Oesophageal conditions Flashcards
1
Q
Describe the anatomy of the oesophagus
A
Muscular tube composed of two layers:
- an outer longitudinal layer
- an inner circular muscle layer
Connects the pharynx to the stomach
Striated (voluntary) muscle in upper portion gradually changes to smooth muscle in lower part to become continuous with muscle layer of the stomach
2
Q
Define achalasia
A
An oesophageal motor disorder of unknown aetiology, characterised by oesophageal aperistalsis and insufficient lower oesophageal sphincter relaxation in response to swallowing.
The normal muscular activity of the oesophagus is disturbed (absent or uncoordinated)
3
Q
What is the cause of achalasia?
A
Inflammatory destruction of inhibitory nitrinergic neurons (ganglion cells) in the oesophageal myenteric (Auerbach) plexus
Results in loss of peristalsis and incomplete lower oesophageal sphincter relaxation.
The exact cause of this inflammatory process is unknown, but possible triggers include infection, autoimmunity, and genetic factors.
4
Q
Summarise the epidemiology of achalasia
A
- Achalasia may occur at any age; however, incidence increases with age.
- The median age at diagnosis is 53 years.
- Achalasia affects both sexes equally.
- Annual incidence 1/100,000
5
Q
Recognise the presenting symptoms of achalasia
A
Achalasia cannot be diagnosed on the basis of history alone.
Symptom onset is insidious, during which time many patients may adapt to significant symptoms by slowly altering their diet or eating habits.
- The key symptom is dysphagia to solids and liquids.
- liquids is common only in oesophageal motor disorders (not obstructions)
- May be intermittent
- Retrosternal pressure/pain- may be relieved by drinking cold water.
- Regurgitation- when in recumbant position. different to GORD- food retained in oesophagous tastes bland not sour
- gradual weight loss- different to malignancy rapid WL
- heartburn- secondary to fermentation of food retained in the oesophagus
- slow eating
- coughing/choking while recumbent- 2/2 regurgitation of retained food and liquids
- recurrent chest infections- aspiration of retained food
- sensation of a lump in the throat (globus)
- hiccups- 2/2 delayed transit of food in the oesophagus and diaphragmatic irritation.
6
Q
Recognise the signs of achalasia on physical examination
A
Posturing to aid swallowing- to manage dysphagia, patients may adopt particular postures, such as:
- arching the neck and shoulders
- raising the arms, standing
- sitting up straight during the meal
- walking around after a meal.
May show signs of complications:
- Aspiration pneumonia
- Malnutrition
7
Q
Identify appropriate investigations for achalasia
A
-
Upper gastrointestinal endoscopy
- low sensitivity for the diagnosis of early achalasia
- essential 1st line to exclude malignancy- causes pseudoachalasia
-
Barium swallow
- loss of peristalsis and delayed oesophageal emptying
- dilated oesophagus that tapers smoothly to a beak-like narrowing at the gastro-oesophageal junction
- advanced disease the dilated oesophagus may be tortuous and sigmoid-shaped with diverticula.
-
High-resolution oesophageal manometry- assesses pressure at LOS. May show:
- Elevated resting LOS pressure (> 45 mm Hg)
- Incomplete LOS relaxation
- Absence of peristalsis in the smooth muscle portion of the oesophagus
-
CXR
- Appearance may suggest achalasia, but test has a low sensitivity and is not diagnostic.
-
Bloods:
- may do serology for antibodies against T. cruzi if CHAGAS DISEASE is a possibility (and blood film may detect parasites)
- presence of myenteric plexus antibodies
8
Q
Algrove syndrome
A
The triple-A (Allgrove) syndrome, characterised by:
- achalasia
- alacrima
- adrenocorticotrophic hormone-resistant adrenal insufficiency
Autosomal recessive disorder that has been mapped to chromosome 12.
9
Q
Define GORD
A
Symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond, into the oral cavity (including larynx) or lung
10
Q
Explain the risk factors of GORD
A
- family history of heartburn or GORD
- older age
- hiatus hernia- reducing competence of the gastro-oesophageal junction and inhibiting clearance of oesophageal acid post-reflux
- obesity/pregnancy- intr-abdominal portion of oesophagus uses diaphragm as a sphincter
- diet: LOS pressure reduced by smoking, alcohol and coffee and some drugs (calcium-channel blockers, nitrates, beta-blockers, progesterone).
11
Q
State some mechanisms that usually prevent reflux
A
- Lower oesophageal sphincter
- Acute angle of junction (angle of His)
- Mucosal rosette
- Sling fibres around the cardia
- Crural fibres of the diaphragm
12
Q
Explain the aetiology of disease of GORD
A
- LOS regulates food passage from the oesophagus to the stomach
- Contains both intrinsic smooth muscle and skeletal muscle.
- Episodes of transient LOS relaxation are a normal phenomenon, but they occur more frequently in GORD, causing reflux of gastric contents into the oesophagus.
- Transient LOS relaxation is more common after meals and is stimulated by fat in the duodenum.
13
Q
Summarise the epidemiology of GORD
A
common- affects between 10% and 30% of people in developed countries.
14
Q
Recognise the presenting symptoms of GORD
A
- Retrosternal burning pain, radiating to epigastrium, jaw and arms.(Oesophageal pain is often confused with cardiac pain.)
- Aggravated by:
- Lying supine
- Bending
- Large meals
- Drinking alcohol
- Pain is relieved by antacids
- Waterbrash (regurgitation of an excessive accumulation of saliva from the lower part of the oesophagus often with some acid material from the stomach)
- Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze +/- pneumonia (rare)
- Dysphagia - caused by formation of peptic stricture after long-standing reflux
15
Q
Recognise the signs of GORD on physical examination
A
Usually NORMAL- can have halitosis, enamel erosion
Occasionally -
- epigastric tenderness
- wheeze on chest auscultation
- dysphonia
16
Q
Identify appropriate investigations for GORD and interpret the results
A
Diagnosis is clinical, supported by testing when required. Heartburn and regurgitation are the most reliable symptoms
- If suspected: PPI Trial
- Further tests are indicated if symptoms do not improve with therapeutic 8-week trial of a PPI
- or if patient has alarm symptoms
If GORD persists:
-
Oesophagogastroduodenoscopy (OGD) and biopsy
- may show oesophagitis (erosion, ulcerations, strictures) or Barrett’s oesophagus
- can exclude malignancy – must exclude for all >55 years
- Barium swallow and meal: sliding hiatus hernia, oesophageal ulcer,stricture.
- Ambulatory 24-hour pH monitoring: assess the degree of reflux.
-
Oesophageal manometry
- evaluates oesophageal contractions and lower oesophageal sphincter function.
- It may detect subtle presentations of oesophageal motility disorders such as achalasia or diffuse oesophageal spasm.
17
Q
State a general management plan for GORD
A
Lose weight, avoid smoking, coffee, alcohol, chocolate, tomatoes and citrus juices.
Avoid tight garments, stooping and large meals.
Elevate head of bed. Avoid of late-night eating if nocturnal symptoms are present.
18
Q
State a medical management plan for GORD
A
Control acid secretion
- H2 receptor antagonists (e.g. ranitidine)
- PPIs (e.g. omeprazole, esomeprazole).
- Antacids (sodium bicarbonate) may be effective in controlling symptoms in mild disease.
- Provides rapid symptom relief and healing in oesophagitis (>80% of patients).
Minimize effects of reflux
- Alginates to protect oesophagus
Improve LOS tone and promote gastric emptying.
- prokinetic agents
- (e.g. bethanechol, metoclopramide, domperidone)
19
Q
State a surgical/interventional management plan for GORD
A
Endoscopy:
- Annual endoscopic surveillance - looking for Barrett’s Oesophagus
- May be necessary for stricture dilation or stenting
Surgery:
- Antireflux surgery if refractory to medical treatment
- eg Nissen Fundoplication: fundus of the stomach is wrapped around the lower oesophagus - helps reduce the risk of hiatus hernia and reduce reflux
- gives excellent results.
- Indicated in approximately 20% of patients with GORD:
- failed optimum medical treatment
- complications of reflux (benign stricture, Barrrett’s oesophagus)
- severe oesophagitis on endoscopy
- ‘large volume’ reflux.
20
Q
Identify the possible complications of GORD
A
- Oesophageal ulceration
- Peptic stricture
- Anaemia
- Barrett’s oesophagus
- Oesophageal adenocarcinoma
- Associated with asthma and chronic laryngitis
21
Q
Summarise the prognosis of patients with GORD
A
- 50% respond to lifestyle measures alone
- In patients that require drug therapy, withdrawal is often associated with relapse- however, there are risks associated with long-term use of these drugs
- 20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
- Oesophageal adenocarcinoma may be a serious though rare complication of GORD.
22
Q
Define Barrets oesophagus
A
A metaplastic change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia (columnar epithelium)
SQUAMOUS → COLUMNAR
23
Q
Explain the aetiology of Barrett’s oesophagus
A
The primary aetiological factor involved in Barrett’s oesophagus is gastro-oesophageal reflux.
However, there is evidence that combined acid and bile reflux are the primary causative agents.
24
Q
Explain the pathophysiology of Barrett’s oesophagus
A
Prolonged exposure of the normal squamous epithelium to refluxate of GORD leads to mucosal inflammation and erosion
This leads to replacement of the mucosa with metaplastic columnar stem cell
25
State the risk factors for Barrets oesophagus
Mix of environmental and genetic factors
* **acid/bile reflux or GORD**
* **increased age**
* **white ethnicity**
* **male sex**
* family history of Barrett's oesophagus or oesophageal adenocarcinoma
* obesity
* smoking
26
Why is Barrets oesophagus potentially life-threatening?
Intestinal cell **metaplasia** caused by Barrets could develop to **low-grade dysplasia**
This is a PREMALIGNANT condition - **high grade displasia** can then develop to **adenocarcinoma**
27
Summarise the epidemiology of Barrett’s oesophagus
* **twice as common in males**
* Prevalence **0.5-2%**
* The frequency of oesophageal adenocarcinoma in men has **quadrupled in the past few years.**
* This may be linked to an **increase in incidence of GORD**
* **3-5%** of people with GORD will develop Barrett's oesophagus
28
Recognise the presenting symptoms of Barrett’s oesophagus
Common symptoms:
* **Heartburn**
* **Regurgitation**
*Patients are likely to experience symptoms of GORD:*
* Nausea
* Water-brash (sour taste in the mouth)
* Bloating
* Belching
* Burning pain when swallowing (dysphagia)
*Atypical symptoms:*
* chest pain
* laryngitis
* cough
* dyspnoea or wheezing- reflux-induced asthma or reactive airway disease
* history of aspiration pneumonia
29
Identify appropriate investigations for Barrett’s oesophagus
1. **Gastroscopy (OGD - Oesophago-gastro-duodenoscopy)**
* ****See abnormal epithelium proximal to the gastro-oesophageal junction.
* Areas of ulceration, narrowing (stricture), and nodularity should be targeted for biopsy because they are more likely to contain areas of dysplasia and adenocarcinoma
2. **Barium oesophagogram**
* May be considered as the initial test in patients with dysphagia in order to evaluate for a mass lesion or stricture before endoscopy.
* Cannot diagnose Barrett's oesophagus.
* Can document other signs of GORD or a hiatal hernia, which are risk factors for Barrett's oesophagus.
30
Generate a management plan for Barrett’s oesophagus
PPI → radiofrequency ablation → endoscopic mucosal resection → oesophagectomy
**_non-dysplastic Barrett's oesophagus_**
* 1st line – **PPI + surveillance**
* Adjunct – radiofrequency ablation
* 2nd line – anti-reflux surgery plus surveillance
**_low-grade (non-nodular)_** **_dysplasia_**
* 1st line – **radiofrequency ablation**
* +/- **endoscopic mucosal resection** (nodular regions)
**_high-grade dysplasia_**
* 1st line – **radiofrequency ablation** +/- **endoscopic mucosal resection**
* Plus – **PPI**
* 2nd line – **oesophagectomy-** definitive treatment option (20-40% will have early adenocarcinoma)
31
Summarise the prognosis for patients with Barrett’s oesophagus
Barrett's oesophagus carries a **30-60x higher risk** of oesophageal adenocarcinoma than the general population
**5-10%** of those with Barrett's oesophagus will develop adenocarcinoma over 10-20 years
Generally, **adenocarcinomas** discovered while screening for Barrett's oesophagus are early-stage lesions and have **good prognosis (5-year survival \>85%).**
32
Define oesophageal cancer and state the 2 main types
Malignant tumour arising in the oesophagus. There are TWO major histological types:
* Squamous cell carcinoma
* Adenocarcinoma
33
Explain the risk factors for oesophageal cancer (adenocarcinoma and SCC)
**_common risk factors_**
* **male** sex (M:F 7:1)
* low **socioeconomic status**
* a diet **low in fresh fruit and vegetables**
* **achalasia** (10-fold risk increase)
**_SCC_**
* **tobacco** use
* **excessive alcohol** intake
* **family history** of oesophageal, stomach, oral, or pharyngeal cancer
* **non-white** race (squamous cell carcinoma)
* **high-temperature** beverages and foods (squamous cell carcinoma)
* **drinking maté** (squamous cell carcinoma)
**_Adenocarcinoma_**
* **GORD and Barrett's oesophagus**
* **hiatus hernia-** 2-6-fold increase due to GORD
* obesity
34
Summarise the epidemiology of oesophageal cancer
Incidence varies widely
M:F = 7:1
average rate for Western countries of 3 per 100,000
* **Squamous has decreased** (decreased tabacco/alcohol consumption) in the west
* **adenocarinoma has increased** (increased incidence of barretts oesophagus) in the west
* Squamous more common in **developing** countries
* Adenocarcinoma more common in **western world**
35
Recognise the presenting symptoms of oesophageal cancer
Often asymptomatic until locally advanced disease- patients present late
_Common symptoms:_
* **dysphagia**
* progressive- initially worse for solids
* most common PC- only occurs after there is an obstruction \>2/3rds of the lumen
* **odynophagia (painful swallowing)**
* one of the signs of a locally advanced tumour with possible invasion of the airway or mediastinum.
* **weight loss**
* often overlooked as broad differentials when not paired with previous 2 PCs
_Others:_
* **Regurgitation**
* **Cough**- may indicate the presence of an oesophagotracheal/bronchial fistula resulting from local tumour invasion
* **Hiccups**- phrenic nerve involvement
* **Choking** after food
* Voice **hoarseness**
* **Fatigue** (due to iron deficiency anaemia)
36
Recognise the signs of oesophageal cancer on physical examination
May be no signs
Metastatic disease may cause:
* Supraclavicular lymphadenopathy
* Hepatomegaly
* Hoarseness
* Signs of bronchopulmonary involvement
37
Identify appropriate investigations for oesophageal cancer
_1st investigations_
1. **oesophagogastroduodenoscopy (OGD) with biopsy**
2. **comprehensive metabolic profile-**
* ****advanced cases with near or complete oesophageal obstruction
* Patients may become severely volume-depleted → hypokalaemia, elevated creatinine and serum urea/nitrogen
_2nd investigations- cancer staging_
* **Staging - CT chest and abdomen**
* indicates size of primary tumour, local invasion, and presence or absence of metastases
* **FDG-PET scan**
* see hyperactivity (hot spot) at primary tumour site and locoregional disease; may also show activity in lungs, liver, or bones suggestive of metastases
* done before EUS to avoid unnecessary testing in patients with metastatic disease.
* **Endoscopic ultrasound (EUS) ± FNA**
* standard pre-treatment test.
* It can identify all the histological layers of the oesophagus and thereby confirm the T-stage with 90% accuracy.
* ****indicates extent of local invasion and presence or absence of spread to lymph nodes
* Other - **bronchoscopy, lung function tests and ABG**
38
Define Mallory-Weiss tear
**Tear/laceration** often along the **right border** of, or near, the **gastro-oesophageal junction**, as a result of **violent** retching, vomiting, coughing, or straining.
39
Explain the aetiology of Mallory-Weiss tear
Factors such as:
* **coughing, retching, vomiting, straining, hiccups**
* **closed-chest pressure** or **cardiopulmonary resuscitation**
* acute **abdominal blunt trauma**
* **alcohol**
* **medications** (aspirin or other non-steroidal anti-inflammatory drugs [NSAIDs])
* **chemotherapeutic agents**
* **oesophageal instrumentation** have been associated with MWT..
40
Explain the risk factors for Mallory-Weiss tear
* **condition predisposing to retching, vomiting, and/or straining**
* GI obstruction
* gastroentiritis
* hyperemesis gravidarium
* bulimia nervosa
* **chronic cough**
* ****whooping cough, bronchitis, bronchiectasis, emphysema, COPD, or lung cancer
* **hiatal hernia**
* ****precipitating factor found to be present in 40-100% of patients with MWT
* retching during endoscopy or other **instrumentation**
* eg NG tube, ERCP
* significant **alcohol use**
* ****reported association in 40-80% of patients
* **previous instrumentation**
41
Summarise the epidemiology of Mallory-Weiss tears
* Most common between the ages of **30-50 years**
* **More common in men** than in women in a ratio of 3:1
* Represents **3-15%** of cases of upper GI bleeding- quite rare
* Recurrent bleeding is common
42
Recognise the presenting symptoms of Mallory-Weiss tears
The classic presentation of MWT consists of a **small and self-limited episode of _haematemesis_**
This varies from **flecks of blood** mixed with gastric contents and/or **mucus**, and blackish or 'coffee grounds', to a **bright-red** bloody emesis
**After** a bout of retching, vomiting, coughing, or any other factors that **increase pressure at the level of the GOJ**
_Other less common presentations:_
* dizziness, syncope
* dysphagia
* odynophagia
* melaena
* haematochezia
* retrosternal pain with interscapular radiation
* midepigastric abdominal pain.
43
Recognise the signs of Mallory-Weiss tears on physical examination
There are no specific physical signs in patients with MWT
44
Identify appropriate investigations for Mallory-Weiss tears
_Initial laboratory investigation- bloods_
* **Hb, Hct, platelets (plt), U+Es**
* evaluate severity of bleeding
* check for anaemia
* **Cross matching/G+S**
* ****those with anaemia at presentation or ongoing bleeding.
* **PT and aPTT, INR**
* in all patients on anticoagulants or those suspected of coagulopathy.
* **LFTs**
* rule out liver disease which may predispose a patient to oesophageal varices
_Other initial investigations_
* **Oesophagogastroduodenoscopy**
* diagnostic test of choice
* should be performed in all patients with upper GI bleed **_after_** stabilisation
* CXR
* Laceration or tear is not visible under conventional radiography
* May be an initial test diagnosis in patients with suspected oesophageal perforation.
45
Generate a management plan for Mallory-Weiss tears
80-90% of the time, the bleeding from a Mallory-Weiss tear will stop on its own
If bleeding is continuous:
1. **urgent evaluation + monitoring**
* phytomenadione (Vit K) IV
* crystalloid fluid replacement
* Blood transfusion (packed red blood cells) for ongoing bleeding/Hb \<80 g/L
* Prolonged PT/INR should be corrected with FFP
2. **Endoscopy**
* Haemoclip placement
* thermocoagulation therapy
* endoscopic band ligation (EBL)
3. **Surgery**
* should be reserved for situations where endoscopic haemostasis of bleeding has failed
* laproscopic/angiotherapy
46
Identify + describe a rare but serious complication of Mallory-Weiss tears
**Boerhaave's perforation**
Oesophageal perforation carries a high mortality secondary to rapidly developing mediastinitis and sepsis.
*Signs and symptoms:*
* **Retrosternal or epigastric pain with interscapular radiation** immediately following an episode of vomiting.
* dyspnoea (due to pleural effusion)
* cyanosis
* fever + sweating
47
Summarise the prognosis for patients with Mallory-Weiss tears
For most patients, bleeding is self-limited, and will have stopped by the time of endoscopy.
**Prognosis is excellent in patients without associated disease or complications.**
Re-bleeding occurs in about **8-15% of patients, usually within the first 24 hours**
*High-risk factors for re-bleeding:*
* old age (aged \>65 years)
* haematemesis and/or haematochezia at presentation
* haemodynamic instability/shock
* alcoholism
* aspirin/NSAID use
* comorbidities (anaemia, chronic liver disease, CAD, COPD, renal failure)
48
Define hiatus hernia
**Protrusion of intra-abdominal contents** (usually stomach) through an enlarged **oesophageal hiatus of the diaphragm**.
49
Explain the 3 causes of hiatus hernia
1. **Congenital**
2. **Traumatic**
3. **Non-traumatic**
* Sliding (80%)
* Paraoesophageal (rolling, 20%)
* Mixed
50
Explain the classification of non-traumatic hiatus hernia
**Type I**
* **Sliding hiatus hernia**
* Protrusion of the gastro-oesophageal junction followed by the body of the stomach
**Type II**
* **Pure para-oesophageal hernia or rolling hiatus hernia**
* Herniation of the fundus or body of the stomach or both into the chest
* maintenance of the gastro-oesophageal junction below the diaphragm.
**Type III**
* **Mixed or combined para-oesophageal hernia**
* Combination of types I and II.
**Type IV**
* **Giant hiatus hernia**
* herniation of one or more other organs, such as colon, small bowel, omentum, and spleen.
51
What symptom can discerne between sliding and rolling hiatus hernias?
**Acid reflux**
**_Sliding (80%) -_**
* the hernia moves in and out of the chest.
* Acid reflux often happens as the **lower oesophageal sphincter becomes less competent.**
**_Paraoesophageal (rolling, 20%) -_**
* **Gastro-oesophageal junction remains intact** so acid reflux uncommon
52
state some risk factors for hiatus hernia
key risk factor = **obesity**
Other risk factors:
things that increase *intra-abdominal pressure:*
* **ascites**
* **pregancy**
* **chronic cough**
* **pulmonary disease**
things that *weaken oesophageal hiatus:*
* chronic **oesophagitis**
* **structural abnormalities** of the oesophageal hiatus or the phreno-oesophageal ligaments
* previous gastro-oesophageal **surgery**
53
Summarise the epidemiology of hiatus hernia
* **Common in WESTERN countries**
* Clinical estimates of the prevalence of hiatus hernia in western populations range up to **50%**
* **70% = \> 70 yrs**
* Particularly common in older obese women
* **50% have symptomatic GORD**
54
Recognise the presenting symptoms of hiatus hernia
Most are **ASYMPTOMATIC**
**GORD symptoms + painless regurgitation** = hiatus hernia
* regurgitation esp when lying down
Patients may present with symptoms of GORD
* **Heartburn**
* **Waterbrash**
NO correlation between the size of the hernia and severity of the symptoms
55
Identify appropriate investigations for hiatus hernia
_Bloods_
* **FBC** - check for iron deficiency anaemia
_Radiology_
* **CXR (first line)** - gastric air bubble may be seen above the diaphragm
* **Barium swallow** – aka upper gastrointestinal series- best diagnostic test
_Endoscopy_
* **Upper GI endoscopy** visualises the mucosa to detect oesophagitis but cannot reliably exclude a hiatus hernia
56
Generate a MEDICAL management plan for hiatus hernia
Medical:
* **PPIs**
* **Lifestyle changes-**
* losing weight
* elevating the head of the bed
* avoiding:
* large meals
* meals just before bedtime
* alcohol
* acidic foods.
57
Explain the SURGICAL management of hiatus hernia- in whih patients is surgery indicated?
**Nissen Fundoplication**
Indicated in the minority, including patients with:
* **complications of GORD** despite aggressive medical treatment
* **pulmonary complications** (e.g. aspiration pneumonia)
* **Rolling hiatus hernia** - prophylactically, even if asymptomatic, because of the long-term risk of strangulation and mediastinitis.
Gastric resection is reserved for patients with irreversible ischaemia or necrosis.
58
Briefly explain a loose Nissen fundoplication
The **stomach is pulled down through the oesophageal hiatus**
Part of the stomach is wrapped (360 degrees) around the oesophagus
Makes a new sphincter and reduces the likelihood of herniation
59
Identify possible complication of hiatus hernia
**Oesophageal**
* Intermittent bleeding
* Oesophagitis
* Erosions
* Barrett's oesophagus
* Oesophageal strictures
**Non-Oesophageal**
* Incarceration of hiatus hernia (only with paraoesophageal hernias)
* This can lead to strangulation and perforation
60
Summarise the prognosis for patients with hiatus hernia
* Generally GOOD
* Sliding hernias have a better prognosis than rolling hernias
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