Benign or malignant disease?
The photo shows the findings in a 65 year-old woman.
A 30-year-old diagnosis.
An elderly patient being investigated for iron deficiency anaemia.
The photograph shows what was found in an elderly patient who was being investigated for iron deficiency anaemia.WHAT IS THE MOST LIKELY DIAGNOSIS? a) Gastritis associated with Helicobacter pylori infection b) Gastric cytomegalovirus infection c) Cameron ulceration d) NSAID-induced ulceration e) Ulceration from a diffusely infiltrating gastric cancer
An easy diagnosis but difficult aetiology
Try your diagnostic skills!
The photograph shows the mucosal appearance throughout the colon in a 49-year-old woman undergoing investigations for abdominal pain and diarrhoea.WHAT IS THE CAUSE OF THE MUCOSAL APPEARANCE? a) Melanin b) Lipofuscin c) Haemosidderin d) Food colourings e) Cyanosis
A classic colonic lesion.
These photographs show a lesion that was resected from the sigmoid colon.
These photographs show a lesion that was resected from the sigmoid colon.WHAT IS YOUR ENDOSCOPIC DIAGNOSIS? a) Hyperplastic polyp b) Tubular adenoma c) Tubulovillous adenoma d) Villous adenoma e) Serrated adenoma
A condition not associated with…?
The photograph shows what was found in a 55-year-old man who was undergoing upper digestive endoscopy because of iron deficiency anaemia.WHICH OF THE FOLLOWING DOES NOT HAVE A RECOGNISED ASSOCIATION WITH THE CONDITION? a) Hypergastrinaemia b) Portal hypertension c) Liver disease without portal hypertension d) Systemic sclerosis e) Bile reflux
A suspicious sigmoid stricture?
Watch the video & decide!
This patient is undergoing an emergency flexible sigmoidoscopy after admission with sudden onset of vomiting and abdominal distension.Watch the video WHAT IS THE DIAGNOSIS? a) Ischaemic stricture b) Crohn’s stricture c) Malignant stricture d) Diverticular stricture e) None of the above This is a most peculiar sigmoidoscopy! There is a narrowing of the lumen in the mid-sigmoid that the endoscopist is able to traverse. On the other side of the stricture you find yourself looking at… small bowel mucosa! The patient has suffered a colonic perforation that has given rise to a fistula into the ileum, so option e is the correct answer. Diverticular disease used to be a condition that was firmly in the surgical camp. However, uncomplicated diverticulitis is increasingly managed with conservative therapy and it appears that we don’t even need to give antibiotics in all cases.1 Only about a quarter of patients develop complications requiring surgery. Remarkably, patients who are well but have free air in the abdomen that is visible on X-ray, may be treated with antibiotics and bowel rest2 and abscesses are usually drained radiologically. In a case such as this, with a combined small bowel and colonic obstruction, surgery is indicated. The traditional operation is the Hartmann procedure with a proximal colostomy. The drawback is that a proportion of patients who undergo this procedure will never have their bowel continuity restored. In view of this, many colorectal surgeons have advocated that a primary anastomosis can be an equally safe but a better alternative in selected cases. There is no evidence from clinical trials to inform us which is the better option. However, the construction of a primary anastomosis is more demanding and requires the sound clinical judgment of an experienced colorectal surgeon to decide when this option is likely to fail. The Postgraduate Course of the UEG Week 2013 dedicated a complete session to the topic of diverticular disease (Diverticular disease: Important, poorly understood and badly managed) and is well worth a look. Just sign in to myUEG, put ‘Diverticular disease’ into the UEG Education Library search box and hit enter! References
- Chabok A, et al. Randomized clinical trial of antibiotics in acute uncomplicated diverticulitis. Br J Surg 2012; 99: 532–539.
- Costi R, et al. Challenging a classic myth: pneumoperitoneum associated with acute diverticulitis is not an indication for open or laparoscopic emergency surgery in hemodynamically stable patients. A 10-year experience with a nonoperative treatment. Surg Endosc 2012; 26: 2061–2071.
The photograph shows what was found in the rectum of a 65-year-old homosexual man who was complaining of bright red rectal bleeding. He admitted to drinking two to three whiskeys per day. He was not taking any medication and his only past history was of prostatic carcinoma, which was treated 2 years previously. There was no relevant family history.How would you initially manage the patient? a) Rectal steroids b) Rectal aminosalicylates c) Cautery using a heater probe or argon coagulator d) Antibiotics e) Surgical resection
These photographs show the stomach (top) and second part of the duodenum (bottom) of a 55-year-old man undergoing gastroscopy to investigate iron deficiency anaemia.What would you organise next? a) Gastric biopsies with immunohistochemical staining for e-cadherin b) Measurement of serum gastrin levels c) An enteroscopy d) A capsule endoscopy e) A colonoscopy
Decide on the Spot!
60 seconds to make the correct decision.
A 16 year old severely handicapped boy is referred for a PEG as he has become increasingly difficult to feed without regurgitation and vomiting.
Should I stick to the Plan?
In the latest case, Bjorn tackles a patient that has returned after previously undergoing Radiofrequency Ablation.Watch the video This patient with a 10cm stretch of Barrett’s found to harbour high-grade dysplasia after several sets of samples has been treated with Radiofrequency Ablation. Three months later she has now returned to assess the response. WHAT WOULD YOU DO NOW? a) Do nothing, this mucosa is still healing
b) Apply APC to the small amount of Barrett’s remaining
c) Apply further RFA to the remaining Barrett’s
d) Remove the nodule at 12 O’clock by EMR
e) Remove all of the remaining Barrett’s by EMR
Plenty of Polyps!
This 30 year old man was referred for a gastroscopy because of indigestion which had resolved with PPI therapy. Can you identify the cause?Watch the video
Which statement is correct?a) These findings are most probably due the PPI therapy b) These findings are most probably due to Helicobacter infection c) This patient most probably has FAP d) This patient most probably has Peutz-Jeghers syndrome e)These findings are most probably due to metastatic disease Please add your answer below! Case submitted by Dr Pradeep Mundre, Specialist Registrar at Leeds Teaching Hospitals.
A suspicious stricture?
This 70 year old patient is undergoing a gastroscopy because of 2 months history of dysphagia. At endoscopy, this stricture is found at the gastro-oesophageal junction.
After you have taken a full set of samples, what single question is the most likely to give you a hint as to the true cause of this stricture?
a) Ask about medication the patient is taking
b) Ask about a history of atopy
c) Ask about a history of heartburn symptoms
d) Ask if the symptoms are intermittent
e) Ask about the alcohol intake
This seemed to have been a particularly difficult case. Although the stricture looks peptic, the wide-spread gastric intestinal metaplasia tells you that the patient has come to the end of a life-time of Helicobacter infection. She now has atrophic gastritis with florid intestinal metaplasia and is of course achlorhydric. Without any gastric acid, how could she possibly have developed a reflux-induced oesophageal stricture !!?
The strictures seen in eosinophilic oesophagitis are in my experience less “membrane-like” and 2-3 cm in length. Furthermore, there are no oesophageal stigmata of the condition (longitudinal furrows, micro-abscesses or trachelisation). Option D (intermittent symptoms) implies oesophageal incoordination. However, if this was the underlying condition, she should not have a stricture. Finally this does not look like a squamous cell carcinoma (option e).
This leaves us with drug induced stricturing (NSAID or biphosphonate). Indeed the patient had recently been started on alendronate! Well done Dr Lekharaju who got the correct diagnosis!
In addition to stricturing, biphosphonate may cause an acute oesophagitis, oesophageal ulceration and even gastric ulcers, presumably due to direct contact of the tablets with the mucosa. It seems that alendronate is particularly hazardous whilst risedronate (a third generation biphosphonate), may be less ulcerogenic. The co-administration of a NSAID and alendronate is especially toxic.
Classically, the treatment includes stopping the biphosphonate and starting a proton pump inhibitor. However, it must be tempting to restart after a couple of months with a lower dose of some other biphosphonate, advice the patient to take the tablets and then eat some food (although you are supposed to take alendronate on an empty stomach) and continue the proton pump inhibitor. Not sure what risk to quote the patient for a relapse. However, if the patient has marked osteoporosis, it may be a risk worth taking?
Pushed for an Answer!
This middle aged woman was admitted following a haematemesis after taking NSAID's for abdominal pain...You explain the unexpected endoscopic and that the result of the biopsies will be available in the next few days. THE PATIENT THEN ASKS YOU WHAT IS THE LIKELY OUTCOME?
- Explain that she will need stop the ibuprofen and start a course of proton pump inhibitor to heal the ulcer
- Ask her if she has noted any spots on the skin
- Ask her if she has a history of kidney disease
- Ask her about a family history of gastric cancer
- Explain that she will probably require an operation
The best way to make the diagnosis…
This is the duodenum in a 45 year old woman who one year ago was found to be anaemic.The patient was fully investigated including a negative Coeliac serology screen and normal duodenal biopsies. Now, she has been re-referred with indigestion. With folate supplementation, her Hb is stable. What would you do now?
a) Reassure the patient
b) Repeat the serological tests
c) Take a new set of samples
d) Request an abdominal CT
e) Check her HLA DQ2/ HLADQ8 status Thank you for your feedback! Coeliac disease is currently diagnosed by blood test and histology. Sooner or later, patients with coeliac disease will produce endomysial antibodies (EMA) and tissue transglutaminase antibodies (tTGA) when gluten is ingested. The IgA tTGA and IgA EMA serological tests have high levels of sensitivity and specificity in the diagnosis. Patients with a positive blood test and those with negative antibodies who are suspected to have coeliac disease should be referred to a gastroenterologist, who will decide if a gastroscopy with duodenal biopsies to diagnose coeliac disease is necessary. In the UK, many patients with vague and non-specific abdominal discomfort are referred for an unnecessary gastroscopy with duodenal biopsies to diagnose Coeliac disease. The reason why an endoscopy is unnecessary is that coeliac serology is an excellent screening test. If a tTG test is negative, the diagnostic yield of a gastroscopy is vanishingly small. Money and resources are better spent elsewhere! Naturally, the condition can be enigmatic and patient can sero-convert "late" and become serology positive when they were initially sero-negative. Naturally, checking the serology every 3-4 months, in someone in which you think is developing celiac disease, is no big deal. In contrast, 3-monthly repeat duodenal biopsies would quickly become burdensome for the patient and expensive for the health service. In this case, the mucosa is a little lumpy (you see this best along the valvulae conniventes) and completely flat. Nevertheless, currently the “correct answer” would be to take another set of samples (no big deal perhaps as the patient is undergoing a gastroscopy anyway). However, I believe that in the future this may be seen as another example of wasteful excess which deprived patients with GI cancer from a prompt diagnosis. In the West we tend to leave the ultimate diagnosis to our histopathologists whilst paediatricians are happy to rely on serology. This case is presented by Camila Adour (Gastroenterology Resident at the "Hospital Naval Marcílio Dias", Rio de Janeiro, Brazil)
A case of hide and seek !
Somewhere within this stomach there is an early gastric cancer.The patient is undergoing the examination because of iron deficiency anaemia. Have a close look at the clip and see if you can spot the cancer. WHERE IS THE EARLY GASTRIC CANCER? a) On the anterior wall of the gastric body
b) On the posterior wall of the gastric body
c) On the anterior wall of the antrum
d) On the posterior wall of the antrum
e) Just above to the pylorus Well done to everyone as you all spotted the cancer! The early gastric cancer is not easy to see on the initial video and I have uploaded a second clip showing the appearances after dye spray. The lesion has now been scheduled for endoscopic resection. As there is no deep, central ulceration and the lesion is “smallish”, I think that the lesion will turn out to be intramucosal. It’s probably best removed by ESD although it would also be possible to remove it using an Olympus cap or the Cook Duette banding device or the “pull within the snare” technique. After all, almost all lesions, perhaps with the exception of flimsy villous adenomas, can be removed by the “pull-within-the-snare” technique. To the patient, I quoted a 1:30 risk of late bleeding and a 1:50 risk of gastric perforation, which would be easily fixed with clips. As I only do about 1 ESD/week I am somewhat rusty and resecting this lesion may take me an hour! If the patient is not fit for a GA and not unusually stoical, the “pull-within-the-snare” technique will have the lesion off within 5-10 minutes. In the event, the patient was unfit for a GA but could tolerate a hybrid ESD whereby I cut around the lesion using a hook knife and then placed a snare around it. The video capture (the last clip) missed the placing of the snare but did capture the closure of the mucosal defect using 15 clips and an Olympus "ligating device".
A Duodenal Disaster?
This is a clip from the resection of a duodenal polyp situated at the junction between the duodenal cap and D2.
The procedure was carried out under general anaesthesia and having seen the video clip of the middle and the end of the procedure, how would you advice the patient after he has come around following the anaesthetic?
a) The procedure went very well and you will be able to go home this afternoon
b) The procedure went very well but we will keep you in hospital for observation over night
c) The procedure probably went well but we will keep you “nil by mouth” and keep you
in hospital for observation over the weekend
d) The procedure didn’t go according to plan and we will now start intravenous antibiotics
and will organise a contrast enhanced CT scan
e) The procedure went very wrong and we are now organising for you to undergo
Thanks to everyone for adding to the discussion ! I have the greatest respect for duodenal EMR’s. It is an unforgiving area to work in. The late bleeding rate approaches 10% following larger resections. The vascular supply is rich and the enzyme-rich environment will make sure that any clot which is "doing a job", is promptly digested. Then we have perforations! The muscle propria layer is extremely flimsy and in this case I think that it’s more a thin tear than the usual punched out perforation we see elsewhere in the GI tract. For this reason the “target sign” is unreliable in the duodenum.
If you look at the video clip carefully, you see a small bubble coming out of the tiny perforation close to the clip. I did struggle to close the defect and in the end the patient had to go to surgery. As there was no “contamination”, drains were placed and the area washed out. Nevertheless, the patient spent a month in hospital as the perforation slowly healed.
A recent audit in Leeds, found that risks increase sharply when lesions larger than 2cm in size are resected. A recent series from Australia put the “danger size” at 3cm. The risk of a perforation can approach 1:30 and for this reason you need nerves of steel, a patient who is fully informed of the risks as well as immediate access to supportive and experienced upper GI surgeons. It is my belief, that this is Tiger Country which should only be entered by the most experienced operators working in a tertiary referral centre.
Resection of this chunky polyp in the ascending colon was never going to be easy ...Attempting to resect this sizeable polyp situated in the ascending colon turned out to be more hazardous than the endoscopist had anticipated. Have a look at the video clip and consider. WHAT WOULD YOU DO NEXT?
a) Re-open the snare and attempt to re-grasp the vessel
b) Inject adrenaline
c) Apply clips
d) Apply a ligation device (EndoLoop)
e) Phone a friendly surgeon Half-way through the resection, which took place in Leeds, blood is beginning to seep through. However, at this point you are committed and there is little point aborting and in opening the snare again. The blood is filling too fast to get any clips accurately placed and there is no stalk to re-snare or ligate. You have only two options, 1) quickly inject adrenaline or 2) use a “coagulation forceps” (or at a pinch a pair of hot biopsy forceps) with the diathermy machine set at “soft coag” at between 60-80 watts. To partially open the snare again and try to stop the bleeding with the tip has the potential to go very wrong as it may act as a needle-knife, quickly slicing through the wall of the bowel. Most admit that I am a little dissappointed with the APC. It never seems to work very well with fast-bleeing vessels. We elected to use adrenaline. Most units will use a concentration of 1:10,000 of adrenaline but it is probably safer to use a concentration of 1:100,000. Unfortunately, when you need adrenaline there is usually little time to fiddle around trying to get the stuff diluted. How much did we inject? In this case 25ml was required before the bleeding stopped. This volume did not particularly worry me as I kept a keen eye on the patient’s heart rate! If the patient’s heart rate starts to creep up, I stop injecting. Once the bleeding has been brought under control, I try to remove all the clot and then either place clips or use the coagulation forceps to secure the haemostasis. After all, that adrenaline will disappear and the bleeding may well start up again. The trouble with clips is that they often get in the way as you continue the resection. For this reason alone, coagulation forceps may be preferable. I should mention that when the diathermy is set to “soft coagulation”, you can expect a slight delay to the coagulation. Typically, you need to have your foot on the blue pedal for about 1.5-2 seconds before you start to see any visible diathermy effect. Once you see some visible sizzling, continue to coagulate for another couple of seconds. In Leeds, I have had a late perforation when dealing with a troublesome oozer in the duodenum. For this reason, I am particularly careful and never “cook” a vessel more than twice and, I avoid its use in the duodenum. And then we are left with the final question which you will always have to face when something goes wrong – “Why were you doing this in the first place ???” Because this is the recurring question which colleagues, patients, upset relatives and lawyers will always ask you after something has gone wrong, you should ask yourself the same question before you decide to “cut”. In this particular instance, I do agree that the lesion seems very chunky and may well be malignant. However, prior samples had indicated that it was a TVA with only HGD and it does seem to lift - although somewhat reluctantly! My cunning plan was to resect a more substantial piece to confirm cancer. Unfortunately, my 2cm resection fragment again only revealed HGD ! In any case, the outcome is clear - an endoscopic resection would be too hazardous (bloody) and surgical resection is now indicated.
An innocent finding?
This nodule was found in the gastric antrum of a 50 year old man complaining of heartburn.WHAT IS THE MOST LIKELY DIAGNOSIS?
a) ectopic pancreas
e) Adenoma WHAT WOULD YOU DO NEXT?
a) reassure the patient
b) take a full set of samples from the lesion
c) request an EUS
d) resect the lesion endoscopically
e) check the serum gastrin and urine 5-HIAA levels Thank you to everyone who have had a crack at this case! Of course, this lesion could be a GIST but the position is typical for than of an ectopic pancreas. Leiomyomas are very uncommon in the stomach (whilst common in the oesophagus). Carcinoids (which should now be called “NET’s”) tend to be less protruding (and yellowish when cut). Gastric adenomas are usually flat and often a little paler than the surrounding stomach. Ectopic pancreas were first described in 1729 and is said to be found in about 14% of autopsy series (seem a very high figure though). This particular lesion is in the typical location, in the antrum on the greater curve. However, ectopic pancreatic tissue may also commonly be found in the duodenum and jejunum (less commonly in the oesophagus or biliary tract). The only thing missing from this case is a central umbilication from the draining duct. This is the first time that I have seen a peculiar fold around the ectopic pancreas. Presumably it has been described before? Although the pancreatic tissue may become inflamed or undergo malignant conversion, it seems far less likely to do so than the true pancreas. In spite of this, I am frequently asked to remove these nodules for "histological confirmation". As it is difficult to distinguish an ectopic pancreas from a small GIST by EUS, the buck is passed to me. Unfortunately, the endoscopic resection is usually more tricky than initially anticipated. As the ectopic pancreatic tissue is situated deep in the gastric wall, the submucosal injection will lift the mucosa around the nodule, whilst the lesion itself does not lift. I have attached a short video of the lift and resection which illustrates the point. As the hazards of an ESD or EMR will outweigh the risk that it's a GIST (when the lesion is as typical as this), I believe that the correct answer to is reassure the patient and decline any proposal of surveillance.
A suspicious colonic lesion!
This flat lesion was found at the splenic flexure in a patient undergoing colonoscopy because of a change in bowel habit.A biopsy is taken indicating that the lesion is a “tubular adenoma with low-grade dysplasia”. WHAT WOULD YOU DO NEXT?
a) I don’t believe the histology and would obtain more samples
b) The lesion is benign and should be removed by piecemeal EMR
c) The lesion may be malignant and should be removed by ESD
d) The lesion may be malignant and an EUS should be organised next
e) The lesion is certainly malignant and surgery is indicated In the West, we are just getting our heads around the concept of two types of “Laterally Spreading Tumours”; the Granular (LST-G) and the Non-Granular types (LST-NG). You probably know that the granular types can grow very large and are most common in the rectum and caecum. In spite of their size, the LST-G is usually a tubulovillous adenoma with a very low risk of harbour cancer (around 1%). The LST-NG lesion can be found anywhere in the colon and have a smooth surface. In spite of their more innocent appearance, they are usually tubular adenomas often with high-grade dysplasia or early cancer. The Japanese have now added to the complexity by introducing another two types of Laterally Spreading Tumours, the “LST-mixed type” (LST-M) which is essentially a LST-G with a dominant nodule and the “Depressed type”. LST-M lesions have a greater risk of harbouring cancer inside the dominant nodule. LST-D’s are the least common lesion and this is a good as an example of the “LST-D” that you would ever find! In fact, all our Japanese colleagues agreed that this lesion was likely to have an invasive component and that it would be difficult to remove it endoscopically in view of its location. The painstaking ESD was achieved by asking the patient to intermittently stop breathing which would give me 20 seconds to cut, following which he could breath normally for another 30 seconds before holding his breath again. It was a huge effort which did pay off! The lesion turned out to be benign and the patient was spared surgery (which at best would have been associated with a 2% risk of death). Why ESD and not a piecemeal EMR? The reason for the decision was our belief that the lesion may harbour an invasive component. An ESD maximised our chances of histological confirmation that the lesion had been completely removed. An EUS, using a high-frequency probe, is as good as (but not better than) a careful endoscopic assessment of the crypt and the vessel pattern. In the future, NBI with magnification is likely to replace dye spraying for the assessment of suspicious lesions (for example using the “NICE system” of lesion assessment) . The reason for this is that when no organised crypts is seen after spraying dye, this may be because the crypts have been destroyed (the Kudo type 5 pattern) but it could also be because mucus has prevented the dye from outlining the crypts. With NBI, a destroyed crypt pattern is also difficult to see but the grossly abnormal capillary pattern associated with a Kudo’s type 5 crypt pattern, remain easy to spot.
Lesion submitted by Dr Andrew Chilton, Consultant Gastroenterologist at Kettering General Hospital, United Kingdom.