Category: Portal Hypertension Bleeds

PBC Bleed 7. The Vesuvius Within Me. Crashing in the Same Car.

Good thing I finally got around this month to describing November’s bleeds 5 and 6 in this continuing realtime account of me and my PBC (primary biliary cirrhosis) because now it’s already time to move along to bleed 7.

This was a rather dramatic one, occurring in the wee hours of January 18, 2013. My hemoglobin [hgb] dropped to a personal worst of 6.1, I landed in the ICU and then on the cardiology floor, and required 3 transfusions. A couple of days ago my hgb was 10.5, mildly anemic, but I feel great.

Why the ICU and cardio unit? Because when your hemoglobin drops that low (normal for post-menopausal women = 11.7 to  13.8), it means none of your organs — including your heart — are getting enough oxygen.

What went right this time was that the Asheville ER got a gastroenterologist in to perform an endoscopy immediately, while I was still actively bleeding. Except for my first bleed, in Huntsville the doctors waited 20 hours or more to ‘scope, after drugs and IV fluids had stopped the bleeding.

You can’t be sure of the source of the bleed if you don’t see the bleed.

The Asheville GI theorized what I had this time around was a Cameron’s Erosion. This is erosion in the stomach near the diaphragmatic haitus which is a hole where the esophagus passes into the stomach. The junction should be below the diaphragm, but if you have a hiatal hernia, as I do, then it is above the diaphragm. Usually, hiatal hernias cause no bother other than indigestion. But I have other things going on as a result of the PBC, namely protal hypertension and gastric and esophageal varices. (If you search “cameron’s erosions” + “portal hypertension” + pbc, Google comes up with 75 results, which in the Googleverse is close to zero.)

Now as it happened, I had an endoscopy and visit planned with my hepatologist, Dr. Brendan McGuire, at University of Alabama-Birmingham’s Liver Center for January 22 and 23. So immediately after leaving the hospital on the 21st, we headed south.

Dr. McGuire scoped me Tuesday morning and reported he agreed with the Asheville doctors. He described the area as not unlike a scrape on a kid’s knee that scabs over, but before it gets a chance to heal completely, keeps getting banged up. He didn’t see the site of my first bleed until a few weeks had passed but thinks this one was in its vicinity if not the same place.

So it could be like I keep crashing in the same car, having the same bleed over and again. Since I wasn’t scoped during bleeds 2 through 6, we’ll never know.

Why not fix the hiatal hernia? Too risky: its position, the sites of the erosion and varices, the amount of scar tissue, the thinness of the veins — lots of reasons.

What can be done: double the dose of beta blockers I’m taking to slow heartbeat and of antacids to reduce stomach erosion. And hope that the Vesuvius within me remains dormant.

And what about my primary biliary cirrhosis? I’m doing just fine there, holding fairly stable. It could be years and years before it is bad enough to warrant a transplant. There is something called a MELD score. Normal people’s is zero. Those near dead of liver failure have a score of 40. I’m at 8. Bleeds don’t factor in.

So all I have to do is hope I don’t erupt.

But what we need now is a little relief from the dreariness of reading about me going on about vomiting blood.

I suggest a segue to youtube to view some loveliness: David Bowie singing “Always Crashing in the Same Car.”

You can choose between this one with a particularly happy Bowie, or the GQ Awards show where Bowie wore sandals with socks, or this with a sassy Bowie around 3:18. Or all and more (like here, where he isn’t playing the guitar and seems not to know what to do with his arms).


PS: Although it doesn’t have much about PBC, this site has a cool diagram of possible diagnoses related to liver trouble.


PBC, Bleeding Varices. Bleeds 5 and 5.5. Or 6.

Yes, it has been months since I last posted, and, yes, my next-to-last post was on this same topic (Primary Biliary Cirrhosis [PBC], Portal Hypertension, My Perfect Endoscopy Results and My Fourth Bleed) in my continuing series of what my experience with PBC is like. I’m beginning to understand why there aren’t so many real-time chronicles of progressively worsening illnesses.

You may recall that back in early October 2012, I had a routine exploratory endoscopy with perfect results, followed a few days later by a bleed I was told was from a tear in the esophagus which was patched up, and no other problems noted.

Bleed 5.

November 6 I drove from Asheville, NC back to Huntsville, AL to spend the 8th with my son on his 23rd birthday. Before dawn on the 8th I started throwing up and defecating black blood. I really, really did not want to go to the hospital. I didn’t want to ruin my son’s birthday. I had so looked forward to this. But even less did I want him to discover me bled out, so I told him, and he insisted I go to the hospital. We ended up visiting in a room of the same hospital where we were 23 years previously, to the day.

Next day, the 9th, another endoscopy. And behold, the GI discovers two varices needing banding. He also reports that he saw no evidence of the tear I was told was the cause of my October 5 bleed, with repeated emphasis on the word tear. Huntsville GI added he wasn’t impressed with the Asheville GI’s work and that I had a good deal of scar tissue. Because my hemoglobin creeps up to 9 (12 is normal lower limit), I’m not transfused and am released that day.

Bleed 5.5 or 6.

Between November 8 and November 20, I felt worse and worse, like I was practicing being dead. I didn’t read or write or sleep, just stared out the window.

I was with my daughter at her doctor’s on the 20th when I started throwing up blood. Again. This time was a bit different; t some red mixed in there with the black, not quite as much as in past bleeds, but enough so I am on the verge of losing consciousness.

It was two days before Thanksgiving, and I had really, really been looking forward to spending it with my family and new friends.

The GI on call from the practice I visited to schedule October’s exploratory endoscopy paid me a visit in the ER. This made the sixth I’d seen from that practice. I never will believe that I had a spontaneous tear after the exploratory and not a nick, but GI #6 is simply preposterous. He claims that with PBC patients, low hemoglobin, as low as 8, is preferable to the normal 12-14 because less blood means less likelihood of portal hypertension. How stupid does this man think I am? He’s the doctor and I am not so I refrained from telling him his job or the role of oxygenated blood in maintaining life. But man, why don’t we just take a few pints of your blood, drop you to 8, and then let’s discuss quality of life.

Fortunately, a new GI did the next day’s endoscopy. She reported that I didn’t have varices that bled. Instead, the bleeding was caused by ulcerations around the two bands placed by the Huntsville GI (who was, you’ll recall, unimpressed by the Asheville group’s work).

So was this Bleed 5.5 or Bleed 6? It wasn’t a varices bleed. But then again, neither was Bleed 4 (the nick bleed).

There was a good thing about Bleed 5.5 or 6. It got me some blood. My hemoglobin had dipped to 6.7, an all-time personal worst for me.

I thought after the doctor visited Thanksgiving morning that I would be able to go home when the second transfusion ended. But a nurse said it would take 12 hours to wean me off the IV which was delivering a drug to help stop internal bleeding.

Despair. In comes Thanksgiving Day hospital turkey.

However, when the hospitalist came around, she said since this was not a varices bleed, I didn’t need to be on that drug, and so didn’t need to be weaned from it. I could leave.


No one can give me an answer beyond bad luck for how in hell two varices burst on November 8 when on October 2 and 5, there were no signs of developing varices.

I’m going to Birmingham to see my hepatologist at UAB in 10 days. It is worth it to me to drive 6 hours for an exploratory endoscopy with someone I trust.


Thanksgiving 2012. My left arm. The other looked about the same.

Primary Biliary Cirrhosis, Portal Hypertension, My Perfect Endoscopy Results and My Fourth Bleed

This post updates my last one, Primary Biliary Cirrhosis, Portal Hypertension, and the Frustration of Knowing There’s No Way of Knowing What I Need to Know, in which I discussed what a relief it was going to be to have an exploratory endoscopy in which either I would discover that I had no varices on the verge of bursting and causing a life-threatening bleed, or if I did have varices, they would be banded and so I would not be at risk — for the time being — of a bleed.

Well, here’s what happened. (Fair warning: This blog isn’t for the weak-stomached today.)

Tuesday morning: endoscopy. Great news! No varices! The GI suggested that maybe I could go a year before the next scope.

Wednesday: Normal life, until evening, when it was a struggle to stay focused enough to watch the debates.

Thursday: I felt really poorly, headache, no energy, unable to focus or think or read, light-headedness. I thought, Gee, it’s a good thing I had the endoscopy Tuesday or else I’d be sure I was starting a bleed.

Friday, 1 am: Urgent need to use the toilet. Expelled globs of old digested black blood, then started throwing up black blood. Simultaneously. Really disgusting. Yelled for help, husband came, call into 911, off I go in the ambulance.

Now, this bleed wasn’t as bad as bleeds one, two, and three because my blood pressure never dropped low enough so that I lost consciousness. I was even able to talk the EMT out of starting an IV in my rolling, uncooperative veins en route to the hospital along winding and bumpy roads.

So what happened? How did I manage to go from A+ to F in the esophageal health department?

Next day the founder and boss of the GI practice did a much slower endoscopy. He found a tear in the esophagus and repaired it with two clips.  He wants to call it a Mallory-Weiss tear, which can follow extreme retching. But the only retching I did was sudden and swift vomiting of blood. In fact, no retching was involved. More like spouting.

He can call it what he wants. There’s no way of ever knowing what caused this tear. But the hospitalist, the nurses, anyone without a vested interest in it being a Mallory-Weiss, is likely to agree with me: I got nicked during the Tuesday morning endoscopy.

It happens. I’m not irate. I know that endoscopy is an invasive procedure and that there are risks. According to the Mayo Clinic, tears happen in “an estimated 3 to 5 of every 10,000 diagnostic upper endoscopies.” It is a good thing that I was conscious, coherent, and creditable, and returned to the same hospital where the exploratory endoscopy had been done. Without a history to work up a diagnosis, this could have been as bad as a burst varices bleed. The mortality rate is 20% when the esophagus is already compromised and because

the diversity of clinical symptoms and signs combined with a lack of individual experience [among doctors] regarding this particular condition may impede rapid identification of this potentially hazardous situation. Accordingly, delayed diagnostic work-up may hinder timely and appropriate treatment with a negative effect on patient outcome.

Well, that’s not real encouraging, is it?

So now what? What do I do in six months’ time?

It is, you see, a classic damned if you do and damned if you don’t, between a rock and a hard place, etc. situation: in trying to eliminate the risk of a burst varices bleed by exploratory endoscopy, I incur the risk of a bleed from the endoscopy itself.

Well, I’ll tell you. I’ll have the scope. But I’ll either have it with the hepatologist at UAB even though that means a five or six hour trip, or maybe I would have it here — but only if the bossman himself does it.

Someone who can do the math can combine these odds, just for fun. Incidence of having PBC in the first place: 2.7/100,00. Incidence of tears in upper endoscopies: 3-5/10,000. Incidence of having PBC and having  a tear following an endoscopy = ???

Primary Biliary Cirrhosis, Portal Hypertension, and the Frustration of Knowing There’s No Way of Knowing What I Need to Know.

I haven’t had a post recently on primary biliary cirrhosis. One feature of this blog is the occasional post on what it is like to have this autoimmune condition.

In the past two years, I had three bleeds as a result of esophageal varices bursting as a result of portal hypertension, itself a result of liver damage caused by damage to the bile ducts.

The first was in August 2010 and I required four transfusions. A year and two weeks later I had my second bleed in August 2011. Then at the beginning of this March, six and a half months later, I had my third. After the second and third bleeds, I had two transfusions.

As you might guess, when August of this year rolled around, I worried. I got through August fine, and September as well, that is, no bleed. Tomorrow I am having an exploratory endoscopy to band any varices that look like they could cause problems.

Twelve hours, and I will have dodged a bullet. Or maybe I will be informed that there was nothing to worry about, that no new varices have developed. But this doesn’t mean varices won’t develop later this month. Or maybe not til November or December. Or maybe never.

This is what I mean by the frustration of knowing there’s no way of knowing what I most need to know.

There’s no predicting these things. You can catch them before they happen with endoscopies — and luck.

Endoscopies aren’t painful, but they require twilight sleep anesthesia, and they are invasive procedures with the usual risks. It just doesn’t make sense to have one every week, or month, or two months. How about every three months? Four? Where to draw the line?

When the varices burst,  there are no warning signs until it is too late to do anything but react. With the third I had an inkling that I had started a bleed when I began to feel faint for no reason. Within 15 minutes I was vomiting blood. When the paramedics arrived, they were hopeful they could get me out the door to the stretcher. It didn’t happen. I stood up, and next thing I knew I was in the ambulance with IVs adding fluids to raise pressure to keep blood going to the organs.

When there is no science, magical thinking takes over. You look for patterns to make sense and end up thinking that if in the past two Augusts you’ve had a bleed, why won’t the pattern continue? If the time elapsed between the first and second was roughly a year, and between the second and third was six months, does that mean the fourth will be six months after the third? — or three months? — or maybe never or maybe there is no pattern.

It’s hard not to think that each day that passes without a bleed simply means you’re one day closer to the next one. Or that every time you don’t feel quite right the next thing to expect will be blood.

And there are places it would be worse to be than others. On a hike in a remote region, alone on the road on a rural highway, up in the air mid-flight. You start to curtail yourself, and let the threat define the parameters of your life.

Whether varices are found tomorrow or not, I’ll be safe from this threat — for a while, anyway. But how long a while?

PBC, Portal Hypertension, and a Bloody Inconvenient Route

My last post before my world changed on August 28 was “Another Bloody August. Mysteries and Muddles. And Hospitalists” about my second sudden gastric bleed in two years and my second misdiagnosis by Huntsville Hospitalists and GIs who insist I simply have bleeding ulcers and refuse to consider portal hypertension, a common complication of liver failure, which is the end result of primary biliary cirrhosis.

If you are new to this blog, you are likely confused. One of my recurring subjects is my life with primary biliary cirrhosis, an autoimmune disorder that causes the bile ducts to self-destruct; the back-up of bile leads to cirrhosis, and cirrhosis to liver failure. At the top of my homepage I recently added a link to a permanent page listing both my postings on this subject and some of the most useful websites I’ve come across. I’ve considered pulling these posts and putting them in their own blog, but for now, they are staying here.

I write about this because it is a rare enough disease that firsthand accounts of living with the illness year after year are hard to come by. The blog format gives a new opportunity to illness diarists, a sort of real-time history of our decline. Readers can extract only the posts tagged PBC and see a sort of sped-up version. Like in my case, my first post about having PBC was two years ago, November 13, 2009,  Varicose Veins in my Esophagus? when I was surprised on my annual visit to Kirklin Clinic to learn I’d have to start having endoscopies to check for esophageal varices. Then I decided it was time to write about this illness because I wasn’t going to be able to ignore it forever.

I was right about that; in August 2010 I had a bleed requiring 4 transfusions, and this year another requiring just 2 transfusions. That one landed me in the ICU, however (two weeks later that creep beat the hell out of my daughter, by the way. He knew I’d been very sick. Prince of a fella, that one. I digress).

This August, the Huntsville Hospital staff GI did an endoscopy 20 hours after the bleed and decided I had ulcers. After all, I had had them last year. Only I hadn’t.  In September I visited another GI in Huntsville who determined that portal hypertension, not bleeding ulcers, was the culprit; he started me on beta blockers. Then in October I took a little break from the domestic violence battles to have another endoscopy by the good man Dr. Brendan McGuire of UAB down at the Kirklin Clinic. He rubberbanded several large varices that could have burst, essentially destroying the vessels.

So yesterday, fresh from the non-trial debacle, it was time to return to Kirklin for my annual November pow-wow and bloodletting with McGuire.

I was worried that I was going to find out that my PBC had advanced since I had had a second portal hypertension burst varices bleed.

But no, my blood chemistry remains stable for a person with PBC.

So why the bleeds?

It’s a mechanical issue, according to Dr. McGuire. The blood wants to get up to the heart and lungs. It wants to go through the liver, but the PBC has blocked its usual routes. It could decide to take stronger, wider vessels in my back, for example, as its detour route. But no, instead my blood has chosen to detour through my stomach and esophagus, taking routes that can’t handle that volume of traffic, stressing vessels not meant to handle such loads. When these routes are stressed to the breaking point, they break, and the endoscopy road crew has to come and clean up the mess and patch up the leaks, About the only thing otherwise that can be done is routine maintenance — that is, endoscopy to check out potential problems and band the varices — block the routes — before they have a chance to burst.

So April I’ll have another endoscopy. And who knows, maybe I won’t have a third consecutive bloody August. That would be nice.


Another Bloody August. Mysteries and Muddles. And Hospitalists.

Update: The current (November 2014) hypothesis among my doctors is that whatever they were called in my past posts — Dieulafoy lesions, Cameron’s erosions, or bleeding ulcers — all these bleeds have their source in the portal hypertension which comes from cirrhosis which is caused by my auto immune system attacking my bile ducts, that is, my primary biliary cirrhosis.

Silly me. I look back on my post from earlier this month, An Uneventful Day, Unlike Last August 2, and wonder. There I wrote about how on August 2, 2010, I had an arterial lesion burst where the esophagus meets the stomach, and how nice it was that this August 2, 2011, was so comparatively uneventful.

Little did I know that just 11 days later I’d be back in the ER. Circumstances weren’t quite as dramatic this time around — no ambulance — and I got only 2 transfusions compared to last year’s 4. But in some respects, this episode of vomiting blood was worse.

Why am I inflicting this on you? Actually, I am writing primarily for my readers who like me have primary biliary cirrhosis. There’s more not understood about that disease than is known, and I feel it might prove worthwhile to use the internet as a way to compile and compare histories.

I accept last year’s diagnosis of a Dieulafoy’s lesion, which I attained after consulting my hepatologist, not content with the GI’s conclusion that I had a spurting gastric ulcer. This year the diagnosis is gastric erosion, but I’m not convinced for some of the same reasons I wasn’t last year. While swallowing is a problem some times, once food hits my stomach, all is well — spicier the better.

It seems too weird I can go a year without a stomach-ache while having such a torn up gut that I end up in the ER — too weird considering I am at risk for esophageal varices as a result of portal hypertension as a consequence of PBC.

My intuition tells me the PBC was at least a contributing factor to the Dieulafoy’s lesion, and to this latest event as well.

So this is what I want to know: has anyone else out there with PBC landed in the ER vomiting blood not from varices?

And Now for the Muddles. And Hospitalists.

I keep copies of my medical records. Last year I discovered from the hospitalist’s history that “I got dizzy, and came to the emergency room.” When I complained that this wasn’t an altogether accurate way of describing arriving via ambulance, lights and siren, IV’s in both arms, on O2, my objections were dismissed. This year, I found out that I had been vomiting blood for 2 days when I came to the ER. Wrong again. First, I’m not an idiot. Second, I told the zillion people who had to have the day’s events recounted, that I had vomited twice that afternoon before coming to the ER.

Why can’t these hospitalists listen?

And what, you ask, is a hospitalist anyway? If you are a slow learner like me and it takes you years to realize your [now ex-] general practitioner is too indifferent to bother with hospitalising her own patients, you are stuck with a hospitalist “managing” your case. In my experience this year and last, they are, at best, obstructionists.

This year’s example of foolishness:

In the triage room, I felt really bad, clammy and sweaty. Then I was on a gurney being rushed to the ER trauma room. It wasn’t like fainting, because it wasn’t gradual (when I’ve fainted, usually things turn black but I can still hear what is going on, and then I’m down). I wasn’t out for long, and the ER staff started getting fluids in me as quickly as it could. Seems to me an obvious case of hypovolemic shock. This happens with blood loss.

But the hospitalist saw things differently. He wanted to know about my history of seizures. I don’t have one. What, this has never happened before? Well, yea, once, last year, when I was throwing up golfball-sized clots of blood. Ah ha, so you do have a history of seizures. No I don’t.  How I hate being in no position to resist.

Next thing I knew I was wheeled away and my head was in the damn doughnut — a brain CT, looking for the cause of my “seizures.” CT was normal (duh), so the next day in comes the EEG woman to stick wires on my head. EEG normal — well a bit of excess in the betas, probably related to anxiety (does exasperation count as anxiety?).

This year, 20 hours passed before I had an endoscopy to look for the cause of the bleeding, compared to last year’s 4. Meanwhile, my hematocrit kept falling. Finally, when it hit 7.3, 32 hours after my arrival, I was transfused, compared to pretty much immediately last year.

Was there a connection between the relative slowness of dealing with the problem (blood loss) this year and the the hospitalist’s obsession with seizures?  I don’t expect to ever know the answer. It was, however, most definitely an annoyance I didn’t need.

An Uneventful Day, Unlike Last August 2

Update: The current (November 2014) hypothesis among my doctors is that whatever they were called in my past posts — Dieulafoy lesions, Cameron’s erosions, or bleeding ulcers — all these bleeds have their source in the portal hypertension which comes from cirrhosis which is caused by my auto immune system attacking my bile ducts, that is, my primary biliary cirrhosis.

I know what I was doing a year ago this afternoon: throwing up copious amounts of blood. I posted about various aspects of my Dieulafoy’s lesion (a burst artery where the esophagous meets the stomach) episode last August, but here I go again.

I suppose this was the closest I’ve come to dying, but we never know, do we? I mean, how many times have we avoided accidents by being caught at a red light or leaving the house a little earlier than planned? Slipped and bruised our limbs when we could have smashed our heads? Etc.

But leaving the hypothetical, losing enough blood to need 4 transfusions, one right after the next, is serious business. Had I been alone, or in a remote area, or in most parts of less-developed nations, I would not have survived. I was lucky in my bad luck: the EMTs arrived quickly and started oxygen and IV fluids to raise my dangerously low blood pressure, and I got to a hospital where an endoscopy procedure stopped the bleeding.

What seems remarkable now is how little effect the whole event seems to have had on me — physically and psychologically. I’ve had colds it took far longer to recover from. And I’ve had other medical crises that took a lot longer to come to terms with.

I’ve concluded there were two factors in this case that, as horrific as the experience was, made it less traumatic than you might expect:

  • I was so impaired mentally that as the crisis unfolded, I couldn’t process it.
  • It was pure bad luck. There was absolutely nothing I should have done, but didn’t, or shouldn’t have done, but did, that had anything to do with anything.

I’ll explain. When I learned later that I had been losing blood all day, I realized  the cause of some odd responses I had had that day. It’s about twenty footsteps from my bed to refrigerator, but each time I got up to refill my drink, I had to lie on the kitchen floor for a while before returning to bed. I didn’t think this worth mentioning to anyone, however. And when my husband told me that I had to go to the ER, I complained that I wouldn’t because I was too weak to go. How’s that for logic?

On the way out the door I said I had to rest, and so my husband went to get the air on in the car, and my son stayed with me. Then I started throwing up blood. I don’t remember seeing anything else until I was in the ambulance, although I am told my eyes were open.

So much I didn’t know. I thought my kids were stroking me gently as I lay still when in fact they were pressing on me with all their weight to keep me from rolling on my back and choking as I flailed about. I could hear, however (hearing is the last sense to go among the dying, interestingly). I was bothered by what sounded like a bell. Later I figured it was the metal oxygen tank.

I was in no pain. Moreover, in spite of all this drama I was not scared or worried. I was too mentally impaired, I suppose. Even when I came around in the ambulance, all I thought was, so this is what the inside of an ambulance looks like. Once in the ER, I was annoyed by the pain of the IVs and by not being allowed anything to drink, and I wanted the blood cleaned out of my hair. Only when it was time to be knocked out for the endoscopy repair job did I get upset. I guess on some level I feared not waking up.

Much later, I asked my kids what they thought when I got hauled off in the ambulance. They told me they thought I was  going to die. That’s all that continues to bother me; I am terribly sad that they went through that.

But there is a difference between being sad for them and feeling guilty, and I know that there was nothing I could have done to prevent what happened. Nothing.

Pure bad luck. There is such a thing.

Today was an uneventful day. It was an anniversary of no importance to anyone — just another day. For that I remain grateful.

Of Dieulafoy’s Lesion, Diagnoses and Doctors

InUpdate: The current (November 2014) hypothesis among my doctors is that whatever they were called in my past posts — Dieulafoy lesions, Cameron’s erosions, or bleeding ulcers — all these bleeds have their source in the portal hypertension which comes from cirrhosis which is caused by my auto immune system attacking my bile ducts, that is, my primary biliary cirrhosis.

one of my posts last month, At Risk for Esophageal Varices and I Nearly Bleed Out from a Gastric Ulcer: How Weird Is That?, I raised these questions: can a burst esophageal varice adjacent to the cardia be mistaken for a spurting gastric ulcer? Is it really possible to have such an awful gastric ulcer and no abdominal pain?

I’ve since had a follow-up endoscopy, this one by my hepatologist, and will have another in a month’s time when the clips that the GI used in his repair fall off. They obscured the full view of what the hepatologist thinks may have been neither a gastric ulcer nor an esophageal varice but something else altogether: a Dieulafoy’s lesion.

So I was a just little bit right, or not altogether wrong. My gut instinct — that I couldn’t really have a gastric ulcer — may prove right, but I got caught up in the either/or fallacy: either ulcer or varices, never knowing there could be other possibilities, like this thing called Dieulafoy’s lesion.

It isn’t surprising that a Dieulafoy’s lesion could be mistaken for an ulcer, expecially when it is spurting blood.

A Dieulafoy’s lesion is an “uncommon cause of major gastrointestinal bleeding”

caused by an abnormally large-calibre persistent tortuous submucosal artery. . . The artery protrudes through a solitary, tiny mucosal defect (2-5 mm), commonly in the upper part of the stomach. It may rupture spontaneously and lead to massive bleeding. It has been suggested that the thin mucosa overlying a pulsating artery is eroded progressively by the mechanical pressure from the abnormal vessel.

So it isn’t a disease or chronic condition. It’s a mechanical failure.

Dieulafoy’s lesions and gastric ulcers can be fixed the same way. If the fix is the same, does it matter whether the problem is a Dieulafoy’s lesion or an ulcer?

I think it does because if it is a lesion and not an ulcer, I don’t have to take drugs to inhibit the development of ulcers, and I don’t have to avoid aspirin, ibupropen, and a host of other painkillers, or make dietary changes. I don’t have to worry about an ulcer recurring, either.

So why did the GI see one thing and the hepatologist another?

I’m not sure, but I suspect what we have here is another example of the simple fact that some doctors are better than others. I know there are people who don’t question doctors because they assume anyone accepted into medical school and who makes it through the training must be pretty bright. That stands to reason.

And yet. . . have a look at the night sky. All stars are bright, but some are a lot brighter than others. That might bear remembering if you have your doubts about a diagnosis.

Recognizing a Dieulafoy’s lesion depends on “awareness of the condition and experience in endoscopy.” Experience comes with time, but awareness — well, that seems to me what separates the good from the best.

Had the GI considered Dieulafoy’s lesion as an alternative to an ulcer, then I would assume the next step would be to consider what was known about my case and compare it to what is known about these lesions.

Here are some distinguishing characteristics of Dieulafoy’s lesions:

  • The most common presenting symptom is recurrent, often massive, haematemesis associated with melaena (51%).
  • Characteristically, there are no symptoms of dyspepsia, anorexia or abdominal pain.
  • Initial examination may reveal haemodynamic instability, postural hypotension and anaemia. The mean haemoglobin level on admission has been reported to be between 8.4- 9.2 g/dl in various studies. The average transfusion requirement for the initial resuscitation is usually in excess of three and up to 8 units of packed red blood cells.
  • Approximately 75% to 95% of Dieulafoy lesions are found within 6 cm of the gastroesophageal junction, predominantly on the lesser curve.
  • A history of NSAID [nonsteroidal anti-inflammatory agents/analgesics] or alcohol abuse is usually absent.


Check, check, check, check, check: all true for me.

Reading Your Ambulance or EMS Report, Part 2

Picking up from where I left off in my previous post, there are a few more boxes left to read on the Ambulance or EMS Report, and then there is a narrative or Assessment.

In the center of my form are vital sign readings. One thing that surprised me at first was that although the EMS arrived at my home at 16:00 and started oxygen at 16:04, the first set of vitals is for 16:15. That must have been when I got loaded into the ambulance. Prior to that, the EMS had to see where I was and what was happening, and get the oxygen started. Then I had to get carried from the house, secured on a gurney,  and then the gurney was carried to the ambulance. While one team member [#709] ran an EKG strip, another [#332] took the first set of vitals and then a minute or two later started the IV.

The team took my vitals every 5 minutes. These included pulse, respiration rate, blood pressure, and oxygen saturation. My glucose was measured and my pupils were marked as =R, which I think means equally responsive or reactive. Skin color/condition was “pale, diaphoretic, cool.” Diaphoretic means sweating. When these three descriptions appear together, something is wrong.

Next is AVPU. This stands for Alert, Verbal, Pain, and Unresponsive. Alert is normal awareness, Verbal means that the patient responds if spoken to, Pain means that patient responds by flinching or pulling away from a source of pain, and Unresponsive means just what it says. Verbal is tried before Pain. Your possible grades are: A, V, P, U.


Reading Your Ambulance or EMS Report, Part 1

Let’s say you too got hauled off in the ambulance and are as morbidly curious as I am and so got hold of the report your Emergency Medical Services team left with the ER.

Now what? How do you read this thing? What do these abbreviations mean?

I spent a fair amount of time googling these questions, and to save you the bother, I’ll walk you through mine. I have a lot of blank boxes on mine, so I didn’t research these, but I imagine the boxes on mine that are filled are fairly routine. I assume too that the forms are pretty standard from EMS to EMS.

The page I’m interested in is headed by the usual stuff: name, date of birth, allergies, medications, relevant medical history.

The first thing I wanted to see was what happened when.  This is documented in a box called Event Times, roughly in the center of the page. In my case, the first time noted (and a 24-hour clock is always used), 1556 [3:56 pm] is next to “Crew TOC.” I found one reference to TOC as “Traffic Operations Center”; what I think is meant here is time the crew received the call from dispatcher at 911. Next, Enroute Scene, also 1556. Then Arrive Scene, 1600. Next, Enroute Facility, 1622. Arrive Facility, 1629. Available for Call, 1702. This tallies well with what my family remembers, that is, that the ambulance got to our house minutes after my husband called 911 [actually, 4], and they worked to stabilize me for about 20 minutes before leaving for the hospital [22, in fact]. Once they got me to the hospital, they were busy for 33 minutes filing reports and cleaning up the ambulance, I guess, before being again ready for action.

How the ER doctor could summarize this timeline as “She became dizzy and came to the emergency room for further evaluation” remains to be seen.

Back to the top of the form.

The first box I get a tick in relates to oxygen delivery: nasal cannula, one of those plastic tubing things that hook on behind your ears so it stays in place while two little tube prongs deliver air to you through your nose.

I’m going to skip a box for now to get to Medications. Interestingly, oxygen is considered one. I find that at 1604, EMT #709 (the crew is identified by numbers, not names) began giving me a dose of 6 using route NC. NC is nasal cannula. I learned that an NC “can only comfortably provide oxygen at low flow rates, 0.25-6 litres per minute (LPM), delivering a concentration of 24-40%,” so I figure a dose of 6 means 6 litres per minute. At 1617 I received 4mg of Ondansetron [an anti-vomiting drug] by way of my IV.

Above Medications is a place for recording information about IVs. The first two boxes are straightforward: Time and By [whom (id number)]. Next is  Cath. This is short for catheter and is what you and I call the needle. In the box beneath that heading I found “18,”  the size of the needle, no cath, that is usually used on adults.

Next heading is Site, for example, right wrist. Under Fluid Type NS is ticked: normal saline. Rate is designated as “open”; this means that the purpose of the IV was to get fluids into me quickly to help restore falling blood pressure that results from blood loss and shock. Something that might appear there instead is TKO or KVO:  KVO is Keep Vein Open; TKO is To Keep Open. In these cases, an EMT explains, “The drip rate is minimal – only to keep the vein open and to prevent obstructions from forming so future infusions will properly flow. TKO and KVO are interchangeable. Wide open: to infuse the fluid as fast as the vein/cannula/gravity will allow.” The next box is  Amt Infused; in my case,  750 ml.

Finally, there is this heading: Attempts. Starting IVs can be difficult. My report shows it took 2 tries to get an IV started. I’ve since learned that most EMS are supposed to make only 2 or 3 attempts at placing IVs before going to the next level, an IO. IV stands for intravascular, vascular means veins. IO stands for  intraosseous, osseous means bone. Let’s put it this way: some of the tools involved in IOs look like mini power drills. I’m not going there. You can if you want. Just click here.

Then we have Cardiac Monitoring and Transmission where it is noted that EMT 709 started a 4-lead EKG on me at 1615. A 4-lead is used for monitoring purposes; should my complaint have been chest pain or something along those lines, a 12-lead EKG reading would have been done.