Upper GI Flashcards
Diagnosis of GORD
Made on symptoms alone
Response to acid suppression
Management of GORD
Weight loss Stop smoking Decrease ETOH, coffee, chocolate, spicy, fatty food Avoid late meals Elevate head of bed Above effective only 20-30%
PPI >H2 antagonist (80 vs 50% efficacy)
What’s barrett’s?
What causes it?
Classification
Intestinal metaplasia of the distal oesophageal mucosa (to columnar mucosa)
Begins at LOS and extends variable distances (can be circumferential or tongues)
Correlates with severity of reflux
Needs 10 years of reflux (often silent)
15% with reflux oesophagitis
Classification
Short vs long segment (<3cm vs >3cm)
Long segment = increased risk of malignancy
Rx Barrett’s - high grade dysplasia on endoscopy
PPI
Endoscopic ablation therapy
Much less mortality now
Rx Barrett’s - no dysplasia
PPI - limited data that it reduces chance of dysplasia
Surveillance endoscopy 6 months –> 3 years
Rx Barrett’s - low grade dysplasia
PPI
Repeat endoscopy 6 months
Rings down a oesophagus
Recurrent dysphagia
What is it?
Eosinophil oesophagitis
What is Eosinophil oesophagitis?
Chronic immune mediated inflammatory disease of the oesophagus
Presentation of eosinophil oesophagitis
Dysphagia, food impaction
Young males
Associated with asthma, atopy
Endoscopy - rings and furrows, tears on dilation
Histology: eosinophil infiltration (proximal and mid oesophagus; eosinophils can be seen in distal oesophagus in GORD)
Rx eosinophil oesophagitis
PPI (85% effective)
2nd line: topical steroids (fluticasone puffer or budesonide slurry)
Elimination diets work well in children (not really in adults - we think its more to do with the air you breathe in)
Oesophageal dilatation if strictures
Last line: oral steroids (budesonide) +/- azathioprine +/- dupilimumab (monoclonal Ab IL4 IL13)
Dupilimumab is recently approved for use
What’s achlalasia?
Incomplete LOS relaxation
Aperistalsis
Presentation of aclalsia
Dysphagia to solids and liquids
Regurgitation especially postural (night), saliva and old food (not acid)
weight loss
Chest discomfort/pain (may mimic heartburn)
aspiration
Investigation achlasia
Endoscopy
- Dilated oesophagus, tight LOS, food in oesophagus
- Done to exclude strictures
Barium swallow - birds beak
Manometry
- Most sensitive
- Incomplete LOS relaxation
- Aperistalsis
Rx achlasia
1) Nitrates or CCB
- Generally not effective as the doses that need to be used have large effects on BP
Definitive treatment
2) BOTOX reserved for old patients or too unwell for other definitive therapy
3) Per oral endoscopic myotomy (POEM) is 1st line
- high response, low mortality
4) Balloon dilatation of LOS - 2nd line
- Done in 15-20 minutes
- High response rate
- Low perforation rate
- Not as longstanding as POEM, often requires repetition
5) Laparoscopic hellers myotomy - 3rd line
- Still a role
- Complex operation
- High mortality
- Good response
What are varices?
Venous collaterals which form in the presence of portal HTN
Hepatic venous pressure gradient (HVPG) of >12mmHg required for formation
HVPG usually >18mmHg before bleed
Rx varices
Endoscopy every 6-12 months (usually at diagnosis of cirrhosis/portal HTN)
If no varices - repeat 12 months
If large varices - B blocker (propanolol, carvediolol)
- Need to reduce the resting pulse by 25% for it to be effective
If grade 2-3 varices - banding
No difference in mortality between B blocker and banding
Rx variceal haemorrhage
Non-aggressive resuscitation. Aim Hb >70.
1) Ceftriaxone, followed by norfloxacin (7 days)
- reduce mortality, rebleeding rate, infection
- bacteria goes straight from azygous vein to vascular supply/Rt heart
2) endoscopy + banding
- Within 12 hours
- Gastric varices: glue injection preferred
3) Terlipressin or octreotide
- Acute
- Usually used for 3-5 days
- CI IHD, vascular disease
4) Sengstaken-Blakemore or linton tube
- Temporary measure (24-48h) due to risk of pressure necrosis. Use only if banding fails and you need to quickly stop bleeding.
- Insert it like an NGT and inflate the balloon to compress haemorhaging varices in oesophagus and stomach
5) Danis stent (bridge to TIPSS or surgical implantation)
- For those who fail endoscopic therapy, usually due to previous band induced scarring. Varix doesn’t suck up the band.
- Tamponades the bleed
- Superior to Sengstaken tube in small case series
6) TIPSS
- CI in encephalopathy, portal vein thrombosis
- Best thing to do if ongoing bleeding after banding but technically challenging
+/- PPI doesn’t change immediately but may reduce risk of post-banding ulcers
Don’t use erythromycin
Risk factors PUD
H pylori NSAIDs Smoking Stress - ICU/comorbid Chemo agents Crohn's Gastrinoma (Zollinger-Ellison syndrome) Immunosuppression like steroids - prevents healing of small lesions, doesn't cause ulcers
Repeat positive urea breath test after treatment for h pylori (amoxycillin + clarithromycin + PPI)
What to do?
Clarithryomycin resistance >10% resistance
If resistant…
1st line: Rifabutin, doxycyline/tetracycline, PPI, amoxycillin
2nd line: levofloxacin (salvage therapy)
Others
Bismuth containing quadruple therapy (not used much anymore)
Culture and sensitivity
Rx H pylori
1st line
amox (<10% resistance), clarithromycin, PPI
Penicillin allergy
Clarithromycin, metronidazole (>30% resistance), PPI
HIgh resistance
Amoxycillin, metronidazole, PPI
Relative NSAID toxicity in terms of PUD
Aspirin >Indomethacin > ibuprofen >diclofenac > COX2 inhibitor
Rx gastric ulcer
Gastric ulcers can be malignancy
Duodenal ulcers are very rare
Repeat endoscopy in 8 weeks
PPI
Rx PUD
Treat H pylori
Modify NSAID - change aspirin to clopidogrel
PPI
How long does a gastric ulcer take to heal?
8 weeks
How much blood to get melena?
150ml
Red PR bleeding from an upper GI soruce. how much?
Varices and duodenal ulcers
>500ml
Bleeding duodenal ulcer Rx
Inject with adrenaline
Heat probe
Vascular clip
Sprays
What’s a classification for ulcers?
Forrest classification of ulcers
High risk of recurrence: Active bleeding, clot, vessel - high risk of bleeding
Low risk ulcers - clean base, flat red spot
Rx high risk ulcer
PPI infusion for 72h after endoscopic therapy (from time of gastroscopy, not from presentation)
- Reduces rebleeding rate, improves mortality
Must be infusion - changes pH in stomach, stops acid from dissolving clot
Can Barrett’s extend overtime?
Yes if they don’t take PPI
But in general it doesn’t if you take PPI
Short segments can regress after 5-10 years PPI
Pathophysiology of coeliac
1) environmental
- Gluten
2) genetic
- HLADQ2 or DQ8
3) immunological
- TTG deaminates gliadin to peptides to presentation by APC to CD4 T cells
Clinical features of coeliac
Diarrhoea +/- abdo pain/discomfort (<50% cases)
Others
- OP
- IDA
- Infertility and recurrent miscarriages
- Weight loss
Diagnosis of coeliac
- Serology
- Small bowel biopsy
- HLA typing
tTG-IgA + Total IgA level
Reason we do total IgA is because 2% of coeliac disease is IgA deficient
Other option is tTG-IgA + DGP-IgG
Serology cannot diagnose Coeliac in isolation.
High risk patients with negative serology should have small bowel biopsy.
Small bowel biopsy (gold standard)
- Villous atrophy with crypt hyperplasia, raised intraepithelial lymphocytes
- Biopsy from the 1st (x2) and 2nd (x4) part of duodenum
- If any doubt, do 2 week gluten challenge then rebiopsy
HLA typing
- Excellent NPV but poor PPV
- Does not depend on gluten intake
- Absence of HLADA2.5, DQ2.2 and DQ8 exclude the diagnosis
- Presence of HLADQ2 or DQ8 indicates susceptibility to disease but doesn’t mean they have coeliac
Management of coeliac
Gluten free diet
- Recovery takes 6 months+
Refractory disease: may respond to corticosteroids
Nutritional assessment: Fe deficiency, folate, B12, Vitamin D, hypocalcaemia, magnesium, zinc
Screen for complications: TSH, LFTs, fasting BSL, DEXA
Vaccinations (higher risk for pneumococcal sepsis due to hyposplenism)
Associations with coeliac
autoimmune thyroiditis (Hashimoto or Grave’s) (5% have coeliac)
T1DM
Down’s
Dermatitis herpetiformis (50% will have coeliac)
Recurrent infertility (will return to normal after GFD), miscarriages at 8/52 (coeliac ab cross placenta and will attack foetus)
Osteoporosis and fractures (chronic inflammation; poor vitamin D, calcium absorption)
Ataxia, epilepsy
Coeliac disease for 40 years
Sudden weight loss and diarrhoea
What do you do?
High risk of small bowel T cell lymphoma (6th decade) or small bowel adenocarcinoma
Do CT abdo pelvis
Why is a gluten free diet important in coeliac?
Reduces adenocarcinoma
Reduces BMD loss and fractures
Improves fertility
Improves mortality
Unfortunately has no effect on T cell lymphoma
Refractory coeliac disease
1% will develop refractory disease
Despite compliance to GFD
Happens in 6th decade
Normal tTG IgA (or IgG)
Diarrhoea and weight loss
Types of refractory coeliac disease
Type 1
- Normal intraepithelial lymphocyte (IEL) phenotype
- Good prognosis
- Responds to immunosuppression - budesonide + azathioprine
Type 2
- Abnormal intraepithelial lymphocytes with monoclonal phenotype - can predict the risk of lymphoma if loss of CD3, CD4, CD8 surface markers on flow cytometry (or immunohistochemistry). Predictive if >80% CD3e+CD8- IELs
- 50% will develop enteropathy associated T cell lymphoma in 5 years with a 5 year survival rate of <50%
- Variable response to rx (chemotherapy +/- ASCT)
IgG4 disease
Systemic, fibroinflammatory disease
Typically affects pancreas, bile ducts, retroperitoneal fibrosis, aortitis
Previously a lot of people have had unnecessary surgery (Whipples) when there’s been lumps in the pancreas
Now must do IgG4 level to confirm its not just IgG4 disease - avoid surgery
Diagnosis IgG4 disease
IgG4 level
Histology/aspirate
Rx IgG4 disease
Don’t need treatment if asymptomatic
Symptomatic (immunosuppression)
1st line: steroids then wean
Recurrence: azathioprine (first line), MTX, mycophenolate
Refractory: rituximab
ERCP indications
Mostly done as a therapeutic procedure
1) Obstructed bile ducts confirmed on USS, CT scan, CT cholangiogram or MRCP
2) Gallstone pancreatitis AND cholangitis
3) Primary sclerosing cholangitis if inadequate imaging
(only diagnostic indication) or biliary obstruction
4) Sphincter of Oddi dysfunction
- Type 1: typical biliary colic + abnormal pancreatic enzyme + abnormal imaging + abnormal LFTs
- Type 2: abnormal imaging + blood tests
If bilirubin >50 in obstructed bile ducts, should avoid which investigation?
CT angiogram (bile ducts won’t show up)
Do MRCP
Complications ERCP
5% pancreatitis (reduced by indomethacin suppository)
1% bleeding
1% perforation
1/1000 mortality
Iron deficiency anaemia or unknown cause or overt GI blood loss
What investigations to do?
Pill cam –> double balloon enteroscopy to treat the lesion (invasive procedure; anterograde requires intubation; retrograde doesn’t)
If negative pill cam, won’t generally proceed to a double balloon. May need CT enterography or MR enterography first to look for funny lesions.
Gastroscopy + colonoscopy miss 5m of small bowel.
Need CTAP if suspicious of malignancy
Why do MRCP over CT cholangiogram for obstructive bile duct?
Jaundice patients
- Do US first but doesn’t show good images around duodenum i.e. CBD or ampulla
- Plain CT may be adequate but 90% gallstones are cholesterol so wont’ be visible on CT
- To show up bile ducts, needs CT cholangiogram. However if bilirubin >50, the contrast that is used in CT is not adequately excreted into the bile ducts if they are jaundiced or have high bilirubin.
- MRCP can be done in jaundiced patients. But may not get good quality images due to breath holding factors, hence if bili is <50, should do CT cholangiogram
- In young PSC patients, MRCP is better because they’re going to need lifelong scanning
When is a red cell scan used?
Not used much anymore
If there is enough bleeding >1ml/min, red cell scan can work. Used when desperate.
Is ETOH a risk factor for PUD?
No
Oesophagus is made up of 2 muscle layers
What are they? What lies inbetween?
Inner circular
Outer longitudinal
Plexus of nerves lie inbetween the two layers and also on the submucosal side
Oesophagus
Upper 1/3 is …
Lower 1/3 is …
Middle 1/3 is …
Straited
Smooth
Mixed
Risk factors for GORD
Age Obesity (central) Hiatus hernia Pregnancy Scleroderma Asthma Smoking Alcohol
Does H.pylori cause GORD?
NO
Protects against GORD actually!
Is GORD genetic?
Yes
Relatives of patients with GORD or Barrett’s are more likely to have frequent reflux symptoms
Mechanism of GORD
Transient lower oesophageal sphincter relaxation
- Some reflux is physiological (burping)
Weak lower oesophageal sphincter
Increased intraabdominal pressure (obesity)
Complications of GORD
Ulceration/bleeding Strictures Barrett's Adenocarcinoma of oesophagus Pharyngeal reflux - sore throat
Is recumbent reflux normal?
No
Its always abnormal
Are GORD symptoms predictive of oeosphagitis or severity of oesophagitis?
No
When to investigate further in GORD?
Dysphagia, weight loss, haematemesis
Refractory to simple therapy 4/52 PPI (8/52 if severe)
No evidence to look for Barrett’s oesophagus in longstanding symptoms
GORD symptoms
Heartburn
Regurgitation of gastric contents, effortness
Non-specific/extra-oesophageal
- Nausea, epigastric pain
- Cough, worsening asthma
- Chest pain
- Sleep disturbance
- Dental problems
Dysphagia in longstanding GORD DDx
Oesophagitis
Stricturing
Malignancy
Should we do surgery i.e. fundoplication in GORD?
Indicated in failed medical therapy
Effective in symptom control
Disadvantages
- Complications and 0.1% mortality
- Everyone gets excess flatus and limited period of dyaphgia
- Occasionally get severe dysphagia, gas bloat, inability to belch, vomit, paraoesophageal hernia
- Can fail with time
What investigations should we do pre-op before considering fundoplication in GORD?
Manometry study
- Make sure its not achalasia or oesophageal hypomotility that’s causing GORD symptoms
Endoscopy
- May show oesophagitis
pH study
- If endoscopy doesn’t show oesopahgitis. Confirms excessive acid exposure. Especially if there are atypical symptoms
2 types of oesophageal cancer
SCC (incidence reducing)
- Smoking
Adenocarcinoma (majority)
- Major risk factor is Barrett’s
How to take appropriate biopsies for Barrett’s?
4 quadrant biopsies at 1cm intervals is required within the Barrett segment
Also should wait after healing as inflammatory changes can interfere with assessment of dysplasia (reactive atypia)
Investigation of oesaphgeal dysphagia
Endoscopy
- Sees mucosa
- Can biopsy e.g. eosinophilic oesophagitis
- Can be therapeutic e.g. dalatation
Barium swallow
Oesophageal manometry
When endoscopy and barium swallow haven’t demonstrated a cause
What’s distal oesophageal spasm?
Synchronous, uncoordinated contractions of SM of the oesophageal body
Presentation of distal oesophageal spasm
Dysphagia
- Often variable
- Cold liquids, large boluses
- May get impaction
Chest pain
Regurgitation
Diagnosis of distal oesophageal spasm
Barium swallow
- Tertiary contractions
- Diverticulae
- Poor passage of bolus
Endoscopy
- Retained food
- Uncoordinated or ring contractions
Manometry
- Synchronous pressure waves
Management of distal oesophageal spasm
Soft foods
Eat slowly
Wash down with water
CCB
GTN spray
PPI
Botox into oesophageal body
Dilatation
Myotomy (POEM)
When to transfuse for upper GI bleed?
Aim Hb 70-90
Aim Hb ≥90 in IHD
How to risk stratify for upper GI bleed pre-endoscopy?
Blatchford score
Score <1 = low risk, OP endoscopy
Urea Hb SBP HR >100 Melena Syncope Hepatic disease Cardiac failure
How to predict risk of recurrent GI bleed and mortality post-endoscopy?
Forrest score
- Endoscopic appearance of ulcer
Rockall score
- Age, haemodynamic shock, comorbidities, diagnosis, recent haemorrhage
- Predicts rebleeding and mortality
AIM 65
- Albumin, INR, mental state, SBP, Age
- Predicts mortality
How soon should we do gastroscopy for non-variceal GI bleed?
Within 24 hours
Data is conflicting re urgent endoscopy for high risk patients - could make things worse as patients are not adequately resuscitated and not had PPI to reduce ulcer stigmata
Should PPI be used in upper GI bleed (non-variceal)?
YES
IV esomeprazole 80mg (push over 15-30 minutes) then 8mg/hr infusion
Pre-endoscopy - reduces rates of high risk stigmata and need for endoscopic therapy
But most evidence is in post endoscopy - given 72h post endoscopy for high risk ulcers is associated with reduction in re-bleeding, blood transfusion requirements, hospital LOS, mortality
Endoscopic treatment options for bleeding PUD
What to do in recurrent bleed?
Dual therapy is standard treatment
Inject with adrenaline AND either clip or cauterize or inject sclerosant
Recurrent bleed
Repeat endoscopy with endoscopic hemostasis
If haemostasis not achieved or recurrent rebleeding following 2nd attempt, consider:
Over the scope clips (OTSC) aka bear claw
Topical haemostatic spray
Refer for transcatheter angiographic embolisation (TAE) or surgery
Where do varices commonly happen?
Oesophageal > gastric
What’s the risk of variceal Haemorrhage? What increases the risk of bleed?
5-15% per year
Increased risk of bleeding
- Large varix (30% annual risk of bleed)
- Child pugh C > B > A
- Red sign, red wale mark
- Ongoing ETOH
- HVPG >12mmHg
- Previous bleed (60-70% annual risk)
What is the preferred endoscopic treatment for gastric varices?
Glue injection!
For oesophageal varices, banding is 1st line
What are the disadvantages of glue injection for gastric varices management?
Embolisation
E.g. splenic infarct, pulmonary infarct
DDx of melena
Variceal bleed PUD (duodenal > gastric) Mallory-Weiss tear Malignancy Reflux oesophagitis Gastric erosion/gastritis
Severe Haematochezia - what are you worried about?
10-15% have an upper GI bleed!
If the suspicion is high, must do gastroscopy to exclude
If the suspicion is moderate, can do nasogastric lavage (coffee ground material or bright red blood in the lavage fluid)
Consequences of undiagnosed coeliac disease
Increased all cause mortality
Impaired QOL - impaired fertility, osteoporosis
What part of gluten is immunogenic?
Gliadin
When to screen for coeliac disease with serology
Persistent unexplained GI symptoms Faltering growth 1st degree relative with coeliac Autoimmune thyroid disease IBS (in adults) Prolonged fatigue Unexpected weight loss Severe or persistent mouth ulcers Unexplained iron, B12, folate deficiency T1DM
Consider
Metabolic bone disorder
Unexplained neurological symptoms (peripheral neuropathy, ataxia)
Unexplained subfertility or recurrent mismarriage
Persistent elevated liver enzymes with unknown cause
Dental enamel defects
Down’s syndrome
Turner’s syndrome
How to monitor coeliac response after starting GFD?
- Repeat ab level after 6/12 gluten free diet
- Antibodies generally return to normal after 12/12
- Mucosal healing takes 18 months-2 years
- Repeat gastroscopy and biopsy is useful in adults to assess/confirm of goal of mucosal remission
Should we screen family members of patients with coeliac disease?
YES
10% risk of also having coeliac disease
Is gluten free diet beneficial for non-coeliac people?
NO
Linked to CV events!! (due to reduction in cardioprotective whoe grain intake)
Is coeliac serology a reliable indicator of disease activity?
No
