Oesophageal Disorders Flashcards
What is the anatomy of the oesophagus?
Muscular tube connecting pharynx to stomach
Measures 18 – 26cm in adult human
Lined by squamous epithelium, guarded by sphincters both ends
Upper 2/3 is straited, affords voluntary control
Distal 1/3 smooth muscle
What is the upper oesophageal sphincter?
Functions to prevent regurgitation into oral cavity and larynx and restricts airflow into the oesophagus during inspiration.
Composed of striated muscles
What is the lower oesophageal sphincter?
Maintains a high-pressure zone between stomach and oesophagus (barrier to reflux).
Physiological sphincter.
Composed of smooth muscles.
Normally located within the diaphragmatic hiatus with 2/3 in the abdominal cavity and 1/3 in the thoracic cavity. Can be displaced proximally by hiatal hernia.
What is involved in swallowing?
Oropharynx, oesophagus and the nervous system
What is the first phase of swallowing?
Oral/Buccal Phase (Voluntary)
- Food is chewed (mastication) and mixed with saliva to form a bolus.
- The tongue pushes the bolus against the hard palate and then moves it posteriorly toward the oropharynx.
- Upper oesophageal sphincter opens.
- This phase is under voluntary control (cranial nerves V, VII, and XII).
What is the second phase of swallowing?
Pharyngeal Phase (Involuntary, Reflexive):
- The soft palate elevates (via CN IX & X) to prevent food from entering the nasal cavity.
- The larynx elevates, and the epiglottis closes over the trachea, preventing aspiration.
- The upper oesophageal sphincter relaxes to allow the bolus to enter the oesophagus.
- This phase is mediated by the swallowing centre in the medulla and involves CN IX, X, and XI.
What is the third phase of swallowing?
Oesophageal Phase (Involuntary):
- Oesophagus distends, causing a contraction proximal to distal. Propagating sequence.
- The bolus moves down the oesophagus via peristalsis (coordinated contraction of circular and longitudinal muscles):
-Two types of peristalsis in the oesophagus (primary and secondary).
-Primary peristalsis: initiated in the pharynx by a swallow. These waves are slow moving and sweep the entire length of the oesophagus.
-Secondary peristalsis: initiated by oesophageal distension by food. These waves are important to remove all the food from the oesophagus if it has not been totally cleared by primary peristalsis. - The lower oesophageal sphincter (LES) relaxes to allow food into the stomach and then contracts to prevent reflux.
- Controlled by the vagus nerve (CN X) and the enteric nervous system.
What are some of the disorders of oesophageal Motility?
Hypermobility / acute diffuse esophageal spasm
Hypomotility
Sphincter dysfunction/ achalasia
GORD
Hiatus hernia
Oesophageal rupture (Mallory Weiss syndrome)
Oesophageal cancer
What is the aetiology of hyper motility/acute diffuse oesophageal spasm?
The cause of acute diffuse oesophageal spasm is not known, and the condition is rare, affecting 1 in 100 000 people.
What is hyper motility/acute diffuse oesophageal spasm?
is a disorder of the esophagus characterized by uncoordinated, excessive, and painful contractions of the esophageal muscles. It falls under the category of esophageal motility disorders, affecting the normal movement of food and liquids from the mouth to the stomach.
What are the key features of DES?
Uncoordinated Contractions – Unlike normal peristalsis, the contractions in DES occur randomly and do not effectively push food down.
Hypercontractility – The esophageal muscles contract too forcefully, leading to pain and difficulty swallowing (dysphagia).
Intermittent Symptoms – The spasms may come and go, and they often worsen with stress, very hot or cold foods, or carbonated drinks.
Chest Pain – Can mimic heart pain (angina) and may be mistaken for a heart attack.
Regurgitation – Food or liquid may come back up into the throat without nausea.
What are the possible causes/triggers of DES?
- Nerve dysfunction affecting the esophageal muscles.
- Acid reflux or gastroesophageal reflux disease (GERD).
- Anxiety or stress.
- Extreme temperature foods and beverages.
How is DES/hypermotility investigated?
- Esophageal manometry – Measures muscle contractions in the esophagus.
High resolution oesophageal manometry shows exaggerated oesophageal contractions - Barium swallow X-ray – Identifies abnormal movement.
- Endoscopy – Rules out other conditions like strictures or cancer.
What are the treatment options for Hypermotility/DES?
Medications:
Nitrates and calcium Chanel blockers to reduce smooth muscle contractions
Balloon dilatation:
Considered for symptom relief
Surgical:
Long oesophageal myotomy (cutting muscle) may be needed for severe cases
What is the aetiology of hypo motility?
Primary Cause:Systemic sclerosis (CREST syndrome)
Pathophysiology:
1. Muscle layer is replaced by fibrous tissue
2. Leads to oesophageal dysmotility
What are the associated features of hypo-motility?
- Weak or Absent Peristalsis – The esophagus does not contract effectively, causing food to move slowly or incompletely to the stomach.
- Dysphagia (Difficulty Swallowing) – More noticeable with solid foods, but can also affect liquids in severe cases.
- Regurgitation – Food or liquids may come back up due to poor clearance.
- Heartburn and Reflux – Weak contractions contribute to gastroesophageal reflux disease (GERD) because the lower esophageal sphincter (LES) may also be weak, allowing stomach acid to flow back up.
- Aspiration Risk – In severe cases, food or liquid may enter the airways, leading to coughing or pneumonia.
- Loss of facial mobility
- Microvascular symptoms e.g digital ischemia, Raynaud’s phenomenon
What is oesophageal hypo motility?
Esophageal hypomotility refers to weak or ineffective muscle contractions in the esophagus, leading to difficulty in moving food and liquids from the mouth to the stomach. This condition is often associated with disorders that affect esophageal motility, such as ineffective esophageal motility (IEM) or scleroderma-associated esophageal dysfunction.
How does hypo motility cause microvascular symptoms?
Weakened peristalsis means food and stomach acid remain in the esophagus longer.
Prolonged acid exposure leads to chronic inflammation and damage to the esophageal lining.
Inflammation triggers microvascular dysfunction, leading to poor blood flow, ischemia (lack of oxygen), and delayed healing.
This can result in mucosal ulcerations, fibrosis, and strictures over time.
What is CREST syndrome?
It is the primary cause of hypo motility. CREST syndrome is a subtype of systemic sclerosis (scleroderma), an autoimmune connective tissue disorder that affects the skin, blood vessels, and internal organs. CREST is an acronym representing five key symptoms:
C – Calcinosis
R – Raynaud’s Phenomenon
E – Esophageal Dysmotility
S – Sclerodactyly
T – Telangiectasia
What are the key symptoms of CREST syndrome?
C – Calcinosis
Calcium deposits form under the skin, leading to painful nodules.
Often seen in fingers, elbows, and knees.
R – Raynaud’s Phenomenon
Episodes of reduced blood flow to the fingers and toes, triggered by cold or stress.
Causes color changes: white (ischemia) → blue (deoxygenation) → red (reperfusion).
E – Esophageal Dysmotility
Weak or absent peristalsis in the esophagus, leading to difficulty swallowing (dysphagia), acid reflux, and heartburn.
Related to esophageal hypomotility and microvascular dysfunction, leading to poor circulation and fibrosis.
S – Sclerodactyly
Thickening and tightening of the skin on the fingers and hands.
Can cause joint stiffness and reduced hand function.
T – Telangiectasia
Small, dilated blood vessels visible on the skin, especially on the face and hands.
Can cause cosmetic concerns and minor bleeding.
What is the investigation for hypo motility according to NICE?
- Initial Assessment: Perform a thorough history and physical examination to evaluate symptoms and identify potential alarm features (e.g., weight loss, anemia).
- First-Line Investigation: Conduct an upper endoscopy to rule out structural or mucosal causes of dysphagia.
- If Endoscopy is Non-Diagnostic: Proceed with esophageal manometry to assess for motility disorders.
- Adjunctive Testing: Consider a barium swallow study, especially if anatomical abnormalities are suspected or if manometry is inconclusive.
Contrast radiology shows diminished peristalsis and this can be confirmed by manometry.
What is the treatment for hypo motility?
The treatment of hypomotility initially involves the treatment of associated GORD.
Smooth muscle relaxants can provide relief from pain and dysphagia
Second line treatments include botulinum toxin injection and/or balloon dilatation
Surgery is rarely indicated
What is Sphincter dysfunction/achalasia?
Cause:Mostly unknown; in South America, linked toTrypanosoma cruziinfection (Chagas disease).
Nerve Degeneration – Damage to the esophageal nerves that control muscle function.
Autoimmune Response – The immune system mistakenly attacks the nerve cells of the esophagus.
Pathophysiology: Failure of lower oesophageal sphincter (LOS) to relax
Food boluses getpartially retainedin the oesophagus
Effect:Impaired oesophageal emptying and dysphagia
What are the pathological changes of Sphincter dysfunction/achalasia?
- Dilatation and muscular hypertrophy above the lower oesophageal sphincter
- Loss of ganglion cells on histology
- Long standing cases can lead to oesophageal elongation, mucosal inflammation an increased oesophageal cancer risk from food stasis
What are the symptoms and signs of progression of sphincter dysfunction?
- Progressive Dysphagia – Initially no frank dysphagia, but slowed eating ( left behind at meals). Difficulty swallowing both solids and liquids. Progresses to obvious dysphagia, retrosternal discomfort, regurgitation and weight loss
- Regurgitation – Food and liquid may come back up, increasing aspiration risk.
- Chest Pain & Discomfort – Due to food retention and spasms.
- Weight Loss & Malnutrition – Caused by difficulty eating.
Nocturnal Coughing & 5.Aspiration – Can lead to pneumonia if food enters the airways.
When these symptoms are reported later in life they must be distinguished from oesophageal cancer.
What are the things to consider when taking a history in reported dysphagia?
- presence of symptom when not swallowing
- Is the difficulty with solids/liquids or both?
- Exact location of symptom
- duration and progression of symptom
- presence of regurgitation between meals
-presence of reflux symptoms - PMH
- Drug history
- social history
What are the investigations of Oesophageal sphincter dysfunction/ achalasia?
- Endoscopy is essential, in older patients, show a secondary cause such as infiltration of the distal oesophagus by malignant disease
- Contrast study confirms delay at the lower spinchter and give a characteristic ‘rats tail’ appearance
- Manometry shows incomplete relaxation of the lower sphincter in response to a swallow.
What is the management of sphincter dysfunction?
Medical treatment with muscle relaxants is usually unrewarding. The three effective methods for achalasia are:
Balloon/ pneumatic dilatation
- Leads to resolution of symptoms in 80%
- May have to be repeated
- carries a small risk of oesophageal perforation.
Longitudinal myotomy of the gastro-oesophageal junction (known to surgeons as the Heller’s cardiomyotomy)
-involves making a lengthwise incision through the muscle layers of the lower esophagus and upper stomach
- open surgery or laparoscope or thoracoscope
-surgeons generally combine myotomy with an anti-reflux procedure because of the increased risk of GORD after the myotomy.
-surgical intervention leads to symptoms relief in 85% of patients.
Endoscopic injection of Botulinum toxin into the oesophageal wall:
- Paralyse the LES
- effective but lasts only for a few months
- repeated injections are possible and this strategy is and effective management plan for those unsuitable for surgery.
What is Barett’s oesophagus?
Barrett’s esophagus is a condition where the normal squamous lining of the esophagus is replaced by intestinal-type columnar cells
What is GORD?
Gastro-Oesophageal Reflux Disease (GORD) is a chronic condition where stomach acid and digestive enzymes flow back into the oesophagus, causing irritation and inflammation. This occurs due to weakness or dysfunction of the lower oesophageal sphincter (LES), which normally prevents acid reflux. However, reflux is particularly a symptom of abnormalities at the diaphragmatic hiatus even though GORD occurs in association with many oesophageal conditions.
What are the common symptoms of GORD?
Heartburn – Burning sensation in the chest, worse after eating or lying down.
Regurgitation – Sour or bitter taste due to acid rising into the throat or mouth.
Dysphagia (Difficulty Swallowing) – Due to oesophageal irritation or narrowing.
What are the pathophysiological features of GORD?
If either acid or strongly alkaline secretions reach the lower oesophagus, the lower oesophageal mucosa becomes inflamed.
Although in most patients this is seen at oesophagoscopy as superficial oesophagitis, two complications may result from long-term inflammation:
1. Stricture – an inflammatory reaction in the mucosa and submucosa and can develop into a fibrous narrowing.
2. Metaplastic change – this leads to the development of gastric-type columnar epithelium in the lower oesophagus known asBarrett’s oesophagus, which is a premalignant lesion.
- patients with Barrett’s oesophagus must have regular surveillance of the lower oesophagus to assess for malignant transformation.
What are the two types of GORD?
1.GORD with concomitant hiatus hernia
2.GORD with normal anatomy
What are the 3 types of hiatus hernia?
Hiatal Hernia – The stomach moves up into the chest, weakening the LES.
1.Type I (Sliding Hiatus Hernia):GOJ movesabove the diaphragminto the chest.
2. Type II (Paraoesophageal Hiatus Hernia):GOJ remainsin the abdomen, but part of the stomach herniates into the chest.
3. Type III (Mixed Hiatus Hernia):Combination ofType I and II, where both the GOJ and part of the stomach move into the chest.
What is the aetiology of GORD with concomitant hiatus hernia/sliding Hernia?
The proximal stomach ascends into the chest through an enlarged diaphragmatic opening, carrying a cuff of peritoneum.
The acute gastro-oesophageal angle is reduced, leading to increased risk of reflux.
Reflux occurs even if the intrinsic lower oesophageal sphincter remains normal
What are the risk factors for the development of hiatus hernias?
obesity
increase in abdominal contents (pregnancy)
ageing
male gender
What are the clinical features of GORD with concomitant hiatus hernia?
Reflux, heartburn, and occasional lower-left chest pain, often occurring shortly after eating.
Rule outcardiac originof the pain.
Vague indigestion: Rarely caused by sliding hernia and requires further clinical evaluation and investigation for other potential causes.
What are the investigations for GORD concomitant hiatus hernia?
- Patients with the recent onset of symptoms, particularly if they are elderly : investigate for possible oesophagogastric cancer.
- Barium contrast studies: Historically used to diagnose hiatus hernia.
- Endoscopy:
- Now the preferred investigation method. Allows visualisation of theoesophagogastric junction(though identification may be challenging).
- Assesses the severity ofoesophagitis.
- Enablesbiopsyfor tissue diagnosis if needed.
What is the management of GORD with concomitant hiatus hernia?
Lifestyle:
Weight loss: Especially for obese patients.
Elevate head of the bed: Reduces nocturnal reflux.
Medications:
Alginate-containing antacids: Reduce stomach liquid volume, decreasing reflux.
H2-receptor antagonists: Examples include cimetidine and ranitidine.
Proton pump inhibitors (PPIs): Examples include omeprazole and lansoprazole.
Next steps if medical management fails:
Consideroperative interventionfor symptom control or if the patient prefers to avoid long-term medication.
What are the complications of untreated GORD with concomitant hiatus hernia?
Oesophagitis – Chronic inflammation of the oesophagus.
Barrett’s Oesophagus – Precancerous changes in the oesophageal lining due to long-term acid exposure.
Oesophageal Strictures – Narrowing of the oesophagus due to scarring, leading to difficulty swallowing.
Aspiration Pneumonia – Acid reflux can enter the lungs, causing respiratory issues.
What is the surgical steps for GORD with concomitant hiatus hernia?
Usually performed laparoscopically known as Nissen’s fundoplication.
Surgical steps:
1. Reduction of herniated stomach: Pull stomach back below the diaphragm.
2. Removal of peritoneal Sac: Remove circumferential sac around the hernia.
3. Re-establish Gastro-oesophageal angle: Restore normal angle to prevent reflux.
4. Suturing Crura: Close intercrural space by suturing the crura behind the oesophagus.
Fundolipication:
Wrap Stomach’s fundus around terminal oesophagus
Increases intra abdominal pressure to compress the oesophagus, preventing reflux
What are the complications post-surgery?
One complication of such a procedure may occasionally be the inability to belch and, in consequence, bloating – a sensation of unrelieved fullness of the stomach.
Some patients experience postoperative dysphagia, which is usually transient.
However, the outcome is usually good
The reported success rate with Nissen’s fundoplication is 80–90% in patients with GORD.
What is the aetiology of GORD with normal anatomy?
Many patients have symptoms of GORD without any demonstrable anatomical abnormality at endoscopy or manometry.
In some obesity is a factor
Others may have hyperchlorhydria with or without a demonstrable peptic ulcer.
In the majority, a definite cause is not identified.
Features of heartburn and dyspepsia are universal, with regurgitation of gastric contents in some.
What is the investigation of GORD with normal anatomy?
Many patients are probably treated symptomatically in general practice without investigation.
However, those with troublesome features should have a barium swallow and/or endoscopy.
What is the medical management of GORD with normal anatomy?
Medical management is often sufficient.
For those with oesophagitis, which is unresponsive to treatment (rare) and for patients who are not keen on long-term acid suppression therapy, an anti-reflux operation, such as Nissen’s fundoplication should be considered.
What is Oesophageal Rupture and Mucosal Tear (Mallory-Weiss Syndrome)?
Oesophageal rupture (also known as Boerhaave syndrome) is a life-threatening condition where there is a full-thickness tear or perforation in the wall of the oesophagus. This tear allows the contents of the oesophagus, including food, stomach acid, and digestive enzymes, to spill into the chest cavity, potentially causing severe infections (like mediastinitis) and shock.
Mallory-Weiss syndrome refers to a tear in the mucosal lining of the oesophagus near the gastro-oesophageal junction (GOJ), often caused by forceful vomiting or retching. Unlike oesophageal rupture, the tear is typically superficial and does not involve the full thickness of the oesophageal wall.
What is the aetiology of Oesophageal Rupture and Mucosal Tear (Mallory-Weiss Syndrome)?
- may not take place if vomiting is artificially induced, or the individual is confused – usually from excessive consumption of alcohol.
- In such circumstances, intragastric pressure forces stomach contents into the distal oesophagus, dilating it.
- The oesophagus may rupture with emptying of stomach contents into the left pleural cavity.
- Because the relatively elastic muscle in the oesophageal wall has a greater capacity for stretch than does the folded mucosa and submucosa, quite often only these are split to produce a longitudinal mucosal tear at the oesophagogastric junction(Mallory–Weiss syndrome).
- These tears are usually managed conservatively once identified.
What is the pathophysiology of an Oesophageal Rupture?
Traumatic injury to the oesophagus, in response to a variety of insults is a serious event with potentially devastating consequences.
After Perforation:
Negative intrathoracic pressure causes air, food, and fluids (if stomach is full) to be drawn into the mediastinum and pleural cavity.
Consequences:
1. Chemical pleuromediastinitis develops initially.
2. Progresses to bacterial mediastinitis.
3. Can lead to septic shock and multiorgan failure if untreated.
Immediate and appropriate treatment is crucial to prevent severe complications.
What are 4 categories of Oesophageal rupture?
1.Iatrogenic
2.Traumatic
3.Spontaneous (Boerhaave’s syndrome)
4.Tumour
What are the clinical features of Oesophageal Rupture?
- The patient will have had an episode of forceful vomiting, which may be recalled
- Vomiting may also have been induced either in a glutton or in someone who is mentally disturbed with a history of excessive eating but with the paradoxical desire not to gain weight (bulimia).
- There will be sharp left-sided pleuritic pain. This is known as Boerhaave’s syndrome and named after Herman Boerhaave, the 18th century physician who first described spontaneous oesophageal rupture.
- Machler’s triad: vomiting or retching (90–100%), chest pain (90%) and subcutaneous emphysema (38%) on examination. Classic triad is unusual as patients may also present with other respiratory or epigastric symptoms.
What are the physical findings of Oesophageal rupture?
- The effect of gastric content within the chest is to rapidly produce signs of severe sepsis with fever and circulatory disturbance.
- A left pleural effusion is present as usually the left posterolateral wall of the lower third of the oesophagus is perforated.
- The course is downhill with all the features of systemic inflammatory response syndrome.
- Occasionally, however, the rupture is localized and the patient is less ill with localized pleural signs and features of sepsis, which are less severe.
What are the symptoms of Mallory Weiss syndrome?
Vomiting blood (hematemesis) – This is often the most prominent symptom.
Chest pain – A dull or burning sensation, sometimes mimicking a heart attack.
Abdominal pain – Often from the intense vomiting or straining that caused the tear.
Lightheadedness or dizziness – Due to blood loss.
What is the management of Oesophageal rupture?
-Detailed history of the presenting episode and past medical history to ascertain fitness for a major surgery should be taken.
-The key aspects of management are early resuscitation, early drainage, antibiotics, aggressive organ support and response to secondary sepsis.
-Parenteral or enteral (jejunostomy) nutrition is used until healing is assured, although patient mortality from oesophageal rupture remains high.
-Non-operative management is feasible in patients with small leaks when the mediastinal and pleural contamination is at a minimum. These patients need careful monitoring with nutritional support in a high-dependency setting.
- surgical management
What is the surgical management of oesophageal Ruptures?
Key Factors:Time since presentation, mediastinal/pleural contamination, patient condition.
Primary Repair:Simple closure + drainage; best within 24 hours; high leak risk.
Repair & Reinforcement:Uses intercostal muscle, pleura, omentum; still high leak risk.
T-Tube Repair:Large bore T-tube placed in esophageal tear for controlled fistula; useful in late/early presentation; wide bore drains in mediastinum, pleural cavities, abdomen.
Resection:Used for strictures; high morbidity in delayed reconstruction.
What are the Two main types of oesophageal cancer?
Squamous Cell Carcinoma (SCC)andAdenocarcinoma (AC).
SCC: More common in the Far East (Japan, China, South Africa).
AC: More common in the West, rising incidence, especially in the UK.
What is the aetiology of squamous cell carcinoma?
High correlation withcigarette and alcohol consumption.
Diet: High nitrosamines (from food preservatives), low vitamins A & B3, iron deficiency.
Achalasia(poor oesophageal clearance) may increase cancer risk.
Geographical variationlinked to environmental and social factors
What is the aetiology of Adenocarcinoma?
Barrett’s oesophagus: Columnar metaplasia from long-standingGORDis a key risk factor.
Incidence of AC has overtaken SCC in the UK (2:1 ratio).
Risk factors: Dysplastic changes, length of Barrett’s mucosa, and history of reflux.
What are the pathological features of oesophageal cancer?
Combination ofnarrowingandulceration.
Spread throughdirect invasioninto nearby structures (trachea, pericardium, chest wall).
Lymph nodeinvolvement (mediastinal, stomach area).
Distant metastases in theliver,lung, andbrain.
What are the clinical symptoms of oesophageal cancer?
Early disease: No symptoms or mild feeling of something stuck.
Later stages: Progressive dysphagia, weight loss (10-15% in 4–6 weeks).
Pain from tumour penetration,productive cough, andhoarseness(recurrent laryngeal nerve involvement).
What are the clinical signs of oesophageal cancer?
Weight loss in clinical exam
Palpable lymphadenopathy ( especially in supraclavicular region).
Signs of liver metastasis: hepatomegaly, jaundice, ascites.
What are the investigations of Oesophageal cancer?
Endoscopy: Gold standard for diagnosis, allows biopsy and cytology.
Endoscopic Ultrasound (EUS): Staging and lymph node involvement.
CT scan: Detects distant metastases and assesses tumor size.
PET-CT: Identifies metastases not seen on CT, crucial for treatment decisions.
Staging laparoscopy: In some cases, for advanced tumors.
What are the screening programs for oesophageal cancer?
Screening programs for oesophageal cancer in the UK are a topic of ongoing research and development, particularly as the incidence of adenocarcinoma (AC) has risen in recent years, largely due to Barrett’s oesophagus (BO) as a result of chronic gastro-oesophageal reflux disease (GORD).
What is the main focus of oesophageal cancer screening in the UK?
The main focus of oesophageal cancer screening in the UK is onBarrett’s oesophagus (BO), a condition where the normal squamous epithelium of the oesophagus is replaced by columnar epithelium, which predisposes patients to adenocarcinoma. The key population targeted for surveillance are those withlong-standing GORDand other risk factors for Barrett’s.
Endoscopic surveillanceis performed to detect early malignant changes.
This includesupper GI endoscopy to assess for signs of dysplasia (abnormal cell growth).
If dysplasia is found,biopsyand further follow-up are recommended.
For those with confirmed Barrett’s oesophagus, the surveillance may be doneevery 2-3 years, depending on the severity of the dysplasia.
What do NHS guidelines suggest endoscopic surveillance for patients with GORD?
NHS guidelinessuggest endoscopic surveillance for patients with GORD who also have additional risk factors, such asmale gender,age over 50, andlonger duration of reflux.
What are the oesophageal motor disorders?
Oesophageal motor disorders are a group of conditions characterised byabnormal motility of the oesophagus.
This can lead to dysphagia, chest pain, regurgitation. The disorders range from failure of relaxation (achalasia) to excessive contractions (hypertensive peristalsis).
What are the three main oesophageal motor disorders?
Diffuse oesophageal spasm
Ineffective oesophageal Motility
Achalasia
What is Achalasia?
Loss of inhibitory neurons in the myenteric plexus →failure of LOS relaxation and absent peristalsis
Clinical features are dysphagia, regurgitation and chest pain and weight loss
Diagnosed with Barium swallow “bird beak appearance”. Manometry(absent peristalsis, high LOS pressure), Endoscopy (to exclude malignancy)
Managed with pneumatic dilation and botox
What is diffuse oesophageal spasm (DOS)?
Pathophysiology:
Motility disorder characterised by uncoordinated, non-peristaltic contractions of the oesophagus, leading to intermittent dysphagia and retrosternal chest pain due to abnormal neural control of 0esophageal smooth muscle.
Clinical features: Intermittent dysphagia to solids and liquids, retrosternal chest pain that mimics angina, and occasional regurgitation, often triggered by hot or cold foods.
Diagnosed using oesophageal manometry, which shows simultaneous, uncoordinated contractions with normal lower oesophageal sphincter (LOS) relaxation, and can be supported by barium swallow (“corkscrew oesophagus”) or oesophagogastroduodenoscopy (OGD) to rule out structural causes.
Managed by Calcium channel blockers (e.g., diltiazem) or nitrates to relax smooth muscle, proton pump inhibitors (if reflux is present), botulinum toxin injections, and in refractory cases, surgical myotomy or peroral endoscopic myotomy (POEM).
What is ineffective Oesophageal Motility (IOM)?
Characterized by weak or absent peristaltic contractions in the distal oesophagus, leading to impaired bolus transit due to dysfunction of oesophageal smooth muscle and abnormal vagal or enteric nervous system control.
Mild, intermittent dysphagia to solids and liquids, sensation of food sticking in the chest, and sometimes regurgitation or heartburn, often associated with gastroesophageal reflux disease (GORD).
Diagnosed by Oesophageal manometry, which shows low-amplitude or failed peristaltic contractions in ≥50% of swallows and may be supported by barium swallow (showing delayed bolus transit) or (OGD) to rule out structural causes.
Managed by focusing on treating underlying causes such as GERD with proton pump inhibitors (PPIs), dietary modifications (small, frequent meals, avoiding triggers), prokinetic agents in select cases, and supportive measures like swallowing therapy if symptoms persist.
