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[Pathophysiology of delirium].
Tajana Zah Bogović1, Dinko Tonković, Ante Sekulić
1University of Zagreb School of Medicine, Department of Anesthesiology, Resuscitation and Intensive Care, Zagreb University Hospital Center, Zagreb, Croatia. tajana.zah.bogovic@mef.hr
Delirium involves complex pathophysiological mechanisms, with neurotransmitters like acetylcholine and dopamine playing key roles. Understanding these factors is crucial for managing delirium, especially in intensive care and postoperative settings.
Area of Science:
- Neuroscience
- Pathophysiology
- Critical Care Medicine
Context:
- Delirium pathophysiology is not fully understood, with limited insights into neuronal and glial cell death biomarkers.
- Neurotransmitter imbalances, particularly involving acetylcholine and dopamine, are implicated in delirium pathogenesis.
- Sepsis and iatrogenic factors like sedatives and benzodiazepines are significant contributors to delirium, especially in intensive care units and postoperatively.
Purpose:
- To explore current hypotheses regarding the pathophysiological mechanisms of delirium.
- To identify key neurotransmitters and biological markers associated with delirium.
- To review common causes and risk factors for delirium, including sepsis and postoperative complications.
Summary:
- Delirium is linked to neuronal and glial cell damage, with neurotransmitters such as acetylcholine, dopamine, GABA, glutamate, and monoamines playing critical roles.
- Systemic inflammatory response syndrome from sepsis is a common cause of delirium in intensive care units.
- Benzodiazepine use increases the risk of postoperative delirium, which, along with other cognitive changes, is more prevalent in older patients.
Impact:
- Highlights the multifactorial nature of delirium and postoperative cognitive changes.
- Emphasizes the need for further research into delirium biomarkers and therapeutic targets.
- Informs clinical practice regarding risk factors and prevention strategies for delirium in vulnerable patient populations.
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