Unresponsive Hypoglycemia Mortality?

S

Simusid

Forum Captain
Messages
336
Reaction score
0
Points
16
66 YOM found unresponsive in bathroom. Unknown down time estimated at over 2 hours. CBG was 18. Very diaphoretic and cold with snoring respirations. D50 administered and pt was verbally responsive in under 2 minutes.

Question: (yes I know "it depends" and "every patient is different") How long can a patient in this condition survive? That is, how much longer could he survive with a glucose of 18? An hour? Three?
 
I tried searching and all I could find was a complicated Neuroscience article about inducing hypoglycemia in rats to cause Neuronal death and from what I gathered at around 5 hours of hypoglycemia you have a 15% chance of neuronal survival and 0% at 7 hours. I am sure this would be accelerated by hypoxia related to seizures.

Also I remember reading that, through various pathways, hypoglycemia lengthens then QT interval and can cause sudden cardiac death.
 
Last edited by a moderator:
This article http://www.jci.org/articles/view/31669 says

"Profound, prolonged hypoglycemia can cause brain death. In studies of insulin-induced hypoglycemia in monkeys, 5–6 hours of blood glucose concentrations of less than 1.1 mmol/l (20 mg/dl) were required for the regular production of neurological damage"

So that gives me a good sense of an answer to my question.

The article presents data that in the case of profound hypoglycemia (< 18 mg/dl) glucose reperfusion may actually cause neuronal damage.
 
Simusid said:
This article http://www.jci.org/articles/view/31669 says

"Profound, prolonged hypoglycemia can cause brain death. In studies of insulin-induced hypoglycemia in monkeys, 5–6 hours of blood glucose concentrations of less than 1.1 mmol/l (20 mg/dl) were required for the regular production of neurological damage"

So that gives me a good sense of an answer to my question.

The article presents data that in the case of profound hypoglycemia (< 18 mg/dl) glucose reperfusion may actually cause neuronal damage.
Click to expand...
True, but the article also stated that the glucose reperfusion fluid was more at the high/extreme end of what they could use. The other thing I read was simply that they were recommending correcting a hypoglycemic patients' blood glucose level to a physiological norm instead of "aiming high" (my words) and achieving/maintaining a hyperglycemic state for post-hypoglycemic recovery.

That was an interesting read, I must say.
 
Unless the Nazis worked on it, has to be anecdotal.

I imagine likelihood is lowered once seizures set in due to apnea, potential trauma from fall, and airway embarassment.
 
There might be some human data to answer this, but if it exists, you might have to dig back to the days of when rapid blood glucose testing wasn't readily available and/or rapid treatment wasn't readily available (insulin wasn't a treatment until the 1st half of the 20th century). Considering that by far the most common cause of hypoglycemia is diabetes meds and that research wasn't common, there may never have been any real human data collected.

The animal based research may be ones best bet.
 
Doubt animal studies are useful.
 
Simusid said:
Yeah, the saddest part is that it occurred AFTER they were informed of the nature of the false readings.
Click to expand...

The failure seemed to be not in the handoff from OR to PACU, but from PACU to SICU. While extremely unfortunate, I think we can also easily imagine how this sort of thing could occur; it seems like a textbook kind of error. Many mistakes can be traced to transfer of care.
 
It sounds like a teaching hospital or larger facility if it had a 40 bed SICU. That is just horrible communication and failure to hand off critical information appropriately. You think you would get them an armband or something saying no capillary blood sugar.
 
silver said:
Would any human study be very useful? The variation in ketone production and utilization of the brain is quite dramatic.
Click to expand...

Hypoglycemia produces ketones? Hm! Never thought.
 
mycrofft said:
Hypoglycemia produces ketones? Hm! Never thought.
Click to expand...

Not sure if trolling me or not...
http://en.wikipedia.org/wiki/Ketotic_hypoglycemia#Hypoglycemia_with_ketosis:_the_broad_sense

Here is the biochem down and dirty:
Hypoglycemia causes the release of glucagon, catecholamines, and cortisol. This stimulates beta oxidation (breakdown of fatty acids) and forms acetyl CoA. At the same time your muscle protein is being broken down and glucogenic amino acids can feed into the CAC/TCA. Acetyl CoA can then feed in to the cycle to produce energy. However we have a problem as the brain needs glucose. So those amino acid derivatives are being fed to producing glucose through gluconeogenesis. You are left with lots of Acetyl CoA, which is converted to ketone bodies. These ketone bodies can provide fuel for up to 1/3 of the brain's required energy. However, levels of the enzyme expression to convert back to acetyl CoA vary in the brain. A person who 'starves' themselves often will have more and can utilize more ketones in these dire emergencies.

Know to explain hyperglycemic/diabetic ketoacidosis:
The body doesn't have insulin, so the cells think they are in the same situation as above. This is pathological though. Gluconeogenesis produces huge amounts of glucose, beta oxidation causes acetyl-CoA build up, which is turned into ketones. Ketones are acidic...etc.
 
silver, I never troll, I just have gaps. Thanks for your patience.

I never had a hypoglycemic patient for whom ketones were an issue since we were already trying to get sugar into them and addressing potential/occurring seizure issues. Is the ketone issue in longstanding hypoglycemia, or in the post-ictal phase of an acute hypoglycemic episode?

I know, I know, the brain can run on ketones. It just sounds very counterintuitive. I feel, despite the science, that this might be more of a petri dish type issue than in a realistic emergency setting. I'll study your link more.

EDIT: OK I read it. Not to be grasping at straws, but "A high level of ketones in the blood, ketosis, is thus a normal response to hypoglycemia in healthy people of all ages" does not give me a picture of how high this is, nor its effects upon the renally, respiratorially, or hepatically challenged patient.
 
Last edited by a moderator:
Last edited by a moderator:
My understanding is that in hypoglycemia ketones aren't at a detrimental level, it is a safety mechanism. However in DKA, the cell thinks there is no glucose as insulin does not allow uptake. Therefore there is no feedback and glucose + ketones becomes 'high.'

I mentioned it in hypoglycemia, because a person's ability to uptake and utilize ketones in the brain varies and ultimately could alter the progressive effects of hypoglycemia. For example, it may take one person 3 hours to get neuronal death vs someone else longer.
 
You must log in or register to reply here.
Back
Top