Hypoglycemia in a patient with Dengue shock syndrome on vasoactive agents, when administered D25W, there was an increase in the blood pressure. Is it just adrenal insufficiency, or is there any other explanation for the response?
Perhaps Herlein JA et al's article may give you a hint or indirect evidence.
Also need to consider the effect of high glucose levels on endothelial cell function.
Two things happened when this patient was treated for their Dengue shock: administration of dextrose and administration of volume. One cannot assume that the dextrose alone was responsible for the improvement.
Second point: research on sepsis and trauma shows that almost all the physiology that happens in 'normal' people is different when subject to stress, including sepsis.
Third point: hypoglycaemic response tachyphylaxis, as seen in diabetics and in the rodent paper highlighted by Victor, is probably not a mechanism in the stressed, counter-regulating patient.
So....who knows?
Martin
Thank you Dr. Platt for the input. Clarification: the patient was administered IV fluids (keeping aside colloid vs. crystalloid debate for the current discussion), but to no significant response.
I have seen a patient whom presented as septic, with a background of total hepatic failure who significantly responded to the administration of 20% dextrose during an hypoglycaemic event, with inotropic support being significantly reduced with an increased and sustained mean blood pressure post administration.
But despite this recovering blood pressure with significantly reducing vasopressor support, the patients lactate and potassium levels significantly increased. I can only assume this was due to cellular release with increased perfusion at a cellular level!
I hope this helps.
Hyperglycemia aggravates hypertension and hypoglycemia should aggravate hypotension. It might indicate adrenal insufficiency however more information needs to be known before a definite correlation can be made.
Glucose is required for cellular metabolism. It makes sense that when there are insufficient stores cellular function decreases. This would be no different for arteriolar smooth muscle function and so it makes sense that when glucose stores are restored BP should normalise reducing inotrope requirements
There is agreeance with Christine's response, but if acute and chronic conditions such as AKI etc exist, then the cellular rebound response of electrolytes such as hyperkalemia can result in catastrophic consequences if the appropriate therapies are not implemented or utilised appropriately.
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