Tag: gastric ulcer spurting blood

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.

At Risk for Esophageal Varices and I Nearly Bleed Out from a Gastric Ulcer: How Weird Is That?

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.

If you’ve read any of my posts on primary biliary cirrhosis (PBC), you were probably surprised by yesterday’s post that there wasn’t some sort of medical muddle involved. Wonder no longer: there was. It’s just that my emphasis was different so I left it for today.

I’ve written about being at risk for esophageal varices as a result of having PBC. These are swollen veins (like varicose veins), caused by portal hypertension (itself caused by cirrhosis [in the case of PBC — there are others. Click through to a site devoted to patients’ experiences with it]) in the esophagus. Left untreated these could “burst and bleed into the gut.”

But I had an endoscopy just this past January that showed only a trace of varices, and in such cases, 96% of people are trouble-free for at least 1-2 years (then they do another scope).

Of course, that means 4% of people aren’t.

So as soon as I regained consciousness in the ambulance, I alerted the chief EMT to tell the folks in the emergency room about this. And when I got there, I told them myself.

I will refrain from elaborating on how it feels while being transfused to have to repeatedly explain primary biliary cirrhosis and spell Urso Forte [the drug I take for it] to the ER nurses, and later my floor nurse and abdominal ultrasound technician.

However, following the endoscopy performed there in the ER trauma room, the GI who did the procedure reported that I lost enough blood to require four transfusions not because any esophageal varices burst, but because of a “gastric ulcer spurting blood.” He repaired it with three hemostatic clips and put me on pantoprazole.

But how weird is that? To be at risk of burst esophageal varices and have a gastric ulcer burst instead?

I reviewed my endoscopy report (high marks to the GI, who actually gave me a copy of my own medical report!) and found the location of the ulcer to be the cardia. Googled that, and discovered it is right where the esophagus becomes the stomach, and, in fact, for many years there was debate as to which organ it belonged to.

Now then, there is a new kid on the block at the hospital: the hospitalist. This person is sort of in charge of patients who come in through the ER and whose regular doctor doesn’t admit or have any role in their care. Like me. It took me two days to get someone to tell me who was really in charge of my case: the GI who did the procedure, or the hospitalist.

When the hospitalist visited me, I explained about my surprise that my bleed was gastric and not related to portal hypertension [PBC]. I told him that I didn’t have a local GI, but that I was under the care of a hepatologist at the UAB med center.

So the next day he returns, and says, “Good news: you don’t have to have a liver transplant.” I thought yeah, duh, but let him continue. He told me he had set up an appointment with the hepatologist who would do another endoscopy. And I said that sounds great, but what about this report from the GI deeming the cause of the bleed to be a gastric ulcer? The poor guy looked confused. I suggested he go back and have another (an initial) read of  my endoscopy findings.

But the hepatologist’s office and I agree that I should be seen by him. I have so many 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? Can portal hypertension cause a gastric ulcer? Will this happen again? And will I have no warning other than feeling steam-rollered before it does?

And just how weird is it, if it was a garden variety gastric ulcer, for this to happen to a person who has to worry about bursting varices?

Stay tuned.