ~60%

Barrett's surveillance: No dysplasia Q3–5y; LGD Q6mo × 2 then Q1y or treat; HGD Q3mo or treat endoscopically. High-dose PPI for life.

Emerging: Stretta RFA (LES hypertrophy), TIF (transoral fundoplication), LINX (magnetic sphincter augmentation)

Active Recall - Management of GERD

References

^[3] Senior notes: maxim.md (GERD surgical treatment, Hiatal hernia sections) ^[4] Senior notes: maxim.md (Barrett's oesophagus section, p. 57) ^[6] Senior notes: felixlai.md (GERD diagnosis and case study, pp. 352–359) ^[13] Senior notes: felixlai.md (GERD medical and surgical treatment, pp. 355–357) ^[14] Senior notes: maxim.md (UGIB therapeutic endoscopy, OGD post-PPI infusion) ^[15] Lecture slides: GC 198. Profuse vomiting of fresh blood and in shock severe upper GI bleeding.pdf

Complications of GERD

GERD is not just about heartburn. If left inadequately treated (or in patients with severe, refractory disease), the chronic exposure of oesophageal squamous epithelium to acid, pepsin, and bile leads to a predictable cascade of tissue injury. Understanding this cascade from first principles is the key to understanding every complication:

Chronic acid/pepsin exposure → mucosal inflammation (oesophagitis) → ulceration → fibrosis (stricture) → metaplasia (Barrett's) → dysplasia → adenocarcinoma

The listed complications of GERD are ^[2]^[13]:

Reflux oesophagitis (erosive oesophagitis)
Oesophageal ulcers
Oesophageal stricture
Barrett's oesophagus
Oesophageal adenocarcinoma

Additionally, there are extra-oesophageal complications (respiratory, laryngeal, dental) and complications related to associated hiatus hernia.

Oesophagitis can develop into ulcer → stricture → Barrett's oesophagus (10%) → metaplasia → adenocarcinoma (7% of Barrett's) ^[3].

Feature	Detail
Definition	Visible mucosal breaks (erosions) in the distal oesophagus caused by chronic gastro-oesophageal reflux, detectable on OGD ^[2]
Prevalence	~20–40% of symptomatic GERD patients have erosive oesophagitis ^[6]; the majority (60–80%) have NERD
Pathophysiology	The oesophageal squamous epithelium has no mucus-bicarbonate barrier (unlike gastric mucosa). When the anti-reflux mechanism fails → acid (HCl) + activated pepsin contact the squamous cells → hydrogen ions penetrate the intercellular spaces → disrupt tight junctions → cell necrosis → visible mucosal breaks. Bile acids (if duodenogastric reflux is present) worsen damage by disrupting cell membranes and promoting inflammatory cytokine release.
Grading	LA classification A–D (covered in previous section). LA C/D = severe; more likely to develop complications.
Clinical features	Heartburn, odynophagia (if severe), sometimes occult GI bleeding → iron-deficiency anaemia
Management	PPI therapy (standard dose for LA A/B; high-dose for LA C/D) × 8 weeks → repeat OGD for LA C/D to confirm healing and exclude Barrett's ^[6]
Key point	Healing with PPIs is excellent (~80–90% at 8 weeks), but relapse rate is ~80% if PPI stopped in severe oesophagitis (LA C/D) — hence the need for maintenance therapy

Why does the oesophagus get damaged but the stomach doesn't? The gastric mucosa has a robust triple-layered defence: (1) surface mucus layer, (2) bicarbonate secretion into the mucus, (3) tight intercellular junctions and rapid epithelial turnover. The oesophageal squamous epithelium lacks all of these. It relies on the anti-reflux barrier to prevent acid contact altogether — when this barrier fails, the epithelium is essentially defenceless.

Feature	Detail
Definition	Deeper mucosal defects extending beyond the epithelium into the submucosa or muscularis, occurring in the setting of severe reflux oesophagitis ^[2]^[13]
Pathophysiology	Erosive oesophagitis (mucosal breaks) → if acid exposure continues → the inflammatory injury penetrates deeper → submucosal vessels are exposed → ulcer formation. Pepsin (activated at pH < 4) is particularly destructive — it digests tissue proteins once the epithelial barrier is breached.
Clinical features	Odynophagia (hallmark — acid directly contacts the raw ulcer base, stimulating exposed nociceptors), haematemesis/melaena (erosion into submucosal vessels), retrosternal pain
Complications of the ulcer itself	Bleeding (can be significant — chronic occult → IDA, or acute → haematemesis/melaena); perforation (rare); fistula formation (very rare)
Management	High-dose PPI to promote healing; endoscopic haemostasis if active bleeding; biopsy ulcer margins to exclude malignancy (Barrett's-associated adenocarcinoma can present as an ulcer)

Feature	Detail
Definition	Fibrous narrowing of the oesophageal lumen resulting from chronic transmural inflammation and scarring ^[2]^[13]
Pathophysiology	Chronic oesophagitis → repeated cycles of ulceration and healing → fibroblast activation → collagen deposition in the submucosa and muscularis → concentric luminal narrowing. Think of it like a scar contracture — every cycle of damage and repair lays down more scar tissue, progressively narrowing the lumen. The stricture is typically smooth, concentric, and in the distal oesophagus (where acid exposure is maximal).
Clinical features	Progressive solid-food dysphagia in a patient with longstanding GERD history. Dysphagia to solids only (not liquids) because the lumen is narrowed but not occluded — liquids can still pass. The patient often learns to chew meticulously and avoid fibrous foods. If very tight (< 13 mm lumen), even semi-solids cause obstruction.
Distinguishing from malignant stricture	Peptic stricture = smooth, symmetrical, gradual onset, long GERD history. Malignant stricture = irregular, asymmetrical, short history of progressive dysphagia + weight loss + anaemia. Always biopsy to exclude malignancy.
Management	(1) Endoscopic dilatation — bougie (e.g., Savary-Gilliard) or balloon dilatation via OGD. May need multiple sessions (progressive dilatation over weeks). (2) Long-term PPI — essential to reduce ongoing acid injury and prevent recurrence. (3) Biopsy — exclude malignancy and assess for Barrett's. Recurrence rate is significant if PPI is not maintained.

Stricture vs Cancer — An Exam Favourite

Any patient with GERD and new-onset dysphagia must have an OGD. A benign peptic stricture is diagnosed clinically (long GERD history, smooth stricture) and histologically (biopsies showing fibrosis without dysplasia). Never assume a stricture is benign without biopsy — adenocarcinoma arising from Barrett's can present as a stricture-like lesion.

This is the single most important complication of GERD from a cancer-prevention standpoint.

Feature	Detail
Definition	Intestinal metaplasia of oesophageal stratified squamous epithelium to columnar epithelium with mucus-secreting goblet cells, as an adaptation to long-term acid reflux ^[4]
Prevalence	Develops in ~10% of patients with chronic GERD ^[3]
Pathophysiology	Why does metaplasia occur? The squamous epithelium is repeatedly damaged by acid → stem cells in the basal layer receive chronic inflammatory signals (IL-1β, IL-6, NF-κB pathway) → instead of regenerating squamous cells, they differentiate into columnar (intestinal-type) epithelium that is more acid-resistant (has mucus-secreting goblet cells). This is an adaptive but maladaptive response — the tissue tolerates acid better, but the new columnar epithelium is genetically unstable and prone to accumulating mutations (p53 loss, p16 inactivation, chromosomal instability) → dysplasia → carcinoma.
Cancer risk	Risk of developing adenocarcinoma is 30–100× compared to the normal population ^[16]. Annual risk: ~0.5%/year ^[4]. ~7% of Barrett's patients develop adenocarcinoma ^[3].
Risk factors for Barrett's	Chronic GERD (> 5–10 years), male sex (M:F = 2:1), age > 50, Caucasian > Asian, obesity, smoking, hiatus hernia, family history
Protective factor	H. pylori infection is protective — H. pylori causes chronic gastritis → parietal cell atrophy → ↓ acid production → less acid reflux → less oesophageal damage ^[4]. This is the "African enigma" — high H. pylori prevalence in developing countries correlates with LOW Barrett's/adenocarcinoma rates.

Complications of Barrett's oesophagus itself ^[16]:

Oesophageal stricture (Barrett's-related)
Oesophageal ulceration (Barrett's ulcers — deeper, more refractory than simple reflux ulcers)
Oesophageal haemorrhage (from Barrett's ulcers)
Adenocarcinoma of the oesophagus

The dysplasia-carcinoma sequence:

Stage	Histology	Management	Rationale
Non-dysplastic Barrett's	Intestinal metaplasia, no cellular atypia	High-dose PPI for life + surveillance OGD Q3–5y ^[4]	Low annual cancer risk; surveillance detects progression early
Low-grade dysplasia (LGD)	Mild cellular atypia (nuclear enlargement, stratification, hyperchromasia) confined to crypts	OGD Q6mo × 2, then Q1y if negative; OR endoscopic treatment ^[4]	~0.5–1.3%/year progression to cancer; endoscopic treatment increasingly favoured
High-grade dysplasia (HGD)	Severe atypia, architectural distortion, but no invasion through basement membrane	Intense surveillance Q3mo; OR endoscopic treatment (EMR/ESD/RFA) — advised ^[4]	~6–19%/year progression to cancer; endoscopic ablation is now preferred over surveillance alone
Intramucosal carcinoma (T1a)	Invasion through basement membrane into lamina propria/muscularis mucosae but NOT submucosa	Endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD)	Low risk of lymph node metastasis (< 2%) → oesophageal preservation possible
Submucosal invasion (T1b)	Invasion into submucosa	Oesophagectomy with lymph node dissection	High risk of lymph node metastasis (~20–25%) — endoscopic resection alone is insufficient ^[1]

Surveillance methods ^[16]:

Chromoendoscopy (Lugol's iodine, narrow-band imaging/NBI)
High-resolution white light endoscopy
Seattle protocol: 4-quadrant biopsies every 1–2 cm along the Barrett's segment ^[4]

Barrett's — Key Numbers for Exams

10% of GERD patients develop Barrett's
0.5%/year risk of adenocarcinoma in Barrett's
30–100× increased cancer risk vs general population
Surveillance: No dysplasia Q3–5y, LGD Q6mo then Q1y, HGD Q3mo or treat
Prague C&M classification for endoscopic grading
Seattle protocol: 4-quadrant biopsy every 1–2 cm

Feature	Detail
Definition	Malignant neoplasm arising from the columnar epithelium of Barrett's oesophagus in the distal oesophagus/GOJ
Epidemiology	Rising incidence in Western countries (parallels obesity and GERD trends). In HK, SCC is still most common (90%) ^[1]^[16], but adenocarcinoma is increasing
Pathophysiology	Oesophageal adenocarcinoma mostly arises from a region of Barrett's metaplasia which is due to GERD ^[1]. The sequence: chronic GERD → Barrett's metaplasia → accumulation of genetic mutations (p53, p16, APC, Rb, DNA aneuploidy) → low-grade dysplasia → high-grade dysplasia → invasive adenocarcinoma
Risk factors	GERD, Barrett's oesophagus, obesity, smoking ^[1]^[16]
Clinical features	Painless progressive dysphagia (solids → liquids, typically when ≥ 75% luminal stenosis), weight loss, anaemia, odynophagia, GI bleeding ^[1]
Prognosis	Poor: > 50% have metastasis at presentation; 5-year survival is just 5–10% ^[16]
Management	Depends on staging — endoscopic resection (T1a), oesophagectomy with lymph node dissection (T1b+), neoadjuvant chemoRT for locally advanced disease, palliative stenting/RT for metastatic disease ^[1]

Why is the prognosis so poor? The oesophagus lacks a serosal layer — this means that tumour invasion into the adventitia encounters no fascial barrier, allowing early spread to mediastinal structures (trachea → tracheo-oesophageal fistula, aorta, pericardium). Additionally, the rich submucosal lymphatic plexus facilitates early lymph node metastasis. By the time dysphagia develops (requiring ≥ 75% luminal stenosis), the tumour is usually advanced.

These result from two mechanisms: (a) microaspiration of refluxate into the airway, and (b) vagal reflex from oesophageal acid stimulation causing bronchospasm/cough without aspiration.

Complication	Pathophysiology	Clinical Features
Aspiration pneumonia	Refluxate reaches the larynx/trachea → enters the lungs → chemical pneumonitis + secondary bacterial infection	Recurrent pneumonia (especially right lower lobe — gravitational preference), particularly nocturnal; chronic cough with sputum; fever
Posterior laryngitis / Laryngopharyngeal reflux (LPR)	Acid + pepsin contacts the laryngeal mucosa (posterior commissure, arytenoids, vocal processes) → inflammation. Laryngeal epithelium is far more sensitive to acid than oesophageal (damaged at pH < 5 vs pH < 2)	Hoarseness, voice fatigue, chronic throat clearing, globus sensation, sore throat. Laryngoscopy: posterior erythema, oedema, vocal cord granulomas, contact ulcers
Reflux-triggered asthma	Oesophago-bronchial vagal reflex: acid in distal oesophagus → vagal afferents → reflex bronchospasm. Also, microaspiration → direct airway inflammation and hyperreactivity	Wheezing, nocturnal cough, dyspnoea — worsened by meals, lying flat. GERD found in ~50–80% of asthmatics. Note: asthma drugs (theophylline, β-agonists) also ↓ LES tone → vicious cycle
Chronic cough	Same dual mechanism as asthma (vagal reflex + microaspiration)	Chronic non-productive cough, often worse at night/post-prandially. GERD is one of the "big three" causes of chronic cough (along with upper airway cough syndrome and asthma)
Dental erosions	Chronic acid in the oral cavity dissolves tooth enamel (demineralisation of hydroxyapatite: Ca₁₀(PO₄)₆(OH)₂ + H⁺ → Ca²⁺ + H₂PO₄⁻)	Erosion of lingual surfaces of upper incisors; sensitivity, discolouration. Often noticed by dentists before GI referral.
Otitis media / Sinusitis (paediatric)	Nasopharyngeal reflux → eustachian tube inflammation	Recurrent ear infections, nasal congestion (especially children)
Sleep disturbance	Nocturnal reflux → micro-arousals; bidirectional relationship with OSA (negative intrathoracic pressure promotes reflux)	Poor sleep quality, daytime somnolence, morning hoarseness

While not a direct complication of GERD per se, hiatus hernia and GERD are intimately related ^[3], and hernia-specific complications are important:

Complication	Type of Hernia	Pathophysiology	Clinical Presentation
Cameron lesions	Sliding (Type I)	Erosions or ulcers occurring in the sac of a hiatal hernia ^[10] — mechanical trauma from diaphragmatic impingement on the herniated stomach	Chronic occult GI bleeding → iron-deficiency anaemia. Often missed on OGD unless specifically looked for at the diaphragmatic impression.
Gastric volvulus	Rolling type (Type II/III) ^[3]	The freely mobile fundus rotates > 180° around the GOJ or along its long axis → closed-loop obstruction ± ischaemia	Borchardt's triad: (1) severe epigastric pain, (2) retching without vomiting, (3) inability to pass NG tube. Surgical emergency.
Strangulation / Incarceration	Rolling type (Type II/III/IV) ^[3]	Herniated stomach (or other organs in Type IV) becomes trapped in the hiatus → venous obstruction → oedema → arterial compromise → ischaemia → gangrene	Acute chest/epigastric pain, signs of obstruction, haemodynamic instability. Emergency surgery required.
Gastric perforation	Rolling type ^[3]	End result of strangulation/gangrene or volvulus	Peritonitis, septic shock. High mortality.
Oesophageal bleeding from oesophageal ulceration	All types ^[3]	Acid exposure from GERD + mechanical trauma at the hernia neck	Haematemesis/melaena; chronic → IDA

Emergency management of hiatus hernia complications: NG tube decompression + emergency surgery (laparotomy/laparoscopy) ^[3].

8. Complications of GERD Treatment

While not "complications of GERD" per se, these are frequently tested and clinically relevant:

(Covered in detail in Management section — brief recap)

Complication	Mechanism
Osteoporosis / fractures	↓ Calcium absorption
Hypomagnesaemia	Impaired intestinal Mg transport
C. difficile colitis	Loss of gastric acid barrier
Community-acquired pneumonia	↑ Bacterial burden in refluxate
Iron/B12 deficiency	Acid-dependent absorption impaired
Fundic gland polyps	Hypergastrinaemia → parietal cell hyperplasia
Rebound acid hypersecretion	Compensatory hypergastrinaemia on cessation

Complication	Details
Gas bloat syndrome (90%)	Inability to burp or vomit, flatus; self-limiting in 4 weeks ^[3]
Dysphagia (50% early, 10% long-term)	Wrap too tight. Ix: Water-soluble contrast swallow. Tx: balloon dilatation or revise ^[3]
Recurrence of reflux	Wrap too loose ^[3]
Slipped Nissen	Wrap slides down, GOJ retracts into chest ^[3]
Perforation → mediastinitis	Iatrogenic during dissection ^[3]
Surgical emphysema	Gas absorbed in mediastinum ^[3]

Stage	Complication	Key Feature	Management Principle
Stage 1	Reflux oesophagitis	Mucosal breaks (LA A–D)	PPI therapy
Stage 2	Oesophageal ulcers	Deeper erosion, odynophagia, bleeding	High-dose PPI; endoscopic haemostasis if bleeding
Stage 3	Peptic stricture	Progressive solid-food dysphagia	Endoscopic dilatation + long-term PPI
Stage 4	Barrett's oesophagus	Intestinal metaplasia with goblet cells	High-dose PPI for life + surveillance
Stage 5	Dysplasia (LGD → HGD)	Cellular atypia	Endoscopic ablation/resection
Stage 6	Adenocarcinoma	Invasive cancer	Staging → resection/chemoRT/palliation
Extra-oesophageal	Respiratory/laryngeal/dental	Aspiration, vagal reflex, acid erosion	Treat GERD + specific symptom management

High Yield Summary

Oesophageal complications of GERD (in order of progression):

Reflux oesophagitis — mucosal breaks; LA classification; heals with PPI
Oesophageal ulcers — deeper injury; odynophagia and bleeding
Peptic stricture — fibrosis from repeated ulceration/healing; progressive solid-food dysphagia; Rx: dilatation + PPI
Barrett's oesophagus — intestinal metaplasia; develops in ~10% of GERD; cancer risk 0.5%/year (30–100× general population); requires lifelong PPI + surveillance
Oesophageal adenocarcinoma — arises from Barrett's; poor prognosis (5-year survival 5–10%); > 50% metastatic at presentation

Extra-oesophageal complications: Aspiration pneumonia, posterior laryngitis/LPR, reflux-triggered asthma, chronic cough, dental erosions, sleep disturbance.

Hiatus hernia complications: Cameron lesions (occult bleeding), gastric volvulus (Borchardt's triad — emergency), strangulation, perforation.

Key cascade to remember: Oesophagitis → Ulcer → Stricture → Barrett's (10%) → Dysplasia → Adenocarcinoma (0.5%/year)

Barrett's surveillance numbers: No dysplasia Q3–5y; LGD Q6mo × 2 then Q1y; HGD Q3mo or treat. Always high-dose PPI for life.

Active Recall - Complications of GERD

References

^[1] Lecture slides: GC 189. I can't swallow oesophageal cancer.pdf ^[2] Senior notes: felixlai.md (GERD section, pp. 349–351) ^[3] Senior notes: maxim.md (GERD surgical treatment, Hiatal hernia sections) ^[4] Senior notes: maxim.md (Barrett's oesophagus section, p. 57) ^[6] Senior notes: felixlai.md (GERD diagnosis and case study, pp. 352–358) ^[10] Senior notes: felixlai.md (Upper GI bleeding differential, pp. 334–335) ^[13] Senior notes: felixlai.md (GERD complications section, p. 357) ^[16] Senior notes: felixlai.md (Barrett's oesophagus complications, pp. 368–369); maxim.md (CA oesophagus section, p. 60)

High Yield Summary

Definition: GERD = troublesome symptoms and/or complications from reflux of gastric contents (Montreal definition). GERD ≠ oesophagitis (most have NERD — normal endoscopy).

Pathophysiology: The dominant mechanism is transient LES relaxations (tLESRs), NOT permanent LES weakness. Hiatus hernia disrupts multiple anti-reflux mechanisms simultaneously.

Classification: NERD (60–70%) > Erosive oesophagitis > Extra-oesophageal disease. LA classification (A–D) grades erosive disease.

Clinical Features:

Typical: Heartburn + acid regurgitation (cardinal symptoms)
Atypical: Chronic cough, asthma, laryngitis, globus, non-cardiac chest pain
Alarm features (dysphagia, weight loss, anaemia, GI bleeding, age > 55 new onset) → urgent OGD

Complication Chain: GERD → Oesophagitis → Stricture → Barrett's (intestinal metaplasia) → Dysplasia → Adenocarcinoma (0.5%/year risk in Barrett's).

Barrett's: Columnar metaplasia with goblet cells replacing squamous epithelium. Prague C&M classification. H. pylori is protective.

HK Focus: SCC still most common oesophageal cancer in HK (90%), but adenocarcinoma (from GERD/Barrett's) is rising.

High Yield Summary

Core differential of GERD symptoms:

Coronary artery disease — most dangerous mimic; shared spinal afferents T1–T6; exclude if cardiac risk factors present
Peptic ulcer disease — overlapping epigastric pain; differentiate by meal relationship and OGD
Functional dyspepsia — diagnosis of exclusion; accounts for 60% of dyspepsia; no structural disease
Infective oesophagitis — immunocompromised; odynophagia dominates; Candida (most common), HSV, CMV
Pill oesophagitis — temporal relationship with medication; mid-oesophageal ulcers
Eosinophilic oesophagitis — young atopic males; food impaction; PPI-refractory; ≥ 15 eos/HPF
Achalasia — dysphagia for solids AND liquids, undigested food regurgitation; manometry diagnostic
Oesophageal malignancy — painless progressive dysphagia is cancer until proven otherwise

When to worry: Alarm features (dysphagia, weight loss, anaemia, GI bleeding, age > 55 new onset) → urgent OGD.

Key differentiating test: OGD for structural pathology; oesophageal manometry for motility disorders; 24h pH-impedance monitoring for equivocal cases.

High Yield Summary

Diagnostic criteria (Lyon Consensus 2022):

Conclusive GERD: LA Grade C/D oesophagitis, long-segment Barrett's, peptic stricture, or AET > 6%
LA Grade A is no longer conclusive (may be normal variant)
AET 4–6% is borderline

Four main diagnostic methods (can be used alone or in combination):

Symptom questionnaires (~80–90% accuracy)
PPI trial (1–4 weeks; therapeutic trial)
OGD (detects complications; normal in 60–80%)
24h pH monitoring (gold standard; AET > 6% diagnostic)

OGD indications: alarm features, age > 55 new onset, PPI-refractory, Barrett's screening, pre-operative

pH monitoring indications: doubtful diagnosis, pre-surgical planning, persistent symptoms despite PPI/surgery

Manometry indications: NOT for uncomplicated GERD; used to exclude motility disorders and pre-operatively (aperistalsis → contraindication to Nissen)

Pre-op triad: Manometry + pH monitoring + OGD (all mandatory before anti-reflux surgery)

Barrett's diagnosis requires TWO criteria: endoscopic documentation of columnar-lined oesophagus + histological confirmation of intestinal metaplasia with goblet cells

High Yield Summary

Stepwise management of GERD:

Lifestyle modification — all patients: weight loss, bed head elevation, avoid late meals, low-fat diet, stop smoking/alcohol, avoid chocolate/coffee/spicy food, avoid tight clothing
Medical therapy — PPI is the mainstay (most effective); H2RA for mild disease; antacids/alginates for breakthrough
Surgery — laparoscopic fundoplication for PPI-dependent young/fit patients, refractory GERD, severe regurgitation, Barrett's

PPI key points:

Irreversibly inhibit H⁺/K⁺-ATPase proton pump (final common pathway)
Give 30–60 min before meals (except dexlansoprazole)
Change acidic reflux to non-acidic BUT do not prevent reflux itself
Step-down to lowest effective dose when possible

Surgical key points:

Pre-op triad: manometry + pH monitoring + OGD (mandatory)
Contraindication: aperistalsis
Nissen (360°) = most durable but more dysphagia; Toupet (270°) preferred in Chinese
Complications: gas bloat syndrome (90%, self-limiting), dysphagia (investigate with water-soluble contrast swallow), slipped Nissen, recurrence
PPI independence rate ~60%

Barrett's surveillance: No dysplasia Q3–5y; LGD Q6mo × 2 then Q1y or treat; HGD Q3mo or treat endoscopically. High-dose PPI for life.

Emerging: Stretta RFA (LES hypertrophy), TIF (transoral fundoplication), LINX (magnetic sphincter augmentation)

High Yield Summary

Oesophageal complications of GERD (in order of progression):

Reflux oesophagitis — mucosal breaks; LA classification; heals with PPI
Oesophageal ulcers — deeper injury; odynophagia and bleeding
Peptic stricture — fibrosis from repeated ulceration/healing; progressive solid-food dysphagia; Rx: dilatation + PPI
Barrett's oesophagus — intestinal metaplasia; develops in ~10% of GERD; cancer risk 0.5%/year (30–100× general population); requires lifelong PPI + surveillance
Oesophageal adenocarcinoma — arises from Barrett's; poor prognosis (5-year survival 5–10%); > 50% metastatic at presentation

Extra-oesophageal complications: Aspiration pneumonia, posterior laryngitis/LPR, reflux-triggered asthma, chronic cough, dental erosions, sleep disturbance.

Hiatus hernia complications: Cameron lesions (occult bleeding), gastric volvulus (Borchardt's triad — emergency), strangulation, perforation.

Key cascade to remember: Oesophagitis → Ulcer → Stricture → Barrett's (10%) → Dysplasia → Adenocarcinoma (0.5%/year)

Barrett's surveillance numbers: No dysplasia Q3–5y; LGD Q6mo × 2 then Q1y; HGD Q3mo or treat. Always high-dose PPI for life.

Gerd

References

Gastroesophageal Reflux Disease (GERD)

Anatomy & Function of the Anti-Reflux Barrier

Etiology & Pathophysiology

A. Mechanisms of Increased Reflux

B. Mechanisms of Impaired Clearance

Classification

Clinical Features

A. Symptoms

Active Recall - GERD: Definition, Epidemiology, Pathophysiology & Clinical Features

Differential Diagnosis of GERD

Active Recall - Differential Diagnosis of GERD

References

Diagnostic Criteria & Diagnostic Algorithm for GERD

Investigation Modalities — Detailed Breakdown

Active Recall - Diagnosis of GERD

References

Management of GERD

Step 2: Medical Treatment

Step 3: Surgical Treatment

Step 4: Management of Specific Complications

Special Situations

Active Recall - Management of GERD

References

Complications of GERD

8. Complications of GERD Treatment

Active Recall - Complications of GERD

References

On this page

Gerd

Definition

Epidemiology

Risk Factors

Anatomy & Function of the Anti-Reflux Barrier

1. Lower Oesophageal Sphincter (LES)

2. Diaphragmatic Crura (External Sphincter)

3. Angle of His (Cardiac Angle)

4. Intra-abdominal Oesophageal Segment

5. Mucosal Rosette (Gastric Mucosal Folds)

6. Oesophageal Clearance Mechanisms

Etiology & Pathophysiology

A. Mechanisms of Increased Reflux

1. Abnormalities of the LES [2]

2. Hiatus Hernia [2][3]

3. Increased Intra-Abdominal Pressure [2]

4. Increased Gastric Volume / Acid

B. Mechanisms of Impaired Clearance

1. Defective Oesophageal Peristalsis [2]

2. Reduced Saliva Production

3. Supine Position / Nocturnal Reflux

C. Impaired Mucosal Defence

D. The GERD Spectrum — From Symptoms to Complications

Classification

1. Clinical Classification of GERD [2]

2. Los Angeles (LA) Classification of Erosive Oesophagitis [2]

3. Relationship Between GERD, Hiatus Hernia, and Oesophagitis [3]

Clinical Features

A. Symptoms

Typical (Oesophageal) Symptoms

Atypical / Extra-Oesophageal Symptoms

Alarm Symptoms ("Red Flags") — Must Trigger Urgent Investigation

B. Signs

Barrett's Oesophagus — As It Relates to GERD

Relationship Between GERD, Hiatus Hernia, and Oesophageal Cancer

Neonatal/Paediatric GERD — Special Considerations [5]

Summary of Pathophysiological Mechanisms

Active Recall - GERD: Definition, Epidemiology, Pathophysiology & Clinical Features

References

Organising the Differential by Presenting Symptom

A. Differential Diagnosis of Heartburn / Retrosternal Pain

B. Differential Diagnosis of Dysphagia (When GERD Presents with Dysphagia)

C. Differential Diagnosis of Extra-Oesophageal Symptoms

D. Differential Diagnosis When GERD Causes Upper GI Bleeding

Diagnostic Decision Tree

Key Differentiating Points — Summary Table

Active Recall - Differential Diagnosis of GERD

Why Is Diagnosing GERD Not Straightforward?

Diagnostic Criteria — The 2022 Lyon Consensus (Updated from 2018)

The Four Main Diagnostic Methods

Investigation Modalities — Detailed Breakdown

1. Symptom Questionnaires (Clinical History)

2. Proton Pump Inhibitor (PPI) Trial

3. Upper Endoscopy — Oesophago-Gastro-Duodenoscopy (OGD)

4. Ambulatory 24-Hour Oesophageal pH Monitoring

5. Oesophageal Manometry (High-Resolution Manometry, HRM)

6. Barium Swallow

7. Additional/Adjunctive Investigations

Integrated Diagnostic Algorithm

Differentiating NERD, Functional Heartburn, and Reflux Hypersensitivity

Pre-Operative Investigations Before Anti-Reflux Surgery

Investigation Summary Table

Active Recall - Diagnosis of GERD

Management Philosophy — First Principles

Overall Management Algorithm

Step 1: Lifestyle Modification (ALL Patients)

Step 2: Medical Treatment

A. Antacids

B. H₂-Receptor Antagonists (H2RAs)

C. Proton Pump Inhibitors (PPIs) — The Mainstay of GERD Treatment

D. Adjunctive Medical Agents

Step 3: Surgical Treatment

Indications for Anti-Reflux Surgery [3][6][13]

Pre-Operative Workup (Mandatory) [3]

Laparoscopic Fundoplication — The Standard Surgical Approach [3]

Complications of Fundoplication [3]

Endoscopic Anti-Reflux Procedures (Emerging) [3]

Step 4: Management of Specific Complications

A. Peptic Stricture

B. Barrett's Oesophagus — Surveillance and Treatment [4]