Posted by Dr Pradeep Mundre
This small 15 mm sigmoid polyp was referred for Endoscopic resection. Patient was fit and well with no comorbidities. What do you think of the surface pattern? Would you offer Endoscopic resection or surgery for this lesion ? What is the predicted histology?
The question is how reliably can you trust the surface pattern? And how much importance do you give to this in actual decision making. I classified this as JNET 3 verging on 2B , but as the other factors and dynamic assessment and lifting were favourable , went ahead with ESD for this lesion. What was the eventual histology?
The lesion was resected Enbloc with ESD - suboptimal lift - specimen size 25 mm x 25 mm. The histology was one of Pt1B Sm invasive adenocarcinoma, moderately differentiated, with depth of invasion at 2.9 mm beyond muscularis mucosa (Deep sm invasion ) with Lymphovascular invasion. Clear deep margin by 0.9 mm , clear lateral margins. He was offered surgery after this due to LVI
Often experts consider other factors such as
In conclusion , although its fair to use surface pattern assessment to differentiate malignant and non malignant polyps, but a decision on endoscopic resectability should be based on various factors than just based on JNET Classification.
Post by Dr Pradeep Mundre
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?
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.
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!
Yes! Gyrate crypts best seen after indigocarmine dye spray (I think).
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 gastric lesion is found in an 85 yr old man. Samples have confirmed a moderately differentiated gastric cancer but the lesion can't be seen on CT. The patient is frail with multiple comorbidities and declines both an endoscopic resection and surgery. However, he does ask how long it will take before he dies from the cancer?
WHAT WILL YOU ANSWER?
a) 1-2 yrs
Definitely too pessimistic!
b) 2-3 yrs
Hmm, perhaps if the lesion is poorly differentiated but it doesn't look it!
c) 3-4 yrs
This is probably how long it will before that cancer is at an advanced stage but patient will probably survive for another couple of years beyond that 'transition point'
d) 4-5 yrs
Probably too pessimistic still!
e) >5 yrs
With limited information this is the only figure backed up by some data.
This question is something of an homage to Sir David Cox who developed the well known 'Cox Regression analysis'. Professor Cox died in 2022. As you know, the 'Cox Regression analysis' basically explores the relationship between the length of survival and more than one variable.
You would expect the following 'variables' to influence cancer-specific survival; histology, size of lesion, stage of lesion and perhaps the macroscopical type of early gastric cancer. Perhaps the location within the stomach also influences survival. There is some data that lesions at the gastric cardia are worse.
Of course we don't have data on any of these 'variables'. However, I know of one paper by Tsukuma et al [Gut 2000;47(5):618-21] which did look at the natural history of 56 early gastric cancers in Osaka, Japan. This paper was actually a riposte to an earlier editorial from Leeds by one of my colleagues arguying that EGC is a 'pseudo-disease [Everett S. Lancet 1998;351:1350–2].
As you would expect, 56 EGC's is not enough for any sub-analysis of the above variables. Also they didn't actually look at survival. They looked at the average time it took lesion to progress from what appeared to be 'early' gastric cancer (i.e. confined to the mucosa or submucosa) as diagnosed by endoscopy.
And here we reach the first issue! How sure can we be that the lesion in the image is an EGC and hasn't started to invade into the muscle propria (thus being advanced)? The lesion is about 2cm across and there is a an organised crypt pattern in the centre (can't comment on the vessel pattern as there are no magnification images). It does look 'early' and I stand at least an 80% chance of being correct in that diagnosis. Incidentally, 'lifting' is not a reliable sign in the stomach as any ulceration of the mucosa will tether it down, regardless of stage of invasion.
The authors were pleased to report that if patients are left for long enough, those EGC's will grow and progress. No surprise there then! But the rate of progression was slow!!! The median time it took for 'early' gastric cancers to progress to advanced gastric cancers (i.e. T2 or worse) was estimated to be 44 months but probably shorter in patients with poorly differentiated cancers. Furthermore, the cumulative 5 year corrected survival in patients who never underwent surgery was about 63%.
The answer to the question is therefore 'e'. This patient is likely to live more than 5 years from diagnosis of his early gastric cancer. Better than expected here is the Kaplan-Meyer curve below !
This patient underwent a CT angiogram for chest pain. The angiogram was unremarkable but the radiologist mentions an 'irregularity at the caecal pole with hyperenhancement and mild adjacent fat stranding' and recommend colonoscopy. After the examination, your patient asks you if you have found anything?
WHAT WILL YOU TELL YOUR PATIENT
a) Reassure the patient
That would be unwise!
b) Tell him to wait for the histology
Strictly speaking 'not wrong' but it's not the best option to choose
c) Tell him that we will organise an MRI scan next
MRI's are requested for rectal cancers
d) Tell him that we will organise an EUS next
Life is too short for EUS!
e) Tell him that we will organise a 'staging' chest/abdomen/pelvic CT
This is precisely what you should do!
Did you notice the lesion next to the biopsy forceps? At initial glance into the caecum, there is nothing to see. However, this lesion was about 20mm in diameter and with that rolled edge. It's clearly malignant and you need to request staging CT's. Histology did confirm a mucinous adenocarcinoma and CT sized it at 4.7cm. Far larger than initially thought! As it was involving the serosal surface, it was staged as T4, N1 (due to several small nearby nodes).
Mucinous colonic cancers are unusual, accounting for about a little more than 10% of CRC's. They are usually situated in the proximal colon. This is not the only reason why they are easy to miss. At the early stages they have an infiltrative, ulcerative growth pattern which easily hides behind bubbles or a pool. These are small but evil little things which are easy to miss and grow fast.
By the way, 'signet ring adenocarcinoma' (where the mucus is INSIDE the cell rather than OUTSIDE of the cells) is another sub-type of adenocarcinoma which may be part of the same spectrum. Mucinous and signet ring adenocarcinoma, share similar molecular features such as MSI-H, CpG island methylator phenotype-high (CIMP-H), and frequent BRAF V600E mutations. Of course microsatellite instability is linked with Lynch syndrome but in this case immunohistochemistry stains revealed normal mismatch repair proteins MLH1, PMS2, MSH2 and MSH6.
This scary looking polyp was found in the sigmoid in a patient on a polyp surveillance programme.
WHAT IS THE LIKELY DIAGNOSIS?
a) Mucosal prolapse
Yes! You can't see any typical gland openings at the tip of this polyp. It's a mucosal prolapse polyp with a serrated lesion at the tip.
b) Adenomatous polyp
It's a battered polyp but without any recognisable crypt openings at the tip and therefore NOT adenomatous.
c) Malignant polyp
Well it looks scary and without an organised crypt pattern. All hallmarks of a malignant polyp. However, this lacks crypts because it's an innocent mucosal prolapse polyp!
You've seen a few examples now of the 'mucosal prolapsing conditions' which include solitary rectal ulcer syndrome and inflammatory cloacogenic polyps. First described in 1985 [GIE 1985;31:196–9] they are usually said to be rare. However, experienced endoscopists know that these are common in the sigmoid. I've never seen a mucosal prolapse polyp outside of the sigmoid and would actually not make this diagnosis elsewhere in the colon.
Histology is usually said to be the way to "confirm the diagnosis and rule out cancer". However, for me it's an endoscopic diagnosis. But I do understand that these lesions do look alarming. For this reason, I sometimes take it upon myself to resect the tip of the lesion, proving to all those of little faith, that the lesion is absolutely innocent.
However, I'm not sure that my surgical colleauges are always reassured by the histology which usually rambles on about 'distorted elongated branched crypts, with fibromuscular obliteration of lamina propria with lots of intramucosal haemorrhages and a splayed and hypertrophied muscularis mucosae". However, the bottom line of that pathology report will read; 'No dysplasia'.
This patient is undergoing a gastroscopy because of dyspepsia.
WHAT IS THE LIKELY DIAGNOSIS?
a) Hyperplastic polyp
It's unusual to see a ulceration on a hyperplastic polyp
Unlikely as the lesion isn't covered with entirely normal looking gastric mucosa
Although there are none of the classical chunky vessels around its neck, there are other smaller nearby lesions with some unusually large vessels
Gastric adenomas are usually flat, plaque-like lesions
e) Early gastric cancer (EGC)
EGC is a good guess and patients with atrophic gastritis often do have nearby small type I gastric NET's. However, this isn't an EGC.
As you well know, gastric NET's are classified as; type I (70%-80% of gastric NET's) linked with hypergastrinaemia secondary to an atrophic gastritis and classically appearing as multiple, small gastric nodules.
Then we have the rare type II gastric NET which account for about 5-8% is associated with hypergastrinaemia from a gastrin-secreting tumour such as in the MEN-1 syndrome or the Zollinger–Ellison syndrome. This was a type II gastric NET which has arisen in a patient with a pancreatic gastrinoma and MEN. Several other much smaller NET's have arisen in the nearby gastric mucosa.
Finally, we have the type III NET (20%) which are solitary, large nodules with a high mitotic index arising in a healthy gastric mucosa. These are the ones not to miss as they need a cancer-like gastric resection.
To remind you of the lessons from Prof Mark Pritchard's Podcast on gastric NET's, you should;
• Look for atrophic gastritis
• Consider using some pH indicator strips to measure the gastric pH (unless pt is taking PPI)
• Identify all the NETs, record their size and number and sample them for histology and grading
• Take antral and corpus biopsies and ask pathologist to do report on the presence/absence of gastric atrophy and intestinal metaplasia and also ask them to carry out immunohistochemistry stains for ‘gastrin’ in the antral biopsies and ‘chromogranin’ and ‘synaptophysin’ in the gastric body samples.
• Look into the second part of the duodenum for the small submucosal gastrinomas which occasionally are seen in MEN-I
• Consider samples for Coeliac disease if the patient has IDA
CONSIDER OFFERING ENDOSCOPIC RESECTION FOR:
• type I gastric NETs if >10-15mm
• type II gastric NET if they’re causing problems (eg bleeding) and/or gastrinoma can’t be resected
• type III gastric NET <1cm (provided that it's no worse grade 1/low grade 2 !)
If that proliferative index comes back surprisingly high (>10%), make sure that the pathologist hasn't inadvertently counted Ki67 positive cells in the nearby gastric mucosa. Atrophic gastric mucosa is usually more proliferative than the NETs!
• Full haematinic screen including B12 and Ferritin of course
• Anti-parietal cell AB & Intrinsic factor AB titres
• Serum gastrin level
• Chromogranin level
• Calcium and PTH level (particularly if MEN1 is suspected)
REQUEST THE FOLLOWING SCANS FOR EVERYONE WITH LIKELY TYPE II AND III DISEASE:
• 68Gallium DOTA-peptide PET/CT scan
• EUS to search for duodenal wall gastrinomas and small gastrinomas within the pancreas which CT can't see and to search for lymphadenopathy close to the NET
a) Reflux oesophagitis
An irregular squamo-columnar junction does suggest previous reflux oesophagitis but in this case there is more...
b) Non-dysplastic short segment Barrett's
Short-segment Barrett's is defined as Barrett's up to 3cm. In contrast, 'ultra-short Barrett's is less than 1cm. We sized the Barrett's as C0/M2 (according to the Prague classification). However, it doesn't look non-dysplastic!
c) Barrett's with intra-mucosal cancer
This would have been my own guess. There is no 'thickness' to the lesion and there is no ulceration, two features which would suggest that the lesion can't be removed endoscopically
d) Siewert II invasive cancer
Of course it may be invasive but that would be a little surprising. Endoscopically, this is IMca. Similarly HGD is unlikely as there is a lot of mucosal irregularity and you can see something has infiltrated below part of the squamous mucosa in the 2 o'clock position.
As you know, most of the time Barrett's neoplasia develops on the right-hand side and in the distal (rather than the proximal) Barrett's segment. In this case, in the 2 o'clock position there is a subtle mucosal irregularity. In fact, there appears to be something infiltrating below the squamous mucosa at this location. Biopsies had suggested IMca and a CT had been reassuring. Because the lesion is endoscopically resectable, we didn't bother with an EUS. The lesion was removed and confirmed as a poorly differentiated adenocarcinoma with signet ring morphology. On the other hand, all margins were clear and there was no LVI (lympho-vascular invasion). In the hierarchy of poor prognostic features, LVI and depth of invasion (>500µm) are the most important whilst poor differentiation is the least important. Nevertheless, I was a little worried when the patient declined surgery...
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
D) Coeliac disease
That duodenal mucosa is unremarkable. The 'polyp' in the 3 o'clock position is obviously the duodenal papilla.
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.
This was found in the duodenal cap of a patient undergoing gastroscopy because of dyspepsia.
APART FROM TAKING SAMPLES, WHAT ELSE SHOULD BE DONE?
a) take a CLO test
b) take gastric biopsies
Will show a Hp associated gastritis
c) take samples from D2
That's a no from me...
d) request an EUS
Never seem to be the right answer!?
e) request a CT
Perhaps if bx against all odds with suggest lymphoma but that would be a long shot
You first guesses when you find funny bumps in the duodenal cap should be gastric metaplasia and gastric heterotopia. Brunner's gland hyperplasia is also common but are never multiple (at least I have never seen a case with more than one nodule from Brunner's gland hyperplasia).
This is a case of foveolar gastric metaplasia in the duodenal cap. Basically, the mucosa in the duodenal cap has become more 'stomach-like' with crypts lined by mucus secreting cells (foveolar cells) which are different to goblet cells found elsewhere in the GI tract.
Gastric metaplasia is common in patients with a history of peptic ulcer disease and is thought to be a defence response or adaption to the presence of excess acid in the duodenum. It's thought that Helicobacter are able to colonise the foveolar gastric metaplasia in the duodenum and this contributes to duodenitis and duodenal ulceration.
So, what should you do next? Do a CLO test for Helicobacters of course!
This 'lesion' was barely visible within in a Barrett's segment on white light. However, after acetic acid and with NBI it's more obvious.
WHAT IS THE LIKELY HISTOLOGY?
a) Barrett's LGD
Usually invisible or just a red, flat patch
Subtle change in crypt pattern but with little nodularity?
This was my own guess but it was wrong...
d) Invasive cancer
Yes, superficial invasion (100 microns) and poor differentiation!
I removed this lesion without worrying too much about the subtle 'depressed' growth pattern and the small, round crypts in the centre of the lesion. However, I was surprised to see the pathology report of a superficially invading adenocarcinoma, with poor differentiation to boot!!! This finding makes the advice on 'further treatment' more complex. As you know, in both the upper and lower GI tract, the finding of 'lymphovascular invasion' (LV) is probably the most 'ominous sign' that a patient needs surgery (or chemo-radiotherapy in case of the oesophagus). Poor differentiation is 'bad', but less bad than LVI.
Depth of invasion is also important and in Barrett's you are 'allowed' invasion to about 500 microns below the muscularis mucosa. The corresponding 'safe margin' in SCC's is only 200microns. In this case the depth of invasion was only about 100 microns, leaving 'poor differentiation' as the only 'bad sign'. The patient wasn't a surgical candidate and refused CRT. This was 3 years ago and so far all is well!
By the way, the histopathologists do have a more difficult job than you perhaps imagine, measuring the depth of invasion in Barrett's cancer. This is because they often see several bands of muscularis mucosa, so called 'duplication of the muscularis mucosa'. Elsewhere in the GI tract, the muscularis mucosa is a single band of smooth muscle. They measure the depth of invasion from the top of the muscularis mucosa down the the deepest point of invasion. However, if there are several bands of muscularis mucosa, which one do you measure from?!? Below is an example to illustrate the dilemma.
You may be surprised to hear that both these polyps (found in the caecum and rectum respectively) actually have the same histology!
WHAT IS THE LIKELY HISTOLOGY OF THESE TWO LESIONS?
But it has gyrate crypts and perhaps villous in places??!
Well done! TSA's are great cameleons !
Slit like or small round crypts? No !
Reasonable guess as the growth morphology is that of a LST-G which are usually TVA's!
Right-hand image does look a little villous, perhaps
The surface appears villous in places and gyrate in other areas. The truth is that it is a bit of both - a 'Traditional Serrated Adenoma' (TSA), first described in 1990 by Longacre and Fenoglio-Preiser (Am J Surg Pathol 1990;14:524–37). TSA's are usually less recognisable and usually somewhat 'cerebriform' (like an exaggerated TVA).
TSAs are the least common of the three serrated colonic polyps ('hyperplastic polyps', 'sessile serrated lesions' and TSA’s) and account for only about 5% of serrated polyps and less than 1-2% of all colonic polyps and are usually found in the distal colon.
Pathologists rely on three typical findings when diagnosing TSA’s: deeply eosinophilic cells, flat top luminal serrations and numerous ectopic crypt foci (all demonstrated in the histology slide below from the Journal of Clinical Pathology 2016;69:6-11).
Genetically, TSA's are more like adenomatous polyps harbouring low-level microsatellite instability (MSI-L) or microsatellite stable (MSS) serrated colorectal adenocarcinomas. They usually contain KRAS mutations rather than usual BRAF mutations which you find in the 'Serrated Pathway' to CRC associated with a high-level of microsatellite instability (MSI-H).
Nevertheless, it’s thought that these precursor lesions give rise to serrated colorectal adenocarcinomas as part of the serrated (accelerated) pathway to cancer.
This lesion was found in the ascending colon and referred for removal.
WHAT IS THE LIKELY DIAGNOSIS?
You must be joking!
You are not serious?
Short slit-like crypts, well Yes but there is more to it!
That non-lifting sign doesn't lie!
Must admit that I didn't like the look of this polyp. Sure, it does have an organised crypt pattern. I think that I can see short slits, making it a TA. This would fit with the fact that it probably is a LST-NG type of lesion (which are always TA's).
However, it also looks, 'chunky' and it's the 'thickness' of the lesion which made me suspicious. For this reason I was not surprised to find the non-lifting sign. As there is no lifting what-so-ever, I suspect that the lesion will turn out to be T2 at least.
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
Those IPCL's do look a little prominent but not ectatic etc
But the stricture is within the squamous part of the oesophagus!
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.
Patient with Barrett's harbouring HGD has been treated with RFA. He has now returned for the second RFA session when this is found.
WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?
a) Benign scarring
Doesn't look benign - Looks evil!
b) Local recurrence of non-dysplastic Barrett's
Barrett's are re-emerging in several places. Doesn't look benign!
c) Barrett's adenocarcinoma
Absolutely! Nodules are never allowed in Barrett's!
Actually, there is a re-emergence of several brown nodules below the squamous mucosa. Biopsies confirmed this as an invasive adenocarcinoma, re-emerging from below the 'neo-squamous mucosa'. Clearly, to try RFA again would be a mistake! The histology showed a 'poorly differentiated' cancer and we are recommending either surgery or chemo-radiotherapy next (CRT). Even if histology hadn't shown poor differentiation, this 'smells' like bad disease to me which we may well 'undertreat' endoscopically.
This is an interesting looking colonic polyp
WHAT IS THE LIKELY HISTOLOGY
a) mixed serrated / adenomatous polyp
And that is what it looks like!!!
b) traditional serrated adenoma
But there are TWO components to this polyp!
c) serrated polyp undergoing malignant conversion
Well something has happened but 'lesion' has beautiful crypts!
Actually, the red bit of the polyp was composed of a tubulovillous adenoma and the rest was a serrated polyp! In other words, a mixed serrated/adenomatous polyp. Clearly the famous "three pathways to colorectal cancer": the APC mutation pathway (50%-70%); the mutator “Lynch syndrome” route (3%-5%); and the serrated pathway (30%-35%) can sometime get mixed up !!!
This lesion, situated in a very spastic sigmoid, has been referred for resection.
WHAT IS THE LIKELY DIAGNOSIS?
a) lesion is not neoplastic
Yes, hard to believe but true!
b) lesion is adenomatous
Lesion is 'battered' but crypts don't look typically adenomatous
c) lesion is malignant
No way, lesion isn't angry red, chunky or devoid of crypts!
I couldn't stop myself! After yesterday's case of a rectal 'prolapse polyp, part of the 'Mucosal Prolapse Syndrome', I had to show an example of a sigmoid mucosal 'traction polyp' (my nomenclature). The mucosa at the apex of this sigmoid fold is traumatised and inflamed but not actually adenomatous! Histologically these lesions also appear somewhat bashed up. This is where pathologists may see 'pseudo-invasion' which is actually movement of crypts due to trauma and inflammation.
The sigmoid colon is the most 'powerful' part of the colon developing the force needed to go to the toilet. Presumably this is the reason that diverticular disease first develop in the sigmoid. The force can also create these pseudo-polyps from patches of inflammation which I presume gets tugged along with each peristaltic wave. The end result is that this is the most difficult part of the colon to make head an tail of polyps.
These are common lesions and if you are a 'therapeutic endoscopist', you will be refer these lesions. In these cases, I don't go overboard by placing a snare far down the 'pseudo-stalk'. If you did, you will find that it's taking a long time to cut through all that healthy sigmoid mucosal fold and you run the risk of a perforation (early or late).
Instead, I just catch the tip of the fold and ask my assistant to close the snare as quickly as possible. Of course, you don't need to worry about a type of chunky central vessel which you may find in an adenomatous polyp. Analysis of a small piece of mucosal apex confirmed a normal mucosa. Hopefully this was enough for everyone to relax ...
This lesion in the low rectum has been referred for endoscopic resection
WHAT IS YOUR DIAGNOSIS?
a) Mucosal prolapse syndrome
b) Sessile Serrated lesion
Looks just like it but it isn't!
c) Traditional Serrated Adenoma
That's a No!
d) Adenomatous polyp
Patient complained of constipation...
e) Malignant polyp
But it's not 'chunky', red and it has crypts ?!?
There is no distinct edge to the 'polyp' and the crypts look normal, although a little splayed out and larger than normal, reminiscent of a serrated polyp. In real life, I had the advantage of knowing that the patient had been sent for colonoscopy because of constipation. I low-risk indication of course.
There is no distinct edge to the 'polyp' and the crypts look normal, just a little splayed out and larger than normal. This 'polyp' is actually part of the "Mucosal prolapse syndrome", first described in 1983 by Du Boulay et al [J Clin Pathol. 1983;36:1264–8].
Obviously, this syndrome includes solitary rectal ulcers, inflammatory cloacogenic polyps but also rectal 'prolapse polyps' such as this. In addition, the 'Mucosal Prolapse Syndrome' includes those prolapsing mucosal folds in the sigmoid and perhaps most surprisingly - GAVE !
In a case like the above, a couple of superficial biopsies will usually reveal the true nature of the lesion as it's easy for pathologists to spot the fibromuscular hyperplasia with overlying epithelial crypt distortion rather than dysplasia.
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!
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;
• Atrophic gastritis/achlorhydria/hypergastrinaemia
• Connective tissue diseases (especially systemic sclerosis and hypothyroidism)
• 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'!
LGD is flat, not nodular!
Good guess! Although your guess actually proved to be wrong
Small crypts + nodule = correct!
e) invasive cancer
Nodule should have been larger and without those small crypt openings
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
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
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?
But it's a IIc lesion with IIIs crypts in the centre?!?
c) Invasive cancer
But there ARE small round crypts in the centre and it DOES lift!!!
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
b) 3 O'clock
But the round crypt openings say otherwise!
c) 6 O'clock
d) 9 O'clock
Where there is hardly any Barrett's?!
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 lesion is being removed from the distal oesophagus
WHAT IS THE LIKELY HISTOLOGY?
a) Hyperplastic polyp
You must be joking!
b) Adenomatous polyp
A gastric adenomatous polyp would surely now be malignant
c) Early malignant polyp
But it's arising from a malignant flat component!!!
d) Advanced gastric cancer
Of course this is all very odd. Clearly this is an advanced cancer at the GOJ. What business do I have in 'attacking' this endoscopically?! Actually, the elderly patient had completed a course of chemoradiotherapy (CRT) for a T2, N0 junctional adenocarcinoma some 30 months previously.
Now he has developed dysphagia and a CT confirmed a 2cm polyp at the gastro-oesophageal junction. Histology had shown 'at least IMca' and he was referred for consideration of an endoscopic resection.
Clearly this lesion can't be cured endoscopically. In fact, the elderly patient is not a candidate for surgery and therefore there is no cure at all. However, I was thinking that as the cancer is mainly polypoidal, perhaps if the nodule could be removed, his swallowing will improve and he will not need a stent and could be offered brachytherapy. Clearly this was all 'speculative' but I'm glad to say that 6 months later, the patient still has not developed any dysphagia and his now starting brachytherapy. No doubt a better outcome than could be offered by a stent?
This is a solitary gastric polyp
WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?
a) Hyperplastic polyp
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!
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:
A polyp found in the descending colon and removed as a single fragment (H&E attached)
WHAT IS THE DIAGNOSIS
a) Tubular adenoma
Yes but you are only partly correct!
b) Tubulovillous adenoma
No way, this is a LST-NG!!!
c) Villous adenoma
Absolutely not - there are no villi!!!
d) Sessile serrated lesion
Looks like it but histology doesn't!
e) Malignant polyp
This is a LST-NG type of lesion (laterally spreading tumour of the non-granular type). They are always TA's (tubular adenomas) and often (but usually not), harbour HGD or cancer. I guess that we can't really be sure about the crypt pattern as this is a non-magnified image. However, looking at the histology slide with narrow crypts, I expect that the crypt pattern is probably IIIs (small round crypts) which goes with TA+HGD. Must admit that I was surprised to find invasive cancer and LVI (lymphovascular invasion) in a small lesion such as this! The last image shows clusters of malignant cells within lymphatics. Of all the 'markers' to suggest that the patient needs surgery, LVI is the most important!