Welcome to First Incision, the podcast about preparing for the General Surgery Fellowship exam. I'm your host, Amanda Nikolic. So let's get started with our team timeout. Our patient today is the colorectal module from the general surgical curriculum. And our patient today, or the topic we are going to be covering, is ulcerative colitis. Ulcerative colitis like most of you will already know is a type of inflammatory bowel disease. The definition of ulcerative colitis is an idiopathic
relapsing inflammatory bowel disease involving the mucosa and the lamina propria. I'll start off just by talking about a few interesting facts about ulcerative colitis to provide a little bit of background.
The cause of this condition is not known. Some of the theories include the hygiene hypothesis, which is the theory that exposure to organisms early in life... provide a normal response to infections or pathogens that are encountered later in life versus really clean environments early in life can cause an aberrant response when exposed later in life.
In addition to this, there may be a genetic contributing factor as identical twins have a 50% chance of having ulcerative colitis if one of the twins is affected and 3% in fraternal twins. Patients are affected in two peaks, so in their 20 to 40-year-old bracket, and then again in their 60 to 70-year-old bracket is the highest rates of incidence or presentations with this disease.
And it's important to be aware that the risk of cancer in these patients will increase after 10 years. And by 30 years, 20% of patients with ulcerative colitis will develop a cancer. 25 to 30% of ulcerative colitis patients will require surgical intervention for their disease, which is where we become involved. Indications for surgery could include intractable disease.
not responding to medical therapy, malignant transformation, fulminant colitis, or side effects of medical management. Risk factors for ulcerative colitis, as I've mentioned, include family history. They also include being in those age brackets with higher incidence of ulcerative colitis, as well as your race or ethnicity with Caucasians having the highest risk of the disease and Ashkenazi Jewish.
descendants also having higher risk of the disease. Interestingly, cigarette smoking is a protective factor for ulcerative colitis. However, I would not recommend patients to take up smoking to control disease. So how do patients with ulcerative colitis present? Ulcerative colitis, the typical picture is that the rectum will nearly always be involved and then there will be proximal sort of retrograde spread of inflammation from the rectum.
This inflammation is typically continuous compared with Crohn's disease where there's typically skip lesions. Patients will present with symptoms that correlate with the severity of their disease and inflammation. Patients can present with bloody diarrhea, urgency and tenesmus, abdominal pain, which can be colicky, constipation due to incomplete evacuation of the bowels.
And hemorrhage can occur, but usually significant hemorrhage is uncommon. It's usually bloody stools. Systemically, they can have symptoms such as weight loss, nausea and vomiting, and abdominal distension. On examination, you may find signs that are related to the abdominal disease and the severity of their abdominal disease, or you may find extraintestinal manifestations.
So talking first about abdominal features of ulcerative colitis, patients, if they have a high amount of inflammation, may be febrile, may be tachycardic. They can have abdominal pain and tenderness. They can have abdominal distension and signs of toxic megacolon or perforation. 50% of patients will present with fulminant disease on their initial presentation with ulcerative colitis. So this is toxic megacolon and potentially evidence of perforation.
In terms of extraintestinal manifestations, about 20% of patients with ulcerative colitis will have some of these. They can include musculoskeletal manifestations. So this can include peripheral arthropathies, which typically respond to treatment, and spondylitis, which is usually unresponsive to treatment. Patients can have hepatobiliary manifestations. In ulcerative colitis, this is usually primary sclerosing cholangitis, PSC, which is an idiopathic, chronic...
progressive fibrotic disorder, which manifests as stricturing inflammation and fibrosis of both the intra and extrahepatic bile ducts. And it's important to know that... PSC plus ulcerative colitis is associated with an increased risk of primary liver malignancy by five times. And this can include cholangiocarcinoma, intrahepatic or extrahepatic.
There can be dermatological manifestations, and this includes erythema nodosum, which are inflamed red nodules, usually on the anterior surface of the lower extremities, and these will usually improve with treatment. And the other type of dermatological manifestation is pyoderma gangrenosum. And these are...
pustules or plaques that will typically break down into ulcerative areas. And these can occur anywhere, typically on the legs, but they're like, especially in spot questions in the exam, to show you peristomal pyodermic angrenosum. And this is really difficult to manage and usually doesn't improve with treatment of the ulcerative colitis. These patients can have thromboembolic manifestations.
which include an increased risk of DVT and PE from the general population, as well as increased risk of cerebral venous and dural sinus thrombosis, which can cause strokes. And lastly, they can have ophthalmological manifestations. This includes episcleritis, uveitis, and scleritis. And uveitis and scleritis can both... cause visual impairment or blindness. So they're important to pick up early and require aggressive treatment.
Next, we'll move on to the diagnosis and workup of ulcerative colitis. Unfortunately, there's no single test which is going to give you a clear diagnosis of ulcerative colitis. It really is looking at the whole picture, which combines the clinical picture. radiological workup, endoscopy findings and histopathological findings. So we'll break it up into blood tests, microbiology, imaging, endoscopy and pathology.
So blood tests for ulcerative colitis, you can do a P-Anker test, which is an antineutrophil cytoplasmic antibodies. And this is a... blood test which helps to distinguish between Crohn's disease and ulcerative colitis as it's much more commonly elevated in UC than Crohn's. Can also send markers of inflammation, such as white cell count, CRP and ESR. But if a patient's well treated and has minimal inflammation, these may be normal. Other blood tests that are important include a...
Full blood count. If these patients are having bloody diarrhea, then they can become anemic. And also liver function tests as a, I guess, basic screening for PSC. Not technically in the blood test group, but I'll mention it here as a fecal calprotectin level. Fecal calprotectin is basically a test looking for the protein calprotectin which is found in neutrophils. So if this is elevated then it indicates that neutrophils have migrated into the lumen of the bowel which correlates with...
disease severity or activity. Another stool test you should do is to send the fecal sample for microbiology. You want to rule out other pathologies or organisms that can mimic
inflammatory bowel disease. So this includes clostridium difficile, E. coli, especially serotype 0157H7, salmonella, shigella campylobacter and entamoeba as well as over cysts and parasites should be sent these can also contribute to flares of ulcerative colitis especially c difficile and the other thing is in immunocompromised patients who are undergoing treatment for inflammatory bowel disease
who present with a flare you always have to think about and rule out, CMV as well. The next investigation is endoscopy. And this really is one of the key factors in diagnosis of ulcerative colitis. It provides you with direct visualization and provides you the opportunity to perform biopsies. It enables you to evaluate the proximal extent of disease.
To determine the severity, and we'll talk about severity scores for the endoscopic appearance, it can help you differentiate between ulcerative colitis and Crohn's disease as they do have different endoscopic appearances. And it also enables you to monitor response to medical therapies. Some nonspecific features you might see in ulcerative colitis, in mild disease that may just be mucosal edema or erythema, an abnormal mucosal vascular pattern, and a loss of the vascular pattern.
In moderate disease, there may be superficial erosions or ulcers and contact bleeding. In severe disease, you can find pseudopolyps and cobblestoning due to inflamed and regenerating mucosa. In patients with chronic ulcerative colitis, you can get that featureless microcolon with mucosal atrophy, muscular hypertrophy, decreased diameter of the lumen and loss of the haustral folds.
The main scoring system I came across for looking at the severity of disease in ulcerative colitis is the Mayo score. And this is a score between zero and three. with zero being normal mucosa with no friability or granularity and an intact vascular pattern. A score of one is mild disease with erythema.
diminished or absent vascular markings, and mild granularity. A score of two is moderate disease with erythema, absent vascular markings, granularity, and contact bleeding, but without any ulcerations. And severe disease, which is a score of three, is marked erythema, no vascular markings, friable, spontaneous bleeding, and ulcerations. I definitely suggest you have a look at some pictures of that.
grading system, as well as what pseudopolyps look like, and also a picture of chronic features with that featureless colon, because I've definitely heard of those coming up in spot questions before. Moving on now to imaging. Patients may, when they present with abdominal pain and distension, have an abdominal x-ray that's performed. This may demonstrate a toxic megacolon with dilation of the transverse colon more than six centimetres. And this is a surgical emergency with perforation imminent.
A CT scan may also be performed, which isn't great for looking at UC. You may see some bowel wall thickening or inflammatory stranding, but this doesn't tell you the diagnosis. It just tells you that there's inflammation. But it also could be helpful if you're looking for potential complications of ulcerative colitis, such as megacolon or perforation or even strictures. In terms of histopathology...
Once you've done an endoscopy and taken multiple biopsies, there are some features on biopsy that can be indicative of ulcerative colitis. Things you might see include mucosal inflammation. There's goblet cell depletion, which compared to Crohn's where that's usually maintained, that's an important differentiating factor. There can be cryptofliebukun distortion, vascular congestion.
neutrophils in the epithelium of the crypts which form crypt abscesses, infiltration of the lamina propria with neutrophils, plasma cells and lymphocytes. mucosal destruction with ulcers and atrophy, and pseudopolyps, which you can see granulation tissue over the exposed muscularis propria. Because remember that ulcerative colitis is just a mucosal disease. So the underlying muscularis should be intact and all of the disease should be limited to the mucosa.
I'll also note here that it's important to take multiple biopsies and in different segments of the colon and the ilium when you're working up a patient. to try and help differentiate between Crohn's and UC or some of the other differential diagnoses of an inflammatory colitis. It can still be difficult, even with biopsies, to be able to determine...
what the diagnosis is. And sometimes you'll get a diagnosis of indeterminate colitis based on all of this, which I'll briefly mention at the end of the episode. But the key here is to take multiple biopsies. As I mentioned at the start of this section, diagnosis of UC can be very difficult. I don't think we'll be expected to
make a diagnosis in our exam, I think it's important to know some of the key differentiating features or key features of UC. So if you're given some of these clues that you know to talk about ulcerative colitis in your list of differentials. I think that diagnosis in general is usually done by the gastroenterologists and we're more involved in the workup and then surgical management of this disease.
And that brings us to our next section of this episode, which is to talk about management of ulcerative colitis. First, I'll talk a little bit about assessing disease severity and activity because that really will guide what... different treatment modalities will be suggested. And then I'll go into the medical and surgical management of ulcerative colitis.
So first talking about disease activity assessment, there's a few different... tools that I've come across for assessing the severity of disease and ulcerative colitis, I'm going to briefly mention the Montreal classification and true love and wits criteria. The Montreal classification combines the extent of disease, which they classify as E, and the severity of disease, which is classified as S. So extent of disease includes E1, E2, and E3.
E1 is proctitis only. E2 is left-sided distal colitis, so only distal to the splenic flexure. And E3 is extensive colitis, which includes proximal to the splenic flexure. The severity assessment is S0, 1, 2, and 3. S0 is clinical remission, and these are asymptomatic patients. S1 is mild ulcerative colitis, and these are patients who have less than or equal to four bowel actions a day with no...
with or without blood, sorry, and without any evidence of any systemic illness and also normal inflammatory markers. S2 is moderate disease with passage of more than four stools a day but minimal signs of systemic. toxicity and s3 is severe where there's at least six bloody stools a day and they're systemic toxicities. This includes a pulse rate of more than 90, temperature of at least 37.5, a hemoglobin of less than 105, and an ESR of at least 30.
The true love and wits criteria looks at either mild or severe. Mild being less than four stools a day with no macroscopic blood and no systemic toxicity. And severe is more than six. bloody bowel movements a day, systemic toxicity, anemia, and raised ESR. So they definitely overlap with the Montreal classification. But it's good to know about those. You'll come across those, especially if a gastroenterologist is talking to you about ulcerative colitis. So treatment is...
pretty much defined by the extent of disease and severity of disease. The goal of treatment in general is to try to induce and promote mucosal healing. But in addition to that, we get involved when you have refractory disease or disease with complications such as perforation or toxic megacolon. Before I go into...
what treatments you use for different disease severity, I want to just briefly go through the different types of drugs or treatments available for ulcerative colitis. This will overlap a little bit with Crohn's as well. So the first group to talk about are the aminosalicylates. You might see these drugs written as 5-ASA, which is 5-aminosalicylic acid.
and it's often given as mesalazine or sulfasalazine, which are the trade names. Mesalazine is just 5-ASA, and sulfasalazine is both sulfapyridine and 5-ASA. The amino salicylates are believed to work by inhibiting the production of inflammatory mediators from both the cyclooxygenase and lipoxygenase pathways.
These preparations are more useful in ulcerative colitis than in Crohn's disease. And they can be given orally or rectally. So if you have a disease that's limited to the rectum, then it can be given as a topical enema. These are really first line in mild to moderate forms of UC and even in Crohn's disease. The next group of drugs to talk about are corticosteroids.
We all know about steroids and their mechanism of action is to inhibit the transcription and development of pro-inflammatory mediators. and also through inhibition of phospholipase A2, which is also responsible for the production of numerous inflammatory mediators. Steroids are used for both UC and Crohn's disease, usually in induction of treatment or for severe disease to induce a mucosal healing.
They should definitely be avoided in the long term due to obvious complications of steroids. They can also be used in acute flares as well. Options include oral, such as enteric-coated budesonide, which can be good for ileal or ileocolonic Crohn's disease, or they can be given, obviously, intravenously if required. And potential complications of steroids in the longer term include weight gain, osteonecrosis, increased susceptibility to infection, acne, facial hair, hypertension.
sleep and mood disturbance, cataracts and osteoporosis. The next group of drugs to talk about are immunomodulators or thiopurines. This includes azathioprine and 6-mecaptopurine. These drugs have good... immunomodulatory effects and control of disease, but they do take two to three months to start working. So these aren't good for induction, but are good for maintenance of remission.
They are both purine analogs, and that's why they're called thiopurines, and their mechanism of activity is to inhibit cell proliferation and suppress cell-mediated events by inhibiting the activity of cytotoxic. T-cells and natural killer cells. An important thing to know about these drugs is that you have to test the patient for TPMT, thiopurine methyltransferase.
prior to starting the drug. Because if the patients don't have this metabolite, TPMT, then they won't break down the drugs and they can get bone marrow suppression. The main complications of thiopurines, azathioprine and 6-MP, is bone myrospression, as I mentioned, pancreatitis, which can occur in between 3% to 15% of patients. hepatitis, fevers and rashes. The next drug to talk about is methotrexate. 6-MP and azathioprine are used...
preferentially over methotrexate. This isn't commonly used, but I'll just briefly mention it. Methotrexate is a folic acid antagonist. Its mechanism of action in inflammatory disease seems to be quite complex, but in general, it inhibits T cell activation and suppression of the intracellular adhesion molecule expression by T cells. It downregulates B cells and inhibits methyltransferase, which leads to deactivation of enzyme activity that is important to immune cell function.
Potential side effects of this disease include hepatotoxicity, ulcerative stomatitis, bone marrow suppression, fatigue. pneumonitis and rarely pulmonary fibrosis and kidney failure. It's also teratogenic and is not advised for people that are considering pregnancy. The next group to talk about are biologic agents. So this includes TNF-alpha inhibitors, anti-integrin therapy, and MABs against different cytokines.
These drugs can be used for moderate to severe inflammatory bowel disease where other treatments have been insufficient and also indicated for complicated perianal Crohn's disease. Basically, they are monoclonal antibodies which target mediators of the inflammatory response. Going into a little bit more detail.
There's two types of tumor necrosis factor alpha inhibitors or TNF alpha inhibitors. This includes infliximab, the brand name is Remicade, which is given as an infusion, and adalimumab, which is... known as Humira, which is given as a subcutaneous injection. And you can measure serum anti-TNF drug levels and anti-drug antibodies to determine your dosing. The anti-integrin therapy...
There's one of these which is called vedalizumab, and this prevents lymphocyte migration into intestinal tissue. And this has a slower onset than the anti-TNF treatments. And the last type, which is the monoclonal antibodies against cytokines, especially interleukin-12 and interleukin-23, include ustekinumab. And this is good for psoriasis. So if patients also have, especially patients with Crohn's who have an extra intestinal manifestation of psoriasis, they could use this drug.
Complications of these drugs include infection, they have increased risk of opportunistic infections, the development of malignancies and lymphomas. and also immunogenicity. So you can actually get the development of psoriasis or other paradoxical immune-related disorders on some of these drugs. And we've got two types to go. Last sort of immunomodulatory type are the calcineurin inhibitors. This includes cyclosporine.
and tacrolimus. These are pretty rarely used from what I've read, but sometimes are used as rescue therapy when there's a really severe episode that's not responding to high dose steroids in hospital. and there's pretty limited evidence for their use. And then the last group to briefly mention are antibiotics, and this includes metronidazole and ciprofloxacin. There's pretty low-quality data, but there is some evidence that they can induce...
remission in luminal Crohn's and ulcerative colitis. So there's a lot of information, but I'll just go into a bit of detail about different disease severity presentations in ulcerative colitis and what drug... regimes or approaches you might use. So for patients with disease limited to the rectum, especially if it's mild, you can use topical therapies and these can be
foam, enema or suppository preparations of some of these drugs, especially mesalazine. And these can show an effect in four to six weeks. You can also give steroids topically as enemas. You can give, obviously, mesalazine orally if patients won't use enemas or fail to respond to the topical therapy. For mild to moderate disease, especially if it extends beyond the reach of topical... then you can give oral sulfasalazine or oral steroids if it's not responding to the sulfasalazine.
If this isn't working or as you're weaning the steroids, they are getting disease recurrence or worsening disease, then this is when you would consider a thiopurine such as 6-MP and azathioprine. But these do take three days. to six months to have maximal effect. And if, again, you're not having any response to these treatments, then that's when you'd be considering monoclonal antibody type treatments such as infliximab.
And for patients who present with severe fulminant colitis, these patients require aggressive treatment. So you'd be giving IV steroids, broad-spectrum antibiotics. You'd be considering IV cyclosporine. If patients aren't responding to treatment after three to five days, then you'd be thinking about emergency infliximab. And again, if there's no response to maximal medical therapy or the patient's deteriorating with toxicity, then that's when you'd be considering surgery.
That does take us very nicely into a discussion about surgery. But before I do that, I just want to take a little bit of a segue into toxic megacolon. This is relevant when talking about ulcerative colitis, but ulcerative colitis is not the only cause of toxic megacolon. So the definition of toxic megacolon is dilation of the colon with more than 6cm size of the transverse colon associated with signs of systemic toxicity.
So the underlying etiology can either be inflammatory, infectious, ischemic, related to cancer or medications. In terms of inflammatory, ulcerative colitis is the second most common cause of toxic megacolon. Other inflammatory conditions include Crohn's, although this is much rarer, and Bechet's disease, which is a type of systemic vasculitis. Infectious causes, the most common cause of...
Toxic megacolon is Clostridium difficile infection. Other potential infectious causes of toxic megacolon include Campylobacter, CMV, E. coli, especially that O157H7 serotype, salmonella, shigella, rotavirus, entamoeba, and yersinia. Ischemic colitis is another potential cause of a toxic megacolon. It can be cancer-related due to an obstructing colorectal cancer, chemotherapy, colonic lymphoma, and in stem cell transplant.
And medications such as antibiotics with subsequent C. difficile infection can cause it, as well as some anticholinergics and antidiarrheal medications. The pathophysiology or cause of toxic megacolon is not well known. There's a thought that the colonic inflammation and diminished smooth muscle contractility can...
cause this and that maybe this process involves nitric oxide. The hallmark microscopically is inflammation that extends beyond the mucosa into the smooth muscle layers and the serosa of the bowel. And the thought is that this then paralyzes the smooth muscle and leads to dilatation. And as the inflammatory process continues and the smooth muscle dilates, that you then get inflammation and local inflammatory mediators.
neutrophils invade and these secrete proteolytic enzymes and other inflammatory mediators. And this then subsequently leads to that systemic inflammatory response and systemic toxicity. And how do patients with acute toxic megacolon present? So they'll present acutely with severe bloody diarrhea and abdominal pain.
They'll be systemically toxic, as I've mentioned, can also have anorexia, malaise, and abdominal distension. The diagnosis is a combination of history, examination, bloods, imaging and sometimes endoscopy, although this is controversial. On history, you want to be asking questions that help you screen for a source or a cause or underlying pathology contributing to their toxic megacolon.
On examination, you're looking for signs of toxicity. So this would include tachycardia, heart rate more than 120, fever more than 38.5, hypotension, as well as abdominal signs such as peritonitis. abdominal distension, reduced bowel sounds, but also important to remember that an abdominal examination may not be reliable in a patient who is immunosuppressed or immunocompromised.
Blood tests are relevant looking for signs of inflammation. So this is a full blood count looking at the white cell count. a CRP or ESR looking for systemic inflammation they may be anemic because of the bloody diarrhea and you also want to be looking at their renal function and lactate as well to help with your clinical
picture. On imaging, you would potentially do an abdominal x-ray to start. This may show a dilated colon with a transverse colon more than six centimetres, as I've mentioned. You may see multiple colonic air fluid levels, blunting or loss of the colonic haustra, and potentially small bowel distension. If this is already perforated, you may also see free gas.
On CT, again, you'll see that colonic distension. An abnormal haustral pattern, you may see pseudopolyps. It's worth looking at a picture of pseudopolyps on CT. Again, there may be small bowel distension and complications such as a perforation or abscess. Endoscopy can also be used, but this is a little controversial as some say it shouldn't be done in the setting of inflammation. A limited sigmoidoscopy without bowel prep.
may be helpful in differentiating the cause of the disease, such as if there's pseudomembranes, this may diagnose C. difficile. In ulcerative colitis, the rectum is always diseased. And you may be able to do a biopsy to rule out CMV or amoebic colitis. But you need to be very careful. Use minimal insufflation as colon diseased in this way can be very prone to... There's a few different diagnostic criteria which include looking at evidence of systemic toxicity.
as well as colonic dilatation with more than six centimetres of the transverse colon. So one of the diagnostic criteria I found that I thought was good was having evidence of colonic dilatation on radiology. plus any three of the following, fever, tachycardia, leukocytosis or anemia, and any one of the following, dehydration, altered GCS, electrolite abnormalities or hypotension.
Once a diagnosis of toxic megacolon is made, then obviously prompt treatment is required. The goals of treatment are using a multidisciplinary team to try and
identify and treat the underlying disorder, medically stabilize the patient, and prevent complications. Treatment includes initial resuscitation as per the CRISPR algorithm, close monitoring, for early identification of any deterioration, you want to be giving the patient IV, rehydration, monitoring and replacing their electrolytes, monitoring their urine output.
Patients may have a daily ABDO x-ray to monitor distension, and it's a little controversial, but often these patients will be placed near by mouth, especially in the initial stages. Patients should have DVT prophylaxis. and intravenous antibiotics to reduce the risk of bacterial translocation. Again, this is slightly controversial but we would definitely do this in my institution.
And it's important to consider if the patient has C. difficile, that they're being treated with metronidazole or vancomycin, and if a patient has a CMV activation, that they're being given IV ganciclovir. Medical management can include IV hydrocortisone as well, which should be started on the diagnosis of toxic megacolon. But if an infectious cause is found, it can subsequently be ceased.
Indications for surgery in the management of toxic megacolon include free perforation, generalized peritonitis, uncontrolled colonic hemorrhage, shock, or clinical deterioration despite optimal medical management. And if there's no improvement after 48 to 96 hours of medical therapy, that may also be an indication to operate. So moving back onto ulcerative colitis, we'll get back on track. Surgery and ulcerative colitis.
The indications for surgery and ulcerative colitis include toxic megacolon or fulminant colitis, as I've just discussed, as well as refractory bleeding. unresponsiveness to medical treatment, also known as intractable disease, perforation, and the development of a malignancy. To be honest, I find talking about surgery and ulcerative colitis quite complex. There's a number of different things that need to be taken into account with your decision-making about what operation the patient requires.
Some of these include whether or not this is an elective or an emergency setting, the age of the patient and whether or not they're going to be considering family as rectal dissection can impact on their fertility. the severity of the disease in the rectum and then there's also decisions that need to be made around you know whether you're going to do a end ileostomy or whether or not you're going to consider an ileal pouch. Again, I think this decision making around that is quite complex.
What I might do rather than going into it now is get one of my consultants who does a lot of IBD surgery on the podcast and we can talk through the different options with him and have a think about. what the indications would be for the different types of operations. The one topic I will talk about, though, is the emergency situation with a perforation or megacolon, as I feel like this is more straightforward and probably more likely what we would be faced with in an exam scenario.
So in this situation, the patient is very unwell. And so the principles are to remove the disease segment of colon and obviously avoid doing an anastomosis or complex pelvic dissection that... is not going to improve the patient's current situation. So in general you want to perform a subtotal colectomy and an end ileostomy. You want to avoid doing an ileorectal anastomosis or a pouch acutely in a sick patient. And you definitely want to be avoiding doing any rectal or pelvic dissections.
in an emergency setting. And this has been demonstrated to have an increased risk of pelvic abscesses, pelvic organ injury, pelvic nerve injury. And in general, this will allow a specialist to perform a future pelvic dissection and reconstruction more safely in the future. A couple of things that should be kept in mind when performing a subtotal colectomy and endaleostomy for these patients.
is to try to preserve the ileal branches of the ileocolic in order to facilitate a potential pouch reconstruction in the future. to try to avoid unnecessary dissection in the pelvis and the root of the mesentery, as this could make it more difficult for pouch reconstruction later. In terms of what to do with your rectal stump you want to try to leave a long rectal stump. It's helpful to try to bring the rectal stump or distal sigmoid into the inferior portion of the vertical midline.
laparotomy wound and this will mean that if it does blow out that it will blow out through the skin and if it looks really inflamed and unhealthy you can actually actually exteriorize it to make a mucus fistula if you're really that worried that it's going to break down probably not the exam answer but the other option is to over sew it and leave it in the pelvis usually with a long
proline suture so that you can find it again and make sure that you leave drains in the pelvis and potentially even a trans anal drain if the rectum is very diseased. You'd be planning on doing a reconstruction only when the patient has completely recovered. is nutritionally replete, is off their high-dose steroids and immunosuppression, if possible, but also that their rectal disease is as controlled as it can be before you're thinking about doing further surgery.
On to our last topic on ulcerative colitis. I just wanted to briefly talk about the colorectal cancer risk and... what the surveillance should be for colorectal cancer in patients with ulcerative colitis. So the risk factors for the development of colorectal cancer in patients with UC include prolonged duration of inflammation or uncontrolled disease, patients who have continuously active disease or inflammation, severe inflammation, pankylitis,
the presence of a family history of colorectal cancer, and also if they have concomitant PSC, as this is a major risk factor. The incidence of colorectal cancer increases with the duration of time that the patient has had ulcerative colitis. So 2% of patients with UC will develop colorectal cancer after 10 years of disease, 8% by 20 years, and 18% by 30 years.
Patients should start colonoscopic surveillance eight years after the onset of inflammatory bowel disease symptoms or immediately if they also have PSC. And the recommended surveillance colonoscopy interval depends on whether they are in a low, intermediate or high risk category. So patients who have... quiescent disease without any other risk factors, they can have a five yearly colonoscopy. And patients in the intermittent risk category, so these are patients with quiescent disease.
No high-risk features, but history of colorectal cancer in a first-degree relative. They should have a scope every three years. And patients in a high-risk category. So this includes patients with primary sclerosis and cholangitis. ongoing chronic active inflammation, prior colorectal dysplasia, evidence of intestinal damage with strictures, pseudopolyps, or a family history of colorectal cancer at...
less than 50 years old, require a yearly colonoscopy. And there are some sort of precursor lesions that can be found in ulcerative colitis that I'll just briefly go through. So this includes dysplasia-associated lesion or mass, and these are called DALM's or D-A-L-M. And these are visibly raised dysplastic lesions within an area of inflammation.
these have a high risk of progressing to a malignancy. And they can be removed endoscopically completely. And if they are removed completely, then surveilled. But if they're... very sessile. You can't remove it. There's multiple areas. And these patients will need a proctocolectomy due to the high probability of an underlying neoplastic or cancerous lesion.
The other two things to mention are flat low-grade dysplasia and flat high-grade dysplasia. These are lesions that are associated with high risk of development of colorectal cancer. So flat, low-grade dysplasia has a nine-time increased risk of developing a colorectal cancer, and it can also actually skip the step of high-grade dysplasia and just progress directly to colorectal cancer.
It can be unifocal or multifocal. And the options are a little controversial, but they include surveillance, which should initially be six monthly until there's no further areas of abnormality left. And they should be done by an expert endoscopist with experience in IBD surveillance using both high-definition white light and chrome endoscopy.
And this should only be done if it's unifocal, if there's not multifocal disease. If there is multifocal disease, then these patients should have a prophylactic colectomy. And if patients refuse, then they need three-monthly surveillance endoscopy. The next group is flat high-grade dysplasia, and this is associated with a 45%. incidence of colorectal cancer at the time of colectomy. So if flat high-grade dysplasia is seen on biopsies, then a colectomy is mandatory in this group.
And as I've mentioned, endoscopy should be undertaken by a specialist endoscopist. It requires adequate biopsies, so multiple biopsies in multiple areas of the colon. And it's sort of... recommended that there's random biopsies every 10 centimeters. And any lesion that's seen, such as any delms or flat dysplasia, need to also have multiple biopsies taken.
Gosh, when I started this episode, I thought there wouldn't be that much to talk about, but we've managed to fill 45 minutes. Thanks so much for sticking with me. It's nice to know that the content that we're covering in this podcast is relevant with ulcerative colitis being one of the longer written questions in the exam last week. It was a question about a patient with an acute flare.
who had failed steroid management, was on infliximab and you had to talk about what the indications were for surgery, what types of surgery and the implications of these different types of surgery on a young female patient. I also just wanted to do a little shout out. We talked last episode about mentors in surgery and I recently found out that one of the surgeons who...
I consider a mentor, whether he knows that he is or not, has been listening to all of the colorectal episodes for this podcast. When he told me that I was really blown away and really grateful. The good news is he says that I'm not saying anything that's widely off the mark. So it's good to know we've got some quality control and I just wanted to shout out that it does mean a lot to me and I'm really grateful for all of his support over the years.
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!