Non Diabetic Hypoglycemic

DrankTheKoolaid

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Had an interesting call recently. Get called for unknown medical. Arrive on scene and receive report from patient spouse in driveway before entering residence that patient 60's YO F with a history of cervical CA and a recent Paracentesis (first incident of abdominal distention) drawing 3L off 5 days prior to my contact with her. Spouse relates patient increasingly weaker and has not eaten for 4 days, including the last 2 days while admitted.

Meds : Tinture of Opium, Omeprazole, Synthroid
Alleriges : None
PMH : Cervical CA, Chronic Colitis, G.E.R.D., Hypothyroidism with thyroid still in place

Patient who appears emaciated with a stated in hospital weight of 42kg at discharge, found inside residence. Patient is pale cool and dry, with slow but appropriate responses which is not her norm as I've known this woman for 15+ year. Patient states has had nausea non stop for the last 4 days without vomiting, but has decreased her appetite to nothing. Patient states attempted to drink juices but due to her chronic colitis the acidity of the juices does not sit well with her so she has been on a water diet.

PX includes purple colored hands cap refill 2 seconds with immediate blood produced from lancet use and feet with lower extremities with venous stasis ulcers (weeping) wrapped in ace wraps (when asked about Una's boots states they were removed 2 weeks ago and replaced with the ace wraps). Bruising noted all up and down arms from In-hospital IV attempts. hypertensive 140's/90's tachy at 110 ST without ectopy, 12 unlabored lungs clear unable to obtain accurate O2 sat, Tympanic temp 96.8 12 lead shows same.

Patient unable to even get into a standing position on her own. Once in truck en route 1h 15m to ED. IV 22ga (lucky to find that) with a BG of LO with 25g dextrose administered. 5 minutes pass and patient relates nausea is now gone. Patient remained pale cool and dry and slow to respond. Second BGL reading LO. 2nd 25g dextrose administered 5 minutes pass with patient global color is improving and speech is beginning to improve wait 10 minutes and recheck glucose. Reading LO. At this point i'm thinking there has to be a equipment malfunction so I test my own, (90 mg/dL) Post Mocha so feeling pretty good about that fyi, and test solution 277 mg/dL so machine is working as intended. Patient receives 3rd 25g dextrose, now sitting upright eyes remaining open and conversing as normal. Just prior to arrival at ED patient color noted decreasing back to pale. Report to ED staff which I get funny looks from the RNs accepting patient into a far corner room. Remained in room to see what ED staff obtained after 3 amps of dextrose. (F)BGL 20 mg/dL. RN no longer make eye contact with me and quickly move her front and center to the nurses station.

With the given history and medications. Whats everyone think about the glucose utilization here. I'll hopefully follow up with the PLN later this afternoon to see what they came up with.

3 amps is a first for me, and to see a 20 glucose afterwards is just baffling
 
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Interesting case. Perhaps insulinoma from ca mets. Also contributing would be poor nutrition and her being in a hyper metabolic state. Perhaps infectious process with the acites. Also note that with the possibility of infection, tachycardia, and temp she is close to SIRS criteria, only thing missing is tachypnea and/or white count changes and you only need one of those two. Also the possibility of her taking too much synthroid.
 
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re

Thanks, I am a bit embarrassed as I am not familiar with the SIRS criteria. But will be intimately familiar after this afternoons reading!
 
As Arovetli notes it seems mostly consistent with a radically hyperactive insulin production, but I'm interested in the lack of change on the fingerstick, despite the appropriate and consistent clinical improvements. I wonder if this could be a byproduct of some inherent limitation in bedside glucometry.
 
Sometimes it's really hard to believe the numbers - but the vast majority of the time, the numbers are correct. That applies to all sorts of monitors.

When pulse oximetry was introduced in anesthesia back in the 80's, it took us many months to feel comfortable believing some of the numbers we saw. We "knew" that there was no way the patient's SaO2 could be in the 80's. How did we know this? Well, we just looked at them of course. We finally came to realize that maybe this machine was a little better than we thought it was.

We did the exact same thing when capnometry came along. Now we're doing it with the BIS monitor which purports to help us determine level of consciousness. Far more often than not, the monitors are spot on.
 
Well, the nice thing is that generally the devices aren't magical black boxes. They work by known mechanisms, they are accurate to known levels, and they fail in known circumstances. Barring a novel error scenario, or gross mechanical failure (you dropped it and it got scrambled), you can usually predict the reliability of the equipment -- my understanding of capillary glucometry is just not deep enough to have an answer here.
 
One of the smart things corky did was check his machine once things got unusual. It sounds like he re-QC'ed it and verified it was functioning. Due to this and the fact that the ED readings were consistent I'd say the machines were right. Although the findings are unusual, all sorts of unusual things happen with metabolic disorders, especially with tumors of endocrine tissue. This is the kind of stuff that makes medicine fun.
 
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A lot of sugar per kilo body weight.

Pt came around clinically before her glucose test did. I have seen multiple instances of seizure at 20 or lower, and all at 20 were obtunded, anxious, diaphoretic, restless. What in the pt could confound the glucose test? Did blood appear normal or pale?

Sorry your long-term patient is in such a mess. Sounds like following the fingerstick with glucose was appropriate since she clinically improved, faster than the test machine did. You treated the pt and won.
 
Would have been nice to hear from the ED staff what the initial venous BG was, especially if it was obtained simultaneously with a FSBG.

Glucometers are pretty darn accurate in the stable patient, but in the shock state (and especially cardiac arrest!), they can be way off. See this article about checking, and correcting, glucose in cardiac arrest.

By the way, was the patient icteric/jaundiced at all? Acute liver failure (hepatic mets?) would be consistent with the decreased LOC and hypoglycemia, as well as ascites. Of course, 3 amps of sugar water doesn't usually correct the cerebral edema...
 
According to PLN, though patient had immediete bleeding with lancet they felt she was not getting enough circulation to show the corrected glucose levels. So basically in a shock state. And Kelly, no the patient was not jaundiced. Sorry I didnt put that in my write up with the history of ascites.
 
Corky, your presentation was one of the best I've seen here. Your face-palm is optional, and no dope-slap today.

More about modern fingerstickhttp://answers.google.com/answers/threadview/id/582772.htmlglucometers from "google answers"

And I quote:


"All modern hand-held "finger-stick" blood-glucose meters are based on
the reaction between glucose and an enzyme that catalyzes the
oxidation of glucose (usually the enzyme called, logically enough,
"glucose oxidase"). In this reaction, glucose is oxidized to hydrogen
peroxide plus gluconic acid...
A newer generation of glucose meters incorporates an electrochemical
cell within the device, and measures the integrated current produced
by the glucose oxidation reaction, a quantity that is proportional to
the amount of glucose present."

ENDQUOTE

Not sure what integrated current is, but I wonder what blood pH or the absence/presence of cells does to the reactions.

EDIT: Bigarse NIH article about glucometry:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2769957/
 
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Where I work we see this alot in drug addics. Heroin is the biggest offender for hypoglycemic non diabetics ( diabeticals as they refer to them selfs around here).
 
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Had a patient with multiple end stage cancers going through alcohol withdrawal (self medicating, can't blame him). He is not a diabetic, but the hospital had him on an D5W drip, which they DC'd before transport to a hospice facility. His glucose had dropped to 66 when I checked it enroute, and they restarted the drip as soon as we arrived at the facility.

There are probably lots of mechanisms by which a patient can have hypoglycemia without being diabetic. Its interesting to hear about a few of them.
 
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