These small spots are a common finding within the oesophagus but
WHAT ARE THEY?
■ Glycogenic acanthosis
Good guess but you haven't understood the histology
■ Aggregates of lymphocytes
Absolutely!
■ Xanthelasmata
Only found in the oesophagus!
■ Hyperkeratosis
Looks different remember?
explanation
These are tiny lymphoid aggregates which are sometimes arranged as longitudinal chains mainly, near the ducts of oesophageal glands. These are most prominent in childhood and they regress. The main differential diagnois is that of 'glycogenic acanthosis' is a benign finding which becomes more common as we age. Histologically, they are composed of hypertrophied stratified squamous cells filled with glycogen and has no link with 'leukoplakia', and has no malignant potential. Below you have histologies of lymphocytic aggregates vs glycogenic acanthosis which tells a thousand words!
This was found in the distal oesophagus of a patient with dyspepsia. You take some samples.
WHAT WILL YOU TELL THE PATIENT?
■ This is a benign finding
Yes it is but do you know what it is?
■ We'll see what biopsies show
It's' a spot diagnosis!
■ This may well need EMR
Very unlikely unless those IPCL's look odd
■ Staging investigations are likely next
Can't imagine!
explanation
This may be a good example of 'we don't see' because we don't know what it is. Intuitively, we all blank this because it's a benign finding. But what is it? It's actually a patch of squamous hyperkeratosis with some underlying basal cell hyperplasia. The normal squamous basal cell layer is 1-4 cells thick but, in reflux oesophagitis thic increase up to 75% of the epithelial thickness. However, many cases of reflux oesophagitis does not exhibit basal cell hyperplasia and conversely, there are cases which will not be due to reflux disease as in this case!
In rodents (!), the finding has been linked with vitamin deficiencies and zinc deficiency. Of course, squamous hyperkeratosis in the mouth is associated with squamous neoplasia [ J Clin Pathol 2005;58:1325–1327 ] and for this reason, I always take some samples. However, I am yet to find a single case of dysplasia within a patch of oesophageal squamous hyperkeratosis !!!
This was found in the mid-oesophagus of a 55 year old woman complaining of dyspepsia.
HOW WOULD YOU CONFIRM THE DIAGNOSIS?
■ Take a biopsy
Absolutely, but throw it away afterwards!
■ Organise an EUS
No need!
■ Request a CT
Often a sensible answer but in this case it's stupid!
■ Organise an EMR
Nope!
■ Organise an ESD
Wrong again!
explanation
If you give this a poke, you will find that it's soft and therefore unlikely to be a leiomyoma. The other pale, submucosal lesion which you often see in the oesophagus are 'granular cell tumours'. Although they can turn large, I've never seen one any larger than a few millimetres in diameter.
How then to prove the diagnosis? Simple, take a biopsy and see the fat flow out of your biopsy site (image below) !!! You can then throw that biopsy sample away (there will only be a normal squamous oesophageal mucosa). Presto - You have just confirmed the diagnosis !!!
This patient had not responded to medication and was referred for a dilatation of this mid-oesophageal stricture.
WHAT IS AETIOLOGY OF THE STRICTURE?
■ Peptic
Nope, this doesn't look peptic
■ Candida
Hm, would not cause a stricture!
■ Pemphigus
Usually causes high oesophageal strictures
■ EoE
CORRECT!
■ Radiotherapy
Doesn't look like it!
explanation
This is a 'barndoor case'! A full house of eosinophilic micro-abscesses (those white spots which look like candida), longitudinal furrows and 'trachealisation', a rather soft sign of eosinophilic oesophagitis
It can by much more of a subtle diagnosis and for this reason you should always take oesophageal samples (1-2 samples at 2-3 different levels) in patients with odynophagia or dysphagia. Unfortunately, this patient did not respond to either a PPI, or oral budesonide but did feel better after the dilatation. By the way, this is what the mucosa normally looks like after dilating EoE. There is lots of fibrosis in the 'lamina propria' and I guess that's why it looks like this after a normal dilatation.
This small lesion was found in the distal oesophagus just above the squamo-columnar junction
WHAT IS THE LIKELY DIAGNOSIS?
■ GRANULAR CELL TUMOUR
CORRECT!
■ LEIOMYOMA
INCORRECT
■ GIST
INCORRECT!
■ NET
INCORRECT!
■ EARLY SCC
INCORRECT!
EXPLANATION
This is the typical appearance of a granular cell tumour (Abrikossoff’s tumour) first described in 1926 by Abrikossoff, a Russian pathologist. These lesions can probably develop anywhere but is mainly found in the skin, mouth and GI tract.
Within the GI tract, the oesophagus is the most common location. Lesions are occasionally multiple (about 10% of cases). Granular cell tumours are said to be more common in women and black people. Superficial biopsies may occasionally fail to confirm the diagnosis as these nodules are submucosal. The differential diagnosis is that of a small lipoma, NET or a leiomyoma (which are much more common in the oesophagus than in the stomach). When detected these lesions are usually referred for endoscopic resection. Unfortunately, as the lesions arise from the deep submucosa, the risk of a local recurrence is high (30-40%). For this reason I now treat the raw EMR surface, immediately post-resection with APC set at low power (30W). By the way, a small proportion of these lesions (<2%) are said to be malignant overall. However, the published literature is confusing as GI and non-GI lesions are frequently combined. Perhaps the only compelling reason for removing these from the oesophagus, is that it is cheaper than surveillance!
Lesion found at the gastro-oesophageal junction
SHOULD I ATTACK OR ABORT?
■ ATTACK!
INCORRECT. SOMETHING HORRIBLE IS LURKING BELOW!
■ ABORT
CORRECT, THERE IS A HORRIBLE LOOKING ULCERATED CANCER SEEN AT CARDIA
explanation
From above this looks like a reactive nodule, perhaps secondary to reflux. Naturally, one couldn't rely on a visual inspection and an EMR seemed indicated. However, on retrovertion (bottom right image), the true nature of the lesion is revealed. There is a depressed, indurated area just at the GOJ (the close-up image at the bottom on the left show some irregular, malignant looking vessels). I diagnosed a type III early gastric cancer (Sievert's type III guess) probably involving the muscle propria (T2 disease) and organised an EUS. Surprisingly, the subsequent EUS upstaged the lesion to T3,N0,M0). I find it tricky to "stage" lesions at the cardia. Even small lesions can be far more advanced that expected.
A 16 year old severely handicapped boy is referred for a PEG as he has become increasingly difficult to feed and often vomits after food. Placement of a PEG tube under general anaesthesia is organised. The GA is difficult as the patient is frightened, very strong and with no understanding of what is happening. After a difficult 30 minutes, the patient is asleep and you discover this impassable oesophageal stricture in the distal oesophagus.
WHAT WOULD YOU NOW DO?
■ Abandon the procedure
But the boy wants to eat!
■ Refer for a radiologically placed PEG
But you have found a 'fixable' cause!
■ Dilate stricture and not place a PEG
Yes! Your job is to help him!
■ Reintubate with a slim endoscope and place a PEG
Forget the PEG!
■ Dilate stricture and place PEG
Keep everyone happy? He doesn't need a PEG!
Explanation
This is a recent "real case" of mine!
Endoscopy is unforgiving, a bit like surgery. You have to make the correct decision within a limited time. Tomorrow, OTHERS will be equipped with a "retrospectoscope" which gives them a perfect vantage point from which they can decide if you did "right" or "wrong". In this case, I went ahead and dilated the stricture without placing a PEG. A day later the patient was back eating solid food as normal and the request for a PEG feeding tube was quietly forgotten. Arguably, this was the "wrong" decision and the "correct" thing to do may have been to simply abandon the procedure, send the case back for re-discussion by our Nutritional Multidisciplinary Team, obtain informed consent and then reschedule the procedure in a month time or so. However, the stricture was clearly the cause for the vomiting, sending the patient back with the job unfinished would have delayed the necessary dilatation, put the patient at further risk of aspiration and subjected him to another traumatic general anaesthetic! Arguably the wrong thing to do! But of course, it could have all gone wrong! Oesophageal dilatations are linked with a 1:100 risk of a perforation. Had the family had an opportunity to consider a dilatation? No! Was the patient 'consented' for this? NO! Had you taken samples to ensure that it wasn't a malignant stricture first? NO (but why would a 16 year old have oesophageal cancer?), Therapeutic endoscopy is an odd mix of "thinking on your feet", accepting that sometimes "things go wrong" and working in a team where you can forgive yourself and where others are forgiving when things do go wrong. As a supervisor, sooner or later your trainee will have a serious complication. Surprisingly, we don't recieve any training in handling this! If it's your trainee, bring the conversation somewhere private. Go for a coffee after the list or ward round and hear your trainee tell the story of what happened. Listen and be sympathetic. Usually, I think that this could have happened to anyone. Of course there are things which 'just happen' to anyone. Like perforating an oesophageal dilatation or bleeding at polypectomy. But 'unavoidable mishaps', are more likely to happen to the unskilled trainee or deskilled colleague! When looking into a trainee's complication, I try to consider the following 6 'dimensions':
Actively considering these elements can give you an insight into why it happened. Furthermore, it may provide a clue as to how to help. Should the trainee have fewer cases on the list? Is further supervision required? Finally, supporting your trainee with the coroners report, speaking to relatives and advice on what to expect at the visit to the coroners court is invaluable to the trainee. This is just some of my thoughts to add to your own !
Here are two cases of a small nodule within Barrett's (top and bottom row). Of course you know that a nodule within Barrett's should ALWAYS be viewed with suspicioun. Naturally, both nodules were sampled as well as the surrounding unremarkable looking Barrett's. One case turned out to be non-dysplastic but the other were reported to harbour IMca.
WHICH NODULE IS DYSPLASTIC?
Case A (top row)
INCORRECT!
Case B (bottom row)
CORRECT!
explanation
On facebook, this proved a very difficult question and only half correctly identified Case B (bottom row) as being dysplastic.
Must admit that I felt uncomfortable about both nodules, as in my book, a nodule within Barrett's is never "right". In the end, I actually removed both. Just to be on the safe side. Incidentally, my own simple 'rule of thumb' when assessing Barrett's is as follows:
This is the oesophagus of a 45 yr old woman 3 weeks into induction chemotherapy for AML when she develops retrosternal pain and fever. Treatment with meropenem, ambisome, itraconazole, aciclovir and intravenous omeprazole is started with improvement of symptoms. This is the lower third of her oesophagus. WHAT IS THE MOST LIKELY DIAGNOSIS? a) reflux oesophagitis b) infective oesophagitis c) squamous cell carcinoma d) adenocarcinoma e) infiltration by myeloid cells explanation
An unusual appearance to the squamous portion of the oesophagus! Lower down, the appearances were unremarkable and healing reflux oesophagitis was therefore unlikely. Stains for fungi and immunohistochemistry for CMV were both negative. However, there were some multinucleated squamous cells and after a long search by our histopathologist, a couple of likely viral inclusions were found. This is a resolving herpetic oesophagitis ! Resolving because the patient had already been on aciclovir for a week when the endoscopy was done. Small miracle that our pathologists found traces of the original infection! This is a common issue with immunosuppressed patients. The haematologists are VERY quick to start a broad range of anti-microbial medication, covering fungi, viruses and bacterial pathogens. By the time the endoscopy is done, the original pathogen is usually suppressed to undetectable levels. |
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