a question about glucose toxicity & DKA (re: cloudedbrains aka Donna)

I was also wondering, couldn't these high bg's (340 mg.dL & above)
put her at risk for DKA?

So what if she goes into DKA or something like that, goes
unconscious, goes to emergency, and then is unable to
tell them about the asthma problem in addition to
the high bg's?

Could bg's this high for a sustained period fo time cause
DKA? I guess it all depends on the person, right?

I found this in the archives:


http://tinyurl.com/yxbnk9
__________________________________________________ _____________
mesage #16:

From: Mack - view profile
Date: Sat, Oct 20 2001 3:18 am
Email: Mack <der...@diabeticnetnospam.com>
Groups: alt.support.diabetes

high BGs can result in DKA which can kill, not instantly mind you but
there is no set time limit to when DJA can result in coma and death.
Low BGs are more frequently more sudden and very dangerous depending
on how low and how quickly one goes low.
__________________________________________________ ____________

i was diagnosed with a fbs of 300. during those days i was drinking a few
half gallons of juice per day. mostly pine applejuice. while my fbs was
300 and that was atleast 8 hours after eating.
i wonder how high my blood sugar was after drinking a half gallon of
pineapple juice.
i was going to the bathroom a lot. always thirsty and always drinking some
kind of juice.
i wish i had a meter on those days before dx.

Tom

dumb_fishie99@yahoo.com wrote in message
<1161113665.357488.135770@m7g2000cwm.googlegroups. com>...
>I was also wondering, couldn't these high bg's (340 mg.dL & above)
>put her at risk for DKA?
>
>So what if she goes into DKA or something like that, goes
>unconscious, goes to emergency, and then is unable to
>tell them about the asthma problem in addition to
>the high bg's?
>
>Could bg's this high for a sustained period fo time cause
>DKA? I guess it all depends on the person, right?
>

DKA is caused by a lack of insulin. High blood sugar is not a cause of
DKA, it is an effect of the same lack of insulin that causes DKA, i.e.

http://www.emedicine.com/med/byname/...toacidosis.htm

"DKA is a complex disordered metabolic state characterized by hyperglycemia,
acidosis, and ketonuria. DKA usually occurs as a consequence of absolute or
relative insulin deficiency . . ."

The body's response to the lack of insulin is to metabolize fats to sustain
life. That results in a surplus of ketones and acid end-products in the
blood. The end products will actually lower the pH of the blood (A
serious condition) Hence the name: "ketoacidosis".

It is difficult to judge exactly how insulin-deficient a person is by merely
detecting high blood sugars.

FWIW, Donna ("cloudedbrains") is taking a steroid. Steroids force the
liver to put extra glucose into the blood. A T2 on steroids can have both
high blood sugar and substantial insulin levels.

Type 2 diabetics are subject to NKH. That makes diagnosis a bit more
tricky since, unlike DKA, there are no ketones in the urine or in the
breath to act as an early warning alarm. Also, NKH tends not to change
the pH of the blood. The pH change produced by DKA is easily detectable and
acts as a strong warning signal.

http://www.embbs.com/cr/dka/pathdia.html

". . .History and Physical:

NKH is a slowly progressive disease and it is not uncommon to have 3-10 day
history of increasing thirst, polyuria, and malaise. Courses of up to three
weeks have been described. Symptoms of an underlying infection may be
present, but in some cases there is little history and the clinician must
consider this diagnosis in the elderly obtunded patient.

Patients usually have evidence of dehydration such as dry mucus membranes,
tachycardia, poor skin turgor, and sometimes a low grade fever. The blood
pressure is usually well preserved unless there is severe dehydration or
infection. Respiratory symptoms are usually absent unless the patient has
pneumonia. Central nervous system dysfunction is relatively common in
patients with NKH. Lethargy and disorientation are common, but frank coma is
rare. It is critical to remember that these CNS symptoms rarely present
unless the effective osmolarity is greater than 340-350 mOsm/L. Patients
with altered sensorium and osmolarity less than this should have a different
etiology searched for. Any area within the brain can be affected, and while
focal neurologic findings are uncommon in DKA, they are fairly common
in patients with NKH. . . ."

(BTW: isn't Doctor-ese fun to read!)

Regards
Old Al