Dijabetesna ketoacidoza kod bolesnika sa cerebrovaskularnim insultom - uzroci, mehanizmi, dijagnostika i naše smernice za terapiju

Aleksandar Jovanović ,
Aleksandar Jovanović
Vladan Perić Orcid logo ,
Vladan Perić
Snežana Marković-Jovanović ,
Snežana Marković-Jovanović
Tatjana Novaković ,
Tatjana Novaković
Slavica Pajović Orcid logo ,
Slavica Pajović
Saša Sovtić ,
Saša Sovtić
Srbislava Milinić
Srbislava Milinić

Published: 01.12.2020.

Volume 50, Issue 1 (2021)

pp. 29-33;

https://doi.org/10.5937/pramed2102029j

Abstract

Although cerebrovascular disease may be a well recognised trigger for diabetic ketoacidosis (DKA), literature data on the precise mechanisms, characteristics, or treatment guidelines are rare. The risk of developing an ischemic stroke is doubled in adults with diabetes compared to people with normal glucose metabolism. It is important to point out that even children with DKA have a significantly increased risk of cerebrovascular insult and that they can have a stroke with a frequency of about 10%. Given the significant overlap of symptoms between these two diseases, it can be assumed that attributing DKA symptoms as a manifestation of stroke is not uncommon, especially in elderly and less communicative patients. In addition, pH, bicarbonate concentration, and anion gap are not routinely measured in all diabetics suffering from stroke, at least not in secondary health institutions.Children who develop cerebrovascular stroke during DKA often at the beginning have a preserved consciousness or only mild confusion or lethargy. After a few hours, with the institution of therapy, however, loss of consciousness may occur accompanied by signs of increased intracranial pressure. It was previously thought that the cause was too fast fluid replacement. Recent data suggest that reperfusion injury may be a more likely mechanism. Although most of these studies relate to younger individuals with ketoacidosis, it is clear that at least some of them may be operative in adult DKA. Literature therapeutic guidelines for adult diabetics with stroke-related diabetic ketoacidosis are almost lacking, although it is clear that they could not be the same as those utilised in population with normal glucose metabolism. In this paper, we have tried to define our treatment guidelines for these particular patients.

References

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