you Welcome to First Incision, the podcast about preparing for the General Surgery Fellowship exam. I'm your host, Amanda Nikolic. In this special guest episode, we are joined by Dr. Chris Wakeman, a colorectal surgeon from Christchurch Hospital.
As you'll hear, Chris also has a lot of experience looking after patients with familial cancer syndromes, and he's talking to us today about a variety of the common familial cancer syndromes, what they are, the decision-making and surveillance for these patients. as well as a little bit about short gut syndrome and some advice at the end. I hope you enjoy this episode.
To start us off, would you like to tell us a little bit about yourself? Good morning. I'm Chris Waidness. I'm a colorectal surgeon in Christchurch. I also work for the Familiar GI Cancer Service. So in New Zealand, we have a national registry for hereditary bowel cancers. So we mainly focus on Lynch and familiar adenose polyposis, FAP. We also look at some of the others to a lesser extent, but they're the main two we manage. Increasingly, we're also managing
patients with multiple polyposis disorders in their families and investigating them and trying to predict who in the family needs ongoing surveillance or surgery. That's one of my roles, one of my hats I wear. I have a mixed practice in Christchurch. I work for the university as my primary employer. So I have an interesting side teaching students and postgraduate students. And I also direct for a trauma at Christchurch. So a varied bag as far as general surgery goes.
So today the plan is to talk about familial cancer syndromes and I'm hoping you could start us off with an introduction about the different types and then we could run through some of the surveillance and management options for the different types of familial cancer syndromes.
So when I think about hereditary bowel cancers, I think about them in sort of the polyposis type bowel cancers, the FAP being the classical MAP, where you get multiple adenomatous polyps. We've also got serrated polyposis syndrome. And then I think about... The other main field, which is more common, is Lynch syndrome. You still get polyps, but it's called traditionally non-polyposis hereditary bowel cancer, and that was to try and distinguish from FAP.
We've also got new developing hereditary bowel cancers, which we still don't know much about. With genetic panels, we are seeing patients pop up with some of the POLI and POLD polyposis disorders. We don't know that much yet about penetrance and how serious that is, and so that's a sort of area of development. And the big one is the serratopolyposis syndrome, and we still don't have a clear...
definition genetically of what defects cause that or what environmental effect. So that's a big area of growth but we don't have clear-cut surgical binary decisions which are so easy in some of the other conditions. So I thought for the next part of the episode, we could take some time to talk about those different familial cancer syndromes. To start off with, could you talk to us about familial adenomatous polyposis?
so fap sort of the classical hereditary bowel cancer we know about with polyposis disorders and it's an adenomatous polyposis disorder it's autosomal dominant we know the gene we've known the gene for quite some time now and it's a it's a large gene which means that there's many different phenotypes of FAP. And if your mutation's at the three or the five primed end of the gene, it tends to be more attenuated, so your polyp load will be less.
If it's in the middle, which is around 1309, then we get the classical FAP. You get thousands of polyps and you get early cancers and they also get duodenal disease and Desmoy disease as well associated with FAP. FAP, it's an interesting disorder because it's also got a high rate of index mutation, so it's not unusual for us to find a patient with thousands of polyps but not have any family history, and they're the index mutation.
about 30 percent of patients present with FAP will be the index mutation. The nice thing in New Zealand is because we're a national registry, anyone who's identified, we can follow and chase compared to other countries where you might have regional or state registries or even the Cleveland Clinic, for instance, has got an amazing registry, but it's the wealthy people.
up to the cleveland clinic it's not a national or a state registry so this gives us real national data when we look at it fap if we know that it's in a family we start genetic testing about 16. and then we'll start having that conversation about prophylactic surgery. Prophylactic surgery for FAP depends on how aggressive your phenotype is.
we know with fap that the penetrance is 100 you will get bowel cancer at some stage in your life you don't have prophylactic surgery and we look at historical data We never quite achieve normal life expectancy because even if we cure them of bowel cancer by prophylactic surgery, you can still get duodenal disease or desmore disease. There's other associated things which we can do well, but we never quite approach normal life expectancy.
prophylactic surgery for bowel cancer say if you've got an aggressive phenotype we know your mother or your father had it then we would gene test your children at about 16 age when they're sort of mature enough to understand the condition and then we start having that conversation thinking about when should we do prophylactic surgery. If they have a classical phenotype, then we'd favour a panproctocolectomy, so take all the colon and rectum out, and we normally would give a young person a pouch.
And some people do it as a three-stage or two-stage procedure, prophylactic ileostomies. Normally would be two in Christchurch. I still... worry about the consequences of a leak from a pouch but there are centers who go straight to the pouch and don't do function because they're a young person they'll cope with a leak but i just worry about the consequences of how the function is going to be the problem with a pouch is it's never perfect
Pouch dysfunction is high. A good pouch is five to seven times a day and one nocturnal motion per week as usual. Great lifestyle, but most people would choose to have a pouch and poop out their bottom rather than have a permanent ileostomy.
I think if you present later in life, after your teenage years, then I personally would just choose to have a permanent stoma myself. But to grow up 18 with a permanent stoma is obviously not a flash. If you have more attenuated FAP, then hopefully you might have rectal sparing.
so that you can do a subtotal colectomy and you don't have to have an ileostomy and you have better function. So we do have those families where they've got more attenuated FAP and we'll map them. And as soon as they start to develop... significant polyps which may be an attenuated maybe 20s 30s even 40s sometimes then you start to say okay right we know you've got mainly colonic polyps there's five rectal polyps let's do
a subtotal you still need to keep surveillance of their rectum because they can grow polyps in the rectum and the conversion rate to lose the rectum and go to a panprocticolectomy is around 30 to 40 percent in a lifetime so you will get a number of patients who do well with a subtotal for the rest of their life. We get some clinical FAPs, so they look like FAP, but we cannot find a mutation when we do gene testing. We tend to treat them just like FAP. They tend to be more attenuated.
The extra-clonic diseases in FAP are also concerned. Desmoid disease, not being a malignant disease, but can have significant impact on their health. And it's a funny disease, you never know how it's going to respond. Sometimes large tumors are growing well and then all of a sudden spontaneously regress or suddenly they race ahead on you. And so it's just a matter of treating them symptomatically. And sometimes we use non-steroidals, traditionally Solnodac, to try and control them.
Is there any way to prevent the formation of desmoid tumours in patients who have surgery for FAP? Not really, no. We've not got anything at this stage. And is there any of the phenotypes that are more likely to develop desmoids? It's more the classical FAP and it will run in families quite often that if you can see multiple generations with desmoid disease. And so when you're...
going to operate on someone, you know that they're going to get desmoid at some stage. But you're right, operating on people does promote desmoid progression, pregnancy does, trauma. So even... Occasionally you get patients who fall over and will get a Desmond in their arm, for instance, or something like that. It's a bizarre disease, we don't really understand it. Some of the other extra-colonical things are supernumerary teeth. Chirpy is very common where you get congenital.
pigmentation of the retina. And that doesn't cause problems, but it can be a way we pick up patients sometimes with FAP. They go in for an eye test and then someone noticed it got chirpy and put two and two together that there's family history of bowel cancer and all of a sudden they get referred to us.
When do you start to surveil or do colonoscopies on patients who have a family history of FAPs? So you genetically test them at 16, but do you scope them earlier than that? I tend to try not to because you don't tend to get bowel cancers. really early. It's very unusual to get below 20. So I try and encourage people not to start too early. The pediatric gastroenterologists do sometimes. And I think it just sets up an institutionalisation that they're too often being colonoscoped.
chasing small polyp numbers which are not significant at that young age. Also, you don't have to start your gastroscopies or durianoscopy until 25 normally. So the other place you can get polyps is around the duodenum, around the ampulla is the most important area. And so we start thinking about... doing that scope about 25. Again, there's a little bit of what gene, what's in your family. And we then use the Spiegelman's score to try and predict.
how often you should be repeated. So hopefully you have no duodenal polyps and then we can come back in five years. The ampullary ones are more important. Once you have an ampullary one over 10 millimeters, then you're looking at probably yearly OGDs. In Christchurch, we're quite aggressive with our management. We've got gastroenterologists who will stent the pancreatic duct and do EMR to try and control that disease.
Other places in the world, and even in New Zealand as well, there is mixed practice where some just observe it, and then when they get too big, then they'll do a whipple. The problem with whipple for polyposis is... Because there's no fibrosis in the pancreas, it's a difficult whipple, it's high leak rates, and it worries our HPV surgeons. It's one of the harder of the whipples to do, but at least they get survival, unlike pancreatic cancer.
Or should we move on then to talk about Lynch syndrome? Lynch syndrome is interesting because, I mean, it was first described by Worthian Seamstress, which I think is a great story. So she was... as seamstress he was a pathologist in the united states and she said oh i'm going to die of endometrial cancer
He said, what? Everyone always dies in my family from cancers, some bowels, some gynae type things. And so he went and took a family history and realised there was an autosomal dominant pattern to this. And so he started investigating and mapping this family. And then Henry Lynch got interested in that family, then took over that practice. He didn't name it Lynch syndrome. He named HMPCC for a start. And he started mapping further families in America with Lynch syndrome. And eventually they...
track down the genes of Lynch syndrome. So Lynch is autosomal dominant. It's not as penetrant as FAP.
and it depends which mutation you have there's four or five different mutations and there's probably more yet and the lynch genes take out your mismatch repair gene so your spell checker And so that's how it increases your risk of cancers and the most common is bowel cancer and then there's endometrial cancer and then a lesser extent urethelial and brain cancers and some skin cancers, mutuari skin cancers.
From a bowel cancer point of view, we don't perform prophylactic surgery like FAP because the penetrates is more like 50-60% in the worst genes. In PMS2, which is the less aggressive gene, penetrates may even be down as low as 20%. So that's why we don't have prophylactic surgery. But you need surveillance. So if you have a family history which looks like Lynch syndrome, and then we do gene testing, and if you've got a genetic disorder, you'll need yearly colonoscopies.
If we can't find the disorder, but you'd look like a Lynch family. Previously, we used to use Amsterdam criteria to classify some of these families. So you'd be Amsterdam positive. So that's looking at three generations, two patients affected, one under 50. I think it is top of my head now.
so we use the amsterdam criteria and there's also bethesda criteria to look at what families are look high risk and we might call them lynch-like or suspected lynch and be more like two yearly colonoscopies because the rates of
endometrial cancer are lower than bowel cancer. We don't offer prophylactic surgery, but I tend to refer all my patients for at least a counselling session with a gynae oncologist to discuss the risks. And depending on the patient's personality, they may have finished their family.
and want to have a prophylactic hysterectomy, oophorectomy, and tubes are also important now. So I think that's important to discuss with them. So if you have your yearly colonoscopies with Lynch syndrome, and you're found to have a cancer then the next question is what operation should you have and lynched tumors tend to be more right-sided they tend to be mucinous they're less likely to spread to your lymph nodes
Not that you want cancer, but a lynched tumour is less aggressive as a tumour. Previously, we used to think that we should do a subtotal resection. So take at least, if you had a right colon cancer, at least go down to the descending colon somewhere. There's a little bit of debate about that now. That does decrease your risk of a second cancer by doing that and obviously makes surveillance easier. But the big change in Lynch syndrome has been discovery with the CAP study.
two in particular we're waiting cap three that aspirin has a huge effect on your rate of lynch syndrome we take aspirin for 10 years it's a market effect on colorectal cancer and sir james burn who's the main steerer of the CAP studies from Newcastle, UK, he feels that maybe we should be less aggressive with how much bowel we take, that if we aggressively place our patients on aspirin, that they may not need those extended resections.
I think it's still worth counselling your patients and having a chat about what they think. What dose of aspirin do you have to put them on? Well, that's the big... question what dose because the the cap one study initially was looking at fap and lynch was a bit mixed it was a bit of an experimental study just get it out there this cap 2 was directed at lynch syndrome and they use big doses of aspirin 600 milligrams once a day
and we're waiting the results of cap 3 which is now a dosage trial because they know it works for lynch so now they've randomized people to different doses so hopefully in the next few years we will have a dosage answer In New Zealand, we just prescribe cardiac-type doses of 100 milligrams. And the reason we use that is because there is some evidence from some of the vascular papers that there was a decrease in non-lynch patients of polyps and cancers.
There's one of the nurses study where they took alternate day 100 milligrams and they did have a decreased rate of colon cancer. So we're jumping the step while we wait on CAP3 and presuming that low-dose aspirin won't cause problems. So James Byrne, he argues that in the previous years before paracetamol, we used lots of aspirin for headaches and we used high dose aspirin for headaches and it didn't cause lots of complications and we shouldn't be so wimpy with our dosage of aspirin.
But aspirin does cause complications. You know, there is risks of bleeding and oozing. And so we have to be careful with what we use. All Lynch syndrome and probably presume Lynch should be on aspirin.
But we do have to counsel our patients. We recently did a national-wide study looking at our Lynch patients to see how many of them are on aspirin. And it was disappointing, despite being told and given information sheets, only about 30% of them were on aspirin. So I think we need to do better with the aspirin. And what are the mutations that have been shown for Lynch syndrome? So we've got MSH6, MLH2, PMIS2, and there's the EPICAM, which is the epigenetic mutations too.
There is some others on the panels which we don't know if they're significant. So when you do a genetic test, you find an abnormality, and then they classify the variants. And so it's something called a VUS, a variant of unknown significance. So a one is probably unlikely. but there is a link. A 6 is highly likely, and then you have the papenomic mutation, which we know for sure. And there's a few out there now which could be Lynch-related, mismatch repair gene, but we're not quite sure yet.
And all those different mutations have slightly different rates of colon cancer or endometrial cancer. As I said before, the one of you have to have Lynch would be PMS2 because your rates of cancers are a lot lower. In some places in the world, they will space out their colonoscopy surveillance depending on which mutation. And PMS2 is the one they really want to space out to even three yearly rather than yearly.
And for people listening, they might have noticed that on the pathology tests that they get for colon cancer resections that we test for mismatch repair. Can you explain what that actually means and how that correlates with the likelihood of a patient having Lynch syndrome? So we check for the immunochemistry in New Zealand rather than MSI. And so we do the IHC and that identifies a loss of expression.
of that mismatched repair gene. And if that's abnormal, we then have to check BRAF. And if the BRAF's positive, then it's a sporadic tumour. If the BRAF's negative, when they have the loss of expression, they're likely a lynched tumour. The next step is we refer them on for genetic testing. And that can take six to 12 months. So there's some time lag for genetic testing. And once you've got a positive genetic test, then you are Lynch syndrome.
Without a positive genetic test, you're suspected Lynch or Lynch-like. And if you have Lynch syndrome or you have a family of Lynch-like patients, when would you start surveilling them with colonoscopy and how frequently would they get colonoscopies? So we'd do a genetic test about age 18 on them. Some families get more anxious and push it into earlier. I think it's hard as a 15 or a 16 year old growing up knowing you've got Lynch syndrome.
you know high risk of cancer it's not quite as bad as FAP knowing that you're going to have to have your bag out especially if your mum or your dad had horrible complications for us nasty colorectal surgeons so about 16 and then starting colonoscopy surveillance between 18 to 20.
We pick on 18 to 20 because that's when you're leaving school to start a trade or go to university. Sometimes you have that long first summer break and that might be a good time if you have to have prophylactic surgery and hopefully you're mature enough at 18 to understand. The one thing we haven't talked about with these autosomal dominant conditions is pre-implantation genetics, PGD. And so in New Zealand, you are offered...
three cycles of PGD. And so this involves a lot of work because it involves a full fertility cycle. So they'll raise your embryos if you've got a partner, and then they will test your embryos for the autosomal disorder. So if they... or Lynch or cystic fibrosis or whatever condition that is and then they will sort the embryos into the effect of non-affected and then offer to put back when you're ready.
because you don't have to do it straight away. They can freeze the embryos. They can put back those embryos and you can stop the line continuing of your FAP or Lynch syndrome. So I think that's something important to discuss with your young... families before they go and have children and then go oh you know my my five-year-olds i've done energetic testing on my five-year-old go hi but they've got lynch syndrome and they're stressed for you know for a long time
where they could have done pre-implantation. It is a lot of work. The woman has to go for a full fertility cycle, but it is covered in New Zealand. So for our next topic, could you talk to us about oligopolyposis syndromes? A big growth in the familiar GR cancer service workload has been oligopolyposis, so multiple polyps.
And especially once you're getting more than 10 large polyps in a young person, in a single colonoscopy, you have to think what's going on here. So we think with oligopolyposis, we think about the age. And we think about what size polyps and what type of polyps are they, adenomatous versus serrated. And if you're young and you're getting 10, 20 polyps removed every colonoscopy, you have to be concerned. And there is different age groups criteria for referring.
And it's a cumulative count as well, a bit like serratopolyposis, a cumulative count. So just say you had 10 on your first colonoscopy, 10 on your second, and you're 40, so you've had 20 under the age of 40, I would be wanting a polyposis. genetic panel be performed just to check. And particularly, we've got a family history as well.
So in New Zealand, the Familial GI Cancer Service helps negotiate those patients. So we take those referrals, we chase their colonoscopies, we'll check their acunary counts, what polyps, what size, check their family history.
and then refer on to the counsellors to get genetic testing for someone we think could have oligopolyposis. And so when you say genetic counsellors, are there people that actually talk to patients about whether or not to do the testing at all and the consequences of if they find something? Yes, that's correct. Because obviously, I mean, especially if you're chasing something like Lynch syndrome, there is a significant mental health issue which could go with it or stress which goes with it.
the patient and the family and so generally genetic testing should be done by a qualified genetic counselor who can talk through the implications and the implications for health insurance or any insurance policies going forward because someplace in the world that can have If you register for your health insurance, you've got a genetic disorder, it may affect what you're recovered for. And so I think counselling is an important component rather than just a random genetic test done by...
Ancestry.com or one of those commercial companies, you can do eugenic testing that way. The problem is there's no counselling and also their understanding of the variants of unknown significance, the VUSs. is very poor. They just say, oh, we found a mutation which might be associated with Lynch. Well, actually, it's a VUS1, which is not significant and unlikely to be involved. And so you don't get that counselling or that knowledge.
There are some new things like methylation, looking at methylation or looking at the actual tumours genes, so not your genes, tumour genes, which the genetic counsellors can help organise tests and it's getting more and more complicated. simple surgeons to manage and we do need the specialist geneticists and genetic counselors to help us with comparing the tumors genes and the patients genes and the VUSs and what's significant what's not
So the other growth area we've had since I started 10 years ago or more for me a GI cancer service is serrated polyposis syndrome. Initially it was called hyperplastic polyposis syndrome and the WHO definition has changed with time. This is serrated polyps, serrated of any class. It can be hyperplastic or serrated style polyps or traditional serrated polyps.
And the cancer pathway is not the classic one we think about with polyps, with adenomatous polyps. And there are alternative pathways to cancer. And it seems to be a little bit slower, but it is concerning. And we do see patients with hundreds of serenity. rated polyps potentially and see cancers associated with these. We don't have a clear-cut genetic disorder. It's not like Lynch or FAP where we can find one or two genes.
test the family and know so we do have to recommend colonoscopies for first-degree relatives with serratapolyposis syndrome sometimes i'm counseling patients who are young in their 30s and 40s have got hundreds of polyps You're having yearly colonoscopies. We're not winning every colonoscopy. You have 30 to 40 polyps removed.
At some point, a subtotal colectomy at least, where you can at least survey them with a flexi-sig, would be preferable to having full bowel prep and a full colonoscopy every year. Decrease the burden of colon, which can change into cancer. It is a big burden, yearly colonoscopies, and the problem is also you create a scarred colon as well where you don't know when you've removed hundreds and hundreds of little serrated polyps.
We don't know the progression, and the different families behave in very different manners. But that's definitely an area of growth as far as polyposis follow-up as serratopolyps. It would be lovely we could just discover the one gene. I'm suspicious there'll be several different variants because you get families where, yes, they've got serrated polyposis, they've had 40 or 50 polyps removed and every colonoscopy you find three or four every year or every two years.
But there's other families, as I say, have hundreds of polyps, and you've got to be really paranoid about them at a young age too. Generally with the serratopolyposis, it's that first colonoscopy. You find, say, 10 polyps. two or three bigger than 10 millimeter or 20 millimeter size polyps so you then you bring them back in a year and hopefully with yearly colonoscopies you reduce that polyp burden so you're only getting one or two then you might better space them out to two yearly colonoscopies
But it can be quite a colonoscopic burden for the country and the patient, yearly colonoscopies. And when would you suspect serrated polyposis in a patient or family member? It's a cumulative count. And so it's... 20 polyps or five large polyps, basically. And they're all serrated sometimes? And serrated of some type, yeah. Do they get mixed polyps? Do they find serrated and adenomatous polyps or are they usually just serrated?
The predominance is serrated polyps, but you've still got a colon, so you can still get an adenomatous polyp. So just because you've had two adenomatous polyps and say 30 serrated polyps. you're not going to say they don't have serrated polyposis some of those other oligopolyposis disorders can have mixed polyposis where you've got both and you're getting large numbers of both adenomas and serrated polyps and again we don't understand the genetic cause of that
there will be an environmental or microbiome effect with some of these and might be combined that you have a low risk genetic disorder but you've got the right microbiome and it makes you more likely to progress to cancer it's probably multifactorial is what i'm trying to say
And in those patients where you don't know what the gene is, is the interval between colonoscopies dependent on the number and types of polyps that you're finding? Yes. Initially, you start off aggressive yearly colonoscopy and then hopefully space it out.
find that and then if they've got SPS then you're going to tell their first school relatives they should at least have a screening colonoscopy to see if they've got polyps and if they've got no polyps then maybe you might say we'll read it in three years or something like that
But we don't really have the science to know how to predict. And again, if you are a first degree relative, is there an age that you might start doing colonoscopies? Top of my head, I'm going to say 25 is a ballpark figure. So it's not as aggressive as FAP? No. No, definitely not. The other topic I was hoping to talk to you a little bit about, because I know you spent some time at St Mark's, is management of short gut syndrome.
Yes, Sir Mark's is a hospital in Harrow, just outside of London, though it has moved since I was there. It was right next to the village of Harrow where the traditional school is. It was set up. in the 1790s by Frederick Salmon as a hospital for the disease of fistulas and anal conditions. And one of the old hospitals has still got the brickwork outside and has that engraved on the outside, which is a very specific hospital.
In the 80s, they got into polyps initially and became a very specialised colorectal hospital. But one of the areas which they have is an intestinal failure unit. I think it's about a 20-bed intestinal failure unit run by the gastroenterologist but with surgical help. And they are one of the national...
areas for transfer of patients with short gut syndrome. So when you're on the intestinal failure run as a surgical fellow, you saw lots of patients brought in from all over the country with all sorts of disasters with short gut. Short guts, it's a huge problem, but it's variable on age as well, and it depends what length. So important things to think about when you're operating and you come across a patient with, say, dead ischemic gut from an SMA is think about where you're losing your bowel.
So is it jejunum? Is it ileum? Can you retain the ileocecal valve? Because that valve will slow your progression of food and does help with short gut. So it's length. is the important thing and so once you start losing significant lengths say more than two meters or getting down to less than two meters you're going to have an element of short gut syndrome and depending on your age you can adapt so if you're old and
old doesn't take much to be old even over 50s getting old as far as short gut syndrome goes your ability to adapt really decreases so if you have less than 1.5 meters of small bowel left and you're say 70, your risk of adaption is going to be minimal and you'll be looking at lifelong TPN.
And is this appropriate sometimes? And that's that hard decision. Oh, I think I'm going to leave a metre of bowel in someone. Is this appropriate in an old person? If it's a young person, obviously you're going to go for it. But you've got to think about what piece of bowel. And it's really important if you're that first surgeon to map and measure and think. Sometimes you might leave them open and redo that mapping the next day when you bring them out of ICU.
try and join them up as much as possible on the second operation if you are doing relooks. Use of stoma is okay because you can reverse them. One of the big new things which has been interesting the last few years is The Auckland University, Auckland Hospital has developed this refeeding system where they can take your intestinal chyme and refeed it down distal lumens of stomas.
to say you've had multiple segments of bowel and you've brought out multiple stomas, you can be feeding distal to your proximal stoma. So think about bringing up double-barrel stomas, which might be amenable to these refeeding systems. In New Zealand, we have a home TPN service. They don't run that many patients throughout the country. But home TPN is very intensive and it does have complications.
TPN is better than it used to be as far as the complications to your liver or PEC lines are a lot better than they used to be. But it's not something you necessarily would want. Sometimes patients don't need full TPN or they might need alternate TPN.
sometimes they just need fluids as well so they might be eating okay so nutrition's all right but they're still losing a bit of fluid by their stomas and so you might need to have a pick line and have alternate day one liter of saline or something like that
So having a nutritional service and referring to a special nutritional team is important. We do a reasonable job in Christchurch, but there is actually a national nutritional team based out of Auckland which will give us advice if we need it or ask for it.
and all home tpn patients do need them the national service tied in so if you're in a regional australia say i'd be thinking about transferring to a bigger hospital home tpn And when you say adaptation, some patients will over time be able to wean off the TPN and eat more normally, or if you can join up a patient and get the colon back into circulation, for example, they may not need to be on the TPN lifelong.
Yes, they might start off on alternate day TPN or alternate day fluids. And at St. Mark's, I remember, there was a visiting surgeon from Melbourne. And on that day, I joined three jejunum to sigmoid. anastomosis and sort of looking like crazy. But their explanation was, if you do that, the patient can at least drink. Nutritionally, they'll still need TPN, but you decrease how much TPN, how much fluids you need to give.
Everyone feels a bit more normal pooing at their bottom and being able to eat and drink a bit more normally. But it did seem crazy. You've only got jejunum straight onto your sigmoid. Well, I always ask the guests on the podcast, what advice do you have for trainees who are preparing to sit for their fellowship exam? I obviously set my part twos a while ago now.
But you need to build up that initial knowledge with your book reading, but then as you get towards the end, you want to keep that big framework. And I used some of the American Absight type. books because they weren't specific enough for our part two. You needed more detail than they gave you for theirs, but they gave you a nice big broad scaffold to build knowledge on.
I remember things like melanoma, which we don't do melanoma in New Zealand. It's more the plastic surgeons, but we obviously have to know part two. And it gave you the, I need to know blestose thickness. all the different details and then I could build my knowledge, go back to my textbooks and build the part two level for us. So keep it broad, build a big scaffold and then get specific stuff, special papers you want to throw in when you get asked that.
Thank you so much for coming onto the podcast. It's been fun. If anyone wants to email me, I'm happy to answer any questions or give me a phone call. It's all good. It's time to close up. Thanks for listening to First Incision. If you have any comments or feedback, send us a message at firstincisionpodcast at gmail.com or follow us on Instagram at firstincision. Happy studying!