Tag: Dieulafoy’s lesion

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.