Chad Ball 00:12
Welcome to the Cold Steel surgical podcast with your hosts Ameer Farooq and Chad Ball. We’ve had the absolute privilege of chatting with some amazing Canadian as well as international guests over the past year. While the topics have been broad in range, whether clinical, social or political, our aims for the podcast continue to remain the same. We hope to inspire discussion, creativity, scholarly research, and career development in all Canadian surgeons. We hope you enjoy our second season as we continue to highlight some incredible guests, deliver detailed masterclass sessions on a myriad of clinical topics and introduce some fresh new features such as debate and companion formats. We hope you relish the podcast as much as we do.
Ameer Farooq 00:55
In this episode, we were joined by surgical oncologist Dr. Carolyn Nessim. Dr. Nessim works at the Ottawa General Hospital and gave us a masterclass on melanoma. We talk about an initial approach to melanoma, staging, immunotherapy, and even get a walkthrough of how Dr. Nessim does your groin dissections.
Chad Ball 01:31
For some of our listeners, maybe who don’t know you, as well yet, can you tell us a little bit about where you grew up and what your training pathway was? And what sort of lead you to Ottawa?
Carolyn Nessim 01:41
Sure. I’m originally from Montreal, was born and raised. And I actually did my bachelor’s degree at McGill in occupational therapy. So I was actually an occupational therapist first, before I was a doctor. I worked as an OT for about two years in New York City. And then while I was working, I was in the Bronx and in Harlem working in pediatrics, with kids that had autism, as well as developmental delays. And the more I worked with them, the more I realized I wanted to do medicine. So I applied while I was in New York. I got accepted to the University of Montreal, and came back home. So I did my medical school and general surgery residency at the University of Montreal as well as a master’s degree. And then I did my fellowship in surgical oncology at the University of Toronto. And as I was doing surgical oncology in Toronto, I kind of had this love for soft tissue tumors. Anything in the soft tissue I liked, so that included soft tissue sarcoma, and melanoma. And so I wanted to do a little bit more in that field. So, I ended up going to the Peter MacCallum Cancer Center in Melbourne, Australia where I did an additional six months doing only melanoma and soft tissue sarcoma. And when I came back from Australia, I basically did what everybody else does. You just put your application out there and call around and email people and I eventually connected with Rebecca Auer at the Ottawa Hospital and told her what I wanted to do and what I was interested in and she’s like, wow, right place right time. We exactly need a sarcoma melanoma surgeon right now and it’s perfect. So, I got the job. Since then, it’s been morphed into additional cancers. So I also treat gastric cancer and neuroendocrine tumor. And I do a little bit of carcinomatosis evaluation. We don’t do high tech surgery but we do carcinomatosis evaluation. So that’s a little bit about me.
Chad Ball 04:09
That’s a really great story. You know, you would have had some obviously great mentors in Toronto, probably Carol Swallow comes to mind amongst others. And then doing melanoma in Australia is probably like, you know, hitting the Mecca.
Carolyn Nessim 04:21
it is, it is. I mean, I picked Australia for a reason. It’s the number one cancer in Australia because there’s like patchy holes in their ozone layer. And we would do the thin melanoma clinic on Thursday afternoons and so no melanoma thicker than a millimeter could come to that clinic and you would just do their wide local’s right there and then when they would come. And then we would do the regular melanoma clinic all day Friday, and it’s pretty impressive. First two hours of the day is tumour work with, you know, 60 people in the room. And then you do the combined multidisciplinary melanoma clinic. So you take the entire unit of that clinic and there’s medical oncology, radiation oncology, plastic surgery, anti surgical oncology, dermatology and nurses. And you all have side by side clinics. We would see about 150 people in that one morning. We’d be done by 1:30pm, having seen about 100 people. And what was really cool is, if you were doing a skin check, and you thought a spot looked funny, well, you just go get the dermatologist and they come with their fancy dermatoscope. And they say, no, that’s fine, go home, or yeah, that’s bad, go to the back room. And then the plastic surgery residents were doing all the biopsies, and it was a really well oiled machine. And then my favorite part of the day was after clinic, we would go to the pub, which was two doors down and everybody would go and it was always a nice blast. So a wonderful experience, loved it immensely, learned a lot and really got to really understand melanoma.
Ameer Farooq 06:10
There’s something to be said about just going somewhere where they do the day in day out and they have a complete, well oiled kind of machinery and set up to do something such high volume like that. So let’s leverage your melanoma expertise and dive right into the topic of melanoma. And I can see firsthand that this is something that lots of trainees struggle with. Mainly because I think so much of it has changed in the last little while. And depending on your rotation, or where you train, you may or may not be exposed to a lot of this during training. So it’s awesome that we can have you on the podcast and let’s dive right in. So, I’ll give you a scenario. So if you have a 50 year old female who presents to your clinic with a new skin lesion that’s been getting bigger, and the GP says, is this query melanoma? How do you approach that patient that comes to you in clinic?
Carolyn Nessim 07:10
So, to be honest, as a surgical oncologist, I usually get them once the diagnosis is made. But if I did get a lesion like that, you know, I always tell family doctors that the most important indicator that it is a melanoma is that the patient noticed it. Because unfortunately, ABCDE, which we all learn in practice doesn’t always apply, especially in nodular melanoma where they’re around and regular and raised and bluish, in tinge and not necessarily so black. Or they can be very pink and purple. So I think, you know, if a patient is concerned about a lesion, and it obviously does not look like it’s seborrheic keratosis, because the majority of the time it’s seborrheic keratosis. If it truly does look abnormal, then you just biopsy it. I don’t think there’s any harm in biopsying lesions that people are worried about. Just take a piece. How to decide what kind of biopsy, so the standard of care or the best kind of biopsy is an excisional biopsy, where you remove the entire tumor with a very minimal margin. You’re not doing a wide local excision, you’re just taking off the lesion to assess it to know what to do as a next step. When lesions are, I’d say about a centimeter and a half or less, you can take them off. If they are larger than that. You don’t want to be doing large excisions in the clinic, because that could affect your lymphatic drainage and mapping for potential sentinel node. So when the tumor is too large, then a punch biopsy is a pretty sure fire way to get a diagnosis.
Ameer Farooq 08:54
So let’s say you know, I’m sure you must occasionally get sent patients that have had, for example, a shave biopsy or something like that. How do you approach that scenario? Because it obviously changes, like it doesn’t give you the information that you really need?
Carolyn Nessim 09:12
Yeah, so that’s true. I think it depends who did the shave, I’ll be honest. If you if you go to Australia, in fact, they do do a type of shave biopsy called saucerization. And really, it’s only because dermatologists know how to do them. And our dermatologists actually do know how to do quite successive, what they call a “deep shave”, where they can still get to the subcutaneous fat, in which case it’s not dangerous. And you can still get the entire information on the lesion. I think we don’t teach that to general surgeons because we had never learned how to do this deep shave. And so for us, it’s much safer and much more reliable to do a punch in a larger region. That being said, you know, there’s a big difference when the deep margin is positive. And you look at the patient, and you see quite significant residual disease leftover versus having a deep positive margin. But when you look at the patient’s skin, all you see is a scar. If margins are positive, and all you see is a scar, the likelihood of residual disease is extremely low. And our group just is looking at this and doing a paper but it is less than 20% chance that there’s actually residual disease and so that thickness is probably quite accurate. It’s very different if you have a positive deep margin on a shave, but there’s obvious residual disease. But I would argue in a thicker melanoma, so let’s say they told me it’s a two millimeter, and your deep margin is positive. Kind of doesn’t really change my management, because that’s getting the two centimeter margin and a sentinel node. Where it gets a bit more tricky is when the deep margin is positive, but they tell me it’s 0.5 millimeters. So in thin melanoma, this is very important. And I do talk a grand rounds and plastic surgery rounds especially because this is a very important concept. If the pathology comes back in situ or a thin melanoma, like a 0.5 millimeter, but the deep margin is positive. And when you look at the patient, you see obvious residual disease, it’s much better to try to excise the entire lesion to really get the full assessment of the lesion. Because unfortunately, what can happen is you treat it like a thin melanoma, you do the one centimeter margin. And if you’re in a certain location where it’s tricky to close it, all of a sudden, it’s being closed with a rotation flap or a keystone flap or some fancy thing. And then lo and behold, the final pathology says it’s a three millimeter melanoma. And now they ask for sentinel node biopsy. And at that point, it’s too late. You can’t do a sentinel node after a rotation flat. The lymphatic drainage has been too manipulated and moved around that you won’t be able to identify the correct node. So the concept of, well I did a lymphoscintigraphy and I can find a node – of course you can find a node. Any area of skin will map to a lymph node, it just happens to not be the right sentinel node. You really want the node that was close to the original melanoma. So I think deep positive margins in thin melanoma has a definitely different approach than a deep positive margin in the thicker melanoma where it really doesn’t change your management at all.
Ameer Farooq 13:14
Okay, that makes a lot of sense. Just to back up again for a second. Where do risk factors, you know, they always teach us these classic risk factors in melanoma like this pale skin and red hair. Does that really even matter for you as a surgical oncologist, or as someone who’s seen a lot of melanoma patients?
Carolyn Nessim 13:35
I mean, it doesn’t change anything in how we treat patients. I think it is important in terms of prevention. I think it would be nice if we had larger campaigns to explain the risk factors of melanoma and to improve prevention. Because, you know, I don’t think people are fully aware that if their redheaded, blond haired, blue eyed pale skin are at higher risk, they often seem quite surprised when I tell them that. So we think that’s intuitive. But it’s not always so intuitive. I’ve also had some, you know, African American patients and Mediterranean patients come with melanoma, and they tell me well, how is that possible? I have dark skin. So I think, you know, there does need to be some awareness of the risk factors. And really it is exposure to the sun. And who are going to impact on the most are younger children. You know, it takes decades for a mutation to turn into a cancer. So really, when patients tell me at the age of 50, but I wear sunscreen every day. And I say well, it’s not about what you did in the last five years. It’s what did you do as a child and did you get some blistering sunburns as a child and they go, oh well, yeah, because back then we didn’t put anything on and it’s like, well, that’s what caused the mutation. So the risk factor is UV light. It is sun blistering type sunburns. And so protection from the sun is very important. In Australia, they have this campaign called the Slip-Slop-Slap campaign. And you know, everybody’s aware of it. And it basically means just wear sunscreen every day, every morning when you go outside. And we definitely don’t have the rates of melanoma as other parts of the world because we are a colder climate. But we still get our significant share of melanoma in Canada. And I do think awareness of risk factors is important. There’s never been any evidence that skin screening for the general population would actually prevent melanoma. And that’s where we have a bit of a bug. But we are starting to study, are there certain populations that should get skin screening on a regular basis from their family physician, and that’s being actually studied in Calgary with a really good group. But it’ll take years before we get the answer to that study, but a very important one.
Ameer Farooq 16:06
The other thing that everybody always talks about, and I think sometimes the significance of which didn’t really dawn on me until I was studying for the Royal College exam is sort of the morphologic subtypes. Can you just briefly go over what the morphological subtypes are in melanoma? And why is it important to really know what those are?
Carolyn Nessim 16:28
So they are important. The most common is superficial spreading, and it’s the one that has the best prognosis. And why that’s important is because superficial spreadings are the ones that have that classic appearance. ABCDE, they’re asymmetrical, their borders are irregular, they’re got multiple colors in them, they evolve over time, and they have a diameter of greater than six millimeters. So superficial spreading is the most common with the best prognosis. And the reason it’s the best prognosis is because it tends to grow in a lateral fashion, as opposed to in a vertical deep fashion, which is more dangerous. The other reason why it’s so important is that not all superficial spreadings are de novo. So the whole concept of a polyp that you know is an adenoma and the adenoma turns into a cancer. Well, we have that in melanoma too. And superficial spreading is that kind in the sense that it could start as just a regular nearby and then it becomes a dysplastic nevi, and then that goes into melanoma in situ and then that turns into superficial spreading melanoma and about 25% of superficial spreadings are like that. So again, it’s about awareness. But that continuum does exist in skin cancer, but mainly only for the superficial spreading and lentigo maligna melanoma subtypes. And that’s why some patients will be like, but I’ve had that thing for 20 years. How can you suddenly now tell me it’s melanoma? So I’ve had the melanoma for 20 years? And you’re like, no, it was a regular nevi before, it just recently changed. And that’s why the recently changed component is very important. Nodular melanomas are the second most common and don’t present like that at all. So nodular melanomas are round, they’re bulky, and they grow quickly. They grow vertically, they grow quickly, and they have the worst prognosis. They weren’t there last week, they’re suddenly there, you thought it was a little bug or a pimple, and it just won’t go away. And it blisters and bleeds and it hurts and sometimes they’re pink and sometimes they’re purple and sometimes they’re black. So they’re very hard to diagnose. But they’re probably one of the worst prognosis. You then have the lentigo maligna melanoma, those ones also somewhat are on a spectrum where they start as in situ disease and then can develop into a malignant melanoma. They’re the ones that tend to be on the head and neck and on the face, especially those patients that are in the sun all the time. Those sunbirds that go to Florida and elderly patients. So that’s the most common sight. But they’re not that frequent, malignant melanoma. So it’s the third most common. Finally, the last most common type would be the Acral lentiginous melanomas, these ones we think are not necessarily associated with sun exposure. We’ve noticed that Acral lentiginous melanoma which is based, you know, it can be on the palms of the hands, soles of the feet, under the nail beds, tend to happen actually more in patients of Asian, Mediterranean or African descent. And we have noted that they more likely have a SEA kit mutation in them and so therefore may not be related to the sun. Those are the most aggressive and with the worst prognosis. You then have a variety of other melanomas like desmoplastic melanoma that can look like a sarcoma, in fact, and many sarcoma surgeons might take off the desmoplastic tumor thinking it’s DFSP and finding out, oh lo and behold, it was a melanoma. You have amelanotic melanoma, which is like in the term, it has no color. And then finally, you can have all of the rarer uveal melanoma and in the back of the retina. You can have you know, mucosal melanoma in the anal canal, or even in the rectum or even in the vagina. Those ones are quite aggressive. So, lots of different kinds, and the list goes on and on. But, you know, those are probably the most common.
Ameer Farooq 20:45
So we’ve gone over most of the history features that I think you’d be asking about in clinic. What are the important things that we should be doing for physical exam when we’re seeing a patient, and evaluating a patient for melanoma?
Carolyn Nessim 21:01
I mean, ultimately, I think that to be perfectly honest, I make sure they have a dermatologist, because the bottom line is, I’m not a dermatologist. And I’m not the best at diagnosing melanoma and much better at treating it once it’s been diagnosed. So when I get a consult, I do a full skin check. And I do look, but in general, I’m focusing on the site of where there was the primary tumor. And the goal is to look at the site, you want to look at the biopsy sites, you want to see if there’s residual disease, or if there isn’t any residual disease anymore. Just looks like a scar. You want to feel along that limb, or on that back between the primary site towards the nodal basin. And you kind of feel deep into the subcutaneous tissues to make sure there’s no intrinsic disease. And then you check the local nodal basin and that would be related to that area. Whether it be the groin, the axila, the neck, or all four depending on the location of the melanoma. So those are the things that I personally focus on.
Ameer Farooq 22:08
Can you define in transit disease versus satellite disease? Like what are the differences between those two?
Carolyn Nessim 22:15
Now, there actually are no differences between the two. It’s just a discussion of location. So there used to be a distinction in the AJCC, where a satellite nodule was anything within two centimeters of the primary. Whereas an in transit lesion was anything more than two centimeters from the site of the primary towards the nodal basin. We still call them in transits and satellites, because that’s how we understand it. But ultimately AJCC has now gotten rid of that terminology, and they’re all kind of the same thing. And they’re called intra lymphatic metastases, because what they truly are, are little spots of tumor within the lymphatic channels. That is what in transits are. And so whether you call it a satellite, a microsatellite, an in transit, there’s whole bunch of terms. The point is they are intra lymphatic metastasis, and they all have the same prognosis, regardless of their location. And so the minute you have in transit disease, you’re definitely a stage three.
Ameer Farooq 23:23
I think one thing that also gets people tripped up a little bit is sort of the staging workup. So if you have someone with a biopsy proven melanoma, you know, you’ve gotten a thickness. What kind of staging workup should you be doing?
Carolyn Nessim 23:39
So, the answer, the quick answer is you shouldn’t be doing any staging workup for most melanomas. So any early stage melanoma with no clinical evidence of nodal disease does not need imaging. Multiple studies have shown very, very extremely low yield and a lot of false positives that you go down these rabbit trails, looking for something that’s not there. And so we actually do not image early stage node negative melanoma. One caveat to that are T4b melanomas, so anything that’s greater than four millimeters and is ulcerated. In those patients, consideration of preoperative imaging can occur because you may find disease and you may find metastases at that stage. In Australia, and they did a very interesting study where they looked at which threshold of a T4B are you more likely to yield something diagnostic. And they found that the cutoff was about seven millimeters. So anything greater than seven millimeters I image pre-op. Anything less than that, I don’t tend to because often it just delays a very important surgery to find no evidence of disease. But I think in certain T4bs, depending on the story, the rapidity of progression, how it presented, if it’s nodular or not, I may do pre op imaging. But for everyone else, if there’s no clinical evidence of disease, you do not require any imaging. And in fact, you know, I advocate this quite a bit in the Choosing Wisely campaign because people do image and it’s really a waste of unfortunate money and time. So the minute you’re node positive, that changes everything. So once you have a positive node. So if they come back with their sentinel node being positive, or they present with palpable nodal disease presentation, then all stage three melanomas should get imaging. In earlier days, before having adjuvant therapy, you could even argue that a 3A may not need imaging because even there, the yield is low. But now in the era of adjuvant therapy, we need to make sure they’re not metastatic before giving them a treatment. And therefore all stage threes are going to get imaging. The ideal imaging if you had whatever you wanted, and it didn’t matter what your province pays for, then you would get a PET scan and an MRI brain as a baseline. If you cannot get a PET scan, then a CT chest abdo pelvis is a good option.
Ameer Farooq 26:39
Any lab work that you would do as part of your workup?
Carolyn Nessim 26:44
Ameer Farooq 26:46
Carolyn Nessim 26:49
Like I don’t do any lab work ever. I don’t do lab work. So, there’s a caveat to that. If you’re a stage four patient, there is some evidence that LDH is very prognostic. And it actually is included in the staging system. So in all stage four patients, it’s M1A, LDH normal or high. M1B, LDH normal or high. Because what we’ve seen is that in patients with a high LDH, they definitely have a worse prognosis than those with a low LDH. So that’s really the only laboratory test that’s really specific to melanoma and could be done in stage four patients.
Ameer Farooq 27:31
See, I remembered something from the Toronto review course. So there you go. We’ve kind of been dancing around this, but can you talk about what the TNM staging is for melanoma? And I think it’s definitely worth going over this again, just because it seems to change quite often. I think there was a recent revision right before we wrote our exams.
Carolyn Nessim 27:55
Yeah, so the eighth edition just recently came out, although recent is now I think, almost two years ago now. But the eighth edition just came out. And the one that keeps changing is the thin melanoma, they can’t seem to decide what’s higher risk or not in the category of thin melanoma. But really, what it is is a T1A is anything less than 0.8 millimeters without ulceration. And a T1B is point eight or more. Or less than 0.8, but has ulceration. That’s the biggest change. So, in the sixth edition, what made you a T1B was ulceration. In the seventh edition, what made you a T1B was having at least one mitosis. And then the eighth edition, they got rid of the mitosis and they put back the ulceration. Um, so I think that it’s because they don’t know and I think it’s because we don’t know. All of these, you have to appreciate that the staging system is based on a massive retrospective review. Albeit international, hopefully quite representative. I actually don’t know if there’s any Canadians in this multi international staging system. But it is a retrospective review, and the eighth edition was on 1500 patients or so. And so what they do is they look at the outcome based on different criteria to determine staging. So a T1B currently is point eight millimeters to one millimeter or less than that if there is ulceration. The rest of the categories have not changed. So a T2A is between one and two millimeters and then A means it’s not ulcerated and B means it is. Same thing T3, is two to four, and T4 is greater than four. A means it’s not ulcerated. And B means it is. When you go into the N category. The N category is thee nodal category and it’s quite complex. But there’s N1, N2 and N3 disease. N1 is usually only one node positive and two is two to three nodes positive and three is greater than three nodes positive, or in transits and satellites and all the rest of it. And there’s a huge combination because then it breaks down into N1A, N1B, N1C. And I mean, I don’t remember it all by heart, I have it on an app on my phone, so that I can stage patients. So yeah, that’s the end stage. I think the newest thing is that even if you have a microsatellite beside the primary melanoma, you’re automatically in a stage N3C, even before doing a sentinel lymph node biopsy. And I think that is one of the biggest changes because you start to debate, do I even need to do a sentinel node biopsy if there’s a satellite beside the primary? The word is still out on that. We still do the sentinel node, but it’s hard to know if it’s valuable because they might give them adjuvant therapy anyway. And then finally, the M stage, the newest addition to the M stages, the M1D stage. So M1A is that the metastasis is subcutaneous, but not where your original melanoma used to be. So for example, if the melanoma was on the leg, but now someone shows up with a subcutaneous spot or a mass on their back, that’s actually not an in transit. That’s a subcutaneous distant metastasis, because it’s nowhere near the nodal basin. And therefore, would be an M1A disease. Also M1A is slightly different, because it can invade muscle and bone. So that’s a little bit different. And then, M1B is lung. M1C is viscera, and M1D, which is the new one, is brain. So CNS metastases, because we do know that that has a significant poor prognosis in melanoma patients. And then they call them LDH normal or LDH high. So they’ve categorized that even further, because as mentioned earlier, LDH high has a poor prognosis. And then finally, in the last edition, there is now a new stage: 3D. So 3Ds are anything that’s a T4B, with N2 disease and above, so that’s really bad disease. Like if you’re a stage 3D, or you’re on the cusp of being a stage four.
Ameer Farooq 32:55
That’s a brilliant overview. And it’s hard to keep track and we’ll link some resources to the eighth edition in the show notes so that people can look at that as well and listen, and then sort of review things as they go on. There’s a couple of points that I wanted to just pick apart there. So the first one was just to clarify, for a thin melanoma, what are the features that would make you consider doing a sentinel lymph node biopsy?
Carolyn Nessim 33:26
I think that’s a tricky question because we don’t have any randomised trials, and we don’t have the best evidence. Currently, the recommendations are any T1B and above, I should get a discussion at the very least, of a sentinel node biopsy. So T1B should have a discussion. It’s not strongly recommended, but at least a discussion. And that is because of what the AJCC showed is that in patients with a point eight millimeter or above melanoma, with no other factors, just the fact that it’s 0.8, had an 8 to 12% chance of having a positive sentinel node. So depending on what your threshold is, to what’s an important significance, positivity rate, and in which some people think 5% or more is significant, you would therefore recommend sentinel node biopsy for all T1Bs because their risk is higher than 5%. So that’s become actually less complicated than it used to be because now we just say, well, T1B and above gets a sentinel node biopsy, or at least you discuss it with the patient and let them choose. What gets a little bit trickier is when you get these really odd consults of a point five with three mitosis or a point six, with microsatellites. Because then you’re like, well, that’s really not good. And it shouldn’t be that way. And should I offer a sentinel node to that patient? So one study that I do refer to a lot, is a large meta analysis that was done by Erin Cordeiro and Francis Wright in Toronto, where they looked at, you know, they did a meta analysis of all the studies that included thin melanoma and their high risk features and sentinel node positivity. And there was actually more patients than the AJCC. It was almost 11,000 patients. And what they showed, interestingly, was that anything point eight or greater, without any other factor was an independent predictor of having about an 8% positivity rate. Ulcer rated melanomas had a 5% positivity rate. Microsatellites had a 28% chance of having positive nodal disease. And having at least one mitosis had a 9% chance of having positive nodal disease. So I still kind of use that study to help me decide when they’re less than point eight. Because we do know that those are still high risk features. I tend to focus more on my toasties and microsatellites, because I think those are an ulceration, because those three seem to be the most significant. But again, it’s just a discussion. I don’t think you can strongly recommend it. The number needed to treat is very, very high, obviously, when it’s only like a 8 to 10% positivity rate.
Ameer Farooq 36:34
So sort of on a related point, with regards to the T staging, what are the margins that you need to have when you’re doing their wide local excision based on their t stage?
Carolyn Nessim 36:48
Yeah, so that’s one of the easiest things in melanoma. If it’s a T1, it’s one centimeter. So anything less than a millimeter, the margin is a centimeter. Anything that’s one to two millimeters, the margin is one to two centimeters. And anything that’s two millimeters or more is two centimeters.
Ameer Farooq 37:08
We all breathe a sigh of relief when when memorizing knots.
Carolyn Nessim 37:14
That’s one easy thing!
Ameer Farooq 37:17
So we wanted to just talk a bit about therapeutic groin dissections. You know, we had the pleasure of interviewing Dr. Wright and going over all the MSLT1 and MSLT2 trials. So we won’t belabor that point again. But let’s talk a bit about therapeutic groin dissections. So we’re talking now about a patient that comes in with obvious palpable clinical nodal disease, or for whatever reason, needs a therapeutic groin dissections. Can you talk a little bit about the relevant anatomy and how you kind of approach that operation?
Carolyn Nessim 37:58
So I think that there are so many schools of thought. Because there’s two things you want to look at number one, how bulky is the node is that recurrent disease? Is it primary disease? Is this a missed sentinel node from the past? Like, they don’t all present exactly the same. And then once you have kind of figured that out, you then have to make the decision of, “am I only doing the superficial grind, or am I going to do a pelvic grind as well?” I must admit, when you’ve got big, bulky palpable disease, I don’t bother with the like weird criteria that has never been proven about “it has to be at least three centimeters or greater”, or “there has to be three or more nodes” or “it has to look suspicious”. If you have a big bulky papable node in your groin, you’re probably getting both. It just makes my life a lot easier. And it’s a lot easier to just have a standard that you follow. And as long as you follow it and you’re comfortable with it, it goes quite well because doing the pelvic node dissection doesn’t necessarily increase much in terms of morbidity. The main lymphedema is caused by the superficial groin dissection, not really by the pelvic dissection. So once someone has palpable nodal disease, it’s very immunogenic. And so it’s a kind of cancer that can really cause enormous amounts of inflammation. And so lymph nodes can feel a little bit bulkier sometimes. It doesn’t mean it’s melanoma. And that’s the same thing if you already had a primary melanoma and then you feel palpable disease at the same time. You should always biopsy that and actually prove it’s melanoma. Before you tell someone you’re going to dissect them because there is morbidity associated with that. And so I actually do an FNA in the clinic. It’s pretty easy. Cytology comes up from pathology, we do our FNA, we send it off. You don’t need a core. You don’t need anything fancy. If it is melanoma, it’ll tell you it’s melanoma. And if it isn’t, it’ll tell you that it isn’t. So let’s say it is melanoma, and then I want to do the groin and pelvic node dissection potentially, my first step is a PET scan. Because the PET scan will show me if there is obvious pelvic disease, and how much disease there is in the actual groin. There is the scan associated to PET scan, it’s good enough quality that I could see in my vein, my artery, and you know, kind of have a sense of how bulky is this node? Is it invading any structures? Does it look easily susceptible? So, assuming that all of that looks good, in some cases of the axila, to be honest, if this was more an axillary node, if they’re very, very bulky, and you feel them kind of creeping on to the pec major, that’s where I start worrying about the brachial plexus. In which case now I’m going to order an axial MRI to make sure that the brachial plexus is okay before going in and taking out these monstrous 20 centimeter nodes. But in the groin, it usually always comes off and I would argue that most melanomas, they kind of push structures aside, it’s very rare that it feeds structures. That’s different when it’s recurrence melanoma or someone who’s had radiation. And now there’s only three that came up. That’s very different than just hey, I have a palpable disease and I’ve never been operated or treated in that area. So I actually do two incisions. I don’t do the Lazy S. I recently looked at my own data. And my infection rate was ridiculous. When I was doing Lazy S, I just felt that everybody was infecting across this crease, or dehiscing or because you know, not everybody’s fit and thin and whatever in our patient population. And so I’ve stopped using the Lazy S. I don’t do that. So I make an incision on the groin, overlying the femoral artery. That’s the best location. And then I go down, and I’m always under the crease. It means a little bit of tunneling at the top part of my groin dissection, but I’d much rather do that with some nice retractors than cutting across the crease. Which often didn’t actually help me anyway, because you can’t really cut it. Like even cutting the inguinal ligament I never found that it helped me anyway. So I do not do that. I never cut the inguinal ligament. So make your incision. First step is raise flaps on either side. Get down to the Sartorius laterally, get down to the adductor medially. Make sure you’re at the most medial border of both muscles, open the fascia, and then find where the two muscles meet inferiorly in a V format and a V shape. That’s the bottom of your dissection. You don’t need to go any lower than where the two muscles meet. Then the next step is you identify the saphenous vein, which is medial. I personally do not ligate the saphenous vein, I was taught by Francis right and I do not do it. There is a belief that it could reduce the risk of lymphedema. Makes the surgery a little bit more complex, a little bit longer because then you have to dissect the saphenous vein throughout the whole procedure. But as long as it’s not thrombosed and it’s looking good, then you can do that. So once I’ve cleared my saphenous vein, I then identify the femoral artery. And with a Lauer, dissect right off the femoral artery just like you would in vascular surgery and the femoral vein. And as you get up to the top, you then identify your inguinal ligament. You clear all the lymph nodes off the inguinal ligament and bring them downward. And then finally, what’s left is the nodal tissue right at the sapheno-femoral junction. And because I don’t ligate the vein, I’m clearing off the Ssapheno-femoral junction. There’s always another little tributary vein that you’ll ligate and ultimately removes the specimen. And now you have a nice, fully resected groin dissection with all your anatomical landmarks that you need to clear while preserving a saphenous vein. It’s okay to ligate the saphenous vein, you just have to realize that you’re ligating it twice. So the first time you ligate is at the bottom of those two muscles there. That’s where you’ll usually find it and move up. And then you’ll ligate it again at the sapheno-femoral junction. And then you can either take the sapheno-femoral junction, you could clip it, you could tie it, you could sew it. There’s a variety of ways to close that off. It’s really surgeon preference. In terms of the pelvic node dissection, I then do a separate encision. So two finger breaths above the inguinal ligament, I’ll make an incision between the ASIS and the pubic tubercle, just like you would for hernia surgery just slightly lower than hernia surgery. And ultimately you open scarpis fascia, then you get on to the external oblique, you open the external oblique, and then you have to cut a little bit of the internals, but ultimately, you’re just spreading the muscle more importantly, so you spread and then you’ll see a bulge. That bulges your peritoneum. So with a sponge on a stick or a peanut, I push the peritoneum aside so that I can enter the retroperitoneal space. Kind of like in kidney transplant surgery or in hip surgery and orthos. You’re really entering the retroperitoneal space. Depending on how bulky the disease is, you might actually see the ureter as well. So you got to make sure that that’s out of the way. But you push everything aside and make sure your peritoneum is aside. The trickiest part here is finding a good retractor to really be able to stay in that space. I found that sometimes, believe it or not, a balfour can help or work. Or even Alexis wounds retractor has sometimes gotten me out of a tricky situation. And deavers are also very useful, and assistants are awesome. Like medical students who are great at doing this. But ultimately, you’re now on top of your iliac artery and vein. So you palpate because you’ll feel the pulse. And that’s what kind of directs you. At least that’s what directs me because I know that I’m in the right space. And then you just clear all the nodal tissue off of the iliac artery, the iliac vein, and move all the way up to where the external and internal vessels meet. So you don’t need to go along the internal iliac, you don’t need to go along the internal like, you just want to go clear all the external iliac nodes up until the bifurcation. And then more medially, you want to clear the obturator nodes. You will feel them. You will feel the obturator canal, the node that just sits right above the inguinal ligament on that point, that’s actually Cloquet’s node. Cloquet’s node is the first node of the deep dissection. And you clear all of obturator nodes and you can usually see the obturator nerves so you know that you’re in the right space. And you take out all of that tissue. And yeah, that’s your deep dissection.
Ameer Farooq 47:38
That’s a beautiful description of that operation. Well, I think we’re getting close to the end here. So I just have a couple more kind of quick snappers here. One thing I want to specifically ask you about postoperatively with their care is, do you leave drains?
Carolyn Nessim 48:16
I do. Um, so I’ve changed quite a bit. I used to do a Lazy S. I used to close the skin with staples. Yes, believe it or not. And I would put two JPs in. And honestly, I didn’t feel like it was, I mean, I was also doing practice, but I just had all these infections, and it was really frustrating me. And I remember a wound care nurse coming up to me and saying, well would you like me to put in incisional back on that? And I go, what’s that? And so she showed me and I was like well, that sounds fantastic. Like maybe that’ll work. From there, I ended up doing this T-bridge incision or two incision technique. I only leave one JP now in the lower groin. I never put one in the pelvic part anymore because I realized it just doesn’t need it. And I put an incisional customizable praveena on top of the whole thing. So pravena is a type of incisional vac that patients can go home with. I actually had to advocate quite a bit for my hospital to pay for this. But it really has reduced our infection rate by 50%. And we actually presented that as an oral presentation to society surgical oncology this past August. Virtually of course because everything is COVID virtual. But I really think it has made such a huge difference and my infection rate has gone way down. I think the groin is a tricky spot. I think it’s not easy to treat once it falls apart. If someone is extremely thin and I’m really concerned that the vessels are completely bare after I finished my groin dissection, I have done a Sartorius flap. And I’d say 30 to 40% of patients will sometimes get a Sartorius flap, depending on the situation or what it looked like or if there’s radiation involved. Or, like, I know they’re going to get post op radiation, there’s probably more in squamous cell carcinoma where they’re really big and bulky and bad. Or in Merkel cell carcinoma, where I really do feel the Sartorius flap protects the vessels in the tissues underneath because the radiation is really going to zap that skin. So that’s kind of my general approach to bridge incision, maybe a sartoria swap. And then one JP that I put only in the lower groin, and the incisional pervena vac. The closure takes as long as the surgery.
Ameer Farooq 50:58
You answered all my questions that I had. That’s brilliant. Yeah, that pravena seems like something that a lot of people are using in a variety of settings. And it seems to really help. You know, obviously, adjusvant therapy in melanoma is a big, big topic, and we can’t do it justice in a single podcast. But can you kind of break it down in your mind how you think about adjuvant therapies, the types of adjuvant therapies and sort of who gets them postoperatively?
Carolyn Nessim 51:23
First thing I want to say is I love adjuvant therapy, because it makes me have a job. Because we were criticized for so many years for doing sentinel node in melanoma because they’re like, why are you even doing a sentinel node? There’s nothing you can even offer the patient. That has now changed and that is really a surgeons dream that you can maybe improve outcomes with not only surgery alone. At least that’s what surgical oncologists thrive on. So I think adjuvant therapy is a super new thing. I think you have to take it with a grain of salt. So far, all trials have only shown an improvement in disease free survival, not yet in overall survival. And I think it’s just because we’re only at three years follow up and we just need a bit more time. I think the curves separate wide enough that I suspect there will be an overall survival advantage. There are two kinds of adjuvant therapy and different kinds of patients. So I’m sure everybody’s aware that melanoma now has a lot of molecular profiling. And there are different mutations that can be found in melanoma. So a BRAF mutation is found in 50% of patients. It tends to be identified in younger patients under the age of 50. However, it can be identified in older patients, and has now a targeted therapy. We know that giving BRAF plus MEK inhibitors have an effect and an improved overall survival in metastatic melanoma. And now it is showing us that giving up a BRAF and MEK inhibitor in the adjuvant setting can also improve disease free survival, and is already trending towards an overall survival benefit in the adjuvant setting. So, you do need to be BRAF positive of course to get these treatments. And so if you’re not BRAF positive, then you only have the other option, which is immunotherapy. Immunotherapy, how I like to explain it to the patients, is a treatment that stimulates your own body and your own immune system to create an army of T cells to fight off the cancer. And that’s really what it does. There are CTL for inhibitors like ipilimumab, which we actually do not really give in the adjuvant setting. There was one clinical trial where ipi was better than placebo, but unfortunately it was also very toxic. And so it’s not really given in the adjuvant setting. But PD-1 inhibitors like Nivolumab or Pembrolizumab both showed benefits in the adjuvant setting and are given. So you have a BRAF positive patient, you have two options. You can give them BRAF plus MEK inhibitors. It’s for one year, it’s an oral medication and it’s given daily. Its main side effect is fever. Unfortunately, the fever can be quite severe, to the point where people come to the hospital and may be hospitalized for that fever. There are now algorithms and new strategies on how to mitigate fever in patients taking BRAF inhibitors. But it’s a significant complication. That being said, the grade 4 or 5 toxicities is only 5%. And the nice thing about BRAF inhibitors is the minute you stop it, the toxicity gets reversed. So very reversible toxicities. Ironically, another toxicity of BRAF inhibitors is getting brand new thin melanomas. So you do need a dermatologist and squamous cell carcinomas and other little skin cancers. You do you need a dermatologist checking your skin if you’re on BRAF inhibitors. And it can have effects on heart and eyes and so they also do see ophthalmologists on a regular basis. The BRAF studies did show benefit in all stage threes. So three A, B and C. It did not include intransit disease, but it did include stage three A, B and C. But you had to have at least a one millimeter deposit in your sentinel node. If it was less than that, then you’re not likely going to get adjuvant therapy. And some people argue that maybe the three A’s, because they have such a good outcome don’t need adjuvant therapy and observation alone is okay. But the minute you’re a 3B or 3C, you’re probably going to get stronger recommendations for adjuvant therapy. If you are BRAF positive, you can still get immunotherapy. So you kind of have to choose between BRAF and immunotherapy. Immunotherapy is an IV therapy, if it’s nivo, you’re getting it once every two weeks. If it’s pembro, you’re getting it once every three weeks. It has a great toxicity profile, once again, four to 5%, for toxicity. And actually a little bit easier tolerated by patients then BRAF inhibitors. I guess the issue with immune therapy is that some of the side effects are basically autoimmune side effects. So colitis, hypophysitis, arthritis. The issue is the endocrine type toxicities. The endocrine type toxicities, like thyroiditis, and hypothyroidism, and diabetes and hypophysitis, if you do get them, it can be permanent and will likely be permanent. So you really have you know, it’s there’s a huge trade off there. So, you know, especially the adjuvant setting, you’re not surely going to die of your melanoma. We’re just trying to mitigate the risk. So you want a toxicity profile that’s reasonable, you know. But some patients have become diabetics and hypothyroids and now they have to live on, you know, all that medication for the rest of their life. Because that toxicity is not reversible. The colitis and the other types of toxicities tend to be reversible with treatment, with steroids and all the rest of it. So there is that option. If you’re BRAF negative, of course there is no option and then you just go to immunotherapy. I think how they choose is based on comorbidity, age. If you already have an autoimmune disease, they’re not going to be keen to give immunotherapy so they’re going to lean towards BRAF MEK inhibitors. At that stage or in COVID, they’ve been leaning way more towards BRAF MEK inhibitors because they’re oral. And so you don’t have patients needing to come for IV therapy to the hospital. So it’s definitely being used more often. Another very interesting concept is that when these clinical trials were done, everyone had a completion node dissection. So they’d have their sentinel node, if it was positive, they would get a completion node dissection, you’d have full staging and then you would decide about immunotherapy or BRAF therapy. The immunotherapy trials, so the pembro trial included 3A B and C. The nivo trial however, was slightly higher risk patients. So it was three B and above and included resected oligometastatic, stage four patients. Um, but I guess, you know, it is kind of tricky to know what to give a BRAF positive patient because they can have both. Really they get to choose. But if you have an autoimmune disease, they’re probably going to not give you the immunotherapy because you might just reactivate that or stimulate that a bit too much. There is a belief that maybe the sustainability of response is higher with immunotherapy. And so sometimes that’s why they lean towards that but there’s no evidence of that right now. In the metastatic setting we see that immunotherapy has a more sustainable response than BRAF MEK inhibitors, unless you have very minimal disease. So, BRAF and MEK have shown sustainable response if you have less than three sites of metastatic spots and a normal LDH. There’s that LDH again, it really is a key factor in deciding prognosis. The other interesting thing that they found is because we don’t dissect anymore, because the MSLT-2 trial came out and now we don’t dissect anymore. So people are kind of getting adjuvant therapy based on the sentinel node alone. So it’s not full staging. But that’s fine, because in general, as long as you have one node positive, you can get adjuvant therapy. But what they’ve noticed is that there’s now local recurrences in the nodal basin that are happening. And that tends to happen more often on patients getting immunotherapy in the adjuvant setting than patients on BRAF MEK inhibitors in the adjuvant setting. And, you know, it’s interesting, we don’t really know why. One of the things that I have noticed, anecdotally, like I don’t have much evidence, but anecdotally, patients on immunotherapy that are responding and doing really, really well, interestingly, will respond in the lung and the liver and everything is disappearing. And the only thing that won’t go away is the damn lymph node in the groin. Or the silly in transit disease on the person’s back. So it seems as though maybe immunotherapy doesn’t seem to penetrate the lymphatic system, as well as it penetrates the bloodstream. And so often, I’m still operating on these patients, because everything will have gone away, except for their nodal disease. And so they’ll be like, but I want them to be NED, so can you go take out the nodal disease? So you’re still operating on nodes, even though we try to stop operating on nodes. We can’t. Because they’re always there. And so it is a very interesting phenomenon. I don’t see that as much with BRAF and MEK patient. Those tend to melt. Like they tend to go away. So there might be, you know, there might be a little mechanism there that we’re not fully understanding. But anyway, I think I talked a lot. But that’s the general gist of adjuvant therapy. It’s a great new thing that we can offer patients. And I think it’s good that you know, the other thing we don’t know is because in the metastatic setting, these drugs are so effective, do you really need to give it now? And that’s what I tell patients, I say that if after the discussion about adjuvant therapy, they don’t feel keen, it’s not the end of the world. And this is why it’s different. I think it’s really different. In most cancers, let’s take away colorectal cancer, because that’s different. But let’s say in breast cancer. In breast cancer, adjuvant therapy’s pretty important. Because if you metastasize, there’s nothing really I can do. I’m going to give you some palliative chemo, but I’m not going to cure you, right? Or I’m going to give you some palliative hormone therapy, but I’m not going to cure you. In melanoma, if you become metastatic, and I give you immunotherapy, and you’re the 50% that responds, you can live like that for 10 years. And I’m not calling it a cure, but man, it’s pretty close. So, you know, if you don’t take it in the adjuvant setting, it’s not the end of the world, because maybe it’ll work in the metastasis setting. And maybe, just maybe, and this is just me theorizing again, maybe for BRAF MEK, when volume disease is very high, like in the metastatic setting, it’ll work for a while, but resistance will develop and then people recur. But, you know, in the adjuvant setting where disease volume is low, maybe that’s where BRAF MEK is gonna work best in immunotherapy. When you think about it, you need to have the antigen presented for the T cell to recognize it. Post surgery, there can’t be that many antigens around. Like, what’s being presented to the T cell? The theoretical cell in the bloodstream, I guess. But it’s not a lot of volume of disease. And so maybe for immunotherapy, having more disease, like in a metastatic setting makes more sense and it might be more effective. So maybe it’s that BRAF MEK is better in the adjuvant setting and immunotherapy is better in the metastatic setting. But who knows, this is just me, after seeing a lot of patients. Very anecdotal. Some evidence about this, some discussion about this. But I do think it’s fascinating, interesting and very curious to see what the next step is to come in adjuvant therapy because there’s a lot more being evaluated.
Ameer Farooq 1:04:49
It really is such a fascinating time to be a surgeon in so many different areas. And I think melanoma is emblematic of that. You know, like you said, it’s sort of like, being in the surgical role and in treating the disease, it’s not going away, it’s just finding different things where the surgeon still needs to be involved in. And really having an understanding of all the whole treatment spectrum and all the different therapies is so important now. I think as a surgical oncologist, that’s where the extra training that you and other surgical oncologists have done is so important.
Carolyn Nessim 1:05:25
And I think that’s great, because I mean, honestly, like I probably every second day will get a text from one of my medical oncology colleagues. They say, have time to chat? Because they’re just so keen, because their drugs are finally effective. Often it requires still a combination. And I have a lot of metastatic patients, right? Because they’re like, okay, this is what we’re gonna do. He’s responding to Pembro, but he has these in transits, and I can’t get rid of them. So you’re going to aisle two while I give pembro, and we’re gonna get rid of this. So it is a lot of collaboration. And it’s working quite well. We have some patients that maybe we’ll do a neoadjuvant approach, because let’s say they’re all ego metastatic. They have two sites of disease, or two sites and an in transit. So technically, fully respectable. But you could, if there BRAF positive, you can give them some BRAF therapy, shrink everything down. And then the surgeon takes it all out. And then they watch and wait. So there’s a lot of different things like that, that have been happening recently. Or for the example that I gave before. Everything’s melting away, except for this small bowel metastases. Can you go and take out the small bowel? Well, sure, I’ll go take out just that one spot, because everything else is going away, except for that one spot. And so those kinds of scenarios are happening more and more. And it’s making my job like really fun, and interesting and challenging. But yeah, it’s definitely a very different approach than just doing your standard wide local sentinel node biopsy surgery.
Ameer Farooq 1:07:07
In closing, I wanted to highlight a talk that you gave for the CAGS meet week talking about disparities in outcomes for melanoma patients. It was a fascinating talk. I was hoping you could briefly give us a synopsis of what you talked about and sort of what you found.
Carolyn Nessim 1:07:26
So we looked at our LIHN. So we’re really just Eastern Ontario. So everybody that drains to our Eastern Ontario in the Ottawa Hospital. And we try to see if socio economic status had an effect on overall survival, diagnosis of disease, the receipt of adjuvant therapy, and how often people are on clinical trials. And if SES had an impact on that. Ultimately, role studies on socioeconomic status for melanoma have shown similar trends. And whether it was American, European, and now Canadian, it doesn’t seem to actually be very different, even though we have a universal health care system, which I thought was very interesting. So patients of lower SES have a lower incidence of melanoma. And there is some theorizing that that’s maybe because they just don’t go to sunny destinations that often because they don’t have the money to go to sunny destinations that often. But when they are diagnosed with melanoma, they tend to be diagnosed at a later stage. And they tend to have a worse overall survival, likely because they’re diagnosed at a later stage because what we saw was that it’s not that they’re not getting the same treatment. So interestingly, even if they’re lower SES, they’re somehow still getting offered adjuvant therapy, still getting offered clinical trials, and still accepting adjuvant therapy. So I don’t think it’s because they’re not accessing the care. So that was a really interesting point that we saw. They often actually got more BRAF and MEK inhibitors, which is oral medication, because the one thing we did see are the people that are lower SES are the ones that live the furthest away from the cancer center. And they lived on average, I think it was like 72 kilometers away or something like that. Whereas the highest decius subgroup lived 20 kilometers away from the cancer center. And so distance seem to keep coming back even in our multivariable analysis that living far away, seems to have an impact on these patients. And so they also had a higher stage, just like it’s been seen in other research, and they also present with more advanced disease. But once they’re diagnosed, it looked like they were actually quite comparative to their higher SES cohorts. So we’re not doing so badly in our region, in the sense that lower SES patients are getting adjuvant therapy, they are being offered clinical trials, and they’re actually accepting it, and they’re taking it. But they still have a worse overall survival, most likely, because they just have worse tumors, they’re just being diagnosed later. And so I think what it might be is that maybe they need more access to family care practitioners, or dermatologists or even just self awareness. Like we were talking before awareness about risk factors. Because especially in the area of Eastern Ontario, a lot of those patients are farmers, there’s a lot of farmers in Ottawa, there’s a lot of farmers in our region, they probably live outside in the sun without a shirt on all the time. Right. So it’s really just giving them the awareness that maybe that’s not the best practice, I know, it can get hot, but like maybe there’s other ways to get around that. But, you know, it really is that they’re just being diagnosed later than the higher SES patients. And so what can we do to try to expedite their diagnosis, whether it’s education and awareness, whether it’s more access to primary care practitioners and dermatologists so that they can go see someone in a reasonable amount of time when they see something on their skin? That’s a little bit worse than instead of just kind of waiting for it to grow, and then saying, oh, god, that’s really bad. Now, I better show up to the doctor’s office. So I think that was a very interesting highlight of our study where we went a step further to look at treatment. And the treatment differences were actually not that different
Ameer Farooq 1:11:46
In closing, one of the questions we always ask our guests is, if you could go back and give yourself advice as a trainee, especially in the light of such a varied and changing practice, like you have, what would that advice be?
Carolyn Nessim 1:12:00
I think, you know, stick to what you really love to do. And I know that’s hard in our environment right now with a limited number of jobs. But I do think you have to be somewhat passionate about the topic that you do. I remember when I first interviewed in surgical oncology as a resident and they asked me, What do you like doing? And I was like, well, I want to do melanoma sarcoma and gastric cancer. And they kind of said, what are you crazy? Those are the three most rare cancers in Canada! There’s no such a job. And I said, well, there could be a job and and they said, well sarcoma, really? And I said well that’s what I love to do. And I think that if you convince someone, I mean, someone that actually said how was melanoma and sarcoma similar, that’s not even similar. And I said sure it is. It’s soft tissue tumors that sit on major vessels and nerves. And I have to dissect the major vessel and the nerve from the tumor. Whether that’s in the armpit, the groin, or the belly, in my mind, that’s very similar. And they looked at me and they said, wow this girl has practiced that answer. But I think that, you know, if you do have a passion, and you can show that you really can bring something along, and you really have a vision of what you want to do. I think that’s where people get engaged. We just share your vision. We all have one, we all know what we want. We all know what we see ourselves doing or what we want to be doing. But if you share that vision, you’re gonna find someone who’s going to be like, Ooh, I like that vision. I’m going to go down her path. So I think you know, obviously study. You know, be good people. I think we all are in general surgery. We’re like the nicest doctors in the hospital to be honest. But yeah, that’s what I would suggest. Try to picture…you know Dr. Auer always said – she’s one of my colleagues and has become slowly a mentor for me – what is your why? Why do you do what you do? Find the why. If you can find the why, you will really move towards that in your whole career. And it really shapes what you do and why you do it. And so finding your why, whether it’s for research, whether it’s for your clinical work, whether it’s for your personal life, like I really think it’s a great concept. Find your why. Because once you find that you kind of know where to go next.
Ameer Farooq 1:14:58
You’ve been listening to Cold Steel, the official podcast of the Canadian Journal of Surgery. If you’ve liked what you’ve been listening to, please leave us a review on iTunes. We’d love to hear your comments and feedback. So feel free to email us at email@example.com or connect with us on Twitter @CanJSurg. Thanks again.