Oesophagogastric Flashcards
What malignancy is H.Pylori responsible for increasing the risk of developing?
MALT (Mucosa Associated Lymphoid Tissue) Lymphoma of the stomach through T cell activation, epigenetic changes and and H-Pylori-regulated miRNA expression.
Describe the anatomical layers of the oesophagus.
- Mucosa (stratified squamous epithelium)
- Submucosa
- Muscularis propria inner circular and outer longitudinal
- upper 1/3 striated
- lower 2/3 smooth
NO SEROSA
Describe the anatomy of the esophagus.
Layers:
Mucosa (squamous epithelium), submucosa, muscularis propria (upper 1/3rd striated, lower 2/3rds smooth) NO serosa.
Length:
~25cm beginning ~15cm from incisors at cessation of pharynx to ~40cm from incisors just under the diaphragm where it becomes stomach.
Narrowed by:
- Upper Oesophageal sphincter (narrowest)
- Aortic arch
- Left mainstem bronchus
- Diaphragm
Other areas of interest:
- Killian triangle; Superior/Lateral: Inferior Constrictors
Inferior: Cricopharyngeus
Site of Zenker’s Diverticulum
- Upper oesophageal sphincter; created by the cricopharyngeus muscle
(most common site of iatrogenic perforation and foreign body.Innervated by RLN. prevents swallowing air. contracted at rest. - Lower oesophageal sphincter;
not a true sphincter. is created by inner circular muscle layer, innervated by the vagus nerve and relaxes with swallowing or gastric distension.
Blood supply:
Arterial:
-Cervical by inferior thyroid artery
- Thoracic by bronchial arteries and vessels directly from the aorta
- Abdominal by Left gastric artery and inferior phrenic artery.
Venous drainage by azygous and hemiazygous veins.
Lymphatics:
Superior = upper 2/3rd
- cervical into deep cervical lymphatics
- thoracic into paraoesophageal LNs and mediastinal LNs.
Inferior = lower 1/3rd
- abdominal into gastric and cardiac and coeliac LNs and into thoracic duct via cisterna chyli.
Describe the physiology of swallowing.
- Oral phase
- mastication
- trough formation
- bolus movement posteriorly
- voluntary control - Pharyngeal phase
- tongue blocks oral cavity to prevent retrograde movement of bolus, the soft palate closes the nasopharynx, the vocal cords close and the larynx moves up with epiglottis flipping over to close the opening to trachea. The cricopharyngeus muscle/UOS opens
- bolus passes pharynx
- reflex initiated by food stimulating tactile receptors in oropharynx. - Peristalsis and relaxation
What are the normal manometry pressures for the upper and lower oesophageal sphincters?
Upper:
Resting
50-70mmHg
Swallowing 15mmHg
Lower:
Resting
10-20mmHg
Swallowing
0mmHg
What are the typical vs atypical symptoms of gastro-oesophageal reflux disease?
Typical:
- burning pain 30-60min post meal (pyrosis)
- worse when supine
- acid brash
- epigastric pain
Atypical:
- cough
- odynophagia (painful swallowing)
- water brash (increased saliva production mixed with gastric acid)
- globus sensation
- aspiration
- hoarse voice
- wheezing
What are some complications of GORD?
Oesophageal:
- Esophagitis
- Barretts
- Oesophageal stricture
Extra-oesophageal:
- Chronic cough
- Asthma (Increased Vagal Tone, Bronchial Reactivity & Microaspiration)
- Laryngotracheal stenosis
- Chronic laryngitis
- Dental erosisons
What diagnostic tests are used in GORD and what information do they provide?
pH Probe
First Test to Diagnose (But Not Mandatory)
DeMeester Score
Components:
Percent Total Time pH < 4
Percent Upright Time pH < 4
Percent Supine Time pH < 4
Number of Reflux Episodes Total
Number of Reflux Episode > 5 min
Longest Reflux Episode
Score > 14.72 Indicates Reflux
Upper Endoscopy
Not Required for GERD Diagnosis
Evaluates Hiatal Hernia, Strictures, Esophagitis, Metaplasia & Malignancy
Manometry
To Rule Out Underlying Motility Disorder
Indications:
If Upper Endoscopy Normal
Required If Planning Surgery
What are the best predictors of success with fundoplication?
- Typical Symptoms
Resolve in 90% of Patients > Atypical Symptoms Resolve in 60-70% of Patients - Symptoms Improved on PPI
- High Oesophageal pH
Describe indications for fundoplication and contraindications
What is a Zenkers diverticulum?
What oral contrast is used when suspected Boerhaaves?
Water soluble - gastrograffin - if aspiration risk though gastrograffin should be avoided as gastrograffin pneumonitis has very high mortality.
Dilute Barium more sensitive
What is the most common site of oesophageal perforation?
It depends on the eitiology;
Most common iatrogenic site is at the cricopharyngeus
Most common overall and in say Boerhaaves is left posterolateral 2-3cm above gastro-oesophageal junction.
What are the management principles for oesophageal perforations?
It will depend on eitiology and location of the perforation, physiology of patient, what damage has been done to surrounding tissues.
Basic tenets are resuscitation and antibiotic cover for GNR, oral flora, anaerobes and fungal.
Management options:
- Non operative for contained leaks
- Drainage alone
- T tube drainage
- Oesophageal exclusion or diversion
- Stents or clips
- Primary repair with buttress
- Oesophagectomy with immediate or delayed reconstruction.
By location:
Cervical:
- explore neck
- place drains
Thoracic:
- primary repair preferred if patient can tolerate it.
- involves thoracotomy, debridement, myotomy to visualise full extent of mucosal injury and repair in two layers using inner absorbable and outer permanent and cover with well vascularised tissue such as intercostal, omental or lat dorsi flap. leak test, NGT past repair, drain chest and close and consider enteral feeding access placement.
(middle third right posterolateral thoracotomy, lower third then left posterolateral thoracotomy).
What is the grading system for erosive oesophagitis?
Los Angeles esophagitis classification system, which employs the A, B, C, D grading system based on variables that include length, location, and circumferential severity of mucosal breaks in the oesophagus
Grade A = one or more erosions limited to mucosal folds and 5mm or less.
Grade B = one or more erosions limited to mucosal folds and >5mm.
Grade C = erosions extending over mucosal folds but over <75% of the circumference
Grade D = erosions extending over mucosal folds and >75% of the circumference.
What is the diagnosis and differentials?
LA grade D oesophagitis (over mucosal breaks and >75% of circumference)
Differentials;
- Barretts
- oesophageal adenoca
- candida oesophagitis
Describe Barretts oesophagus.
This complication occurs as a result of chronic pathological acid exposure to the distal oesophageal mucosa. It leads to a histopathological change of the distal oesophageal mucosa, which is normally lined by stratified squamous epithelium to metaplastic columnar epithelium. Barrett’s oesophagus is more commonly seen in Caucasian males above 50 years, obesity, and history of smoking and predisposes to the development of oesophageal adenocarcinoma. Current guidelines recommend the performance of periodic surveillance endoscopy in patients with a diagnosis of Barrett’s oesophagus
How often do you surveillance patients with Barretts oesophagus and what is the surveillance biopsy protocol?
The Seattle protocol is to biopsy using 4 quadrant biopsies every 2cm of the Barrett’s mucosa .
This samples only a small fraction of the lining but offers the possibility of recognising dysplasia. Ideally the biopsies from a given segment of Barrett’s oesophagus should be submitted to pathology in a separate container to enable the focusing of subsequent biopsies on the area if dysplasia is identified.
The finding of low grade dysplasia (LGD) warrants a follow-up endoscopy within six months to ensure that no higher grade of dysplasia is present in the oesophagus. If none is found, then yearly endoscopy is warranted until no dysplasia is present on two consecutive annual endoscopies.
The finding of high grade dysplasia (HGD) in flat mucosa should lead to confirmation by an expert GI pathologist and a subsequent endoscopy within three months. HGD with mucosal irregularity should undergo endoscopic mucosal resection. Although the natural history of HGD is variable, there is a five year risk of EAC exceeding 30%. It is because of the high risk of prevalent cancers that these patients are often evaluated as if cancer is present. Staging procedures with endoscopic ultrasonography, CT scans, and PET scans have been performed although there is not sufficient evidence to warrant their routine application
What is the Prague classification for Barretts oesophagus?
Grading Criteria used when reporting extent of disease (i.e. C5M7)
C Value: Circumferential extent
endoscope depth at GOJ Minus depth at the proximal-most circumferential extent
M Value:
Maximum extent
endoscope depth at GOJ Minus depth at the proximal-most maximum extent
What are the different causes of dysphagia?
Can be broken down into where the level of dysphagia is:
Oropharyngeal Dysphagia:
- UES Dysfunction
- Neuromuscular Disease – Most Common
- Oropharyngeal Causes
- Cerebrovascular Disease
- Parkinson’s Disease
- Neuropathy
- Myasthenia Gravis
- Oropharyngeal Carcinoma
- Congenital Web
- Zenker Diverticulum
Oesophageal Dysphagia:
- Motility Disorders (Achalasia, DES, Scleroderma, DM)
- Oesophageal Carcinoma
- GORD
- Schatzki Ring
- Strictures – Most Common Cause
Oesophagogastric Dysphagia:
- Achalasia
- Gastric Carcinoma
- Stricture
Paraesophageal Dysphagia/Physical Obstruction:
- Thyromegaly
- Left Atrial Enlargement
- Postoperative Scarring
- Lymphadenopathy
How is dysphagia graded?
Dakkak & Bennett Dysphagia Score
Grade 0: No Dysphagia
Grade 1: Dysphagia to Solids
Grade 2: Dysphagia to Semi-Solids
Grade 3: Dysphagia to Liquids
Grade 4: Aphagia
When would you use gastrograffin vs barium swallow when doing an oesophagogram?
Barium Swallow
- Pick Up Masses
- Caustic to Tissue
- Best Initial Test for: Dysphagia or Odynophagia
Gastrografin Swallow
- Not Caustic
- Best to Detect: Perforation
What is viewed in A and in B?
A is the z line (transition zone between squamous oesophageal lining and columnar gastric lining) this one is regular.
B is a Schatzki ring (a circular membrane of mucosa and submucosa that forms at the squamocolumnar junction of the distal esophagus. Schatzki rings appear as thin membranous structures that do not contain any muscularis propria. The upper surface is covered with squamous epithelium, and the lower surface is covered with columnar epithelium. Schatzki rings are always associated with hiatal hernias).
What is shown here? What can it cause?
Arteria lusoria - Abberant right subclavian artery coming directly off aorta after the left subclavian.
Can cause dysphagia lusoria and also causes non recurrent right ‘recurrent’ laryngeal nerve.
What is an oesophageal web?
Thin membrane of oesophageal tissue (usually anterior cervical oesophagus). Can be caused by various syndrome or a Zenker’d diverticulum.
How do you classify hiatus hernias?
Sliding vs paraoesophageal.
Sliding Hernia
Type I: Gastroesophageal (GE) Junction Herniated Above the Diaphragm
Most Common Hiatal Hernia (95%)
Paraesophageal/Rolling Hernia
Type II: Part of the Stomach Herniated Above the Diaphragm Next to a Normally Positioned GE Junction
Least Common Hiatal Hernia
Type III: Combined Type I & Type II
Most Common Paraesophageal Hernia (90%)
Type IV: An Intraabdominal Organ Other than the Stomach is also Herniated Through the Hiatus (Spleen/Colon)
Spot diagnosis. How is it treated?
This is a fluroscopic xray of the lateral neck showing a Zenkers diverticulum.
it is a false diverticulum (only involves mucosa and submucosa not all the layers). It is a pulsion diverticulum causes by increased pharynx pressure due to impaired relaxation of cricopharyngeus upper oesophageal sphincter and a natural weak point at Killian triangle bordered by the circopharyngeus inferiorly and the inferior constrictors supero-bilaterally.
If symptomatic (e.g. with halitosis, dysphagia, regurgitation) or if >1cm then repair.
Repair may be open (surgical) vs endoscopic.
Cricopharyngeal Myotomy & Diverticulum Repair
Through a Left Cervical Incision
Diverticulum Repair:
Small (< 2-3 cm): Diverticulopexy
Fixation to the Prevertebral Fascia
Moderate (3-5 cm): Diverticulopexy vs Diverticulectomy
Large (> 5 cm): Diverticulectomy
Endoscopic Diverticulotomy
Endoscopic Division of Septum (Including Cricopharyngeal Muscle)
Rigid Endoscopy Requires Neck Extension Although Newer Flexible Endoscopy Does Not
Previously Required At Least 2-3 cm Length Although Newer Techniques Permit Treatment of Smaller Lengths
Lower Complication Rates but Higher Recurrence Rate
Spot diagnosis
Epiphrenic diveritculum (<10cm of GOJ). They can be true or false diverticulum, can be multiple and are pulsion diverticulum due to motility disorder. Usually associated with a hiatus hernia as well. 0.6% chance of malignancy.
What is demonstrated here?
This is a manometry study of the oesophagus. It shows 3 different patterns of achalasia. Type 1 shows no contractility with incomplete LOS relaxation, Type 2 shows pan oesophageal pressurisation and Type 3 shows premature spastic contractions.
What is achalasia? What is the pathophysiology?
Achalasia is an oesophageal dysmotility characterised by incomplete relaxation of the lower oesophageal sphincter with oesophageal aperistalsis.
It is due to an autoimmune destruction of the neural ganglion cells in the myenteric plexus with T cell and eosinophillic infiltration .
If someone has taken a tryp to Mexico/south america consider parasitic infective cause of achalasia by Trypanosoma cruzi causing Chaga’s disease.
What are some complications of achalasia?
Aspiration
Weight loss/malnutrition
SCC of oesophagus
What is pseudoachalasia?
Similar appearance to achalasia on fluroscopy and similar symptoms but is due to malignancy not underlying motility disorder.
What is Allgrove syndrome?
- Autosomal Recessive Disorder
- Triad: Achalasia, Adrenal Insufficiency & Alacrima (Reduced Tear Production)
What is this manometry showing?
There is a failure of the LOS to relax but there is a preserved peristaltic wave so this is in keeping with oesophago-gastric junction outflow obstruction.
What is this the classic appearance of?
Corkscrew oesophagus in keeping with diffuse oesophageal spasm. It is uncordinated diffuse contractions with no peristalsis. Characterised by premature rapidly propagated contractions from impaired inhibitory innervation.
What is demonstrated in this manometry?
This shows a coordinated high amplitude contraction with peristalsis. This is consistent with a jack hammer or nut cracker oesophagus. Due to excessive cholinergic drive.
What is shown in this manometry?
Absent contractions. No peristalsis. Consistent with connective tissue disorder like systemic scleroderma.
What are the so called ‘minor disorders of peristalsis’?
Ineffective Esophageal Motility (IEM)
≥ 50% of Swallows Ineffective
Most Often Caused by Distal Damage from Chronic GERD
Often Have More Mild Symptoms & Require Less Intervention
Manometry
Chicago Classification – Version 3:
Normal Integrated Relaxation Pressure (IRP)
≥ 50% of Swallows Ineffective
Tx: Control of GERD
Fragmented Peristalsis
≥ 50% of Swallows Fragmented
Often Have More Mild Symptoms & Require Less Intervention
Manometry
Chicago Classification – Version 3:
Normal Integrated Relaxation Pressure (IRP)
≥ 50% of Swallows Fragmented
(DCI > 450 mmHg with > 5 cm Break)
Poorly Described in Literature
What is demonstrated in this image?
This is an oesophageal manometry study. This swallow is normal showing the swallow, the normal amplitude peristaltic wave and relaxation of the LOS just preceding the peristaltic wave to allow the GOJ to receive the bolus.
When it comes to foreign body ingestion, which ones require emergent, urgent and non-urgent endoscopy?
Emergent Indications:
Esophagus:
- Sharps
- Button Batteries
- Complete Obstruction (Drooling/Cannot Handle Secretions)
- Causing Airway Compromise
Stomach/Duodenum:
None
Urgent Indications:
Esophagus:
- Blunt Objects
- Food Impaction
Stomach/Duodenum:
- Sharps
Either:
- Magnets – Some Recommend Observation if Only a Single Magnet
- Long Object > 5-6 cm
- Superabsorbent Polymer
- Lead-Containing Products
Non-Urgent Indications:
Esophagus:
- Coins (Can Observe 12-24 Hours)
Stomach/Duodenum:
- Button Batteries (Can Observe for 48 Hours – Remove if Not Passed)
- Blunt Objects with Diameter > 2.5 cm
What is the danger of button batteries? How would you manage the patient who has swallowed one?
When impacted in oesophagus or retained in stomach can cause necrosis and erosions and perforation from electrical current.
Initial Management:
Indications for Radiographic Localization:
Age ≤ 12 Years
Battery Size ≥ 12 mm or Unknown
Single Small Battery: Observe at Home without Imaging
Treatment:
Esophageal Impaction: Emergency Endoscopic Removal
Stomach Location:
Symptomatic: Endoscopic Removal
Asymptomatic:
*Asymptomatic Indications Debated
Age < 5 Years & Battery Size ≥ 20 mm
Remains in Stomach After 4 Days & Age < 6 Years or Battery Size ≥ 15 mm
Intestinal Location:
Asymptomatic: Observe
Symptomatic: Surgical Removal
https://starship.org.nz/guidelines/foreign-body-ingestion/
What is the diagnosis? Who does it effect most commonly? What are the characteristic endoscopic appearances?
Eosinophilic oesophagitis. It is a chronic immune mediated/antigen response with eosinophilic inflammation.
Men aged 20-30s with atopic hx of allergies, asthma, eczema. Also associated with IBD and coeliac.
Characteristic appearance like in this stem picture is most commonly the linear furrows but can also have white plaques, stacked rings “feline oesophagus” appearance, strictures or oedema.
Spot diagnosis
Oesophageal candidiasis. Treat with fluconazole.
Define the pathology seen here.
This is Barrett’s Oesophagus. It is defined as intestinal metaplasia of the oesophagus from normal squamous epithelium lining the oesophagus to columnar epithelium with goblet cells.
What is this and what are the risk factors for its development?
This is an SCC of the oesophagus. Typically found in upper 2/3rd of oesophagus.
Risk factors include:
- Alcohol
- Tobacco
- Hot tea
- HPV
- Achalasia
What is this and what are the risk factors for its development?
This is an adenocarcinoma of the oesophagus. Typically found in lower 1/3rd of the oesophagus.
Risk factors include:
- Barretts
- GORD
- Obesity
- Tobacco
This is an endoscopic image of the oesophagus. What are the differentials?
- Leiomyoma (benign tumour of muscularis propria)
- Leiomyosarcoma
- Lipoma
- GIST
- Enlarged lymph node creating external compression
If this lesion is seen on barium swallow. What is it most likely and how do you biopsy it?
This is a typical lens shaped impression on distal oesophagus of a leiomyoma. You diagnose them on OGD or imaging and do not biopsy these as complicated the removal of them later. They can usually be removed by enucleation (unless have been scarred down with previous biopsy).
If a patient has dysphagia, weight loss and red flags for oesophageal cancer. You notice they also have palms and plantar surface of feet that look like this..what might they have?
Tylosis with oesophageal cancer. Rare autosomal dominant disease that has 40-90% increased risk of developing oesophageal SCC and they also have hyperkeratosis.
Require screening OGDs every year from age 20.
Describe the different kinds of fundoplications.
Nissen is a posterior 360 degree wrap.
Dor is an anterior 180 degree wrap
Toupet is a posterior 270 degree wrap.
Describe each of these findings post fundoplication.
A) Normal Nissen,
B) Partial Fundoplication,
C) Disrupted Fundoplication,
D) Twisted Fundoplication,
E) Migrated Fundoplication,
F) Slipped Fundoplication,
G) Paraesophageal Hernia
What are the lymph node stations for the stomach?
1: Right Pericardial Stomach
2: Left Pericardial Stomach
3: Lesser Curvature
4: Greater Curvature
4sa: Short Gastrics
4sb: Left Gastroepiploic
4d: Right Gastroepiploic
5: Suprapyloric
6: Infrapyloric
7: Along Left Gastric Artery
8: Along Common Hepatic Artery
8a: Anterosuperior CHA
8p: Posterior CHA
9: Celiac Axis
10: Splenic Hilum
11: Splenic Artery
11p: Proximal Splenic Artery
11d: Distal Splenic Artery
12: Hepatoduodenal Ligament
12a: Hepatic Artery
12b: Bile Duct
12p: Behind Portal Vein
13: Posterior Surface of the Pancreatic Head
14: Root of the Mesentery
14a: SMA
14v: SMV
15: Paracolonic
16: Paraaortic
16a1: Aortic Hiatus
16a2: Celiac to Left Renal
16b1: Left Renal to IMA
16b2: IMA to Bifurcation
17: Anterior Surface of Pancreatic Head
18: Inferior Margin of Pancreas
19: Infradiaphragmatic
20: Esophageal Hiatus
110: Paraesophageal in Lower Thorax
111: Supradiaphragmatic
112: Posterior Mediastinum
When assessing an UGIB and the ulcer is seen. What is the risk classification used for quantifying risk of rebleeding?
Forrest classification.
I Active Pulsatile Bleeding (Highest Risk – 80%)
IIa Visible Vessel (50%)
IIb Adherent Clot (15-25%)
III Clean Ulcer Base (< 5%)
What treatment options are available for perforated peptic ulcer disease?
May Consider Conservative Management (NGT, ABX & PPI) if Presentation Delayed (> 24 Hours), Contained & No Peritonitis
Stomach:
Stable: Same as Refractory Tx
Unstable: Biopsy & Graham Patch or Wedge Resection
Duodenum:
Small (Most < 1 cm): Graham Patch
Pyloric Exclusion with Gastrojejunostomy Indications:
High Risk for Leak
Too Large
Poorly Controlled DM
If Known Ulcer Diathesis: Add Highly Selective Vagotomy
Contraindicated if > 24 Hours, Unstable or Extensive Peritonitis
“Giant” (≥ 2 cm):
No Consensus on Specific Repair
Options:
Roux-en-Y with Roux Limb to Ulcer Edge
Requires Kocher Maneuver & Debridement of Ulcer Edge
Serosal Patch with Jejunal Loop
Antrectomy & Billroth II Reconstruction
Primary Repair & Triple-Tube-Ostomy
Gastrostomy, Retrograde Duodenostomy & Feeding Jejunostomy
Requires Kocher Maneuver to Minimize Tension & Debridement of Ulcer Edge
Tube Duodenostomy
Preferred Procedure if Unstable
Procedure:
Debride Ulcer Edges
Place Malecot Catheter Through Defect
Purse-String Suture Around Catheter
Mobilize an Omental Pedicle
Wrap Omental Pedicle Around the Tube & Secure at the Base
Bring Malecot Externally to Drain
What is this image showing and what are some treatment options?
This is a gastric emptying study showing time points 0 min, 1 hr, 2hr, 4hr post. This image is showing delayed gastric emptying.
Treatments available include;
- Acute Exacerbation Tx: Reglan or Erythromycin
- Chronic Tx: Dietary Changes (Multiple Small Meals with Low-Fat & Low-Fiber)
- If Fails: Reglan, Domperidone or Erythromycin
- Options if Fails:
Venting Gastrostomy
Pyloroplasty
Gastric Electrical Stimulation/Pacemaker
What are the types of gastric volvulus?
Organoaxial: Around Longitudinal/Long Axis
Antrum Rotates Anterosuperiorly with Fundus Rotates Posteroinferiorly
Greater Curvature Rests Above the Lesser Curvature
Most Common Rotation
Mesenteroaxial: Around Short Axis
Antrum Rotates Above the GE Junction
Typically Not Associated with a Secondary Anatomic Defect
Complex: Aspects of Both Organoaxial & Mesenteroaxial
What is the TNM staging for GIST?
Spot diagnosis.
GAVE (Gastric Antral Vascular Ectasia)
How do you manage UGIB from oesophageal varices?
Resuscitation
- early ICU involvement
- tricky fluid balance in cirrhotics
- early intubation
- aggressive correction of coagulopathy
Cessation of haemorrhage
- antibiotics ceftriaxone 2g IV
- terlipression 2mg IV every 4 hrs
- early OGD with banding +/- sclerotherapy
Back ups balloon tamponade, TIPS, surgical shunt.
Prevention of rebleed
- continue abx for 7 days
- continue terlipressin for 3-4 days
- beta blocker e.g. nadolol
- PPI
- Repeat endoscopy and band ligation every 10-14 days until varices eliminated
- portal venous decompression
(liver transplant if decompensated, TIPS if poor liver function as bridge to transplant, surgical shunts if not liver transplant candidate Warren selective distal spleno-renal shunt preferred elective option)
Describe when and how you would use a Sengstaken-Blakemore tube. What are some complications of its use?
This is used for control of oesophageal variceal bleeding when other measures like terlipressin, antibiotics and banding have not succeeded and may be used as a temporising control of haemorrhage until transfer to a facility with expertise to perform TIPS etc and in some cases may be all thats required to stop the acute haemorrhage (up to 50%).
It is inserted usually under general anaesthesia at time of OGD via the nose or mouth and the gastric balloon is inflated first and put on 250g of traction and if bleeding not controlled then oesophageal balloon can be inflated. The balloons need to be clamped securely.
It can cause mucosal necrosis, perforation, aspiration or be unsuccessful in cessating the haemorrhage.
In what patients would you recommend screening for oesophageal varices? And how regularly would you screen them?
In decompensated cirrhotics, or compensated cirrhotics with liver stiffness on elastography >20kPa or thrombocytopaenia <150.
If no varices and liver disease inactive then recommend OGD every 3 years
If no varices and liver disease active or if small varices with no red signs and liver disease inactive then OGD every 2 years.
If small varices with no red signs and liver disease active then OGD every year.
If high risk varices i.e. varices with red signs or large varices (>5mm) then commence carvedilol or nadolol. If contraindicated then perform variceal ligation and repeat OGD every 1-2weeks until obliterated then 3-6monthly for 1 year then annually thereafter.
If established on long term beta blocker therapy then no need to continue screening.
What classification system do you use for oesophageal varices?
Many out there. Most widely accepted is Baveno classification
size
- small <5mm
- large >5mm
red signs
- present
-absent
high risk = red signs or >5mm.
What are these, how are they classified, what is the aeitiology and how are they treated?
These are large gastric varices in the fundus.
Gastric varices are classified as fundal vs ectopic from gastroepiploics.
Aeitiology:
Fundal - if isolated (i.e. without oesophageal varices) then sinistral hypertension from splenic vein thrombosis. If associated with oesophageal varices then likely portal hypertension.
Ectopic varices portal HTN.
These are treated like oesophageal varices for the GOJ ones but are poorly managed with endoscopic measures for gastric varices outside the GOJ. Can try cyanoacrylate injection as polymerises to form a firm clot. Otherwise splenectomy may be required.
