Here are three colonic polyps. One is a TA+LGD, another a TA+HGD and the final is a TVA+HGD
WHICH POLYP IS THE TVA?
a) A
Nope, this one has slit-like crypts typical of a tubular adenoma (TA). In fact, most small polyps are TA's. Presumably there is a progression from TA→TVA→Cancer apart from depressed lesions (IIc lesions) which go directly from being TA's to cancer.
b) B
It's a little difficult to see the crypt pattern without a close-up. However, you don't need to! Look at the growth morphology. This is a LST-NG and they are ALWAYS TA's!
c) C
Yes! Gyrate crypts best seen after indigocarmine dye spray (I think).
explanation
Most 'laterally spreading TVA's are of course LST-G's. However, this doesn't have the usual cobblestoned appearance of a 'laterally spreading tumour of the granular type'. It's rather 'chunky' in fact. That's because its harbouring HGD! A rare beast indeed as almost all laterally spreading TVA's only harbour LGD.
This is the stomach of a middle aged lady undergoing gastroscopy because of anaemia.
WHAT IS THE DIAGNOSIS?
a) HP associated gastritis
This is beyond gastritis! The fundal mucosa is pale and atrophic rather than red and inflammed!
b) Atrophic gastritis
The fundal mucosa does appear atrophic apart from a few scattered red patches which is all that remains of the normal gastric lining. But how about the antrum?
c) Autoimmune gastritis
Correct!
D) Coeliac disease
That duodenal mucosa is unremarkable. The 'polyp' in the 3 o'clock position is obviously the duodenal papilla.
Explanation
Those red spots in the gastric fundus is what remains of the more normal gastric mucosa whilst most of the surrounding mucosa is atrophic. In contrast, the antrum is unremarkable, as is the duodenum. This is an example of a 'body predominant' gastritis and your endoscopic diagnosis should be an autoimmune gastritis! The antral G-cells, found deep within the antral pyloric glands are pumping out huge amounts of gastric which is leading to ECL cell hyperplasia and multiple small NET's. In fact, most patients with type I gastric carcinoids have an autoimmune gastritis! The anaemia was due to vitamin B12 deficiency.
A somewhat scary dilatation.
WHAT IS THE LIKELY AETIOLOGY OF THE STRICTURE?
a) peptic stricture
There are no linear reflux ulcers!
b) eosinophilic oesophagitis
yes! Long and fusiform stricture and mucosa 'splits' in a frightening way
c) SCC
Those IPCL's do look a little prominent but not ectatic etc
d) adenocarcinoma
But the stricture is within the squamous part of the oesophagus!
explanation
Eosinophilic oesophagitis was first described in 1978 and is widely regarded as an allergic condition. Food allergy may play a significant role and the majority of sufferers have either personal or family history of other allergic conditions.
In contrast, Lymphocytic oesophagitis is much more recent, first described by Rubio et al in Sweden in 2006. As yet there is no consensus on how many lymphocytes are needed to make the diagnosis. Extrapolating from EoE, I take 2 samples from the proximal, middle and distal oesophagus respectively, in all patients with inexplicable dysphagia. LyC oesophagitis is still regarded as something of an entity "in search of a disease". For this reason it's difficult to know if the reported increasing prevalence is simply due to the pathologists being on the lookout and more oesophageal samples (correctly) being taken in patients with dysphagia. There is an association with old age, female gender, smoking, reflux disease and primary esophageal motility disorders. Clinically oesophageal rings, webs, nodularities, furrows and strictures have been described in both conditions. Personally, I think that they look subtly different! I suggest a LyC oesophagitis when there is subtle dilatation of the intrapapillary capillary loops within the squamous oesophagus. In my experience you don't usually see this in EoE. For this reason, a lymphocytic oesophagitis would have been a very reasonable guess in this case. Those IPCL's do look a little dilated don't they? Of course, strictures are supposedly far less common in LyC oesophagitis than in EoE. WHAT IS THE MOST LIKELY DIAGNOSIS?
a) Portal hypertensive gastropathy
Doesn't really look like 'snake skin' does it?
b) HP associated gastritis
HPAG is a great mimicker but not this time
c) Gastric vascular ectasia
Absolutely, affecting the whole stomach!
d) Lymphocytic gastritis
LyC gastritis is ulcerative!
e) Linitis plastica
Another great mimicker but this is a vascular issue rather than mucosal infiltration!
explanation
Of course, this is a case of Gastric Vascular Ectasia. As the whole of the stomach is affected, I don't think that we can call it 'antral' ectasia. Gastric antral vascular ectasia “GAVE” (watermelon stomach) has been described with; • Cirrhosis • Atrophic gastritis/achlorhydria/hypergastrinaemia • Connective tissue diseases (especially systemic sclerosis and hypothyroidism) • Diabetes • Heart failure • Chronic renal failure It has been proposed that the underlying link between all the different conditions associated with GAVE may have autonomic dysfunction in common leading to prolapse of the antral mucosa through the pylorus. Must admit that I'm sceptical! A study suggested that a “punctuate pattern”, as seen in this clip, is typical of cirrhosis whilst a “striped type” was more common in non-cirrhotic cases. Indeed this patient had NASH cirrhosis. Portal hypertensive gastropathy probably has a different aetiology and is a different condition as gastric antral vascular ectasia can develop with a normal portal pressure. Patients with vascular ectasia of course usually present with iron deficiency anaemia. Patients with bleeding from GAVE were previously treated with antrectomy. Now, the first line treatment is “thermal therapy”. Octeotride and oestrogen-progesterone have also been used in small series but would now only be considered if endoscopic therapy fails. It is far easier to treat these lesions using the argon coagulator than the heater probe. Using a banding device may be quicker in patients who tolerate gastroscopies poorly. RFA is also effective but is VERY expensive. This patient attends for Barrett's surveillance WHAT IS YOUR DIAGNOSIS?
a) Barrett's without dysplasia
A nodule within Barrett's is NEVER 'normal'!
b) LGD
LGD is flat, not nodular!
c) HGD
Good guess! Although your guess actually proved to be wrong
d) IMca
Small crypts + nodule = correct!
e) invasive cancer
Nodule should have been larger and without those small crypt openings
explanation
My 'rules of thumb' when assessing Barrett's is as follows: 1) crypts look different in a distinct patch but the area is flat = LGD 2) areas of superficial ulcers within the Barrett's = widespread LGD 3) crypts look different and there is a distinct nodule = HGD 4) crypts are tiny small and there is a nodule = IMca 5) there are no crypts and there is larger nodule = invasive cancer Of course this isn't fool proof ! After all, it's very difficult to distinguish HGD from IMca even on histology! However, it gives you a starting point on how to assess Barrett's and what you should enter on that Histopathology request form. Remember that your pathologists need your help! This lesion was found at gastroscopy WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?
a) Siewert I SCC
Nope!
b) Siewert I adenocarcinoma
Lesion isn't centred 1-5cm above the GOJ
c) Siewert II adenocarcinoma
Yes! Lesion staged as T2,N0 on PET-CT
d) Siewert III adenocarcinoma
Lesion isn't centred 2-5cm below the GOJ
explanation
This lesion is clearly malignant with a rolled edge and surrounding mucosal ulceration. It was confirmed as a Siewert II adenocarcinoma, T2,N0. Cancers at this location are becoming more common. They are easy to miss, particularly if you don't slow down as you traverse the gastro-oesophageal junction (GOJ) and/or retrovert at a distance. On retrovertion you need to pull the scope back up so that you can have a close view of the cardia. Siewert et.al. developed the classification as follows:
Of course it can be difficult to determine where the epicentre of a cancer is, particularly on imaging. At endoscopy you are in a unique position to accurately record the correct Siewert type of the cancer. It makes a difference because the Siewert type has implication for treatment! Siewert I lesions are treated with oesophagectomy and gastrectomy as these lesions usually metastasise to nodes in the mediastinum. Siewert II are 'true' junctional cancers and mainly metastasise to nodes in the abdominal nodes but in around 15-20% of cases, there are mediastinal nodes. For this reason, patients with Siewert II lesions are only offered gastroectomy (without oesophagectomy) IF there is no mediastinal lymphadenopathy. Arguably, any borderline mediastinal nodes should probably be sampled before or during surgery before a final decision is made not to clear the mediastinal nodes with the resection specimen. Patients with Siewert III cancers are usually offered total gastrectomy plus a distal esophagectomy (to get clear resection margins, a so called R0 resection ) as these lesions spread to peritoneal nodes. This is a video clip of a small lesion removed from the sigmoid colon. WHAT IS THE MOST LIKELY HISTOLOGY?
a) TA+LGD
But it's a IIc lesion with IIIs crypts in the centre?!?
b) TA+HGD
Absolutely!
c) Invasive cancer
But there ARE small round crypts in the centre and it DOES lift!!!
explanation
You may call this a "flat elevated lesion with a central depression (IIa+IIc lesion) or simply a depressed lesion (IIc lesion). Frankly it doesn't matter because both a part of the same 'family' of evil little b.....ds. They are always TA's and the small, round crypts (Kudo type IIIs crypt pattern) tells you that the lesion harbours HGD. This is because as dysplasia progresses from low to high grade, crypts get smaller and more withered. Of course they eventually disappear altogether as the lesion develops into a cancer which no longer follows any 'instructions' to form organised crypts. However, the crypt pattern is still discernible in the centre AND the lesion lifts well. Both of these tells you that the lesion is likely to still be benign. Ultimately, the pathologists called it a TA+HGD. However, there was mucinous differentiation in the centre of the lesion. Could these little shits be the early stage of mucinous colonic cancers? Quite likely! Imagine how easily they are missed when hiding behind a fold or below a shallow puddle !!! WHERE IS THE BARRETT'S CANCER?
a) 12 O'clock
Eagle eye!
b) 3 O'clock
But the round crypt openings say otherwise!
c) 6 O'clock
Nope!
d) 9 O'clock
Where there is hardly any Barrett's?!
explanation
Of course the lesion is situated at 12 O'clock. There you can see a subtle mucosal nodularity with an irregular vessel pattern. It was removed by 'suck within the cap' EMR and confirmed as an IMca. This is a solitary gastric polyp WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?
a) Hyperplastic polyp
Spot on!
b) Hamartomatous polyp
A bold guess but wrong!
c) Cystic fundic polyp
Too red and should be several of them!
d) Adenomatous polyp
But there is no defined crypt pattern?!
e) Malignant polyp
May be a 5% chance that you are right!
explanation
A missing piece of information, which I perhaps should have provided, was the H.pylori status of this patient! This lesion was arising from a H.pylori associated gastritis.
Most polyps found in a stomach with Helicobacter pylori associated gastritis are hyperplastic (inflammatory). They appear angrily red (because they have lots of capillaries) and often with white fibrin caps, making them look a little like mushrooms. A small proportion of hyperplastic looking polyps are actually malignant. In my experience, these 'stealth cancers' are most common close to the gastric cardia and are always solitary. Conversely, multiple inflammatory polyps in the antrum and gastric body are almost certainly benign. Of course, this is a 'solitary' hyperplastic polyp, close to the fundus. Perhaps not unexpectedly it harboured some (low grade) dysplasia (histology below). The dysplasia is in the crypts lined by deep purple/blue cells rather than the normal light pink cells. The contrast is probably best seen in the second histological slide where the dysplastic part is towards the top of the slide and the non-dysplastic is at the bottom half. If the H.pylori test is negative, and particularly if the patient is taking a PPI, the polyp is more likely to be a 'Fundic gland polyp' (cystic fundic polyp) which are full of cystic spaces and therefore look a little translucent like frog-spawn. Rarely polyps are hamartomatous as in Peutz-Jeghers polyps and the polyps arising in patients with 'Cronkhite-Canada syndrome or in Juvenile polyposis. In many cases these lesions have an odd but distinct surface crypt pattern or, alternatively look again look translucent like frogspawn. It's rather difficult to explain the appearance of a hamartomatous polyp and for this reason, I have attached some images below (after the histology slides). Another polyp, most likely to arise in an atrophic gastritis with patches of intestinal metaplasia, is an adenomatous polyp of the 'intestinal type'. To remind you, there are at least 4 types of gastric adenomas which all have an organised and regular surface crypt pattern:
These linear lesions were found in a 50 yr old patient undergoing colonoscopy to investigate her loose stool.
WHAT IS THE LIKELY DIAGNOSIS?
a) Crohn's disease
Does give linear ulcers but should be larger and deeper!
b) Ischaemic colitis
Also gives linear ulceration, often on the ante-mesenteric border.
c) Collagenous colitis
Absolutely!
d) Ulcerative colitis
Doesn't give linear ulceration and surrounding mucosa wouldn't be normal
e) Lymphocytic colitis
Perhaps one could develop into the other?
explanation
Actually, this patient had collagenous colitis! I suspect that the acute injury are linear tears in the mucosa which then granulate as in the images above. Finally, you are left with linear scars as in the image below. Pure speculation but seems logical ! At colonoscopy, the mucosa is often unremarkable but there may also be mild, patchy erythema or linear cracks. Histology reveals the typical thickening of the subepithelial collagen layer from the normal 3-6 μm to more than 10 μm as well as lymphocytic infiltration of the epithelium and the lamina propria. Rectal biopsies are not sufficient to make the diagnosis as normally the collagen layer is particularly thin here. Samples from the rectum and sigmoid confirms the diagnosis is more than 90% of cases. Interestingly, patients with eosinophilic oesophagitis may also develop some fibrosis in the lamina propria which also 'cracks' in a spectacular way when a dilatation is carried out.
This polyp is pretty when viewed by the endoscopy but stunning below the microscope!
WHAT IS THE HISTOLOGY?
a) Tubular adenoma (TA)
This polyp is prettier than that!
b) Tubulovillous adenoma (TVA)
Endoscopically it could be but histology says otherwise!
c) Villous adenoma (VA)
Absolutely!
d) Traditional Serrated Adenoma (TSA)
Endoscopically Yes, but histologically No!
e) Sessile Serrated Lesion (SSL)
Would be unusal for an SSL to be 'subpedunculated'
explanation
Endoscopically it can be difficult to recognise a villous adenoma. Unless you submerge the lesion to see the villi rise up like the arms of a sea anemone. Apparently, they are quite difficult to 'process' by the pathology lab as well. They are fragile and those beautiful villi, easily become damaged.
Of course, villous adenomas are regarded as 'high risk lesions'. The other high risk findings often used as surrogate markers for cancer in guidelines are: having 3 or more adenomas, polyps 10mm or larger, and polyps harbouring high-grade dysplasia. However, if you have to make a choice of the two strongest predictors of future cancer risk, a study in Gastroenterology found that it would be; finding a polyp 2cm or larger and resecting a polyp found to harbour HGD [Gastroenterology 2019;158(4);875-83].
This colonic polyp was removed as a single fragment from a 60 year old lady. You can see the mucosal defect in the last image. The patient asks you what will happen next?
WHAT WILL YOU REPLY?
a) Can't tell, we will have to wait for the histology
You can do better!
b) In all likelihood there will be a site-check in 4 month or so
You are missing something!
d) You will probably need an operation
You've spotted the desmoplastic reaction!
explanation
The polyp looks very suspicious but did seem to lift and I therefore decided to go ahead and removed it using a stiff, large snare. It took a little longer than expected for the snare to cut through. Of course, the mucosal defect should be blue. In this case it's yellow! The polyp was malignant, invading about 1mm into the submucosa and you are looking at the 'desmoplastic' reaction generated by the cancer.
Apart from the sometimes deceptive 'non-lifting sign', there are two further signs that a lesion may be malignant. First, it may look smaller and smaller as you inject below the lesion (see example below). Another sign is that your blue sub-mucosal injection appears to lift the lesion until you retrovert and have a look at the other side. If you then find that it hasn't actually 'crossed the mid-line', there is fibrosis below the lesion preventing the fluid to disperse evenly. I was not entirely surprised to learn that the patient declined surgery. After all, he was 86 years old! He lived another 7 years and never developed any sign of bowel cancer. By the way, there is a theoretical risk of tumour seeding if the lesion is perforated during resection. However, when the perforation is done with a red-hot tool such as a knife or snare, the risk of seeding is surprisingly low. I have perforated a handful of cancers but have never had a case of late disseminated peritoneal disease. My Japanese colleagues (off the record), agree that the risk is there (some have seen it) but is low. If you decide to sample a suspicious looking polyp, you shouldn't use the same forceps to sample another lesion. This is because if cancer cells become lodged in the biopsy forceps, which are then used to sample another location and them become stuck in the biopsy, the histopathologist will diagnose cancer in TWO locations when in fact, there is only a single cancer.
This was found on the anterior gastric wall in an elderly patient with iron deficiency anaemia
WHAT IS THE MOST LIKELY DIAGNOSIS?
■ Gastric ulcer scar
Quite possible but you would take samples surely?
■ Gastric erosion
But there is a nodule in the centre?
■ Benign gastric ulcer
But there is no 'ulcer' in the centre?!
■ Early gastric cancer
Surely, the most likely diagnosis?
explanation
Gastric folds are being pulled into this 'lesion'. Of course most EGC's are depressed or flat elevated with a central depression. This is not easy to classify into the Paris classification system. I guess that you can argue that its' an elevated lesion with a central depression? Anyway, at the centre of the lesion there is a nodule! Not an ulcer! It's most likely an EGC. In fact, the lesion was resected endoscopically and proved to be poorly differentiated invasive cancer with a positive deep margin ! As the patient was 84 yrs old, no surgery was offered. That was 6 years ago and the patient remains well with only an unremarkable scar in the stomach to remind him ! Wonderful !
These peculiar colonic lesions were found in the colon of an asymptomatic patient.
WHAT ARE THEY?
■ Inflammatory polyps
Absolutely!
■ Adenomatous polyps
These are too long and peculiar looking to be adenomatous!
■ Hamartomatous polyps
No way!
This lesion was found in the transverse colon of a patient with iron deficiency anaemia (IDA).
HOW WILL YOU APPROACH IT WITH APC?
■ Zap the centre first
Absolutely, ablate the central feeding vessel!
■ Start in periphery and work towards centre
Would work but take longer than neccessary
■ In a spoke an wheel pattern starting in the periphery
Would also work but would take longer
This patient attended for dilatation of his biopsy confirmed peptic oesophageal stricture. Clip has been speeded up somewhat. WHAT WOULD YOU ORGANISE NEXT?
■ A clinic appointment
To ask pt about the swallowing? Hmm, somethings missing!
■ Another dilatation in 2 weeks time
Stricture not very tight and the dilatation should last longer
■ an early follow up OGD for biopsies
The mid-oesophageal stricture is peptic but what of the mucosa below?
explanation
The background to this case is a recent audit which we did in Leeds on missed upper GI neoplasia. We have had several instances of oesophageal cancers being missed when the endoscopist focused too much on the 'task in hand'. For example, we have had several SCC's missed when the endoscopist was carrying out a Barrett's surveillance endoscopy. This is another example of a missed (intramucosal) adenocarcinoma, glimpsed about 10 seconds into the clip in the 3 O'clock position. With mid-oesophageal peptic strictures there is often a stretch of Barrett's below which of course must be assessed and sampled at the earliest convenience. Of course, one can argue that when the job is to do something therapeutic, such as placing a PEG or removing a large polyp, it is 'permissible' to miss a cancer elsewhere. After all, the objective is not to undertake a careful diagnostic examination but to 'do a job'! I'm a strong believer that 'diagnostic' examinations and 'therapeutic' examinations must be clearly separated when you are looking at 'missed lesions. There is a distinct 'therapeutic window' during all endoscopic procedures done without a general anaesthetic. In the upper GI tract, it's up to 20-30 minutes and in the colon I think that it's up to 45-60 minutes. Your patient will not thank you for wasting the valuable minutes of your therapeutic window on carrying out a full diagnostic examination. Of course, after your therapeutic procedure you should consider if an early diagnostic gastroscopy or colonoscopy is needed. But carrying out a full assessment of the squamous portion of the oesophagus at the time of a Barrett's surveillance examination doesn't add much to the procedure. Similarly, when a mid-oesophageal peptic stricture is found, one should realise that the reason that the peptic stricture is in the middle of the oesophagus and not the gastro-oesophageal junction, is probably that there is a a Barrett's segment below the stricture. It doesn't add much time to the procedure and that IMca could have been spotted earlier! Previous biopsies have confirmed that this rectal polyp harbours TVA+HGD. It's removed by piecemeal EMR and at the end of the 2min video clip you see the end result. WHAT WOULD YOU DO NEXT?
■ Place clips
Always clips !
■ Wait for histology
And of course, you have requested an 'urgent report'!
■ Request EUS
Life is too short for EUS!
■ Organise an MRI
For local staging and confirmed T2,N1 cancer
■ Request staging CT
Looking for mets in the Chest+Abdomen+Pelvis - proved negative!
explanation
The learning point of this video clip is the EMR defect; it's white (image A) !!! Perhaps the picture below explains it better. Normally my EMR defects are blue (because I mix indigo carmine dye into the submucosal mix). In 'image B' below, the white arrow in the second image shows you what a 'healthy EMR defect should look like. IF you cut too deep, you can see the white, linear fibres of the muscle propria layer (red arrow). Of course this is a warning sign that you MUST carefully close the defect with lots of clips. Actually, next to the tip of the red arrow you can see a black 'micro-perforation' where the full thickness of the muscle layer has been breeched. Naturally, this is were your first clips goes!
Anyway, the mucosal defect in the video clip is just - white, without any linear muscle fibres. This is fibrosis! I have seen fibrosis like this below large sigmoid polyps which have been yanked about with the forceful sigmoid peristalsis. However, the more usual reason for this appearance is that you are looking at the fibrous tissue below a cancer, called 'desmoplasia'. Consequently, if I see a fibrous tissue in the base of the lesion I would do the following: Place clips (because I always do) Fast-track the histology Organise an MRI Request staging CT (chest+abdomen+pelvis) The ultimate diagnosis? Histology confirmed that the polyp was malignant and the imaging (of course requested at the time of the resection), confirmed a T2, N1 carcinoma. A week later, we had a full diagnosis. Unfortunately, the patient turns out not to be a surgical candidate. There is rarely unbridled joy after the endoscopic removal of a CRC ...
This polyp was found in the sigmoid.
HOW IS IT BEST REMOVED?
■ Cold snare polypectomy
Wouldn't be my first thought!
■ EMR
I agree - single fragment EMR!
■ ESD
Would just add time and expense to procedure (unless you need practise, I guess)
explanation
This 10-12mm polyp is covered with a beautiful gyrate crypt pattern typical of a TVA. The risk of cancer deep within, in spite of the normal surface is far below 1%. But it's not 0% and it would also be a little difficult to cut through this amount of tissue. For these reasons, I think that 'cold snaring' would be wrong.
At the other end of the spectrum, we have an ESD. It would ensure a single fragment resection but would take about 20 minutes or so. The in between the two, we have an EMR. If course, a single injection of 3-4ml would lift this nicely and then a 15mm snare would resect it, single fragment, within a minute. I think that the best method of removal of polyps up to about 2cm, is by EMR as polyps up to this size can usually be removed as a single fragment. This patient is on a surveillance programme due to alcoholic liver disease but has never had a bleed. He is maintained on a non-cardioselective β blocker. WHEN WOULD YOU RECOMMEND THE NEXT SURVEILLANCE EXAMINATION?
■ None, this patient should be offered banding
Correct, if you decide that there are 'red signs' or the varices are grade II or III
■ In 12 months time
Correct, if you decide that there are no 'red signs' and that the varices are grade I
■ In 2-3 years time
Would only be correct if there are no varices at all!
explanation
I must admit that I don't like the current surveillance guidelines for patients with portal hypertension. This is a good example why! Although the LFT's had remained stable and the patient had remained abstinent, you could argue that there are 'red signs'. Of course, the presence of 'red signs' predicts progression of varices [J Hepatol 2003;38:266–72] and because the patient is already on a β-blocker, band ligation should now be started. The truth is that 'red signs' are common and have a poor agreement value between endoscopists.
If you decide that there are no 'red signs', and that the varices are grade I only (which depends on the degree of inflation of the oesophagus), the recommendation is to offer surveillance in 1 year. Finally, if you decide that the varices are now grade II (or III), variceal band ligation would be the logical next step. Thus, you can make an subjective argument for any of the above three treatment options. Of course, what you decide will be judged in hindsight. If you decide that these are not red signs and the patient re-presents with a bleed in 6 months time, you could be open to criticism for missing signs of progressive liver disease. Surely, in the modern era of FibroScans, it's possible to predict progression of portal hypertension non-invasively!!! Five years ago, the BAVENO VI workshop only mentioned in passing, that surveillance endoscopies may be avoided in patients with elastography values <20 kPa and a platelet counts >150,000 as these patients are at low risk of progression. Similarly increasing size of the spleen is another warning sign and could be looked for when these patients attend for screening for HCC's. The American guidelines suggest that there is no need to offer patients with untreated viral cirrhosis a screening endoscopy to search for varices IF elastography is <20 kPa and the platelets are >150. They concede that annual elastography and platelet counts may be less predictive in other causes of cirrhosis. However, the American guidelines advice continued surveillance if varices have been found in the past, particularly if liver injury is ongoing. The next Baveno conference in October 2021 will hopefully recommend non-invasive monitoring rather than endoscopy. It would be cheaper, less arduous for patients and offer less subjective findings! The now rather dated BSG guidelines are summarised in the graph below.
■ Inflammed granulation tissue
Was my first too! But it doesn't quite look right ...
■ Adenomatous polyp
Adenomatous polyps are usually smooth topped
■ Malignant polyp
An intramucosal cancer arising from the anastomosis
explanation
This patient had in the past undergone a Billroth II operation. You can see that the nodule is arising from the surgical anastomosis. Distal gastrectomy is a well-known risk factor for developing an anastomotic cancer later [Sitarz R. World J Gastro. 2012;18(25):3201–6]. The risk of anastomotic cancer steadily increases after surgery. About 15 years after surgery, the risk exceeds that of the background population (age- and sex-matched). For this reason, surveillance has been suggested to start 15 yrs after surgery. The case for surveillance was strengthened by the fact that dysplasia can often be found in random biopsies from the anastomosis several years before cancer develops. In spite of this surveillance in not recommended. A surveillance study in Amsterdam traced 500 patients who had undergone a distal gastrectomy for benign disease and only detected 10 cancers (6 were in an early stage). Furthermore, there was no survival advantage in the screened group after 10 years follow up [J Clin Pathol. 1984;37:748–54]. Other studies have also put the cancer yield by surveillance at around 2% and concluded that regular surveillance could not be recommended [Am J Surg 1977;134:581-4], [ Lancet 1977;ii467-9] [ Scan J Gastro 1981;suppl 16:169-71]. Nevertheless, my practise is to always take do 'opportunistic screening' by obtaining 6 biopsies or so from the gastric side of the anastomosis when I come across a case. On first glance the nodule appears to be inflamed granulation tissue only. However, there is an odd cleft in the centre and the base from which it arises is also nodular. The polyp was removed and was confirmed as harbouring intramucosal cancer. Of course, after finding dysplasia (which often does not progress) or IMca, these patients should be offered surveillance.
This was found at gastroscopy in a middle aged patient with anaemia
WHICH STATEMENT IS CORRECT?
■ The severity is related to the severity of the underlying disease
This is generally thought to be the case!
■ Its generally more marked in the distal vs the proximal stomach
It's the other way around actually
■ Beta blockers don't help
Beta blockers do reduce gastric perfusion
■ The condition is irreversible
A reduction in portal pressure improves the condition
explanation
Congestion secondary to portal hypertension is thought to be the primary cause of Portal Hypertensive Gastropathy. However, other factors may also play a part such as mucosal protective mechanisms, inflammatory response, local vascular tone, hepatic function, gastric mucosal perfusion, endotoxin, and gastric sucrose permeability, have been suggested to influence the development of Portal Hypertensive Gastropathy. However, because Portal Hypertensive Gastropathy is a dynamic condition which improves after liver transplantation or after TIPS, suggests that it IS portal hypertension which is the primary driver.
There is a correlation between Portal Hypertensive Gastropathy and Child-Pugh stage, HVPG (hepatic vein pressure gradient), MELD score, albumin level, bilirubin, platelet count, INR and even survival [Bang CS. BMC Gastro 2016;16(93] You are right, there is also a small oesophageal varix visible! These polyps were found in the stomach of a 40 year old man on a Barrett's surveillance programme WHAT WOULD YOU ADVICE?
■ We should eradicate your Hp
This patient is VERY unlikely to have H.pylori
■ We should remove these endoscopically
An unnecessary job unless one look wonky, like perhaps that single red one!
■ We should stop you PPI
But the patient has Barrett's ?!
■ We should stop you PPI
That's what I would do !
explanation
Of course, this is a Fundic Gland Polyps/Cystic Gland Polyps . They are usually multiple, somewhat transparent sessile polyps, usually in the 1-5mm in diameter and located in the body and fundus.
Histologically there are cystically dilated glands lined by gastric body type mucosa. Of course, there is no need to sample these. A study patients with FGPs reported that they can be diagnosed with a high degree of accuracy based on endoscopic appearance alone (J Clin Gastroenterol 2003;36:399-402). The sporadic polyps are caused by activating mutations of the beta-catenin gene. Not sure how an APC gene mutation (you may remember are involved in FAP), could give rise to FGP’s though! Furthermore, I don't know how the use of PPI's can be linked to the development of FGP's. Presumably its something to do with the prolonged hypergastrinaemia and enterochromaffin cell-like (ECL) hyperplasia? I have seen a couple of cases of cancer developing within a FGP. In both cases the patient had FAP and the polyps were markedly larger than all the surrounding cystic fundic polyps. There have been case reports of dysplasia arising within sporadic fundic gland polyps. A few series have reported a <1% risk of sporadic FGPs harbouring dysplasia (Am J Surg Pathol 1998;22:293-298, Eur J Gastroenterol Hepatol 2003;15:1153-6, Endoscopy 1995;27;32-37). I must admit that I don't believe the figure of <1% risk of dysplasia in a sporadic FGP. I suspect that these series consist of rather selected cases. Of course by only selecting polyps 10mm or larger, you would be filtering away 99% of the FGP's, leaving only the 'far above average risk lesions' behind. Nevertheless, the BSG recommend sampling some of them to confirm the diagnosis but not to set out on any attempt to remove them. Of course, this advice is different to the advice for Hyperplastic polyps which ARE usually linked with H.pylori and also a greater risk of developing cancer. The BSG advice is summarised in the algorithm below. Sporadic FGPs are not associated with either H.pylori gastritis or atrophic gastritis. In fact, it has been proposed that H. pylori infection may have an inhibitory effect on the development of FGPs. Of course, you wouldn't stop the PPI in a patient with Barrett's. Actually there is no evidence that patients with unstable Barrett's are any more or less likely to progress to cancer if they stop their PPI. However, there must be a point (I presume) when the use of PPI is beneficial in the 'evolution' of Barrett's. Are patients on a PPI less likely to develop Barrett's or to develop damage the stem cell DNA? Not sure! The BSG do recommend a colonoscopy in patients below the age of 40 yrs. to rule out the possiblity of FAP. However, as the average age of colorectal cancer in patients with 'attenuated FAP' is 55 yrs, I would personally recommend a colonoscopy in patients above the age of 40 yrs. This is the GOJ of a 60 yr old woman with dyspepsia. WHAT IS YOUR DIAGNOSIS?
■ Reflux oesophagitis
No this is a nodule not an ulcer!
■ Hyperplastic/reactive nodule
Hyperplastic nodules have villous surface!
■ Unremarkable Barrett's
A nodule within Barrett's is always suspicious!
■ Adenocarcinoma
Absolutely!
■ Squamous cell carcinoma
No abnormal vessel pattern within nearby squamous mucosa!
Explanation
Actually, this patient was on a Barrett's surveillance programme. Five years earlier a small IMca had been removed following which annual surveillance had been reassuring. However, then this lesion was found and referred for removal.
Histological assessment of the resection fragment reported early invasion into the submucosa (which is 'allowed' provided that the depth of invasion is less than 500 microns (0.5mm). There was no LVI but unfortunately, there was poor differentiation. Of course, the 'worst' feature to find is probably LVI. Poor differentiation is worrying but less worrying than LVI. The reason for this is that 'poor differentiation' is a rather poorly defined entity. For example, how many crypts should be involved to call something 'poor differentiation' rather than 'focally poor differentiation'? Anyway, the patient was young and ultimately underwent an Ivor-Lewis which confirmed that the EMR had been curative with only some HGD remaining within the residual short stretch of Barrett's. We urgently need a prospective study following this type of Barrett's patient closely over time with regular EUS and CT to see if we can detect the small number of patients who subsequently turn out to have lymphnode involvement
Patient has turned up to have his 'green' PD stent removed but I'm astounded to find two stents poking out of the papilla and they are both green !?
WHAT SHOULD I DO?
■ Remove the stent with a twist in it
Turned out to be correct!
■ Remove both stents
A dangerous attitude?
explanation
After scrutinising the X-rays, I concluded that the Pancreatic Duct stent was the 'single pig-tailed' stent (the one with the twist). Furthermore, the other one was draining bile. Obviously, the reason for the pig-tail is to stop the stent from migrating up the duct. PD stents are more likely to migrate than CBD stents and therefore the pig-tailed stent was more likely to be the PD stent even before I confirmed this on the images taken at the time of ERCP.
Well, this is one of the reasons why I don't like having stent removals on my list. Shouldn't it be the job of the person who placed to stent to also remove them?! |
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