Uncategorized

Mesenteric Ischemia Review in NEJM

This is a neat little review. 

While I am contemplating 345px-Ischemicbowel.PNGto actually starting a podcast that would review the GI literature in some detail on a monthly basis, i will prepare myself by posting a few reviews of the articles that sparked my interest/I feel are important for a gastroenterologist to be aware of.

I start with the March 10th Issue of NEJM, which has a nice summary article on Mesenteric Ischemia. Now if you are looking for a quick-guide to how to diagnose it or how to treat it – this is NOT the article for you. But if you want the details on exact specificity/sensitivity of different imaging modalities ( it happens to be 85% Sensitive-90% specific on Ultrasound, for example, and CTA is 95-100% Accurate) – then this is the article for you – you can download it and file it away for when you need the info. It is too bad that the authors did not want to make a table such as this (found and cited elsewhere):(which they cite as reference 26)

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But I understand that the aim here was to give a more “comprehensive” view on what mesenteric ischemia is for the general reader.  It has nice figures with examples of CTA with acute embolus to SMA, as well as chronic mesenteric ischemia with occlusion of SMA in setting of a celiac stent occlusion.

For the endoscopists amongst us, nothing is more true:”…endoscopic examination does not reach the majority of sections of the small bowel that are most frequently involved in mesenteric ischemia…” so dont scope of VCE these patients for no reason.

And now for clinical pearl:

Lawrence Brandt – a professor at Albert Einstein College of Medicine – one of the first persons to expose me to the wonderful world of gastroenterology loves to talk about non-occlusive mesenteric ischemia – NOMI  – Overall mortality is 50% – Mostly in patients with cardiac disease/complications/recent cardiac surgery. Papaverine hydrochloride through a catheter infusion can be considered. Not sure where else we can use Papaverine for a GI condition (let me know if you know).

To remember NOMI, Dr. Brandt usually brings up is a person in their 70s, with HTN, has an MI with hypotension, then stented, was put on beta blocker, and clopidogrel/aspirin, then develops severe abdominal pain. Exam is with mild tenderness, labs are unhelpful. INR is 2.1, everything else is ok. What’s the diagnosis? – NOMI!  Why? – vasoconstriction that is persistent,as a reaction to a previous insult, even if precipitating event is gone.

 

References as cited or linked.

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Article · CGH · Uncategorized

HCC in the absence of Cirrhosis

We often talk to
Hepatocellular_carcinoma_1.jpgour patients with cirrhosis regarding the risk of HCC, and putting aside the debate as to the efficacy of screening for such, most of our patients get the ultrasound twice yearly, +/- AFP every so often, and we cross our fingers and hope for the best, given how non-existent effective therapy for HCC is (other than resection).

This article in CGH – which regained the title of my second most favorite GI journal this week, is an article from the Texan folks, discussing HCC in the absence of cirrhosis.

This is a review of the Veteran’s Affairs database (boy would I love to get my hands on that!), 2005-2011 diagnoses of HCC, which was limited to 1500 random charts (obtained from a total of 10,695 HCC diagnoses).

~80% of the patients diagnosed with HCC had cirrhosis. Which means ~20% did not. Who are these remaining folks?

Many had metabolic syndrome, NAFLD, but some had no risk factors whatsoever.  It is interesting that in the cohort of 43 patients with what authors defined as “No cirrhosis – very high probability” – many still had some fibrosis.

In any case, logistic regression to look for associations and risk factors for HCC in absence of cirrhosis was conducted. Results:

NAFLD, HCV, HBV, Alcohol abuse, Metabolic syndrome, Others (hemochromatosis, autoimmune hepatitis, A1-AT deficiency). Idiopathic – only in 13 out of 194 patients!

Conclusions: 

  1. Glad to know that we are aware of major risk factors for HCC even in the absence of cirrhosis.
  2. No evidence as of yet to expand the risk pool to screen patients without evidence of cirrhosis.
  3. If chemoprevention is ever developed, now we know a good population to apply it in ( ex – Maybe Metformin?.
  4. It would be nice to have a large data dump of such patients on a national level, and include other variables in analysis, such as factors associated with good outcome or poor outcome. I suppose we can wait for the next paper.
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