A case of mistaken histology?
This patient originally presented with a small gastric ulcer. One of the samples taken on admission was reported as "suspicious of diffuse type gastric cancer" and further biopsies are advised.Two weeks later the gastric ulcer has healed, leaving a scar on the greater curve. WHAT IS YOUR ENDOSCOPIC DIAGNOSIS? a) the appearances are reassuring and the histological impression was probably due to sampling the inflamed mucosa close to the ulcer
b) the ulcer scar is suspicious and the likely site of cancer
c) the red patch on the lesser curve is suspicious and the likely site of cancer
d) both the scar and the red patch are suspicious and this patient probably has two small cancers
e) on close scrutiny, the whole stomach appears abnormal - this patient has a linitus plastica involving most of the stomach At the time of the endoscopy, I decided that the ulcer scar seemed innocent and decided to examine the rest of the stomach in more detail. The red patch on the lesser curve did catch my eye. This proved to be the focus of a “poorly differentiated adenocarcinoma. In addition to the samples taken from the lesser curve, I also took a set of samples closer to the cardia to help the surgeons plan their operation. Unfortunately, one of the 6 samples taken closer to the cardia also proved positive and the patient subsequently underwent a total gastrectomy. Surprisingly, the lesion was only found to be 2cm in diameter and was staged pT1b (i.e. invading into the submucosa but not involving the muscularis propria), none of the lymphnodes were involved. C is the correct answer! If the patient had not presented with a benign GU, he would probably have presented a year or so later with advanced cancer! If the location the original biopsies had been better documented, a lot of confusion could have been avoided! Whenever, you suspect that you may be dealing with a diffuse type, poorly differentiated adenocarcinoma, you should select “Jumbo forceps”. These are larger than normal but cost the same. All reputative manufacturers of biopsy forceps should be able to offer you a larger version for this type of cases. Nevertheless, I would recommend taking lots of samples. In the case above, I took 34 “Jumbo samples”. If you still draw a blank, the next option would be a full thickness laparoscopic wedge biopsy aimed at most suspicious area. If this also draws a blank, you may be dealing with a funny patch of gastritis !
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 (126.96.36.199.14)
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
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
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.
HOW WOULD YOU ADVICE YOUR PATIENT?
- 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
- 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
- this lesion is probably best removed but it can probably be done endoscopically
- this lesion will probably need to be removed surgically
- this may have arisen somewhere else in the body and a full body scan may well be required next
This nodule was found in a 45 year old woman presenting with some vague indigestion.
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.
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.
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
DiagnosisThis 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.
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?
Aberrant crypt foci
Familial adenomatous polyposis
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.
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.
a) Hyperplastic polyp
b) Serrated adenoma
c) Tubular adenoma
d) Tubulo-villous adenoma
e) Villous adenoma
This lesion was found in the duodenum of a 45 year old man with an inherited condition.
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
This lesion had previously been found in the terminal ileum. Biopsies had been reported as normal mucosa only.
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.
a) Ulcerative colitis
b) Crohn’s disease
c) Solitary rectal ulcer syndrome
d) Extra-gastric B-cell lymphoma
e) Rectal prolapse
This sessile lesion was found at the gastric cardia in a 50 year old woman presenting with dyspepsia.
b) Hypertrophic gastropathy
c) Villous adenoma
d) MALT lymphoma
These are the findings in a 65 year old woman undergoing investigations for anaemia. Her only medication includes ibuprofen for backache and tamoxifen.
b) CMV gastritis
c) Gastric lymphoma
d) Linitis plastica
e) Gastric metastates
This shallow ulcer was found in the ascending colon in an elderly patient who had undergone a sigmoid cancer resection one year earlier.
a) NSAID induced colonic ulceration
b) Ischaemic colitis
c) Crohn’s disease
d) Early colonic cancer
e) Colonic metastasis
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.