Primum Non Nocere

To the patient I couldn't help the other day.

I'm sorry we couldn't help you. I know you don't quite believe what I said and I know your personal opinion remains strong. Though you leave frustrated and disappointed, I hope you at least trust me that what we suggest is what we think is best for you. Your best interest was my only priority.

After all, our first rule is Primum Non Nocere- First Do No Harm.

One reason this was a busy week, was an exceptionally high number of hypo_glycemia patients we saw this week. I saw 4 myself, all post-gastric bypass. The high volume is undoubtedly from the many publications my colleague has on this topic, creating a major (crazy) referral bias. My 2nd publication on this topic should come out in Endocrine Practice this month. The referral bias lends itself to another problem which I shall not go elaborate too much, but let's just say when patients are coming from as far as Alabama and Texas, they expect to see you, get the mixed-meal test (fully expecting positive results), CT and/or ultrasound, then the calcium stimulation test, then the surgeon, then have surgery, and be discharged all within a week. Granted, it's expensive to fly in and stay in town, but you can't rush these things. And this leads to high expectations.

The fundamental issue with hypo_glycemia is one needs to fulfil Whipple's triad: 1) Documentation of low serum glucose (less than 50 mg/dL), 2) Concurrent symptoms of neuroglycopenia, 3) Resolution of symptoms with glucose treatment.

It's a fact that serum glucose can drop below 50 mg/dL in normal, lean healthy subjects, and therefore presence of symptoms at the same time needs to be well documented. In the case above, my patient had symptoms at a glucose level of 91 mg/dL, and she's trying to talk me into sending her to pancreatic surgery. She's convinced that 90-100 mg/dL is too low for her. I would not be acting in her best interest, if we took out part of her pancreas, based on available data.

The next step once this has been documented, is to know what the c-peptide and insulin levels were to ensure this was insulin-mediated. Once shown, imaging should be the next step. Because no study has 100% sensitivity, we tend to do a CT, ultrasound, and sometimes endoscopic ultrasound (no head-to-head comparison, but thought to be the most sensitive of all) if the first test was negative.

If nothing clear lights up to suggest insulinoma, a selective arterial calcium stimulation test is usually the next step, to regionalize the problem. 0.025 mEq/kg of calcium is injected into the vessels feeding the pancreas, while insulin levels are measured in the hepatic vein to look for doubling or tripling of insulin.

Only in well-defined cases, do we consult the surgeons. And even then, treatment is not always surgical, as nesidioblastosis may recur and so we reserve that for the refractory, severe ones.

My personal total is now 18 patients, probably the highest amongst the fellows in my division, since I have an interest in this condition. Something that occurs less then 6/1,000,000. Perhaps because of the bias, I must say though that I'm unnerved at the number of bypass patients I've seen presenting with hypoglycemia. Some are clearly not real, and yet there appears to be something, from the altered anatomy, that causes their symptoms that are not glucose-mediated. The ones that are real, what IS the best treatment? Beats me... just 2 years ago when I drafted my manuscript on this subject, we thought surgery should be firstline. Now, with the recurrences we see, I don't think so anymore.

It's a challenging medical mystery. Why this happens. How to treat it. Why patients feel the way they feel. Made more challenging when they come with preconceived notions that they will definitely have surgery.

(if I seemed vague about this condition, it was intentional due to the rarity of it and not wanting anyone to Google my blog. But if you have a medical background you probably know what I refer to. Reference here)