Musings from Gruber: Mesenteric Ischemia

A Case:

60s F with PMHx HTN, PAD, LGIB, RA p/w chest pain.  Pt notes 3 months of diffuse intermittent belly pain, worse with eating and reports a 30 lb weight loss, due to loss of appetite. Belly pain a/w episodic chest pain and palpitations that gets better once abd pain subsides.  Pt notes vomiting and bloody diarrhea all night 2 days ago. Pt given sublingual nitroglycerin by EMS with some relief of pain.

Vitals: 149/94 125 afeb 100% (on RA)

Physical: nontender abd, no rectal exam documented
EKG: ST 130; ?st depression V2?
CXR: unremarkable
Initial labs: Bicarb 22.5; AG 22; BUN/Cr: 84/2.5; WBC 9; H&H: 11/34
Potential Hospital Course:
In view of nontender abdominal exam, ekg without acute findings, neg trop- pt admitted to telemetry.  A few hours later, pt c/o belly pain again and had mild tenderness now. Repeat labs showed bicarb 15, ag 19, h/h 8/24  lactate 4.8, vbg 7.15/23. Pt eventually gets CTA revealing pneumatosis, portal venous gas c/w mesenteric ischemia. Pt goes to OR and found to have dead gut

Discussion:
Were there warning signs on initial presentation that this pt had a life threatening abdominal problem?
  1. History of abd pain with weight loss with bloody BM concerning and requires workup (ex: CT abdomen).
    • Could be malignancy
    • Abd pain with eating could be post prandial angina seen with mesenteric ischemia.
    • Bloody bm could be lower gib or presentation of mesenteric ischemia
  2. Latched onto her presenting c/o chest pain and worked pt up for acs but her belly pain with chest pain should have prompted consideration of aortic dissection, mesenteric ischemia, malignancy, gerd.  AD and ME are dxs that need to be ruled out quickly as they can kill you quickly.  They both require CT with iv contrast (regardless of creatinine) to make dx
    • Pitfall: Assuming alternate dxs (such as chest pain or infectious colitis) when you get the nonspecific early findings of mesenteric ischemia
    • Response or lack of response to sl ntg doesnt help in making dx of cad.
      • esophageal spasm and other abd problems may respond to ntg
      • mi may not respond to ntg
  3. No rectal exam was done but pt has h/o lgib and reported bloody diarrhea
  4. Initial labs appeared unremarkable ie bicarb 22.5 and ht 34 and wbc 9 but pt did have ag 22 indicating  metabolic acidosis.
    • Close to normal bicarb in face of elevated anion gap may be due to coexisting metabolic alkalosis due to vomiting and dehydration.
    • Regardless, AG of 22 indicates metabolic acidosis and cause of this requires workup and ruling out mesenteric ischemia in face of abd pain.
    • Case similar to prior EMRounds post where pt had very elevated AG which was not worked up and subsequent drop in bicarb, elevated osmol gap lead to diagnosis of ethylene glycol ingestion
    • Abnormal labs (ie cpk, bicarb, AG, hyperk) need to be addressed and repeated to see if they are improving or getting worse, usually after intervention
  5. BUN elevated out of proportion to creatinine indicates either upper gi bleed or that pt is very dry and needs fluids
    • This pt was probably very dehydrated from vomiting and needed ivf
  6. Lactate should have been sent in ED.
    • Important to remember that lactate lacks sensitivity especially in early presentation of mesenteric ischemia.
    • Do not rely on lactate to rule out mesenteric ischemia
  7. Mesenteric ishemia must be on your differential in any pt who presents with belly pain and has metabolic acidosis
  8. Consider vascular cause of abd pain in pt with h/o peripheral vascular dx
    • Pts with abdominal pain with vascular cause (ie AD, ME) may be NONTENDER
  9. We commonly use “cognitive forcing strategies” with chest pain to make sure we consider worst case causes of CP (ie aortic disseciton, pulm embolus) and should do the same with abd pain (ie could this be mesenteric ischemia or dissection?)
  10. CT findings in early mesenteric ischemia may be nonspecific (such as bowel wall thickening, bowel wall dilatation or mesenteric edema)
    • As with any disease, making the dx early in the presentation before it becomes obvious is challenging but this is where we can have the greatest impact

2 comments

  1. Addendum: Priya pointed out that the a-g decreased on the repeat labs but the bicarb decreased. This typically happens when the pt is given normal saline which closes the gap by increasing the chloride without affecting the bicarb. So now you have a non-anion gap met acidosis. This frequently happens in pts in dka who receive lots of NS. In this mesenteric ischemia case, the pt was getting worse and the bicarb decreased but the a-g was improving. So an important point is to not just look at the a-g which can be very misleading as to the pt getting better, but to look at the bicarb and the lactate as an indication of how the pt is doing

  2. Thank you for taking the time to write this Dr. Gruber. We don’t often get the opportunity to understand how an attending processes and thinks through a case so this was extremely helpful, informative, and educational.

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