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 patient developed bloody stool whilst on holiday in Africa. They continue on return home and he undergo a flexible sigmoidoscopy. Of course, stool samples are obtained (last image).
WHAT IS THE PATHOGEN?
a) Clostridium difficile
Can be seen moving down a microscope
b) Salmonella enterica
Can give bloody diarrhoea but its not it!
c) Entamoeba histiolytica
Rasberry stool, to be examined warm
d) Campylobacter jejuni
May also give bloody stool but that's not it
e) Vibrio cholerae
Hmm, rice-water stool...
explanation
Let me give you some more clues! Classically, there are 'flask-shaped' ulcers found on resectional histology in which the mucosal surface ulcer is rather narrow with a wider, necrotic submucosal component in which the amoeba multiply. Stools have been described as like "Raspberry jam" and when examined whilst still warm, something can be seen moving. Of course PCR is the best way of confirming the diagnosis.
This patient had amoebic dysentery! Mild cases can resolve without metronidazole.
Patient was complaining of indigestion and reflux symptoms.
WHAT IS YOUR DIAGNOSIS?
a) Normal oesophagus
Not quite normal is it?
b) Reflux oesophagitis
This doesn't look like reflux!
c) Adenocarcinoma
Actually the correct answer!
d) SCC
Red nodules, even if surrounding by squamous mucosa are adenocarcinomas (usually)
explanation
You may be surprised to hear that the small nodule at 3 O'clock turned out to be an IMca! It was removed endoscopically. Of course, it's the question then arises; "Should we offer RFA". The BSG recommends this for patients with Barrett's harbouring flat dysplasia. However, in this case there is only a tiny, tongue of Barrett's in the 6 O'clock position! Actually, we just gave this a quick blast of APC (at a fraction of the cost of RFA) and it was gone. However, the patient remains on annual surveillance!
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 patient with ulcerative colitis has developed a polyp in the transverse colon. The lesion has now been sent for an endoscopic resection.
WHAT WOULD YOU DO?
a) Abort!
Smart!
b) Attack!
You are creating a problem of your own making!
explanation
Some would say; "if you can remove the lesion in that colitic colon, then 'do it'! The problem is that nothing may appear "irresectable" giving plenty of time, determination and poor judgement.
Many studies looking at outcomes of polypectomy in UC, excluded polyps >1-2cm or flat polyps. Other studies have included polyps arising outside of the colitic field or only have a short follow up period of a few years. Actually, most are coming to believe that when dysplasia develops in the colitic colon, it's not a 'random' case of bad luck. It can be the result of a long process of progressive DNA damage! At some stage we will be able to have a look at the state of the stem cell DNA in patients with conditions such as Barrett's, Colitis and atrophic gastritis. I think that we are in for a surprise ! In addition, did you spot the small focus of invasive cancer in the 2-3 O'clock position? Surprisingly, this was only T1 disease!
A polyp found in the transverse colon
WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?
a) Tubular adenoma
You are half correct!
b) Tubulovillous adenoma
On the left side, the crypt's are slit-like rather than gyrate
c) Villous adenoma
VA's are soft like sea anenome !
d) Serrated polyp
No, the crypts are not large, round openings!
e) Malignant polyp
Yes, there are no crypts on the right-hand side !
explanation
Did you spot that cancer has developed on the right side of this tubular adenoma (TA). On the left side, the crypts are slit-like whilst on the right hand side, the crypt pattern has been destroyed (Kudo type V crypt pattern). The Haggitt stage was I and I took particular care in removing the polyp with a large margin. The cancer was only 4mm in diameter. Perhaps the smallest adenocarcinoma of the colon you will ever see ?
This is the scar following the piecemeal removal of a sigmoid polyp some 6 months ago. It was a 15mm tubular adenoma harbouring high-grade dysplasia. Samples from the EMR scar has showed 'distorted glands' only.
WHAT WOULD BE THE CORRECT FOLLOW UP?
a) organise an immediate follow-up
WTF ! This not a normal scar! You absolutely need to organise more samples, and perhaps a CT !!!
b) organise a follow-up in 6 months time
Would have been a mistake !
c) organise a follow-up in 12 months time
Would have been a big mistake!!!
d) organise a follow-up in 3 years time
May have cost the patient his life!!!
explanation
The first EMR was piecemeal and histology could of course not confirm that the resection had been complete. Indeed the 'index histology' reads oddly mentioning "frequent mitotic figures" and "back to back glands". To a gastroenterologist these words does not sound particularly alarming.
However, the pathologist was trying to say "this looks like cancer but I can't actually make that diagnosis" !!! Indeed this doesn't look like a normal EMR scar! The whole area is indurated as if there is an infiltrative process below the mucosa. Histology was reassuring mentioning some distorted crypts only. Sadly, the endoscopist was content with the reassuring repeat histology and did not reflect on the worrying endoscopic appearances. He did NOT organise a second round of post-EMR samples and the patient returned 2 years later with an advanced cancer. The take home messages from this sad story?
A 21-year-old man presents with a past history of intermittent abdominal pains. For the last year he has suffered with more frequently bouts of abdominal pains and more recently he has started to vomit some 30 minutes after eating. He has been started on lansoprazole for a couple of months with no response. At gastroscopy (photograph) there is a severe gastritis and a tight pylorus requiring dilatation to examine the duodenum (which was unremarkable).
His blood results are as follows: Hb 11.2 g/l MCV 105 fl WCC 11.9 x 109 Plat 395 x 109 Basal gastrin 180 pg/ml (<75) WHAT IS THE MOST LIKELY DIAGNOSIS?
a) Hp associated gastritis
Doesn't explain all the 'issues' !
b) Zollinger-Ellison syndrome
There is a simple explanation to that elevated gastrin level!
c) Crohn's disease
Well done!
d) Gastric lymphoma
The antrum would do but how do you explain the macrocytosis?
e) Diffuse type gastric cancer
Could look like this but he is a bit young isn't he? !
explanation
Although the patient has a raised gastric level, this can be explained by the lanzoprazole. The macrocytosis is more difficult to explain. An autoimmune gastritis would be expected to be worse in the gastric body than in the antrum. In fact, the only other possibility is that the patient has terminal ileal Crohn's disease, causing malabsorption of B12 as well as a Crohn's gastritis. This was indeed the case! Actually, the diagnosis had already been confirmed by antral biopsies before I carried out the dilatation! Wouldn't like to dilate a diffuse type cancer !
An odd lesion in the middle of the oesophagus of a 55 year old woman. WHICH OF THESE POSSIBILITIES IS THE MOST LIKELY?
a) Papilloma
Papillomas look more warty and I've never seen them ulcerate
b) Leiomyoma
Statistically the most likely benign lesion probably!
c) GIST
Are very rare in the oesophagus!!!
d) NET
Are also very rare in the oesophagus!
e) SCC
Not likely as the IPCL's are regular and the lesion isn't brownish!
explanation
GIST's are extremely rare in the oesophagus whilst common in the stomach. In contrast, leiomyomas are common in the oesophagus and rare in the stomach. However, this looks odd and the previous biopsies had not been able to get to the bottom of the diagnosis. Are we missing a SCC? However, it looks like something from deeper layers were breaking through the mucosal surface. In contrast an SCC should start growing at the surface and in time invade deeper. The 'intrapapillary capillary loops (IPCL's) dilate up, become irregular and eventually completely disorganised in SCC's. At the same time the oesophageal wall takes on a brownish tint on NBI.
I decided to remove it and it turned out to be a leiomyoma. I presume that it had got traumatised or perhaps by pressure necrosis ended up with a funny surface. Don't think that I have seen an oesophageal NET as yet. Presumably they are very rare in this location. By the way, I've uploaded an example of a T2 mid-oesophageal SCC in the clip below. The lesion looks smallish but is already beyond endoscopic cure and Lugol's shows up a large area of background dysplasia which looks orange rather than brown after Lugol's dye spray.
55 yr pt with a Barrett's nodule is referred for an endoscopic resection. I'm surprised to find 4 abnormalities within his 10cm stretch of Barrett's
WHICH OF THESE IS THE MOST LIKELY TO BE ENDOSCOPICALLY RESECTABLE?
a) Lesion A
I agree! Of these 4, A is the only one which isn't ulcerated and therefore is least likely to be invading deeply.
b) Lesion B
Would be my second guess as the ulcerated area seem superficial
c) Lesion C
Don't like the ulceration!
d) Lesion D
Would be my least favourite lesion to attack as the ulceration suggests deeper invasion and poor lift into my cap.
explanation
This may be something of a record, 4 synchronous lesions! Clearly A, B and D are malignant. At first, ulcer C seem more innocent without an elevated edge but on closer assessment, it also has a slightly elevated rim.
Of these 4, A is the only one which isn't ulcerated and therefore is least likely to be invading deeply. Of course, they are assessed together as there is no point in EMR'ing one only. Either all are curable endoscopic means or none are ! Rather than going ahead with attempting to resect these, I actually bailed out and took samples from each lesion. Biopsies showed invasive, poorly differentiated adenocarcinoma at each location! Clearly, this patient has multifocal 'bad disease' which endoscopy is unlikely to cure in my opinion. I believe that surgery is a far better option and the patient is currently awaiting his oesophagectomy. If you still are not convinced of the pitfalls in trying to deal with ulcerated Barrett's lesions, have a look at the lesion below. Two rounds of sampling had indicated that the lesion harboured HGD. However, I failed to remove the lesion and ultimately the patient underwent an 'Ivor-Lewis'. You can see the histology yourself. The 4mm surface is literally the tip of the iceberg and below you can see the cancer (red line) invading up to the muscle propria.
This polyp found on the lesser gastric curve.
WHAT IS THE MOST LIKELY DIAGNOSIS?
a) Hyperplastic polyp
HP polyps are usually subpedunculated and angry red
b) Intestinal metaplasia
IM is also 'pale' but not 'flat elevated'
c) Gastric adenoma
Would be my first guess!
d) Early invasive cancer
This is a plaque without a depression or dominant nodule to suggest invasive cancer
explanation
Of course, this could have been rather easy to miss! An insignificant pale, plaque-like lesion but with distinct borders best seen after indigo carmine dye spray (as usual). Endoscopically this is what a gastric adenoma looks like and it was removed endoscopically. Somewhat surprisingly, histology reported a small spot of IMca and therefore its at actually an early cancer - not invasive though!
Most invasive, gastric EGC's are of course shallow depressions as in the example below. In fact the lesion below was invading into the middle of submucosa and was confirmed as poorly differentiated. Afterwards the patient underwent a distal gastrectomy where no further cancer was found. 'Poor differentiation' is the least reliable and lymphovascular invasion (LVI) is the most reliable predictor of nearby lymphnode micro-metastases.
This polyp on a short stalk was removed from the colon
WHAT IS THE LIKELY HISTOLOGY?
a) TA
At the edge, the crypts are clearly sli-like but how about the centre?
b) TVA
Doesn't look like gyrate crypts!
c) VA
Doesn't look like a sea anenome!
d) TSA
TSA's do have crypts but this lesion doesn't in the centre!
e) Early cancer
Was my own firm diagnosis!
explanation
The head of the lesion is clearly of concern. There are 'horns' on it! Of course, the devil has horns but as it was arising from a stumpy stalk. I went ahead and removed it. Somewhat surprising our pathologists called the lesion TA+HGD!
Admittedly, there was disagreement between our histopathologists and 2 out of 5 believed that it was an invasive cancer. Endoscopically, the lesion is clearly malignant and at the very least it's an intramucosal cancer (IMca). Of course, our UK histopathologists are unable to make the diagnosis of Intramucosal cancer in the colorectum because this is not a diagnosis recognised by the 'Vienna classification'. Elsewhere in the GI tract, intramucosal cancer is a diagnosis which our pathologists are 'free' to make. It makes no sense whatsoever to me !
This lesion was referred for resection just beyond the pyloric ring. It seemed to lift well but rather to my surprise, the snare cut through the base of the lesion (bottom image on the left). It took some further lift and a stiff snare to scrape the lesion of the muscle propria layer.
WHAT IS THE LIKELY HISTOLOGY?
■ Adenoma
Adenomas are usually not umbilicated ...
■ Brunners gland hyperplasia
I don't bother to remove those and they are not umbilicated!
■ Gastric heterotopia
Is usually found at this location but never require EMR
■ NET
Of course it is - it's umbilicated !!!
■ Early malignancy
Would be VERY rare in the duodenal cap!
explanation
The lesion is umbilicated... As you probably remember, umbilicated lesions in the duodenum are usually NET's. For some reason, they look different to NET's found elsewhere in the gut, where thin vessels are usually seen crawling up their sides. In the photograph below, you can see that at the very earliest stage (first image), there is no central indentation. However, very soon a subtle central dip develops (second image) which at the advanced stage (when I was tasked with removing the lesion), it has a deep central pit which was intermittently bleeding.
This proved to be a WHO grade I NET (neuroendocrine tumour, with a mitotic rate <2%). These lesions always seem to be tethered down close to the muscle propria and can be difficult to remove without taking a chunk of muscle propria with it. Duodenal NET's should of course be discussed at the 'neuroendocrine MDT' and usually end up having: 1) Measurement of plasma chromogranin A (pCgA) levels. CgA is produced by all cells derived from the neural crest and high levels are found particularly in patients with metastatic disease. 2) A ‘gut hormone screen’ (measurement of gastrin, glucagon, vasointestinal peptide, somatostatin and pancreatic polypeptide levels). 3) Finally, an ‘octreotide scan’ (somatostatin receptor scintigraphy) or, even better, a PET/CT scan using peptides that bind to somatostatin receptors (68Gallium-DOTA-TOC/NOC/TATE).
This is an odd looking sigmoid polyp which is seen arising from a broad stalk.
WHAT IS YOUR ENDOSCOPIC DIAGNOSIS?
■ Tubular adenoma (TA)
But the crypts don't look slit-like do they?
■ Tubulovillous adenoma (TVA)
Was my first thought but it doesn't look quite right...
■ Villous adenoma (VA)
If your bx forceps disappears into the polyp it's a VA
■ Traditional Serrated adenoma (TSA)
You'd be excused if you got this wrong - these are rare beasts!
explanation
My initial endoscopic diagnosis was that of a TVA. However, it looked a little "exaggerated". Actually it turned out to be a "traditional serrated adenoma" (TSA).
TSA's are rare and mysterious polyps. They only accounting for about 1% of colorectal polyps and are most common in the sigmoid and rectum. Endoscopically they can appear as “exaggerated” tubulo-villous adenomas or as villous adenomas. In the image below, I've put four examples of TSA's together to illustrate how differently these can appear ! It has been proposed that because one-third of "serrated cancers" are found in the distal colon and perhaps these cancers arise from TSA’s! However, genetically, TSA's are more like adenomatous polyps harbouring low-level microsatellite instability (MSI-L). They usually contain KRAS mutations rather than the BRAF mutations which you find in the 'Sessile Serrated Lesions'. For this reason, it's perhaps unlikely that they contribute to the 'Serrated Pathway' to cancer. By the way, a recent paper has highlighted that patients with TSA's are also at greater risk of 'high risk polyps', elsewhere in the colon.
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!
Two gastric polyps (labelled A & B) were both removed from the stomach of a 60 year old woman who complained of indigestion.
WHAT IS THE LIKELY DIAGNOSIS?
■ Both are hyperplastic
But the look different to each other!
■ NET + HP polyp
Well done ! And presumably you know which is which?
■ Both are NET's
But they look different!
■ HP + Adenoma
How about those fine vessels seen in the second image?
■ Both are adenomatous
But they look different!
explanation
You can see the thin vessels crawling up the side of polyp A. This appearance is typical of a gastric NET. Polyp B has a more villous surface with a few white spots - all typical of a hyperplastic gastric polyp. Some of these may contain some malignant cells which somehow generate a hyperplastic/reactive/inflammatory reaction around themselves. However, most hyperplastic gastric polyps are benign and arise secondary to a Helicobacter pylori gastritis. For this reason, you should always do a CLO test in these cases.
Every few weeks, I look up the notes on Prof Pritchard's' Podcast on gastric NET's to remind myself of the workup of these cases. As you remember, you should take samples to confirm an atrophic gastritis whenever you find a gastric NET. In this case, the patient did NOT have an atrophic gastritis. Instead, there was a Hp associated gastritis which is the reason for the second polyp. We realised that what we had was a TYPE II gastric NET! Analysis confirmed that the 17mm was WHO grade II. The finding of anything else than an innocent Type I gastric NET means that further imaging was required. A little late in the day of course but fortunately, the following imaging investigations were unremarkable:
Anyway, below is a reminder of what to do at gastroscopy, when you have a case of gastric NET:
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 was referred for a flexible sigmoidoscopy because of PR bleeding. However, the only abnormality found was a sore anal canal. Samples are taken of course.
HOW WOULD YOU NOW ADVICE THE PATIENT?
■ We'll see you in clinic once histology is to hand
But there is a degree of urgency here!
■ Symptoms may improve with 'anusol'
No they will not!
■ We will try topical mononitrate first
You are barking up the wrong tree!
■ We will organise a scan next
Yes, a rectal MRI revealed something important!
■ Inject 80mg of triamcolonone
You are missing the point!
explanation
Actually, this isn't a case of haemorrhoids or an anal fissure. Histology reported; " Within hyperkeratotic epidermis there are scattered individual highly atypical infiltrating malignant cells with frequent apoptosis and moderate clear cytoplasm. There is no ulceration or significant inflammation."
Actually, this is a case of Perianal Paget's disease, - a VERY rare condition!!! You'll remember that a 'puckering' of the skin around the breast areola is associated with underlying breast cancer. This was first reported by Sir James Paget in 1874. However, a few years later, the same phenomenon was described elsewhere, so called "extramammary Paget's disease". In descending order of frequency, this has been described at; the skin of the vulva, perineal skin, perianal skin and the skin of the scrotum. Paget's disease, is usually NOT a primary cancer of the apocrine glands of the skin. It's almost always secondary to a nearby cancer of the rectum, anus or prostate. In this particular case, further imaging revealed a nearby prostate cancer! ! 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!
During a Barrett's surveillance OGD, I notice this small red spot at 6 O'clock.
WHAT IS THE LIKELY HISTOLOGY?
■ Reflux ulcer
I don't think that you get this within Barrett's without dysplasia!
■ LGD
Clear crypt pattern, not that different from surrounding mucosa? Good guess!
■ HGD
Quite possible and would have been my guess IF there was some nodularity associated
■ Early cancer
Impossible as lesion has an organised crypt pattern!
explanation
Previous surveillance samples, 3 years earlier had not revealed any dysplasia. However, that red spot shouldn't be there! A reflux ulcer is unlikely as the Barrett's is there because it protects the food pipe from acid. Of course it does this by developing crypts with Goblet cells which secretes protective mucus (of course the pathologists call this process 'metaplasia'). Early texts usually stated that ulceration is common within Barrett's. In my experience, ulceration within Barrett's only happens when dysplasia develops. With the arrival of dysplasia, you begin to see a disappearance of the Goblet cells and of course when the Goblet cells start to dwindle, so does the protective mucus.
In the bottom zoom image you can see that there is a distinct surface crypt pattern at the site of the red spot. Therefore the cells can't be too disorganised, making cancer unlikely. Actually this turned out to be a spot of LGD. I would have guessed HGD/IMca (pathologists struggle to tell the difference) if there was a visible nodule at the site of the red spot. Isn't it interesting that even at the very earliest stage of dysplasia, the unstable cells signal the need for more oxygen to nearby vessels?
This lesion was found in the ascending colon.
HOW WOULD YOU DESCRIBE IT?
■ Flat elevated lesion (IIa)
Only lesions 10mm or smaller are referred to as 'IIa lesions'
■ Flat elevated lesion with a central depression (IIa+IIc)
But that depression dissappear when lumen is inflated!
■ Laterally spreading tumour of the non-granular type (LST-NG)
But the surface is 'cobbled' not smooth!
■ Laterally spreading tumour with a central depression (LST-D)
LST-D's are always TA's (and therefore have a smooth surface)
explanation
Lets just state something from the start! A flat elevated polyp is of course a IIa type of lesion BUT when larger than 10mm in diameter is no longer referred to as a IIa lesion. Now, it's a 'Laterally Spreading Tumour'!
There are 4 types as follows:
In this case the crypts are gyrate, (type IV crypts), making it a TVA. Laterally Spreading Tumours with a gyrate crypt pattern are all TVA's and almost never harbouring more than LGD. OK but it looks depressed in the centre doesn't it? No, it isn't depressed in the centre! It's simply they way the large lesion has folded itself. This is something of a 'trick question' as I deliberately didn't inflate the colonic lumen fully in the first image. When the lumen is inflated, you can see the true shape of the lesion; a LST-G ! A meta-analysis in 2013 by Voorham et al. [Voorham QJM. AM J Gastro 2013;108(7):1042-] concluded that pedunculated polyps were more likely to harbour KRAS mutation and APC mutations than flat lesions, and that flat lesions were more likely to harbour BRAF mutations. Depressed lesions and LST-NG’s were particularly unlikely to contain KRAS. Below are some examples of LST's 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 sizeable polyp was discovered at the ileo-caecal valve and was referred for resection. Samples have not been taken to avoid tethering down making the endoscopic resection uneccessarily difficult. HOW WOULD YOU APPROACH THE LESION?
■ Back off and take some samples
Yes, and perhaps request a CT!
■ Attempt an EMR
You first need to decide what this is!
■ Consider removal by ESD
Can't be adenomatous, it's growing out of the TI!
■ Underwater EMR
Would also be ill advised
■ Refer for surgery
If this is what you think it is, then Yes!
explanation
In most cases, I would say 'if it lifts it will shift'. However, in this case I wouldn't bother with a test-lift. The reason is that the thing is growing out of the terminal ileum. You don't get adenomatous polyps growing out of the TI! This must be something else! In fact the true lesion may be larger than the red nipple-like polyp. Even though there are no large 'tell-tale' vessels running up it's side, the only thing of this size, growing out of the TI, is a NET! A lymphoma was my second guess. TI NET's are often bad news and should be considered for surgical resection. There is another odd thing about NET's growing in the terminal ileum. The WHO grading system doesn't seem to relate to the aggressiveness of the lesions behaviour ! This was only WHO grade I (proliferation index was only 1.8%) but on a full analysis after the right hemi-colectomy, the NET was found to be a invading into the muscle propria layer and with metastatic deposits in 2 out of 12 resected lymph nodes (T2,N1) as well as ulcerated deposits of NET in the nearby pericolic fat on the serosal surface. The moral of the story? In the terminal ileum, 'well differentiated NET' doesn't mean that it's well behaved! |
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