The issue of factors contributing to cerebral edema in DKA is as Dr.
Fischer outlined, not clearly defined from the literature. The best work
to date from Duck & Harris suggests that the two important contributing
factors, from their retrospective review were, a total fluid rate of >
4000 ml/sq. Mt and a sodium that does not rise as expected with
hydration. It's interestting to note that on Harris data from rabbit
models of DKA, crebral edema was demonstrated in virtually all the
cases. This suggests that occult cerebral edema probably occurs in many
clinical situations that we are not aware of. Intuitive concepts like
rate of fall of sugar or osmolarity have not been consistently shown to
be causative factors.Mel's recent study in 1995 supports this too.
I also agree with Dr. Steele that the assessment of hypovolemia and
severity of dehydration is exaggerated in an acidotic state because of
catecolamine induced vasoconstriction and tachycardia. To that I would
also add that because of Kusmaal respirations and mouth breathing the
mucous membranes appear drier than due to pure dehydration.
My personal experience of about 5 cases of cerebral edema is quite
varied. All except one were hyperosmolar (> 320mosm/L) on presentation.
Some had received aggressive fluid resuscitaion at referring ED's. There
was one whose blood sugars were actually in the 300-400 range on
presentation who subsequently developed cerebral edema and herniated.
Dr. Baxter's case confirms this variable experience.
I believe, as Dr. White said that if they are hypotensive on
presentation they deserve isotonic fluid boluses upto 40-60 ml/kg, as
long as total fluids is not > than 3000-3500 ml/mt sq/day. If they are
hyperosmolar (> 320) I correct over 48 hours. It is imprtant to be
vigilant all the time for any complaints of HA, worsening lethargy,
blurry vision, or a corrected sodium that does not rise with hydration.
These may be early signs of impending cerebral edema.
Hope that helps
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