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(English captions by Andrea Matsumoto from the University of Michigan)
ERCP (Endoscopic retrograde cholangiopancreatography) pictures and we had the pictures of just the
bile ducts and they were trying to figure out where the liver was and it’s a little
tough for me to figure out a way to show that but I did my best.
This is a picture of the anatomy, and this is, in grey, the ERCP scope going down the
bowel just opposite the Ampulla of Vater and then a catheter going up into the bile duct.
So when you see the scope down here and the catheter, the common bile duct is going up
here and then just in the hind of the liver it branches so you have the left ducts and
the right ducts and the gallbladder is in there someplace.
Now I tried to take some of those ERCP pictures and tried to superimpose a liver…sort of.
So here is the ERCP scope coming down, here’s the catheter going in, this is the common
bile duct, here’s the bifurcation at the left and the right, and then the bile duct
is up in here, and here’s the cystic duct with the gallbladder.
This is the other normal one I showed you.
The ERCP scope here, the rest of it’s probably coming over here, the patient is twisted a
little bit to show this better so the catheter is down here, this is the common bile duct,
here’s the bifurcation, the left ducts, the right ducts, here there is no gallbladder.
This is the one with the sclerosing cholangitis.
Here’s the scope, this is the catheter, here’s the common bile duct with all the
dilations and strictures, and in this case the liver lobe should be bigger here and bigger
here, these are the intrahepatic ducts.
I’ll try to get these posted on CTools for you also but I was trying to show you the
relationship here of the liver to where these bile ducts are.
Okay. [Student question: with the ERCP are you trying to avoid getting any of the dye
into the pancreatic ducts?]
She he’s asking about, are we trying to avoid the pancreatic ducts?
It depends on what your goal is.
We were talking about cholestatic liver diseases so we really want to look at the bile duct.
As Michelle Anderson and Grace Elta will tell you later this week, the pancreas is a very
touchy organ and one of the risks of ERCP when we’re messing around the Ampulla or
injecting dye into the pancreatic duct is can we create pancreatitis?
So if, at all possible, you want to avoid the pancreatic duct.
It’s just the two of them come together there and we can't avoid it completely.
Especially for anything having to do with the biliary system, you’re really trying
to look only at that.
But we do inject into the pancreatic duct and you’ll see a number of pictures tomorrow
about that.
Both today and a lecture on Thursday are things that I put together as kind of a miscellaneous
group of GI topics that kind of pick up some common problems that really don't get treated
that well in our other general lectures that are doing more on physiology and the whole
organ.
Actually this talk originally was one of your colleges a number of years ago who in the
post sequence comments said ‘I got all the way through a GI course and I still don't
know what hemorrhoids are.’
I can fix that so we’re going to talk about several different topics today.
Today we’re going to talk a little bit about hiatal hernia, which you’ve heard about,
a little bit more about gas, constipation, some about diverticuli, which I believe you
had something in your pathology section on also, and hemorrhoids.
A hiatal hernia means that the top of the stomach is above the diaphragm through the
hiatus where normally just the esophagus goes.
It’s an anatomic abnormality
Normally you have the lower esophageal sphincter right at about the hiatus of the diaphragm
and there are various ligaments that try to hold that in place along with a little fat.
That really keeps everything in there and helps also keep the lower esophageal sphincter
closed.
When the diaphragm hiatus widens or there is a lot of pressure in the abdomen some of
the stomach will go up into the chest cavity.
That’s a hiatal hernia.
Very common, some of my radiology colleagues say if they push hard enough on the stomach
they can probably create a little bit of a temporary hiatal hernia in just about anybody.
Patients are very proud of the fact I have a hiatal hernia and I tell them well, so do
most other people and it doesn't mean much, don't worry about it.
You can see it endoscopically because here we’ve got the pearly pink of the esophagus
and this is the lower esophageal sphincter but then you’re looking at the pinker rugal
folds of the stomach and there is another indentation there, that’s the edge of the
diaphragm.
You can go down into the stomach and turn around and look back.
Here’s the diaphragm edge, here’s the lower esophageal sphincter, so from there
to there is the hiatal hernia.
The radiologist can see it, they can tell where the diaphragm is, they can see the lower
esophageal sphincter, and here’s this.
So radiologists on various barium studies will comment the patient has a hiatal hernia.
It’s usually benign.
It does make you more predisposed to acid reflux and it's complications because the
lower esophageal sphincter doesn't work as adequately when it’s up in the mid chest
because it’s relationship and the twist and the bend and it’s relationship to some
of the ligaments is different.
So you can get more acid reflux and because the hiatal hernia, because this is trapped
a little bit, acid can sit in that stomach pouch and you can sometimes get gastric ulcers
up there, they’re called Cameron’s lesions, and we will occasionally see those in patients.
That’s about all that a hiatal hernia does.
You are more educating and reassuring your patients.
I wanted to make a few more comments about gas because these are things that patients
will ask all of you about.
Your relatives may ask all of you about it so you need to be prepared with a little information.
Gas is another common, physiologic function of the bowel but it can make people upset
or worried and it’s been the source of many elements of humor.
It’s a normal constituent, it helps cause bowel sounds.
Anything that goes in has to come out, so any air that you air swallow has to come out.
Everybody passes flatus many times a day but most of us are not aware of it, some people
become very aware and they are complaining about what is probably normal gas.
If you infuse gas into the GI tract it actually goes through much faster that liquid and solid,
nobody’s figured that out yet, exactly how but it does.
So how do you get gas in the intestine?
When you air swallow, three quarters of that is nitrogen, 21% oxygen, and you will generate
some CO2 as gastric acid is neutralized in the duodenum.
A lot of that CO2 and a bunch of the oxygen is actually soluble across the small bowel
membrane and gest absorbed and goes out in the lungs but the nitrogen is not.
The nitrogen is going to make it all the way down into the colon.
Plus we’ve already talked about the bacterial fermentation can generate a number of gases
in the colon.
So from carbohydrate you can get methane, carbon dioxide hydrogen gas, proteins and
sulfur containing compounds from things like onions can create hydrogen sulfide, which
is the smelly component, and other sulfur based volatile compounds.
Yes the colon can absorb some of these but not all of them so this is the mixture that
comes out.
If you have lots of carbohydrate malabsorption you’re probably going to pass out lots of
gas.
Cows do this all the time, that’s what’s going on in their rumen.
When you look at grazers, horses, ponies, cattle, they are eating grass.
Mammals don't have all the enzymes to break down all of those complex carbohydrates that
form cell walls in grasses so you have to rely on bacterial fermentation.
The cattle do in it their rumen, the ponies do it in their cecum.
They produce a fair amount of methane.
There have been suggestions made about a way to improve our natural gas supple is to bag
the cows and gather the methane but nobody’s figured out how to do this efficiently yet,
but it’s coming.
It’s recyclable: you plant the grass, you feed the cow, you gather the methane and milk,
yeah okay.
This is just an example of showing that when you infuse gas over 180 minutes how much is
evacuated and how fast.
You can see that at a slow rate it comes out slowly, the faster you put it in the faster
it comes out.
Gas, for some reason, seems to travel through the gut pretty rapidly.
Now most times at any one time in your gut there is a relatively small amount of gas.
Here you are seeing little bits in some of the colon, there’d be an air bubble in the
stomach, which is all swallowed air, and little blibs in parts of the small bowel, and there’s
some down here in the *** but that’s fairly small.
We’ve shown you pictures of patients who have an obstruction, they will continue to
swallow air and there may in the colon be some gas generated.
Here you’re seeing huge loops of small bowel, they’re small bowel because you can see
the valvulae conniventes all the way across and they’re in the middle of the bowel,
and then you’ve got colon with the big haustral folds.
This person clearly has excess gas.
To get gas like this you either have a distal obstruction or the bowels stop moving, an
ileus, bad dysmotility.
In surgery service you’ll see some patients after an observation have prolonged ileus
and it’s really difficult to manage.
This is primarily in the colon.
Right colon, transverse colon, you see little haustral folds here and here but there is
nothing that goes all the way across, and then there’s the descending colon.
Clearly too much gas.
There is a little bit in the small bowel here but not distended to the same extent.
Most people, it turns out, who complain of gas symptoms actually have relatively normal
amounts of gas.
Instead, they have a sensation of increased gut distension or increased flatus.
You can however get true increases in gas if you have excessive air swallowing or excessive
bacterial fermentation of carbohydrate.
Gas symptoms that people come to you complaining about are bloating, belching, enlarged abdomen,
passing excess flatus, things like that.
Bloating is one of the less loved symptoms of gasteroenterologists.
It’s very common and we often can't make people really happy about their symptom because
there are many different causes.
Clearly you want to look for altered motility and obstruction but you can have it produced
from the intake of a number of foods that generate carbohydrate fermentation.
You can have an altered gut flora such as bacterial overgrowth in the small bowel where
you’ll get gas production.
You get abnormal sensations of the amount of fullness that’s in the bowel and visceral
reflexes.
People who are constipated may have so much stool in their colon they feel full and bloated
even though it’s not gas even though it’s actually stool.
Then there is this sensation that’s been described where people simply relax the anterior
abdominal muscles and their diaphragm comes down and they bloat out but they actually
don't have anything in there.
This is actually what’s often seen on the x-ray of patients who come in to see us in
GI clinic and complain of gas and bloating.
An absolutely normal x-ray and I often will do this and show it to the patients and say
‘yes you’ve got a problem but it’s not too much volume of gas.’
Most of it is this abnormal sensation, it may be due to poor compliance of the stomach
or gut, it’s often in obese patients and I remind them there’s a lot of other stuff
in there.
It can trigger the sense of eructation and belching and what happens when you feel full
and bloated is the anterior abdominal muscles will relax.
Patients come in and say ‘I’m okay in the morning, I have breakfast, by lunchtime
I’m feeling kind of full, by the end of the day I look like I’m eight months pregnant,
and I’m fine the next morning.’
That is not ascites, that is not constipation, that is not fat, that is relaxation of the
anterior abdominal wall going out and then coming back.
Here is a study that was done with three-dimensional CT scanning and tagging air and then subtracting
everything.
This is a patient, and these are real patients, who complained of tremendous bloating
You can see that the distance here between the iliac crest and the diaphragm in the morning
was quite high and the distance between the vertebrae and the anterior abdominal wall
was fairly small.
The green are all the pockets of gas which could be identified.
Later in the day when they said they were totally full and bloated there was a little
extra gas here when you added all this up, but primarily the diaphragm had come down
and the anterior abdominal muscle wall has gone out.
That was accounting for why they were wearing loose trousers, putting their waistband down
around their lower hip, things like that.
Now a patient who has dysmotility of the bowel, this is a patient with pseudo-obstruction,
very very poor motility throughout the entire bowel, probably also has bacterial overgrowth
and is generating bacteria that is generating gas.
This was in the morning before they had a high carbohydrate meal, and this was later
in the day.
There is a tremendous increase in the actual amount of gas that’s there but, these patients
are actually quite rare.
Belching is another thing that people do when they feel like there’s too much air and
it’s a reflex response of letting air going back up the esophagus.
It’s not rumination, it’s not vomiting, it’s completely separate.
It may release gastric air and people feel better.
You have to do it when you’re up right because in your stomach you’ve got liquid, you’ve
got an air fluid level.
When you’re upright the gas is on top.
When you’re lying on your back the esophagus is actually more posterior and the gas is
usually anterior, so people can't actually belch very well when they’re lying flat.
If they turn over and they're prone or they sit up they can.
Now the problem is that sometimes when some people belch they actually swallow more air
when they’re beginning to belch than they get rid of.
That’s been tested with xenon washout studies where you can use radioactive xenon to actually
calculate the volume.
Prior to the belch they actually subconsciously swallow additional air, then the ileus relaxes,
and air is released up, but the net loss may not be all that much or may actually be negative.
So, continued belching can actually generate more net air in the stomach.
You can try to convince patients not to belch as much because it may make it worse.
Use a straw or some device so that when they’re taking in fluids they’re not sipping and
sucking in as much air.
Have liquids with their meals, don't be sipping beverages all day long.
With things like chewing gum and sucking on candies you’re continuously swallowing and
each of that is air swallowing.
Gas from carbonated drinks probably plays a very minor role in most patients.
Other gas symptoms due to reflex relaxation, reassure the patient.
Lower gas, flatus, that’s normal, but clearly if you’re generating air swallowing, or
if you’re generating flatus in the colon that’s going to cause a problem.
It can be due to changes in intake or changes in gut bacteria.
If they complain of really noxious flatus ask them about their diet because that usually
requires their taking in a lot of high sulfur-containing products.
Meat is all protein contains sulfur groups, and all of the onions and cabbage family members
have a lot of sulfur containing compounds in them.
Cabbage, brussel sprouts, lots of onions, some people just get a ton of noxious gas
from that and if they stop those it’ll go away.
We have to educate people on what kinds of foods can cause flatus, milk being a common
one but then there are these other items we already talked about, lactose.
Here are other things to ask about, if people are taking a lot of these they can get excess
flatus.
That’s my history when somebody comes in.
I’m asking what they’re putting in their mouths, see if there is anything I can suggest
they do a dietary exclusion and see if it solves the problem.
Treatment of gas, there is really poor evidence for any of this.
Reassurance, reduce air swallowing, suppress belching, try promotility agents like metoclopramide.
For some people who really complain of a lot of upper that may help.
There are side effects from metoclopramide so it’s not necessarily what we want to
give everybody.
Simethicone is the anti-gas agent when you see Gas-X or antacids that are anti-gas it’s
simethicone.
What it does is reduce surface tension on bubbles so it makes smaller bubbles and they
might pass through easier.
We actually use simethicone when we’re doing endoscopy, particularly when we’re down
in the duodenum.
You have bile acids coming in there, they’re detergents, sometimes we just have difficulty
seeing because of all these bubbles.
We’re putting air in and they’ve got detergent there and we are generating air bubbles.
We throw some simethicone down through the scope and the bubbles all disappear, it’s
wonderful.
Try to identify some foods, this is where if all else fails try some probiotics, we
have no idea which ones work better for whom.
There is some evidence that Pepto-Bismol and zinc can both block the production of some
of the hydrogen sulfide, you have to take them about four times a day, that’s for
the really end stage patients.
Then consider do they have a malabsorptive disorder that you need to find out and treat.
Constipation is another difficult problem that everyone has to deal with no matter your
specialty.
I can't tell you how many people come in to see me about their chronic liver disease and
say ‘oh by the way, can you deal with my constipation, can you deal with my bloating?’
And I go ‘oh god please, I guess.’ [Laughter]. We can deal with this.
Constipation is less than three stools a week, usually difficult to pass, there is often
straining or a sense of incomplete evacuation.
The prevalence of self-perceived constipation is at least 10-20% in the average American
population but sometimes that means you have to define constipation for your patient.
If they’re passing soft stool, it’s easy to pass, and they’re having three stools
a week that’s fine.
That’s perfectly normal.
Occasional constipation, depending on how your diet changes, is a part of normal life
for most humans.
The arctic explorers who were living on meat had a big problem with constipation.
The pathophysiology we’ve talked about is liquid material enters the cecum from the
ileum.
The colon reabsorbs electrolytes and water, it salvages some carbohydrates, it moves material
in a timely fashion to the ***, but if you have imbalances in this function you can
either have too much liquid stool coming around or too much hard stool coming around.
You can have slow colon transit.
This is where your history of the medications s patient’s on are key.
Some of the most common causes are we put people on narcotics, calcium channel blockers,
anticholinergics, cholestyramine and then are somehow surprised they come in complaining
of constipation.
If you’re going to start one of these drugs talk to the patient about the side effects.
You might not need to give them anything right now, but make them aware of that so that you
can help them when it develops.
Motility decreases, primarily diabetes or hypothyroidism, and idiopathic.
Increased bowel sodium and water absorption is probably the cause of constipation in some
of our patients.
We just don’t understand the mechanisms or why that happens.
Insufficient fiber.
Fiber is an unabsorbed complex carbohydrate.
It increases stool bulk and a clinical observation is that bulkier stools, patients tend to move
that stuff through in better time and they tend to be less constipated.
We don’t quite understand that but the human colon clearly evolved with hunter-gatherers
who had a very high fiber diet.
They were out there eating a lot of plant stuff that had tons of fiber in it because
we can't digest it.
In addition, some fibers are fermented to osmotically active compounds, which adds water
to the stool.
As I said, may improve colonic motility.
Insufficient bile acids.
We’ve talked about if you get rid of all the bile acids in the colon you may get constipation.
It’s usually not a problem unless you give people cholestyramine, then that’s an expected
complication.
There also are patients who can't pass stool well because they have problems in the ***
*** area with the musculature at the *** sphincter, or pelvic floor dysfunction.
That’s a highly specialized area.
If patients say I have to sit on the toilet for an hour, it’s really difficult to push
things out, then you probably need to refer them to somebody who can do the testing for
these maneuvers.
Psychological factors and eating disorders are part of this but we don't completely understand
that one either but most of those folks are on a low fiber diet, which probably isn’t
helping.
I talked about the enterohepatic circulation of bile acids with a little bit getting into
the colon, which probably keeps our stools somewhat loose.
Cholestyramine binds that up and a predictable side effect in virtually everyone that takes
it is harder, less frequent stools.
So, treatment.
Look for any underlying factors of course and add fiber.
For an average person with average constipation in the United States, where we generally have
low fiber diets, advice is always start with fiber.
You can advocate high fiber foods but many people just can't eat enough of them or their
lifetime diet is so different.
You can't change your lifetime diet very well so then adding purified fiber, which is sold
over the counter.
You start with a small dose and you just keep working up slowly until the stools are big
and bulky.
The only problem of course is that some of those patients will develop flatus.
They will not like you.
Then we have osmotic agents, these should work in everybody, just depends how much you
have to give.
You can use Milk of Magnesia in small doses.
You can give sorbitol or lactulose, which are sugary syrups if you can measure out by
the tablespoon.
The one we really have all started to use a lot is a thing called Miralax, polyethylene
glycol.
It’s a non-absorbable, small molecular weight, osmotically active material.
It was developed originally for colon prep procedures but now they purify and sell it
on its own.
You are basically adding an osmotic agent to the colon.
Again, you start with the one capful a day that it says is the dose and you just keep
increasing slowly until patients are having soft stools.
This you cannot get gas from.
These you can get gas from.
Promotility agent.
Sometimes we use that in addition in people say, who have very bad diabetes, and they
have motility problems as well, but it has limited efficacy in the colon, it’s better
in the stomach.
Then you have stimulant laxatives.
They used to have both motor and secretory effects.
There are some people who failed all of these other things, you have to use them on a regular
basis.
We used to think they did something to the colon motility, by destroying it, now we think
the problem is these folks have an underlying dysmotility that we can't identify and that’s
progressing over time, they just need to use these.
Patients say they don't want to be dependent, tell them ‘you’re dependent already, your
colon isn’t working, these will help your colon work.’
Okay, and then monitor what’s going on.
Now, a part of our job as physicians is also to get rid of myths that our patients may
have.
There are a lot of myths out there.
One myth is that having one stool a day is required for normal health.
It’s not.
There is a wide range of normal that really helps with a lot of your patients.
They discover they’re not as abnormal as they thought they were, you don't need to
do anything else.
A control trial was done on exercise, doesn't work.
Not on regular people, regular constipation, regular types of exercise.
Now patients who do marathons, who do lots of running, they can get all kinds of bowel
problems.
They can get ischemia in the bowel, they can have bleeding, they may well have very altered
motility.
There are individuals who say for them exercise makes a big difference but, in general, for
most people where it’s been studied this is not going to be a cure.
But exercise is always good so I wouldn't discourage it.
Drinking more water.
What happens to the water that you are all drinking right now?
It gets into your small bowel, what happens to it?
It’s absorbed, where does it go?
Out the kidneys.
You can't get water into the colon just by drinking water.
You have to have an osmotic agent to hold it there.
So just telling people to drink eight glasses of water a day in most cases is not going
to solve their constipation.
Eight glasses of water and some Miralax a day will probably work quite well.
Colace.
It’s on every hospital’s formulary, it’s part of the standard orders that you will
be taught to write for every patient because people come into the hospital and they get
constipated.
The only controlled studies ever done showed no effect on increasing frequency or size
of stool.
I would love to have that removed from every hospital’s order set and put in Miralax
instead, based on science, but it’s still there so you can order it.
There are some individuals who have been on it a long time and they will tell you ‘if
I stop it I will get constipated again.’
Again, there are probably a few individuals for whom it works but in general it has really
limited efficacy.
I wanted to talk a bit here when we're talking about the colon about the complication called
diverticuli.
Also extremely common, most middle aged and older Americans have at least a few of these.
When people say, ‘oh my doctor did this colonoscopy and time me I have diverticuli.’
Okay, join the average American population.
Diverticuli are out-pouchings.
They do not contain all the elements of the bowel wall and they occur at places where
the perforating arteries go through the muscle.
So the blood vessels come in on the mesentery track around in the serosa or just below the
serosa, and penetrate into the inner layers.
This is why the mucosa is more vulnerable to ischemia hypotension.
It's the last thing on the line getting oxygen.
It also means that at the places where the artery penetrates through the muscle you have
a weakness and as pressures in the colon mount over time you can get mucosa and the serosa
bulging out as a diverticulum.
Very, very common and often they’re have a little draping artery right over them.
So it can start like this and works its way all the way through.
When you’re doing colonoscopy, that’s the lumen there, you’ll see the side openings
which are diverticuli.
Extraordinarily common, we see them all the time.
Sometimes they get really, really big.
When you get this many big ones there may be a disease of the elastic tissue or something
else going on there.
This is part of the colon.
There’s the fat on the outside and the lumen and these are all these huge wide mouth diverticuli.
This is that patient who, before surgery, had a barium swallow.
Barium went through the bowel and then they waited a couple of days till the barium had
gone out of the colon and took an x-ray.
This is barium stuck in all of these diverticuli because it can't get out and now you see the
barium lighting up all the diverticula.
This is just showing you how big they can get.
This is somebody with scleroderma.
At surgery, here’s the sigmoid colon up here.
You’ve got fat around that and, in this case you have all these little blue diverticuli
going off.
These are all normal.
Just happens to be you’re seeing it.
Now, what kind of complications can occur?
Well considering the number of diverticula per person multiplied by the middle-aged and
older population of the United States there could be one hundred million, two hundred
million diverticuli out there.
That means when a problem occurs, even if it's rare, we see a lot of it.
We see a lot of people with complications of diverticuli.
Given the number of diverticuli out there, the probability of getting a problem from
your diverticuli or any one of them is fairly low.
So we can do two things.
First of all, stool can get in there, and it does.
If it ulcerates the mucosa and erodes into that underlying artery you get a diverticular
bleed.
This is not a subtle bleed.
This is not hemoccult positive stool.
This is bright red blood and clots pouring out of the *** usually because it’s under
arterial pressure.
Just like a duodenal ulcer bleed can be a really big bleed.
It’s an artery, okay?
Diverticular bleed, I’ll show you some pictures.
Second thing is if you obstruct that narrow neck you’ve got colonic material inside
which is loaded with what?
Bacteria.
Normally you’ve got bacteria in the lumen of the bowel, some if it’s getting washed
out in the stool.
Stools are 50% bacteria.
But the diverticulum is a blind end so you have bacteria in there growing away and if
they, again, ulcerate through they can perforate through that thin wall of the diverticulum
and cause a little abscess outside.
That’s diverticulitis.
You have diverticuli, if one gets infected and perforates that’s diverticulitis.
You often have to explain the difference to patients.
So diverticulitis.
Here you’ve got a large bowel with some diverticuli.
One of the underneath is perforated and bacteria and fecal material then leaks out into the
peritoneum.
This nice thing is this is often happening down in the sigmoid colon.
There’s a huge omentum there and usually the omentum covers it all up so you get a
contained abscess.
Michael Mulholland, I think, had a case he was talking to you about in his lecture about
somebody who got free air.
Because of course if this perforates out into the open peritoneum you get spillage of gas,
stool, and everything else out into the peritoneum.
But most cases, the omentum plasters over this and you get a contained abscess, which
is why the patients come in with some pain and a fever but they’re not critically ill,
they don’t have peritonitis, they don’t need to go to the OR (operating room) right
away.
We can usually clean that up with antibiotics.
Now of course it can get big and if it gets big and you don’t take care of it, it can
erode into other things close by like the bladder, the ***, things like that.
It can rupture and that’s where you get free air and you get peritonitis because you
get fecal material and bacteria spreading throughout the entire abdomen.
That can happen but that’s much less common.
Probably 95+% are going to be a contained abscess.
This is a CT scan.
Here is the iliac crest.
The spine is down here.
This is the anterior abdominal wall with a muscle.
This is a sigmoid colon.
You’ve got a thickened wall from inflammation.
You’ve got some air pockets and diverticuli and it happens that there is a inflammation
here which is causing thickening of that wall of the colon.
The colon wall should be very thin but here you’re seeing the mucosa, this is the outside
that’s very thickened.
Sometimes there’s so much edema there that you actually get an obstruction because the
wall of the bowel next to this abscess has so much edema it gets thickened.
So some people will come in with constipation, they haven’t passed any bowel movements
because there’s so much edema here things can't get through.
They also have pain, this is an infection they have a fever and a white count.
If it perforates it can travel other places so you can actually get fistulas into small
bowel, skin, bladder, whatever.
These are complications of diverticuli that can occur but they’re fairly uncommon.
If you see a fistula to another part of the bowel, you see a fistula coming to the outside
world, you see a fistula going into the bladder, a diverticular abscess is one of the things
that can do that.
What’s the other one?
Crohn’s.
Yeah those would be the two top players.
TB can do it but TB in the bowel is very rare in this country.
They can then bleed.
They don’t do the same thing together.
It’s a rule, I don’t know who made it up or why, but it’s a rule.
We don’t see bleeding diverticuli and diverticulitis in the same patient at the same time.
You get one or the other.
I can't promise you wont get the other at sometime in the future, but you get one or
the other.
Again, you have a draping arterial around the outside and if an ulcer erodes into it
you get arterial blood being pumped into the lumen.
This is usually in the sigmoid, you can have diverticuli anywhere in the colon, they can
be on the right side, but the most common location is the sigmoid.
Pumping blood into the sigmoid, you’re going to put that out as bright red blood pretty
rapidly.
Here’s looking in at a diverticulum.
In this case there’s just a little bit of blood there and we can actually sometimes
treat that.
Here its been treated but the radiologist can also do it by an angiogram and finding
the bleeding area.
There are a couple ways we can try and get it to stop.
The thing that saves us on these is most people stop on their own eventually.
You just have to keep them resuscitated and transfused and alive until they stop bleeding.
We do have some things we can do, especially in people who have recurrent bleeding.
Again, myth busing.
Clinical teaching says that people with diverticuli should avoid nuts, seeds, popcorn, etcetera,
to reduce the chance these might obstruct the bowel and cause diverticulitis.
Get rid of that recommendation.
There was never any data to support that.
It was a hypothetical thing that got put in the literature decades ago.
There is no evidence and there actually was a study to try to look at this.
This is part of the physicians’ health professional follow-up study, which was started probably
in the 1960s.
Following 47,000 men, they were mostly men because most physicians at that time were
men, and there was an inverse relationship between the intake of these foods and development
of diverticulitis or other complications.
Please don’t torture your patients by telling them they can’t have their raspberry jam,
they can't eat peanuts, they can't eat popcorn, for this reason.
You may have other reasons you don't want them eating them but not for this.
So I’m going to finish up with hemorrhoids, which is way at the other end.
This is a very old illustrative manuscript showing that people had trouble with hemorrhoids
way back then.
This is somebody looking at external hemorrhoids.
They could look in the eye, they could look in the nose, they could look at the hemorrhoids.
You have to understand the *** anatomy for this.
If you look as the distal *** there's the dentate line, which I’ve outlined in orange,
where you go from squamous epithelium to columnar epithelium.
You have the internal and external *** sphincters going around.
There are cushions of vascularized tissue above the dentate like and just here externally.
It is thought that those help for a tight seal when the sphincter closes to help seal
it so you don't leak any liquid or gas unnecessarily.
Otherwise we can’t figure out why that tissue is there because the only other problem is
it causes trouble.
When these blood vessels dilate and the tissue expands that’s an internal hemorrhoid or
an external hemorrhoid.
If you have something on the skin it can hurt.
You’ve got sensation just like on the rest of your skin.
Internal hemorrhoids are above the dentate line.
You can biopsy, you can push at things here, it doesn't hurt.
The surgeons deal with anything below the dentate line, we often deal with anything
above.
You really need good sedation to do anything below the dentate line.
It hurts.
So these are vascular cushions of soft tissue with large vascular channels.
Injury, age, passing of hard stool, fragments or damages these cushions or their supporting
structures so they sag.
They sag forward and in toward the middle.
Straining when you bear down hard increases venous pressure and that will also cause engorgement
of those vessels.
Once the tissues start to swell and prolapse then the passage of stool keeps pushing it
down more and more.
With trauma to the surface you can get epithelial damage leading to ulceration, bleeding, and
sometimes pain.
With external hemorrhoids the worse pain comes when some of those veins thrombose and then
people will come in with severe pain of a hemorrhoid and that’s because it’s thrombosed.
The surgeons can actually open that up, pull out the clot, decompress that, under good
anesthesia.
So internal hemorrhoids come from above the dentate line, external hemorrhoids below.
Here’s a slide.
This is where the tissue has been prolapsing and pulled forward.
Here is an external hemorrhoid right here.
Theses are pictures of extremely large external or prolapsed internal hemorrhoids.
When you just look, clearly those are bad hemorrhoids.
Now from the inside if you’ve got an endoscope and you’re looking back at the *** the
*** sphincter’s down here.
Here are hemorrhoids and they’re prolapsing down through the *** canal and out.
Actually this is an exterior view, right there’s somebody’s hand.
On the internal side you can see these big purple-ish hemorrhoids.
These are relatively modest ones.
They may not be causing the patient any problem but if the surface gets a little excoriated
it can ooze, you can see little bits of bright red blood, you can see streaks of blood on
the stool or the toilet paper.
If you have a really huge hemorrhoid and the whole surface ruptures you can have a big
bleed but that’s actually pretty uncommon.
You get pair or irritation from prolapsed internal hemorrhoids or ulcerated or thrombosed
external hemorrhoids.
You get small amounts of bright red blood.
You can get a major bleed but that's pretty uncommon.
When you have the prolapsing hemorrhoids, they’re going all the way through the ***
sphincter, you can't get a tight seal so these patients may have problems with liquid or
stool incontinence to make their lives even more miserable.
What’s the management?
There’s very little evidence-based therapy.
Again, most of these things were grandfathered in generations ago.
Clearly you’d like to reduce straining if this is somebody who’s been constipated
and strains that may help.
You want to soften the stool, we’ve talked about that.
For pain or irritation there’s all kinds of things you can buy out there.
Very little good evidence-base to say whether they help or not.
Primarily they’re giving the patients something to do and a lot of this gets better on their
own.
But they can help.
If you have a really painful external you can get one of these doughnut ring seats so
the hemorrhoids are sitting over the hole.
That can help.
You can get rid of them.
You can sclerosis these.
You can put rubber bands around them just like we do around varices.
And, surgery can cut them out.
This is really done by surgeons.
If you have painful, or prolapsing, or otherwise difficult hemorrhoids, once you make the diagnosis
you send the patient to a surgeon.
Here is just an example of rubber band ligation.
There’s a rubber band and just like with a varix that will necrose this tissue and
at some point the band will fall off.
You will hope that the blood vessel behind that thrombosed.
Occasionally it doesn't.
So if you see somebody coming into the emergency room who’s pouring out blood from the ***
one of the pieces of history you want to know is, did you have something done to your hemorrhoids
in the last few days?
Was this where the rubber band came off and the necrosed tissue came off and the blood
vessel behind was not yet thrombosed?
Okay, I will finish up with iron deficiency anemia on Thursday.
See you tomorrow.