This patient is under surveillance after having had two previous EGC's. The stomach has been sprayed with indigo carmine dye when this lesion caught my eyes. WHAT IS THE LIKELY DIAGNOSIS?
■ Likely to be gastritis only
The non-staining is suspicious and rarely lie...
■ Likely to be a patch of intestinal metaplasia
There appears to be a crypt pattern in the centre but it can still be neoplastic!
■ Likely to be neoplastic
Non-staining, slightly raised and in an 'unstable stomach' - surely!
explanation
Clearly this is an unstable stomach having given rise to two previous EGC's. In patients attending for surveillance, I always spray indigo-carmine dye throughout the stomach using a spray catheter. I then look carefully at any spots where the dye seems to have slid off. This is such a 'lesion' which was confirmed as a subtle EGC. After my samples had confirmed my suspicion it was removed by ESD and was confirmed as HGD/IMca. I consider the both as the same histology as one pathologists HGD is another pathologists IMca. There was no LVI. However, I was surprised to find that one mucosal resection edge was involved by cancer. Looking back at the clip, I think that it's the 4 O'clock border which has an irregular extension which I failed to spot.
Most EGC's look like this, a shallow depression with a subtle elevated margin. I find the crypt pattern more difficult to interpret. However, as you know, the more destroyed it is, the more likely the lesion is to be poorly differentiated.
■ 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 patient is undergoing a set of oesophageal dilatations of a radiotherapy induced stricture. Three set of samples, a total of 18 biopsies have been obtained from the stricture which have all been reassuring. A CT has reported: "Distal oesophageal mural thickening extends throughout the length of the previously demonstrated bulky oesophageal tumour. No focal abnormality to suggest recurrent disease and presumably appearances are all radiotherapy related". In the video clip, the stricture is seen to be dilated to 20mm. WHAT WOULD YOU DO NEXT
■ Organise the next dilatation in a weeks time
She WILL need more dilatations but you've missed something important!
■ Take another set of samples from that stricture
It does look concerning still but there is something even more concerning here!
■ Take another set of samples from the more proximal oesophagus
You've spotted it!
■ Take samples at the distal oesophagus (below the stricture)
That odd, fleshy lump at 6 O'clock below the stricture has been sampled already. More samples is never wrong but there is something even more important to sample first!
explanation
On intubation, I glimpsed something just below the upper oesophageal sphincter. I deliberately didn't dwell on it in the video, simulating the previous intubations when a synchronous lesion had been missed. In the explanatory clip below, you get a better view of her second SCC. CT staged the second lesion as no worse than T2, N0.
The moral of the story? It's when we are distracted that we run the risk of missing things! In this case, the previous endoscopists had approached the endoscopy as a case of dilatation and switched off their eyes! 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 This subcentimetere polyp was discovered in the rectum of a 60 year old woman undergoing a bowel cancer screening colonoscopy following a positive FIT. Considering the endoscopic appearance and the degree of lifting, WHAT WOULD YOU DO?
■ This is a benign adenoma but it's too close to a large vein for removal
Don't worry about the vein!
■ This is a benign adenoma which I would remove
Doesn't look benign!!
■ This is a likely early cancer which I would remove
Yes it looks evil but should you attack?
■ This is an invasive cancer which I would only sample
Can't argue with that!
explanation
That vein looks intimidating but don't be intimidated! It's not a 'show stopper'. it will move out of the way. However, that polyp does look nasty as there is no definite crypt pattern in the centre, just a swirly surface. However, the lifting is good, suggestive that we stand a good chance of clearing the lesion endoscopically ...
And at this point you can either go ahead and remove the likely early cancer. The advantage is that you get the correct diagnosis whilst biopsies are often inconclusive. The reason why surface biopsies are often unable to confirm invasive cancer is because your pathologists rely on seeing invasion of malignant tissue below the muscular mucosa. The underlying muscularis mucosa is usually NOT included in surface biopsies. However, this is a good example of the potential disadvantages of going ahead to resect the lesion. As you'll see in the video below, I removed it. Histology reported that the lesion was indeed an early rectal carcinoma, 6mm in diameter and with clear margins. However, the deep margin was 'only' clear by 200 microns which of course our pathologists would call a 'positive deep margin'. A 1mm (that is 1000 micron) is the 'accepted' definition of a 'clear surgical margin'. Secondly, there was of course a small focus of LVI. There is usually something to keep you awake at night after removing an early cancer. The disadvantage is obviously that you don't know what to tell the patient!!! - Is my cancer gone or not? - I'm sorry but I'm not sure! - Couldn't you keep a close eye on me with regular colonoscopies and CT's? Well, we could but there is absolutely no evidence that this will save your life IF you still have cancer cells inside of you... Fortunately, there is a study under way in the Netherlands to answer this very question! At the moment, we know that LVI is 'bad' and that the normal next step would be to offer the patient surgery. This patient presented with an emergency GI bleed. WHAT IS THE DIAGNOSIS?
■ Benign gastric ulcer
Hmm, multiple GU's ?!
■ Ulcerated GIST
Multiple ulcerated GIST's. Really?
■ Adenocarcinoma
Multifocal adenocarcinoma ?!
■ Lymphoma
Too crater-like !!!
■ Melanoma
Got it!
explanation
There are actually several odd lesions in the stomach. Apart from the 'multi-focality', the lesions look a little like craters on the moon. Of course, this is what metastatic disease looks like. The dark colour clinches the diagnosis of melanomatous deposits. Here is a link to Sanjeev's and Ashok's case published in Digestive and Liver Disease [2020;52(12):1512] which is an even better demonstration of that dark pigmentation. Malignant melanoma has a peculiar predilection for the gastrointestinal tract. Melanoma can spread anywhere and is the most common metastatic tumor of the GI tract. More often the haematogenous spread is to the small bowel or colorectum. Gastric metastases are uncommon. It’s one of the more common findings in the small bowel of younger patients with anaemia. In an old post mortem series, the prevalence of GI metastasis in patients with melanoma was only 0.9% in 1000 melanoma patients (Arch Surg 1964:88:969-973). However, when you look at cases with advanced disease, up to 50% will have GI metastases (Cancer 1964;17:1323-39). As one may expect, the most common presentation is with anaemia or obstructive symptoms. Interestingly, surgical resection has been linked with a longer survival! Of course, its important to distinguish between a primary GI mucosal melanoma and metastatic melanoma. The criteria for a diagnosis of primary intestinal melanoma include 1) no evidence of concurrent melanoma or atypical melanocytic lesion of the skin, 2) absence of extra-intestinal metastatic spread of melanoma, and 3) presence of intramucosal lesions in the overlying or adjacent intestinal epithelium In a small series, the 5 year survival was 38% (Arch Surg 1996;131 :975-980). Without surgical intervention, the prognosis used to be grim and Amer et al. (Gynecol Obstet 1979;149:687-92) reported a mean survival time of 9.7 months, whilst others have reported an even shorter median survival of 4.7 months. Nevertheless, it is perhaps likely that case selection is the reason for the apparent survival benefit of surgery. The new checkpoint inhibitors and other immunotherapies are revolutionising the treatment of advanced stage disease.
This 50 year old lady presents with dysphagia and a distal oesophageal stricture is confirmed. Intubation is a little tricky due to a pharyngeal pouch but we managed to intubate the oesophagus after the successful passage of a guidewire. After you have obtained a set of samples (last photo), the patient asks what will happen next.
WHAT IS YOUR REPLY?
■ Too early to tell, we will await analysis of the samples first
It's not too early to tell - the signs are there!
■ Whilst we await histology, I will request at CT
Good man! And organise a cancer MDT discussion!
■ The analysis will probably be reassuring and in all likelihood a dilatation is next
Sadly, this is unlikely !
■ The pouch is more likely to be the main problem than the stricture
No, that's not it!
explanation
The stricture doesn't look quite right does it? Somewhat 'nobbly' and without associated reflux oesophagitis. This stricture looks malignant ! There is one more concerning feature which you may have missed...
The vocal cord on the left-hand side is weaker than the right! On direct questioning, the patient confirmed that her voice had recently changed and become more hoarse! This patient had an advanced oesophageal cancer with metastases to the high lymphnodes on the left causing a recurrent laryngeal nerve paralysis! Out of the four options, organising a staging CT and referral to the UGI cancer MDT is the correct course of action! This patient has been referred for an oesophageal dilatation after biopsies have been reassuring WHAT WOULD YOU DO?
■ Abort and take more samples
You are a wise as a fox!
■ Dilate to 12mm
Hmm, cautious but not cautious enought !
■ Dilate to 15mm
Seems reasonable but you've missed something!
■ Dilate to 18mm
You are clearly brave but look again!
■ Dilate to 20mm
If this stricture was benign, I would also aim for 20mm but it isn't!
explanation
Of course this stricture doesn't look right! There is a peculiar plaque-like area in the 10 O'clock position. The dilatation was cancelled and another set of samples were requested together with a CT. Samples indicated that this was a case of poorly differentiated intramucosal cancer and an EMR was organised. Have a look at the clip below. Clearly this lesion is firmly tethered to underlying structures and is beyond endoscopic cure. Some options may pop into your head such as injecting some fluid below the lesion or using the 'pull-within-the-snare' EMR technique. The problem is that these will not change the basic fact that endoscopically the lesion is beyond endoscopic cure! You run the risk of 'muddying the waters' with scrappy histology reporting 'intramucosal cancer at least' and with uncertain margins. Far better is to recognised the endoscopic irresectability of the lesion which provides a clear steer towards the 'next treatment level'. In this case the patient wasn't a surgical candidate and was offered chemo-radiotherapy (CRT).
This patient presented with odynophagia and this is the appearance of the oesophagus from 2014
WHAT WAS THE INITIAL DIAGNOSIS IN 2014 ?
■ Candidiasis
These lesions or to 'fleshy'!
■ Reflux oesophagitis
The lesions are too 'fleshy'!
■ Eosinophilic oesophagitis
Doesn't explain the 'lumpiness' of the mucosa
■ Oesophageal papilloma
A papilloma gone mad !
explanation
This is a case from Pradeep Mundre at Bradford. The correct diagnosis was 'Diffuse oesophageal Squamous papillomatosis'. Unfortunately, by 2021 the patient re-presented with worsening symptoms was was found to have developed a 'basaloid squamous cell carcinoma' (photo below).
Squamous Papillomas and Squamous papillomatosis of oesophagus Papillomas are finger-like projections that histologically have a central fibrovascular core surrounded by proliferative squamous epithelium with keratin outside this. Of course these are usually small and isolated. However they can become larger and rarely there is diffuse changes as in this case, and term 'oesophageal papillomatosis' is applied. There is little in the published literature on oesophageal papillomas with just a few published case series. Aetiology is unclear as to why some grow large whilst the vast majority remain tiny. Published literature has been conflicting with regards to association of oesophageal papillomas with HPV infection. Clinical relevance, natural history and whether this is a premalignant lesion, remain a matter of debate. There has been a few case reports of progression/ association with squamous cell carcinoma, especially with diffuse squamous papillomatosis. In other organs, the causal link between human papillomavirus infection and cervical, anogenital, and some oropharyngeal malignancies has been established by both molecular and epidemiological data. Management Owing to paucity of evidence, it is unclear how to manage this. I guess we can translate knowledge from other areas and use this in oesophagus Isolated small papillomas are easy to ablate with a quick 'zap' of APC. For larger areas of more diffuse papillomatosis, ablative techniques, such as APC ablation or cryoablation or radiofrequency ablation may all be considered. However biopsies or even EMR may be prudent of more 'chunky' areas to rule out possibility of 'prevalent' dysplasia/malignancy. Bjorn has treated a couple of patients with very large areas of oesophageal squamous papillomatosis with APC ablation. Of course, it's quite daunting when you start and it takes a special patient not to freak out when belching up the fumes of vaporised mucosa (a GA would make it easier for the patient of course). However, these lesions actually turn out to be easy to ablate and you will be surprised at the progress when the patient returns for a re-check (usually about 3 months later). However, most patients will probably require 3-4 sessions when the surface area involved is extensive as in this case. Of course, it's difficult to give a general advice about management. Clearly the risk of an elderly patient living long enough to develop a SCC must be small. Conversely, in a young patient, ablation to try to clear the oesophagus will avoid the need for surveillance and is probably justified. Reference Alomari et al Successful Treatment of Extensive oesophageal Squamous Papillomatosis With Cryotherapy, ACG Case Reports Journal: March 2019 - Volume 6 - Issue 3
Just a bit of fun! Five 'gastric ulcers', three of which are malignant.
WHICH 3 ULCERS ARE CANCEROUS?
■ ABC
Bloody hell ! You are good!!!
■ BCD
Good guess but one is of these is benign
■ CDE
Good guess but two of these are benign
■ ACE
Good guess but one is of these is benign
explanation
Image A is a diffuse type gastric adenocarcinoma, which is strictly speaking not an ulcer (they rarely ulcerate of course). These are notoriously difficult to pick up and only show up as either a tiny pale submucosal spot, a red patch as in this case or as a more extensive patch of inflamed gastric mucosa.
Image B was a T2 gastric cancer in which initial biopsies had been entirely benign, only reporting 'reactive atypia'. However, endoscopically there is a rim of thickened, red indurated mucosa surrounding the ulcer. Image C is an early gastric cancer pulling on the nearby gastric folds. It was removed endoscopically and turned out to be intramucosal only. Image D is of an entirely benign 'giant' gastric ulcer. ‘Giant gastric ulcers’ are (arbitrarily) what we call ulcers which are ≥3cm in size. In our Leeds series of 111 ulcers, 42 were malignant (34 adenocarcinomas and 5 lymphomas as well 3 rare tumours). In our series, logistic regression revealed that the (predictable) predictors for malignancy were; 1) increasing patient age, 2) larger size of giant the gastric ulcer and 3) the endoscopist making a diagnosis of a likely malignant ulcer. Finally E is an ulcerated fibroid polyp and not an ulcerated GIST! Of course you can't tell the two apart on endoscopic grounds! A middle aged patient presents with obstructive jaundice. There is a history of upper abdominal pain for 2 months and jaundice for about 4 weeks. She has also lost some weight loss and had night sweats. On examination she is apyrexial, obviously jaundiced and slightly tender in the epigastrium Hb 98 MCV 71 WCC 4.17 Plat 338 CRP <5 (<10) Amylase 102 (<110) Bili 75 µmol/L ALT 910 iu/L ALP 302 iu/L Albumin 37 g/L INR 1.0 An abdominal ultrasound is carried out (images below) If you work outside of the UK, and actually do abdominal ultrasound examinations you will be able to see that the gallbladder is extremely thick walled and hyperaemic. There is also intrahepatic biliary duct dilatation but the CBD is of normal calibre (6mm) and no stones can be seen. I haven't included the images showing that the pancreas, pancreatic duct, liver, abdominal aorta, spleen and kidneys were all normal. WHAT IS YOUR CLINICAL DIAGNOSIS?
■ Biliary colic
There is no pain!
■ Acute cholecystitis
How then do you explain the jaundice?
■ Choledocholithiasis
Would explain the jaundice and a CBD stone can be missed on US
■ Ascending Cholangitis
But there is no fever, raised WCC or CRP !!!
■ Acalculous cholecystitis
Sure no stones seen in the gallbladder but why the jaundice?
explanation of the case (so far - there is more to follow!!! )
Choledocholithiasis should be your clinical diagnosis at this point. This is because the ‘strong likelihood criteria’ are fulfilled as follows;
To search further for gallstones, a CT scan was then requested (below). You can probably tell from the CT that The gallbladder is confirmed as thickened with some extrinsic compression of the bile duct at the porta hepatis to explain the intrahepatic ductal dilatation already seen on ultrasound. The distal bile duct is confirmed as collapsed with normal appearance of the pancreas, kidneys, adrenal glands and spleen. WHAT IS NOW THE DIAGNOSIS?
■ Mirizzi’s syndrome
Absolutely
■ Choledocholithiasis
Nope, no stones seen within the CBD
second explanatation (and yes there are further developments around the corner)
The CT report essentially describes a Mirizzi syndrome type 1. Pablo Mirizzi was an Argentinian Surgeon who first described the obstruction of the common hepatic duct (CHD) by an impacted stone in the cystic duct or Hartmann's pouch of the gallbladder. In Mirizzi syndrome type I there is no fistula between the gallbladder and CHD whilst type II-IV have a fistulous communication. Of course its difficult to tell on imaging if there is a fistula. For this reason the subtype of the Mirizzi syndrome is usually something discovered at surgery.
The patient does undergo a laparoscopic cholecystectomy but to the surgeons surprise there are no stones found within the thickened gallbladder or within the bile ducts. The gallbladder is analysed and the pathologists report that the: “Gallbladder measures 52 x 30 x 20 mm. The serosa is congested and wall thickness is 3 mm. No stone and no focal lesions. There is subacute cholecystitis with myofibroblastic proliferation of the wall and mild acute on chronic inflammation” Strangely enough, the jaundice does not resolve after surgery and for this reason an MRI scan is carried out which confirms a stricture at the common hepatic duct with mild intrahepatic ductal dilatation. At this point we decide to carry out an ERCP to sample the stricture and place a stent. Now you have all the pieces in this jigsaw and should know what's going on! WHAT DID WE MISS?
■ Primary cancer of the gallbladder
No cancer found in resection specimen!
■ Cholangiocarcinoma
You missed something on the video!
■ Gastric cancer
Well done, you spotted this on the video?
■ Duodenal cancer
But the duodenum look fine on video?!
FINAL EXPLANATION
Thanks for sticking with this case until the end! Actually, you did have an opportunity of getting the diagnosis when you heard that the gallbladder histology showed; "markedly thickened wall but with only mild inflammation of the gallbladder mucosa" ...
Of course, this doesn't make any sense! In acute cholecystitis there should be an INTENSE inflammation of the mucosa. So why is the gallbladder wall grossly thickened? A second look into the deeper aspects of that thickened gallbladder wall led to a revelation ! The 'second look histology' reported a 'poorly differentiated diffuse type adenocarcinoma deep within the gallbladder wall with single and files of small neoplastic epithelial cells (histology slides below). The pathologists reported that the tumour did appear to be coming from outside the gallbladder. Of course in the video you should have noticed that the gastric antrum was abnormal, a little indurated and thickened. The samples taken from the gastric antrum confirmed the same diffusely infiltrating adenocarcinoma. Those with VERY sharp eyes, would have seen the antral thickening on the initial CT which wasn't commented upon by the radiologist! So what was the final diagnosis? A diffuse type gastric cancer invading into the gallbladder, cystic duct and hepatic duct ! This may a good time to remind you of the management of gallstone related disease. The 'infographic' below from J Int Care Med 2016;31(1):3-13 summarises everything !
'Banding EMR of this junctional lesion is not going to plan! Biopsies had diagnosed IMca at least but both EUS and CT had been reassuring. WHAT WOULD YOU CONSIDER NEXT?
■ Inject below lesion and try again
It will not work here and (rarely works at all)
■ Change to a wider cap
Will not work!
■ Remove lesion by ESD
You are asking for trouble!
■ Bail and declare that lesion is beyond endoscopic cure
There is no shame in admitting when you are beaten!
explanation
Although EUS and CT had both been reassuring, this lesion is clearly tethered down to the oesophageal wall. The lesion is extending too deeply for endoscopic cure. Trying to 'push the boat out' by attempting removal by 'pull within the snare' technique or ESD will fail and will run the risk of perforation, potentially resulting in the upstaging of the lesion. Bail out ! I'm carrying out a dilatation (20mm) of a distal gastric stricture. WHAT IS THE LIKELY AETIOLOGY OF THE STRICTURE?
■ Benign pyloric stricture
But the stricture is pre-pyloric!
■ Anastomotic stricture
Doesn't look like an anastomosis!
■ Radiotherapy stricture
But why giving radiotherapy to the stomach?
explanation
The mucosa in the 4 o'clock position looks pale and atrophic. This is a 'scar' left after treatment of a gastric lymphoma. Of course, the scar would look the same following Hp eradication of a MALT lymphoma. However, this was after following chemoradiotherapy (CRT) for a 'Diffuse large B-cell lymphoma. Which is a far more nasty lymphoma and patients present with more advanced stage at diagnosis, and have a worse prognosis (about 75% of patients are alive at 5 yrs) than with a MALT lymphoma. This patient was treated with 6 cycles of R-CHOP chemotherapy and radiotherapy 30 Gy in 15 fractions. The risk of stricturing after gastric CRT is around 5%. My dilatations to 20mm didn't do much and the patient had to come back for a dilatation to 25mm before symptoms improved.
This ulcer was found on the lesser curve of a middle aged man with dyspepsia. Biopsies are taken and stained with H&E (below)
WHAT IS THE AETIOLOGY OF THAT GU?
■ Benign GU
Don't you think that the mucosa look odd near to the ulcer?
■ Lymphoma
Yes! That odd atrophic mucosa next to the ulcer look weird but not "carcinoma weird" !
■ Adenocarcinoma - intestinal type
With a 'standard cancer', the surrounding mucosa should be thickened and red not atrophic looking
■ Adenocarcinoma - intestinal type
This was actually my own diagnosis but histology shows lots of small round lymphocytes not ballooned up signet ring cells.
EXPLANATION
There are only two possibilities here. Of course the ulcer itself doesn't tell you much. The mucosa surrounding the ulcer tells you more! With a benign ulcer, you would expect a thin rim of 'reactive' mucosa (looks red and a little villous). In the case of an intestinal type of adenocarcinoma a broad band of surrounding mucosa is red, indurated and thickened. In gastric lymphomas, the surface area of abnormal mucosa is usually far greater than the surface area of the ulceration. There are usually areas of atrophic and inflamed mucosa. Mucosa infiltrated by a diffuse type adenocarcinoma could look like this BUT it's unusual for it to ulcerate!
This patient has a MALT lymphoma ! Of course, I took samples for Helicobacters. Of course not every MALT lymphoma is linked with HP infection (about 2/3 cases are though). In this case our haematologists were optimistic of a good response to Hp eradication because all the 3 good prognostic criteria were met:
Here are 5 oesophageal strictures.
HOW MANY SHOW A CANCER?
■ 1 photograph
Try again!
■ 2 photographs
YES! Well done!!!
■ 3 photographs
No, image C does look dodgy I admit but was benign...
■ 4 photographs
There are 4 dodgy looking strictures but not all 4 were malignant !
■ 5 photographs
One stricture (image D) definitely looks benign!
explanation
Actually there are 2 cancers in there (case A and E). In order the aetiologies of the strictures are:
A = Adenocarcinoma B = Post radiotherapy stricture C = Peptic stricture D = Post ESD stricture E = Squamous cell carcinoma
This is a C2M4 Barrett's under surveillance
WHAT IS THE LIKELY HISTOLOGY?
■ Non-neoplastic Barrett's
Nodularity within Barrett's is always bad!
■ LGD
Visible nodularity is never truly just LGD
■ HGD/IMca
A good guess but you are missing something!
■ Invasive cancer
Yes! That small ulcer is the spot of invasive cancer!
explanation
Of course you should initially scrutinise the right-hand part of the Barrett's between 12 and 5 O'clock or so. Furthermore, dysplasia is most common in the distal rather than proximal Barrett's. However, in this case the subtle nodularity is situated in the 11 O'clock position. That is why I call this an 'unusual case' of Barrett's
I don't think that LGD is visible endoscopically or possible to recognise even by AI systems. However, in this case there is a definite nodularity and HGD/IMca seems the most likely diagnosis. However, worryingly there is a small depression in the centre of the lesion (seen best on NBI) without any crypt pattern at all. That is the location of the poor differentiation and invasion below the muscular mucosa. Furthermore, biopsies revealed LVI and the patient subsequently had chemoradiotherapy (CRT). CRT is a great option in elderly patients but I do worry when young patients opt for CRT. This is because they are at high risk of developing further lesions and they have decades of life expectancy ahead of them for this to happen. The ultimate staging was T1b, N0 disease. I've attached a reminder about TNM staging because it's easy to forget it unless you see it every day!
Monz found this lesion in the terminal ileum. WHAT IS THE MOST LIKELY DIAGNOSIS?
■ Hyperplastic polyp
Nope, those are very rare in TI
■ Adenomatous polyp
Uncommon in TI and there are no adenomatous crypts!
■ Neuroendocrine tumour
Perhaps the most common lesion in TI with those typical little vessels!
■ Small leiomyoma
Could be but those little vessels say otherwise
■ Small GIST
Must exist but I've never seen one!
explanation
At diagnostic colonoscopies, I do try to intubate the terminal ileum. Not to 'practise' but to detect pathology such as this rare lesion at an early stage! These do have a real malignant potential and in fact usually present late with bowel obstruction.
The tell-tale sign are those tiny vessels climbing up around the edges of the polyp and the pale appearance. Of course, this is a terminal ileal NET! The lesion was removed by Monz Ahmed and histology confirmed that it was an NET. Of course, the MOST IMPORTANT issue is the WHO Grade of the lesion. This is because small bowel NET's (excluding the duodenum) are often malignant. The lesion was WHO Grade I (i.e. 1-2% mitotic figures only) which is reassuring but a CT is probably still warranted to look at those nearby lymphnodes. By the way, in the histology below, you can see how close the lesion is on the abutting deep edge. This is the common finding after your endoscopic removal and can be disconcerting. Studies have reported that if you resect lesions using a 'banding device' you can usually get a confirmed (but shallow) clear deep margin. However, neither Monz or I would use a banding device in the terminal ileum. The muscle propria layer is too thin and you are likely to end up with a full thickness resection if you tried. 'Banding resections' are probably best reserved for the oesophagus, stomach or colorectum!
Three colonic polyps to choose between !
WHICH IS THE MOST SUSPICIOUS?
■ A
I agree! Looks like cancer!
■ B
Looks too pretty to be evil !
■ C
On size criteria, the risk is probably about 1:7
explanation
B has a lovely brain-like crypt pattern of a rather pretty TVA. Of course, C is difficult to assess as the surface crypt pattern may not reflect was is lurking deep inside. Data from the NHS Bowel Cancer Screening Programme (see table below) puts the risk of cancer in a >45 mm at 15%. For this reason, the polyp should be removed in as few fragments as possible.
However, A is the polyp which I think looks most suspicious. It has a suspicious central nodule and on the NBI image (top-right), I don't see an organised crypt pattern in parts of the polyp. This is a superficially invasive cancer which was just invading into the muscular mucosa (sm1 invasion)! it lifted well enough for a resection. Again single fragment resection would be paramount when removing this polyp. Below is a table which I received from Matt Rutter a few years ago. It links size with histology for polyps resected on the NHS Bowel Cancer Screening Programme
This 60 year old patient is undergoing a gastroscopy because of early satiety and weight loss. A CLO test was negative
WHAT IS THE LIKELY DIAGNOSIS?
■ Amyloidosis
Could indeed look like this BUT you'd expect the patient to be on haemodialysis!
■ Autoimmune gastritis
Indistinguishable from Hp gastritis but doesn't explain the symptoms
■ CMV gastritis
Possible but more common in children
■ Gastric lymphoma
Could be but you would normally expect ulceration
■ Diffuse type gastric cancer
Yes! The mucosa appears 'swollen' as it's infiltrated by malignant cells spreading between and below the crypts
explanation
As you know, the so called "Lauren’s classification" divides into two types of gastric cancer; the more common 'intestinal type' and the less common 'diffuse type'.
Actually the molecular workup done by “The Cancer Genome Atlas” Research Network" has actually identified four subtypes:
Intestinal type gastric cancer is becoming less common, probably because of the reduced prevalence of H. pylori, whilst the incidence of diffuse type cancers is not falling. There are other recognised differences between diffuse and intestinal type gastric cancer. The 'diffuse type' affect younger patients, the sex ratio is identical whilst the 'intestinal type' is more common in men. Presumably this means that known mutagens such as smoking and alcohol does not predispose to diffuse type gastric cancer? 'Diffuse type' cancers are more common in the proximal stomach and can be inherited as part of B-cadherin mutations. Finally, 'diffuse type' cancer develop BELOW the surface epithelium making them very difficult to spot. There is no irregularity of the overlying crypt or vessel pattern in these lesions. However, late detection is probably not the only reason why diffuse type cancer have a worse prognosis.
As you know, colonoscopy protects less well against future cancer in the right hemi-colon, than cancer elsewhere in the colorectum. Here are 5 lesions, all found in AC. Four are malignant and one isn't ...
WHICH ONE IS NOT A CANCER?
■ A
SM3 invading CRC with very little adenomatous tissue present
■ B
Cancer arising in an SSL !
■ C
A very superficial CRC removed by ESD
■ D
Yes! This is a 'caecal patch' in UC
■ E
Nope, its a mucinous carcinoma!
explanation
You can probably tell that the first lesion is a cancer because of it's nobbly surface and lack of crypt pattern in places. It was a sm1 invasion T1,N0 cancer (i.e. invading up to the muscularis propria layer but didn't invade into it).
The second lesion is a sessile serrated lesion with a small cancer at it's edge. The staging was identical to the first lesion (sm1 invasion T1,N0 cancer). The third lesion was a superficial carcinoma (sm1 invasion only) and the only in the series actually removed endoscopically. The fourth lesion is the 'odd one out'. It's actually a 'caecal patch' in a patient with ulcerative colitis, only affecting the rectum. The final lesion was a 'mucinous adenocarcinoma'. Interestingly, analysis of the initial biopsies reported 'TA+LGD'. Don't believe everything those pathologists tell you! Your eyes don't lie! There is a further interesting twist here. After another set of samples, got the pathologists to agree with our endoscopic diagnosis, we were surprised that the patient was turned down for surgery due to severe comorbidities. Rather begs the question what was the point in putting the 85 year old gentleman through two colonoscopies !!! Anyway, that was 4 years ago and he has still not developed any symptoms from his cancer!? A recent CT confirmed that it was slowly growing and was now annular but without any evidence of spread or obstruction. Interesting and clearly turning someone down for surgery is not necessarily a 'bad thing' ! Still leaves me wondering why they keep scanning the poor bloke though? Below I've attached a reminder about the 'Kikuchi staging' which your pathologists should use to stage superficial flat cancers.
You are called into a neighbouring endoscopy room to advice on this lesion at the recto-sigmoid junction.
WHAT WOULD YOU DO NEXT?
■ Carefully assess and take samples
Yes but in what way would you 'more carefully' assess this?
■ Attempt to remove it now
Well, you would realise that it doesn't lift !
■ Attempt to remove it at a dedicated session
Noo! You missed it !
explanation
This lesion does look completely different when viewed in retroversion (image below). In retrovertion its obvious that it's malignant. Clearly the correct way ahead is to take some better targeted samples and refer to the next colorectal cancer meeting. If you hadn't assessed the lesion in retrovertion, samples would have revealed a TA+HGD only (this is actually what happened), delaying the correct management. The moral of the story is: always view all of the lesion before deciding on where samples should be taken from.
Aha! Are we not told that; "polyps which will be resected endoscopically shouldn't be sampled as it makes removal difficult"? The problem is that when patients have to wait long for their resection, it makes sense to take a few samples or at least do a 'test-lift'. Having to wait 3 month for a resection only to be told that the lesion is likely to be malignant is a disaster scenario. It's then better to exclude cancer as far as possible before asking the patient to wait months for the removal. Of course, its true that it can make a resection more difficult but it's hardly ever a showstopper !
This 3cm polyp was removed from the sigmoid colon. After returning to the recovery area the patient is complaining of severe low abdominal pain.
WHAT WOULD YOU DO NOW?
■ Keep in 'recovery area' for observation
Not 'wrong' a such but you can do more!
■ Bring back into endoscopy room to apply more clips
Now is your chanse to do this before that peritonitis takes hold!
■ Organise a CT
In my experience, it often muddies the water and adds little useful information in this scenario
■ Admit, organise a CT and start AB's
Not 'wrong' but placing clips is more important than any of this
explanation
Large sessile colonic polyps are a particular challenge for endoscopists. That surface crypt pattern may not be an accurate reflection of what is hiding inside! When there is cancer hidden at the centre of the polyp, this will induce a fibrotic response (the pathologists call this a 'desmoplastic response') which can tether the polyp to the muscle propria layer. Large polyps being yanked about by peristalsis can also develop fibrosis beneath even if they are benign (example below of an entirely benign VA+TSA harbouring LGD only with dense fibrosis in its centre). Of course, non-lifting is usually obvious when the lesion is small or flat but can be impossible to see below a large sessile polyp.
The first sign that something is amiss is when in spite of 20-30 seconds of yellow pedal power (i.e. a blended cut/coag/pause diathermy cycle), the polyp is still in place! When this happened, I used to curse under my breath, re-set the diathermy and with a strong hand and a further 30 seconds of diathermy, I would usually 'win' the battle and the polyp would fall off. Unfortunately, this would often turn out to be a 'Pyrrhic victory'. There would either be quite alarming bleeding or a perforation. Nowadays, I believe that these large, sessile polyps are best removed by ESD. In a slow, controlled manner you can then dissect below the lesion. If you encounter fibrous tissue you can attempt to dissect around it, abandon or (if you've got the balls) attempt to continue the dissection in the same plane through the fibrous tissue. Of course, you can also deal with those chunky vessels, one-by-one in a more controlled manner. Back to the scenario in question. If I think that there could be any risk that I've perforated, I would bring the patient back into the procedure room to place LOTS OF CLIPS. In truth, I did immediately recognise the peri-colonic fat in the middle image on the right and closed the perforation without delay. That white base to the upturned polyp in the last image, is a sizeable chunk of muscle propria layer. Anyway, provided that there is no peritoneal contamination, the perforation has been thoroughly closed with a virtual 'suture line' of clips and the patient is young and 'sensible', I would observe them for another few hours in recovery and discharge provided that they remain free of abdominal pain. Beware of the patient who remains in pain but claims to be comfortable because he is desperate to get back home... Of course, the patient must understand my verbal and written information that there may have been a small perforation which I have closed with clips but that he/she must return to hospital if further pain develops. Of course, my standard post-resection information leaflet always advice patients to return to hospital if bleeding or pain develops up to 2 weeks after the resection. No antibiotics, no scans, no admission!?! Controversial of course and I must stress that this is my own management strategy. I believe that my way of dealing with micro-perforations is safer than admission (exposing the patient to all the in-hospital hazards of multi-resistant bugs, Covid-19 etc), reduces the risk of 'over-treatment' (CT scans after EMR's or ESDs' always look alarming to the radiologists with gas in the wall of the bowel and the peritoneal cavity which means that surgeons will be reaching for their knives) and cheaper (of course). By the way, I am no great fan of the over-the-scope (OVESCO) clips for three reasons; a) time is of the essence in perforations and with the OVESCO clip you loose time but having to withdraw the scope to attach the device and b) it is very cumbersome and it can be difficult to reach the lesion and c) you only get one chance to get the clip in the correct position. With 'normal clips, it doesn't matter if a clip goes on a little wonkily, you just place another one!
This 13mm colonic lesion has been referred for resection
WHAT IS YOUR PREDICTED HISTOLOGY?
■ Benign adenoma
No way! This looks like cancer!
■ SM1 cancer
This was our own diagnosis although the non-lifting was of a more advanced lesion!
■ SM3 cancer
Doesn't really look like it but this was the CORRECT answer!
■ T2 cancer
Wrong because the lesion should then have NO crypt pattern
explanation
Histology had 'informed us' that this was a TA+HGD. But of course, Endoscopically this IS A CANCER! 'Newbies to endoscopy' may wonder how I can be sure?
Simply, this is what early colorectal cancer looks like !!! Of course, some cancers are hidden deep within larger, sessile or pedunculated polyp and can not be glimpsed from any disturbance of the polyp surface. That is a separate issue and no amount of experience can help you with the chance finding of cancer buried deep within such a polyp. Attempting to find the words to describe the features which are 'malignant' is difficult. Firstly the lesion is firm! If you can reach it with a finger, you will find that it's hard to the touch. If you can poke it with the biopsy forceps you will find that it moves like a solid disc of firm tissue. It's also the elevated margin surrounding an angrily red centre which has a different crypt pattern is another feature. Actually, there does appear to be some sort of crypt pattern in the centre. Endoscopically we had diagnosed sm1 invasion (i.e. invading into the top 1mm of the submucosal layer). Surprisingly, it didn't lift at all and because the patient was not a surgical candidate, we offered a 'full thickness resection' (images below). Rather surprisingly, the final diagnosis was of sm3 invasion with LVI! With time you will find that removing cancers endoscopically never leaves you with absolute 'peace of mind'. There is always some adverse feature to keep you awake at night! |
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