A dental debacle ...

This patient woke up with retrosternal pain and dysphagia. This was found at endoscopy!?!

WHAT WOULD YOU DO NOW? a) It will probably be possible to remove these endoscopically using a rat-toothed forceps or stent retrieving forceps
b) It will probaby be possible to remove these using a Roth net or a polypectomy snare
c) As it will not be possible to remove these endoscopically, an attempt should first be made to push them into the stomach
d) As it will not be possible to remove these endoscopically, an attempt should be made to place them close to the upper oesophageal sphincter
e) it will probably not be possible to remove these endoscopically and surgery should be the first consideration Thank you to everyone who contributed to this case. Surprisingly, dentures is one of the most commonly found foreign bodies in the oesophagus (excluding food bolus obstructions), this may be as dental wearers are thought to have reduced oral sensation.  Patients usually present with dysphagia or pain.  Even Horner’s syndrome has been described due to compression of the stellate ganglion!  In general, endoscopy has an excellent success rate (>95%) in removing foreign bodies.  However, the success rate is far lower for dentures.  The largest series I could find on the topic is still small and only constitute 21 cases [J Otolaryngology 1998;27(4):190-4].  In this series it proved possible to manage 16/21 cases endoscopically.  For this reason, option B is most likely to be correct.  In addition, this was only a half dental plate which is less hazardous to retrieve than a full sized dental plate (which may well be impossible to swallow). Complications are frequent and include mucosal tears, haematomas and even perforations, usually at the upper oesophageal sphincter.  To reduce the risks as far as possible, an overtube should be used and only gentle traction should be applied.   Unfortunately, most dentures or dental plates will not fit into the overtube.  An edge may protrude sideways as the overtube is withdrawn.  For this reason it is important to abandon the attempt if there is resistance on withdrawing the endoscope+overtube.  I have added the footage of the removal of the dental plate. At the upper oesophageal sphincter, I inflated lots of air in the stomach and asked the patient to belch it up, attempting to synchronise the withdrawal of the overtube with the patients belch. It worked and after a quick rinse, the patient put his teeth back in and an vouched to never fall asleep with the dentures in again.  We'll see about that. I suspect that alcohol had something to do with it. By the way, there is an interesting case report of a laser being used to cut the denture into smaller pieces which could subsequently be retrieved.  Don't think that APC would work as the dental plate does not conduct electricity. If the dentures can not be removed endoscopically, using a rigid oesophagoscope is unlikely to be successful.  Oesophagotomy and oesophagectomy may be the only two options if the dentures are impacted an can neither be retrieved nor pushed into the stomach (which would be "plan B").  Time is of the essence as if the diagnosis is delayed, oedema and pressure necrosis may ensue, making oesophagectomy the only remaining option.

A plethora of polyps

This 75 year old patient was found to have no less than 15 polyps in the ascending and transverse colon!

In addition there were a few smaller, polyps on the left side. There was no family history of colorectal cancer.  This patient had been referred to me to clear all colonic polyps over 2-3 examinations.  HOWEVER, WHICH OF THE 15 POLYPS SHOULD I REMOVE AT THE FIRST EXAMINATION?
a) The most proximal polyps (1,2,3)
b) The polyps on the longest stalks (4,5,6,7)
c) The five smaller sessile polyps (
d) The two largest sessile polyp (8 and 10)
e) None of the above, the patient should be referred for a right hemicolectomy

When this patient was referred, our endoscopy trainee was itching to start removing the “easy wins”.  By this I mean the polyps on a long and inviting stalk.  However, larger, sessile polyps are more likely to harbour cancer.  Furthermore, cancer developing in the head of a polyp has a longer path to travel to come close to the underlying muscular propria (and become stage T2).  For these reasons, the correct answer is “polyp 8” which is the largest lesion.  This polyp did indeed contain Haggitt stage 3 cancer.  Although Haggitt stage 3 is usually reassuring, in this particular case there were malignant cells seen within lymphatics and the patient proceeded to a right hemicolectomy (which did not reveal any lymph node metastases).  Data from our English Colorectal Cancer Screening Programme has revealed some interesting data on the link between size and cancer risk.





Number of polyp cancers




Total number of polyps




Percentage  polyp cancers by size group




































































Size not recorded
































 I must admit that this data makes me a little uneasy about discarding sub-centimetre polyps without histological analysis.  My braver friends tell me that if the polyp looks funny, you can still retrieve if for histological analysis.  However, I also remember the endoscopists equivalent of “sods law” which is that the more you hope that nothing goes wrong (i.e. when scoping Royalty, litigation lawyers or Professors), the more likely a mishap! 

A tricky polyp!

This polyp was found in a difficult position at the caecal pole!

HOW WOULD YOU DEAL WITH IT ? a) Remove by hot biopsy
b) Remove by cold snare
c) Remove by snare polypectomy
d) Remove by endoscopic mucosal resection
e) None of the above

Thank you to everyone who has entered a comment!  This polyp was referred to me for resection!   An understanding of the different adenomatous crypt patterns came in handy as I realised that the “polyp” was not covered with adenomatous mucosa.  Removing it would have been a mistake as it is indeed an inverted appendix! 

True adenomatous polyps are not infrequently found close to the appendix orifice.  The way I deal with these lesions is to inject a few ml of my usual submucosal injection solution (40ml of a colloid, 2ml of adrenaline 1:10.000 solution and 2ml of indigo carmine dye).  If the adenoma lifts out of the appendix orifice, it can be removed.  If I find it anchored down into the appendix orifice, I conclude that it can not be removed endoscopically. 

By the way, you may think that a small polyp at the caecal pole in a patient who has previously undergone an appendicectomy, would be easier to deal with?    Surprisingly the opposite is true!   The previous appendicectomy may have weakened the caecal wall making an polypectomy hazardous.   A friend told me how he found himself looking at the peritoneum after removing a small polyp from the site of a previous appendicectomy!

Case presented by Dr Rakesh Kumar Jha at Narayani Sub-Regional Hospital (NSRH), Birgunj, Nepal  If you are looking for even more endoscopy cases, check out Twitter: @Bjorn_Rembacken

Appropriate advice

This was found in the stomach of a 75 year old man undergoing a gastroscopy because of an iron deficiency anaemia.

At the end of the examination, the findings are explained and you tell the patient that we will be awaiting the analysis of the biopsies. The patients then asks for your opinion of what is the most likely outcome once the histological analysis is to hand.
  1. in view of the small size and your age, this is unlikely to be anything to worry about and it's unlikely that you will need any further examinations
  2. this will probably need to be watched and you will be offered regular surveillance and if the lesion is found to be growing further tests may be required
  3. this lesion is probably best removed but it can probably be done endoscopically
  4. this lesion will probably need to be removed surgically
  5. this may have arisen somewhere else in the body and a full body scan may well be required next 
Thank you to everyone who has contributed to the discussion around this case!   It’s was a particularly difficult differential diagnosis and I did not fully believe the biopsies which indicated that there was only low-grade dysplasia within the lesion.  Ectopic pancreas are much smaller, perhaps 5-8mm in diameter.  In fact, all you see in these cases is the orifice of the duct whilst the pancreatic cells are situated deep in the mucosa.  Most early gastric cancers do appear somewhat depressed with a distinct edge (IIc growth pattern) similar to that of a basal cell carcinoma on the skin.  This appears as an “exaggerated” flat-elevated lesion with a central depression.  It’s almost like a caricature of an early cancer.  The only feature which betrays its true benign nature is how a contraction wave easily deforms it.  This is a soft lesion whilst cancers, carcinoids and GIST’s are very firm and would not have been deformed by the biopsy forceps or a contraction wave.  I do squeeze every lesion which I resect to determine if it feels soft or hard.  This lesion was removed endoscopically and was found to be a gastric adenoma harbouring no more than high grade dysplasia.  Similar to gastric cancers, adenomas arise in stomachs ravaged by decades of Helicobacter associated gastritis.  You will find these lesions in patchily inflamed stomachs with florid intestinal metaplasia, usually in a patient undergoing the examination because of an iron deficiency anaemia (presumably due to malabsorption of iron from the associated achlorhydria).  In contrast to the colon, there are far more gastric cancers than gastric adenomas.  In the colon the opposite is true; there are far more polyps than cancers.  For this reason, it is thought that most gastric cancers do not develop from gastric adenomas.  Should they be removed at all?  This would depend on the age and comorbidities of the patient.  You should think twice before removing any lesion in any patient who may not be able to cope with a 4 unit blood loss.  In this case, the patient was fit and the lesion sufficiently scary looking without a clear crypt pattern it its centre to warrant resection. How about EUS and CT prior to resection?  When considering lesions which appear endoscopically resectable, I can not remember a single occasion when a CT or EUS contributed anything which analysis of the EMR specimen wouldn’t have provided.  For this reason, the new BSG guidelines on Barrett’s no longer advocate EUS and CT staging before EMR for Barrett’s nodules. Perhaps the greatest significance of these lesions is to have a very good look around for synchronous early gastric cancers.

This nodule was found in a 45 year old woman presenting with some vague indigestion.

This nodule was found in a 45 year old woman presenting with some vague indigestion. Biopsies had been unhelpful and only reported that the “squamous mucosa appears hyperplastic”. WHAT I THE MOST LIKELY DIAGNOSIS?
b) Squamous cell papilloma
c) In-situ squamous cell carcinoma
d) Squamous cell carcinoma
e) Verrucous carcinoma Thank You to everyone who had a crack at this case! When I first saw this lesion, I was concerned that it may be a verrucous carcinoma.  There also seemed to be a lot of candida but there was no clinical evidence of any immunosuppression.  Although histopathologists are close friends, never to be entirely trusted, it seemed unlikely that they had completely missed a cancer?  I asked them if they could assure me that this was not a “verrucous carcinoma”?  One the basis of the biopsies, that would be an unlikely diagnosis, they replied.  Nevertheless, the appearances were sufficiently frightening for me to organise an EMR of the more nodular areas. With the EMR fragments to hand, our histopathologists were more helpful and reported;  “Histology shows thickened squamous epithelium with a papillomatous surface. There is keratinisation with foci of parakeratosis and occasional dyskeratotic cells.  Keratohyaline granules are seen in the superficial layers of the epithelium.  There are scattered koilocytes but no epithelial dysplasia or malignancy.”
I had to phone them up to ask what this meant in English.  They explained that “koilocytes” are abnormal squamous epithelial cells in which the nuclei are markedly enlarged, irregular, dark-staining or surrounded by a clear zone.  What do they signify?  Infection by the human papilloma virus (HPV)!
The diagnosis was now clear, this was a squamous cell papilloma and the lesion turned out to be positive for HPV subtype 16. Perhaps making the diagnosis was the easy bit.  How should I now advice my patient?  After all, HPV infection is implicated in some 40% of squamous cell carcinomas in the mouth and throat.  Furthermore, HPV 16 (or 18) is particularly nasty and associated with a 200 times increased risk of cervical carcinoma.  Verrucous carcinomas have also been linked with HPV infection. I decided on an ambitious plan to ablate the lesion by APC (we don't have laser in Leeds), set at a high level (95W).   This turned out to be tedious and unpleasant for both patient and myself.  The smell of burning tissue was overwhelming.  Furthermore, the patient suffered severe retrosternal pain and felt shivery and unwell for several days after each session.  Luckily, after 5 APC ablation session, hardly anything is left of the original lesion.  Was it worth it?  No idea!  But I will keep the patient under 2-yearly surveillance for a while and do the next case under general anaesthesia!

This 25 year old woman presents with a 6 month history of dysphagia.

What would you do now? a) take a full set of oesophageal biopsies
b) inject botox into the lower oesophageal sphincter
c) carry out a balloon dilatation
d) refer for further investigations
e) refer for surgery

I recall a case just like this. A desperate young woman had been admitted for investigations of her dysphagia. I found the oesophagus to be dilated and atonic with a tight and non-relaxing lower oesophageal sphincter. Based on the history and endoscopic findings I diagnosed achalasia and injected the sphincter with 100 units of botox.  Within a week her symptoms had improved and she was very grateful. However, the referring physician was appalled as he thought that all possibility of "confirmation" by manometry had now been thwarted. In the event it had not. The manometry finding which confirms the diagnosis is that of an atonic and non-propagating oesophagus rather than of a non-relaxing sphincter (a bonus if found but not essential).  Furthermore, it takes about a week for the botox to take effect, which gives the referring team ample time to organise further investigations. However, the surgeons also don't like botox as it causes some fibrosis which makes a myotomy more difficult. The "correct answer" depends on your local surgical waiting times. Is it acceptabe to let these patients wait more than a week for their symptoms to be treated (this is how long it takes for botox to take effect)?  Of course, if your surgeons can organise a myotomy within this time, go ahead and refer your patient. If they can't, I would propose to inject botox.  Why such a hurry?  The reason for my own sense of urgency in these cases is that I have seen a patient with achalasia, on waiting list for investigations, die from aspiration pneumonia. How about doing an oesophageal dilatation? I think that we should now stop doing dilatations for achalasia. Forcibly rupturing the sphincter with a large size balloon is effective but too hazardous. I can not justify a perforation rate of up to 1:10 to my own patients. By the way, is it neccessary to "confirm the diagnosis" with manometry?  Personally, I don't think so, in a case as obvious as this. Elderly patients with "presby-oesophagus" may be a different matter but if their symptoms respond to a therapeutic trial of botox, does it matter what the manomery shows?

This is the 12 cm stretch of Barrett’s of a 55 year old man undergoing a Barrett’s surveillance examination.

This is the 12 cm stretch of Barrett’s of a 55 year old man undergoing a Barrett’s surveillance examination. The mucosa has been viewed by white light, NBI and after indigo carmine dye spraying. ACCORDING TO YOUR ENDOSCOPIC INTERPRETATION OF THE MUCOSA, WHICH OF THE FOLLOWING STATEMENTS IS MOST LIKELY TO BE CORRECT? a) The Barrett’s is unremarkable and full set of samples is likely to confirm stable mucosa
b) There is probably low-grade dysplasia and a full set of samples should be taken
c) There is probably high-grade dysplasia/IMca which we should be able to resect with EMR
d) There is probably high-grade dysplasia/IMca which we should be able to ablate with RFA
e) There is probably multifocal invasive cancer and surgery is indicated


This is what unstable GI mucosa looks like in both the upper and lower GI tract. In the colon the endoscopic appearances are easily mistaken for active colitis. The only question is; how unstable?  The nodularity with a range of different surface patterns indicate that this is at least HGD/IMca.  However, the surface area is large and in a few places, there is probably early invasive cancer which RFA will not be able to reach.  To remove all of the dysplastic mucosa endoscopically by piecemeal EMR may be possible but will be complicated with tight stricturing.  As the Barrett’s may well already have foci of invasive cancer, the EMR would have to be done in a single session rather than “multi-stage”, spread over a 6-9 months.  Of course, successful, single fragment removal by ESD is elegant until there is a perforation, when the approach seems reckless as it may have turned a case of early cancer into a case of incurable contamination of the mediastimum. Currently, the “correct answer is E”, i.e. to refer this patient for an Ivor-Lewis oesophagectomy.  But is it the best answer?  We are looking at an operation associated with a 1:20 risk of death and 1:2 probability of morbidity.  Of course, EMR will cause a tight stricture which will take a long time to sort out.  Perhaps spending a couple of months undergoing weekly dilatations and living on liquids is a price worth paying for having a near zero risk of dying and an oesophagus which remains connected to the gastric cardia.

This was found in a 55 year old man undergoing a gastroscopy because of indigestion.

What is the likely diagnosis?
a) Helicobacter associated gastritis
b) CMV infection
c) Gastric lymphoma
d) Multiple hyperplastic polyps
e) e-cadherin mutation with multifocal cancer
This used to be a common finding at our open access gastroscopy service in Leeds (option a is correct).  It’s so called “Octopus sucker gastritis” where the HP associated gastritis is evident as multiple small erosions each giving a ring-like impression from the oedematous mucosa.  Our open access endoscopy service used to run two evenings a week and all weekend.  In all we carried out some 10.000 such examinations each year.  The outcome?  Apart from funding the research into Helicobacters of several of my colleagues, very little.  As far as I know, the risk of dying from gastric cancer in Leeds remained stable.  Of course, we found the odd peptic ulcer which would have been picked up by testing for Helicobacters anyway.  We did see “the worried well” with dyspepsia returning every 18 months or so for another endoscopy.  The “reassurance” of a normal endoscopy seemed to last no longer than 2 years.  The challenge for the next generation of doctors will be to NOT spend millions on the investigation of “the worried well” or those with anxiety or healthcare-seeking personality disorders who use up a disproportionate amount of our health care resources.  In fact, gastroenterologists do not receive training in how to manage patients with irritable bowel syndrome.  We focus to much on trying to “fix” the symptoms and not enough time on supporting the patients coping mechanisms.  I recommend Prof Drossman’s presentation  (click this link to watch it).  We are living longer and health care interventions are getting every more expensive.  Unless we are able to focus resources where we get the “most bang for the buck”, you will be paying the full cost of your own cataract extractions, hip replacements or colonic surveillance when you need them.

This was found in a 60 year old man undergoing a surveillance colonoscopy because of long-standing colitis.

What is the likely diagnosis?
Normal mucosa
Aberrant crypt foci
Familial adenomatous polyposis
Multiple DALM’s

This video clip illustrates one of the pitfalls of the new UC Surveillance policy in the UK.  To reduce the number of biopsies taken, we are encouraged to use dye spraying to identify small adenomas.  The problem is that with dye spraying all sorts of minor mucosal irregularities are found.  This is an example of some slightly more prominent lymphoid follicles, i.e. normal mucosa.

With age, virtually all of us will develop aberrant crypt foci, small hyperplastic polyps and the odd tiny adenoma.  With dye spraying these may be detected and samples taken.

You can imagine the scenario; an elderly patient has undergone many years of unremarkable surveillance, the colitis has been quiescent for a decade but when he attends for his surveillance colonoscopy, 3 tiny adenomas are detected and sampled.  Histology will read; chronic ulcerative colitis with multifocal dysplasia (as 3 tiny adenomas was sampled). 

As all three lesions were virtually removed by the biopsy forceps, a follow-up colonoscopy will not be able to find the “lesions” again.  The best outcome would be a few years of intensive (i.e. 6-monthly), surveillance.  The worst possible outcome would be a pan-proctocolectomy.

But surely, it’s possible to histologically distinguish a DALM from a sporadic adenoma?  Unfortunately, there are no reliable histological criteria which we can rely upon to detect a colitis-associated lesion!   In addition, there are no accepted endoscopic criteria either!  However, I believe that DALM’s are usually smooth surfaced, flat elevated (IIa type) lesions (different to the common carpet-like LST-G lesions composed of multiple small nodules giving the polyp a “crazy paving” appearance. 

This lesion was found in the duodenal cap in a 50 year old woman undergoing endoscopy because of anaemia.

Have a look at the first video and decide which you think is the most likely diagnosis!

My endoscopic diagnosis is: 

a) Brunners gland hyperplasia
b) Pyloric gland adenoma
c) Duodenal carcinoid
d) Primary duodenal carcinoma
e) Metastatic deposit Both brunner’s gland hyperplasia and pyloric gland adenomas are small polypoid lesions (usually smaller than 1cm).  Without a history of FAP, a primary duodenal carcinoma would be extremely rare and in FAP there should be other adenomas surrounding the lesion.  Carcinoids are usually small submucosal yellowish nodules whilst this is a somewhat more scary looking nodule.   I must admit that my own guess would have been that this was a secondary deposit from, for example a primary colorectal cancer.  However, this was not the case!  Biopsies confirmed that it was a carcinoid with a mitotic index <2%.  Both an octeotride scan and CT were reassuring.   By the way, carcinoids are now called “Neuroendocrine tumours” (NETs).   Although they can develop in various organs such as bronchus, thymus, kidney, ovary and testes, the majority (75% to 90%) occur in the GI tract.  About 38% of all GI NETS develop in the small intestine, where they are 6 times more common in the ileum than in the jejunum.  In view of, or perhaps in spite of, the low mitotic index and the reassuring cross sectional imaging, the lesion was referred for endoscopic resection (SECOND VIDEO).  However, what do you believe is the preferred treatment of this lesion? 
a) This is clearly a benign lesion and the patient can be reassured and discharged
b) This lesion could turn malignant in the future and yearly surveillance is indicated
c) This lesion should be resected endoscopically for a full histological analysis
d) This lesion should be resected surgically as it is likely to be malignant after all As a rule of thumb, all NETs larger 1cm or larger should be removed.   However, as NETs arise from diffuse enterochromaffin cells, which are found deep to the surface mucosa, they are difficult to remove endoscopically.  Furthermore, the majority of NETs in the jejunum and ileum are malignant and should be removed surgically!   In the duodenum, I would go by a size threshold of 1cm, if larger, it shoul be removed.  In this case, there was every indication that the lesion was benign and the patient was very reluctant to agree to a hazardous and extensive surgical resection.  For this reason endoscopic resection was decided upon. In spite of the reassuring histology, the endoscopic appearances are worrying.  The size and nodularity suggested to me that it had turned malignant already.  However, perhaps against better judgement I proceeded with the endoscopic resection.  The “pull within the snare” EMR technique is the endoscopic equivalent of a nuclear weapon – utterly powerful and with a huge destructive potential!   As expected, the lesion did not lift well but could nevertheless be removed as a single fragment by this method.  In the THIRD VIDEO you can see that I am particularly anxious to close the mucosal defect.  Why do you think this is?
a) There is a high risk of bleeding after duodenal EMR
b) The resection has resulted in a micro perforation which must be closed
c) In this particular case there is a high risk of late perforation When the resection fragment falls away you can see that it has a round disc of muscle propria in its centre.  Although this is a firm indication that you have perforated, evidently the muscle propria layer is intact in the mucosal defect!   Clearly, I have partially resected through a surprisingly thick layer of muscle propria !  Unfortunately, there was some bleeding which I had to treat with the tip of a “coagulation grasper”.  The heat damage will further weaken the already weakened muscle propria layer!   Unless I can close this mucosal defect, this patient may well will suffer a late "thermal" perforation.   Unfortunately it proved impossible to close the defect with either the clips made by Olympus or Boston Scientific.  The mucosa was simply too firmly stuck down to be pulled over the mucosal defect.  Instead, I had to resort to the “purse –string closure method”.   This method is more powerful but always messy and takes a longer time to achieve.   Luckily the resection had been carried out under general anaesthesia and I could take my time to successfully close the defect.  The Ultimate histology?   Tumour cells were seen invading into the disc of muscle propria which confirmed that the lesion had undergone malignant conversion in spite of the low mitotic rate!  What next?  As up to 40% of lesions are multiple, she will need a capsule enteroscopy.  Furthermore, there is a strong association with other synchronous tumours of the gut.  Second malignancies have been reported in between 10% and 29% of cases (most commonly colorectal adenocarcinomas).  The patient should also be offered a colonoscopy. There were multiple levels in which this case could have become a disaster.  However, the patient recovered without incidence but remains reluctant to undergo surgery!   Perhaps disaster was not averted after all?

This polyp was found in the rectum of a middle-aged man undergoing colonoscopy screening for bowel cancer.

This polyp was found in the rectum of a middle-aged man undergoing colonoscopy screening for bowel cancer. In spite of it’s “classical” appearance it can not easily be categorized according to the Kudo classification. What is your endoscopic diagnosis?
a) Hyperplastic polyp
b) Serrated adenoma
c) Tubular adenoma
d) Tubulo-villous adenoma
e) Villous adenoma
This is a “traditional serrated adenoma” (TSA) with its typical “thick spaghetti in a ball appearance”.  It has been proposed that serrated lesions give rise to up to one-third of colorectal cancers (CRCs).  A cancer pathway which is distinct from the classical adenoma– carcinoma sequence.  In fact, research on serrated polyps has contributed to the current understanding that there are several ‘’pathways’ to CRC.  Cancers arising in traditionally serrated adenomas are typically situated distally whilst the ‘Sessile Serrated Lesions’ (SSL’s) are situated proximally and may account for the evidently low protection against future right-sided future provided by colonoscopy.
Histologically, TSA’s have a complex tubulovillous or villous morphology where the villi are elongated and with bulbous tips.  A recent study described a characteristic pattern of budding of proliferative crypts situated perpendicular to the long axis of villous structures.  Tthe authors called this “ectopic crypt formation and suggested that this is related to loss of (normal) anchorage of crypts to the underlying muscularis mucosa. This is the most characteristic histological feature of TSA’s.  Within TSA’s both conventional “adenoma-like” dysplasia and serrated dysplasia has been reported.  When the dysplasia is found within adenomatous crypts, it’s staged low-grade vs. high-grade.  However, there is no consensus on how serrated dysplasia should be graded in TSA’s.  
Serrated lesions are currently classified by the WHO into 3 types: 1) Hyperplastic polyp; 2) Sessile serrated adenoma or Sessile serrated polyp, with or without cytological dysplasia; and 3) Traditional serrated adenoma.  
Small hyperplastic polyps have been recognized for many years.  They are usually found in the recto-sigmoid and probably have little or no malignant potential. Autopsy studies have reported prevalence rates in the range of 25 – 50 %.  Interestingly, the overall prevalence of serrated lesions increases only slightly with age during adulthood in contrast to conventional adenomas, where the prevalence increases sharply with age. “Giant hyperplastic polyps”, larger than 10mm” on the other hand, are usually found in the proximal colon and are probably a distinct and more sinister entity.  
The colon polyp map used to be simple, “if it looks adenomatous – take it out but if it looks hyperplastic – ignore it”.  This is no longer correct and instead I would propose; “remove everything which is 10mm or larger”.    Submitted by Paula de Azevedo Lopes, Rio de Janeiro. 

This lesion was found in the duodenum of a 45 year old man with an inherited condition.

What is your endoscopic diagnosis?
a) this is an adenoma which does not require removal
b) this is an adenoma which should be removed endoscopically
c) this is an adenoma which should be removed surgically
d) this is a carcinoma which should be removed by a limited surgical resection
e) this is a carcinoma which should be removed by a Whipple’s procedure
Duodenal polyps often have a scary “rodent ulcer – like” appearance (a Kudo’s IIc type of growth pattern).  In spite of their frightening “depressed” appearance, they are usually benign.  In my experience the “volume” of the lesion (i.e. the chunkiness in terms of width and thickness) is a better guide to the presence of cancer.   Polyps with a larger volume have a greater risk of harbouring cancer.  In this particular case, the adenoma still has a well developed crypt pattern in it's centre making cancer unlikely.  Although these lesions are almost ubiquitous in patients with Familial Adenomatous Polyposis, they rarely turn malignant.  The overall lifetime risk of periampullary cancer in patients with FAP has been estimated at 3%–4%.  For this reason the British Society of Gastroenterology recommend 3 yearly screening above the age of 30.  However, this guideline is now 10 years old and rather than a blanket recommendation it would make more sense to tailor the surveillance interval to the patients Spigelman score.  The higher the score, the more frequent surveillance.  
Having spent many years resecting FAP related duodenal polyps, I am beginning to loose heart.  The risk of delayed bleeding in this area which is bathed in pancreatic juices, approaches 1:10.  The risk of perforation can be up to 1:50 and local recurrence is almost guaranteed.  If you consider an ampullectomy, you can add a 1:30 risk of acute pancreatitis to the above.  The best thing we can offer these patients is early surveillance, starting in the mid-20’s when it’s still possible to ablate the polyps by APC.   Oops, almost forgot.  The correct answer? As the lesion is single and below 3-4 cm in size, endoscopic removal should be possible.  The more fundamental and important question is (which I always ask myself):  Would this particular patient be able to cope with a complication?   In this case the answer is Yes.  He is young and is likely to survive the complications (a rapid 6 unit haemorrhage, severe acute pancreatitis or emergency surgery because of biliary peritonitis).  

This lesion had previously been found in the terminal ileum. Biopsies had been reported as normal mucosa only.

My job was now to determine the nature of the lesion and, if indicated, remove it.  Please have a look at the video.  Once you have decided what type of lesion this is, answer the following question;   WHAT IS NOW THE CORRECT COURSE OF ACTION?
a) This is an innocent lipoma which can be left alone
b) Although this is a lipoma it should be removed endoscopically for confirmation
c) This is a carcinoid and can be left alone
d) This a carcinoid and should be removed endoscopically
e) None of the above Ileal neuro-endocrine tumours although uncommon usually arise quite close to the terminal ileum.  In this case, I made an endoscopic diagnosis of a carcinoid (the lesion was too firm for a lipoma) and I progressed to resect it.  Histology confirmed an 8mm carcinoid with a low mitotic count and a positive deep margin (which, in my experience, is usual when carcinoids are removed by EMR).  In view of the deep margin, the patient underwent a surgical ileal resection. There was no carcoid remaining within the ileum but one of the 15 lymph nodes contained a metastasis.  The correct choice would have been e (leave the lesion for surgical resection). Ileal carcinoids are outside the remit of of endoscopic resection.   The reason for this is that these lesions tend to undergo malignant change early.  It is well recognised that once the patient become symptomatic, these lesions are usually  quite large (often >2 cm).  When they have reached this size, ileal carcinoids have usually turned malignant. In a total of 35 618 NET, registered in the Surveillance, Epidemiology and End Results (SEER) Programme, local spread was found in 41% of cases and distant metastases in 30%. In up to 40% of cases the tumours were multiple. Patients with liver metastases may develop the carcinoid syndrome (flushing, diarrhoea and endocardial fibrosis) as serotonin, secreted by the tumours is inactivated by the liver. The overall 5-year survival rate is around 90%.  However, the prognosis is worse in carcinoids with high-grade histology, liver metastases and other distant metastases were it drops to below 40%. The presence of the carcinoid syndrome is not known to influence prognosis. Carcinoid are now classified according to the proliferation index Ki-67 and/or mitotic index.  Low-grade G1 tumours have a mitotic index (Ki-67) at 2% or below (mitotic count <2 per 10 HPF), intermediate-grade G2 tumours (Ki-67 3-20%, mitotic count 2-20 per 10 HPF) and high-grade G3 tumours (Ki-67 >20%, mitotic count >0%).  In spite of it's lymph node metastasis, this lesion had been classified as a low-grade carcinoid!  

This is the rectum of a 65 year old man complaining of rectal bleeding.

Six years earlier he had undergone a successful course of radiotherapy for a gastric MALT lymphoma.  He takes medication for diabetes but is otherwise well.  This lesion was found in the low rectum. 
What is your endoscopic diagnosis?
a) Ulcerative colitis
b) Crohn’s disease
c) Solitary rectal ulcer syndrome
d) Extra-gastric B-cell lymphoma
e) Rectal prolapse
I must admit that my initial thought was of a rectal prolapse.  However, on closer scrutiny the mucosa seemed infiltrated by some process which was ulcerating the mucosa in places.  In the stomach my first thought would have been of a lymphoma (infiltration+ulceration=likely lymphoma).  Indeed, the correct answer turned out to be "d",  a recurrence of the patients B-cell lymphoma!   With the entry in his case notes stating that the treatment had been successful, I did not consider this possibility.  However, it is noteworthy that haematologists do not talk in terms of “cure” for lymphomas.  Successful treatment brings the disease into “remission” but it is doubtful that any patients can ever be told that they are completely cured.  
Of course, MALT lymphomas (sometime called "MALTomas") usually affect the stomach. However,  virtually any mucosal site containing lymphoid tissue can be afflicted. This is because the cancer originates from lymphocytes situated in the marginal zone of “mucosa-associated lymphoid tissue”.  
Gastric MALT lymphomas are commonly associated (70–98%) with chronic Helicobacter pylori gastritis.  In other sites, chronic immune stimulation is also thought to be involved in the pathogenesis.  In the stomach up to 60% of patients will achieve remission with eradication of the Helicobacters.  Patients who are Helicobacter pylori negative are treated with radiotherapy which induces remission in up to 90%.   In this case, the primary lymphoma  started in the stomach but relapsed outside the stomach.  A CT revealed that there were other deposits elsewhere in the abdominal cavity.  He was started on chemotherapy (usually CHOP with rituximab).  If you would like to watch this video in a larger format, please click on this sentence!  

This sessile lesion was found at the gastric cardia in a 50 year old woman presenting with dyspepsia.

What is the most likely diagnosis?
a) Hyperplastic polyp
b) Hypertrophic gastropathy
c) Villous adenoma
d) MALT lymphoma
e) Adenocarcinoma
This sessile lesion is composed of glassy, nodules not dissimilar to “frog-spawn” or cystic fundic polyps as seen in patients with FAP.  It is the typical appearance of “Hypertrophic gastropathy”.  A condition of unknown aetiology which is given the eponym “Menetrier’s disease” if associated with a low protein level.  I have seen this condition in three guises; (1) affecting the whole of the gastric fundus+gastric body in a patient with transfusion-dependent anaemia, (2) in the gastric fundus+body and the duodenum and (3) affecting the cardia/proximal fundus only.  To my knowledge, this proximal – type has not previously been described?    At the end of the video-clip you can see the process beginning to spread down the greater curve.  Any attempt at endoscopic resection would of course be futile and for this reason, I decided to simply resect a few nodules for histological support (“histological confirmation” is a misnomer which I can no longer bring myself to say).   It has been assumed that Helicobacter can drive the process and there have been reports of improvements in symptoms.  For this reason, eradication of Helicobacters is usually advocated.  Patients presenting with transfusion dependent bleeding are usually treated with gastrectomy.  PS. If you would like a higher resolution copy of any of my "Case of the Month" video clips, please send me an email:  bjorn.rembacken@gmail.com

These are the findings in a 65 year old woman undergoing investigations for anaemia. Her only medication includes ibuprofen for backache and tamoxifen.

These are the findings in a 65 year old woman undergoing investigations for  anaemia. Her only medication includes ibuprofen for backache and tamoxifen. 
What is the most likely diagnosis?
a) NSAID induced gastric ulceration
b) CMV gastritis
c) Gastric lymphoma
d) Linitis plastica
e) Gastric metastates
The ulcers are too thickened and indurated for CMV or benign ulceration.  Linitis plastica causes ulceration but in my experience rarely ulceration.  A gastric lymphoma could look like this and would be the main differential diagnosis.  The gastric wall is studded with nodules which have ulcerated.  This is a common appearance in metastases.  However, the appearance is not pathognomonic of metastatic disease,  primary cancer could look similar (have a look at last months video case for example).  However, in this case there are numerous deposits making metastasis the most likely diagnosis.  Infiltrating lobular carcinomas of breast is particularly associated with peritoneal disease.   The mean interval between  primary diagnosis and the metastatic presentation was  7 years in a retrospective analysis (Ann Surg Onc 2005;12(11):886-94).  In view of the long interval, it is particularly  important to highlight the endoscopic diagnosis of "gastric metastasis" to your histopathologists.  This should prompt them to obtain the original histological slides of the primary breast cancer to compare the microscopic appearances with your biopsies.   Gastric metastasis is of course bad news and the mean survival was reported as 28 months in the above study.

This shallow ulcer was found in the ascending colon in an elderly patient who had undergone a sigmoid cancer resection one year earlier.

The patient is asymptomatic but takes numerous medications including the occasional over-the-counter NSAID. 
a) NSAID induced colonic ulceration
b) Ischaemic colitis
c) Crohn’s disease
d) Early colonic cancer
e) Colonic metastasis
I made an endoscopic diagnosis of early colonic cancer.  However, none of the 8 samples taken could confirm anything else than "inflammation".  It seemed difficult to disagree with our histopathologists as 8 samples obtained from this 8mm indurated patch would surely be sufficient to make a reliable diagnosis. 
For this reason an immediate repeat endoscopy was not organised and it was not until 6 months later that the patient returned for a follow-up examination.  The ulcer was now much larger (about 2cm across) and a second set of samples confirmed that the lesion was indeed an adenocarcinoma.  The earlier sigmoid cancer and the new (i.e. metachronous) lesion were histologically different and a colonic metastasis was therefore considered unlikely.  The patient underwent a right hemi-colectomy and the final diagnosis was of a T3, N0, M0 adenocarcinoma. 
We are beginning to understand that colonoscopy may not protect well against right-sided cancers.  This is thought to either be due to poor visualisation of the right hemi-colon or because lesions arising from this part of the colon are difficult to spot at colonoscopy.  Indeed, this case illustrate how difficult it can be to detect an early right sided cancer.  What has not previously been described is that it can also be difficult to diagnose an early right-sided cancer histologically !   From this case, I take home a simple lesson: I should rely more on my  endoscopic diagnosis than the  histological impression.  

This is the appearance from the mid rectum in a patient complaining of a change of his stool which now comes out more "ribbon-like" than usual.

What is the most likely underlying diagnosis?
a) microscopic colitis
b) ulcerative colitis
c) Crohn's disease
d) a circumferential adenoma
e) Disseminated cancer
I must admit that this appearance baffled me.  I managed to squeeze through the narrowed rectum to find that the more proximal colon did not appear normal.  There were diffuse areas of induration and in several places there appeared to be nodules of tissue attached to the serosal surface of the colon. I made a diagnosis of peritoneal carcinomatosis and put the rectal appearance down to severe lymphoedema.  
As always I stated the Endoscopic diagnosis on the histopathology request form. One of our GI histopathologist contacted me the following day to say that only some odd crypt loss could be found and asked me if ischaemic colitis would fit the clinical diagnosis (!).  
I emplored her to take further cuts and congratulated myself on taking a full completement of samples from ALL parts of the colon (14 samples were taken).  One hour later the histopathologist phoned me back to say that she had found malignant cells nestling within lymphatic channels deep within the mucosa.  Two weeks later the patient developed malignant ascites but the primary cancer had not been found when I wrote this. 
The moral of the story is simple. ALWAYS MAKE AN ENDOSCOPIC DIAGNOSIS! At worst you will be proven wrong - but will learn something in the process.  At best, the correct diagnosis will be considered - even if the histopathologist has to go back to his microscope and look again! 

How do you manage oozing following snare polypectomy?

Bleeding following snare polypectomy is always treacherous.  It starts as an innocent but immediate trickle but within a few minutes becomes a pumping, arterial bleed.  You can save yourself 30 minutes of anxiety but quickly re-opening the snare and grabbing the resected stump.   Then apply a little bit of “coagulation power” (for example 25W), advising you assistant that the snare should NOT be closed as you apply the heat.  If your assistant has closed the snare too tightly, it can be a little difficult to disentangle it.  If you struggle, fully open the snare and insert the endoscope beyond the stalk and then try to work the snare free.  In these cases, I usually apply some other means of haemostasis aftewards.  Consider applying a few clips across the resected stump or use the Olympus “ligation device”. 
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