Melclin
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Called at 2330 to an 82YOM, conscious collapse and cannot get up.
Pt present GCS 15, L sided hemiplegia, mild difficulty swallowing, aphasia and a BSL of 3.9mmol/L (70mg/dl).
Per our guidelines, this is hypoglycaemia but its clearly not causing his presentation.
I was wary about treating it at all but I was told by my clinical instructor to do so. I then suggested that I give him 2.5-5 grams and do another BSL from there. I was told to give the full 15 gram intial dose per guidelines. I didn't, instead giving 10 grams and found his next BSL to be 14.1 (255).
Not happy.
Q.1 Thoughts about treating hypoglycaemia in ?stroke pts? According to most medical texts a BSL of 3.9 is not really even hypoglycaemia. Profound hypo has to be treated, but at what point do you start shying away from treating?
Q.2 Regarding the association between hyper-G and increased mortality, is that more as a biomarker showing damage, predicting worse outcomes or is it the actual hyp-g causing the issue and as such will iatrogenic hyper-g cause problems?
I'd look it up myself but its so frustratingly hard to do research now that I've lost my journal privileges.
(FYI, this chap turned out to be having an intracerebral bleed and was admitted for observation).
Pt present GCS 15, L sided hemiplegia, mild difficulty swallowing, aphasia and a BSL of 3.9mmol/L (70mg/dl).
Per our guidelines, this is hypoglycaemia but its clearly not causing his presentation.
I was wary about treating it at all but I was told by my clinical instructor to do so. I then suggested that I give him 2.5-5 grams and do another BSL from there. I was told to give the full 15 gram intial dose per guidelines. I didn't, instead giving 10 grams and found his next BSL to be 14.1 (255).
Not happy.
Q.1 Thoughts about treating hypoglycaemia in ?stroke pts? According to most medical texts a BSL of 3.9 is not really even hypoglycaemia. Profound hypo has to be treated, but at what point do you start shying away from treating?
Q.2 Regarding the association between hyper-G and increased mortality, is that more as a biomarker showing damage, predicting worse outcomes or is it the actual hyp-g causing the issue and as such will iatrogenic hyper-g cause problems?
I'd look it up myself but its so frustratingly hard to do research now that I've lost my journal privileges.
(FYI, this chap turned out to be having an intracerebral bleed and was admitted for observation).
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