Etiology
The pathophysiology of delirium is not very well defined, however several theories have been proposed.
Cerebral Hypoperfusion
Neuroimaging studies have provided evidence that delirium may manifest as a result of widespread brain dysfunction rather than a localized dysfunction. It has been suggested that a disruption to cerebral blood flow affecting a large portion of the brain may play a part in the development of delirium. Subcortical and occipital regions have been noted to display even greater cerebral blood flow disruption during and after acute delirious states. This cerebral blood disruption may have several different etiologies including: microemboli migration post surgery, inflammation or changes in hormone levels.
Neuro-Anatomical Changes
Neuro-anatomical changes have been noted in different patient populations experiencing delirium. One study revealed that 61% of critically ill patients were found to have gross white and gray matter lesions or ventricular enlargements. These cellular changes may explain some of the long term cognitive and behavioural sequelae of delirium.
Sepsis
Sepsis has been associated with the development of delirium as well. It is thought that acute CNS dysfunction may be a result of the degradation of the BBB by the associated septic inflammatory cascade.
Sedative and Analgesic Use
There has been lots of proposed mechanisms of delirium development surrounding sedative and analgesic use. The most common theory involves the use of benzodiazepines which bind GABA receptors in the brain and decrease CNS arousal. This can lead to unpredictable neurotransmission and cerebral functioning resulting in neuronal atrophy and long term cognitive impairment.
Neurotransmitters and Hormones
Many different neurotransmitters and hormones, such as serotonin, catecholamines, cortisol etc. have been suggested to have a part in the development of delirium. Their exact mechanism isn’t very clear in the literature, as both increased and decreased levels of these substances appear to be able to cause delirium.
NOT LIKELY TO HAVE ONLY ONE CAUSE!
It is important to note that delirium is not likely to have one single cause and that not one etiological pathway has been linked to a specific subset of delirium. Therefore, a thorough assessment of a patient's potential multi-factorial causes of delirium is essential.
Cerebral Hypoperfusion
Neuroimaging studies have provided evidence that delirium may manifest as a result of widespread brain dysfunction rather than a localized dysfunction. It has been suggested that a disruption to cerebral blood flow affecting a large portion of the brain may play a part in the development of delirium. Subcortical and occipital regions have been noted to display even greater cerebral blood flow disruption during and after acute delirious states. This cerebral blood disruption may have several different etiologies including: microemboli migration post surgery, inflammation or changes in hormone levels.
Neuro-Anatomical Changes
Neuro-anatomical changes have been noted in different patient populations experiencing delirium. One study revealed that 61% of critically ill patients were found to have gross white and gray matter lesions or ventricular enlargements. These cellular changes may explain some of the long term cognitive and behavioural sequelae of delirium.
Sepsis
Sepsis has been associated with the development of delirium as well. It is thought that acute CNS dysfunction may be a result of the degradation of the BBB by the associated septic inflammatory cascade.
Sedative and Analgesic Use
There has been lots of proposed mechanisms of delirium development surrounding sedative and analgesic use. The most common theory involves the use of benzodiazepines which bind GABA receptors in the brain and decrease CNS arousal. This can lead to unpredictable neurotransmission and cerebral functioning resulting in neuronal atrophy and long term cognitive impairment.
Neurotransmitters and Hormones
Many different neurotransmitters and hormones, such as serotonin, catecholamines, cortisol etc. have been suggested to have a part in the development of delirium. Their exact mechanism isn’t very clear in the literature, as both increased and decreased levels of these substances appear to be able to cause delirium.
NOT LIKELY TO HAVE ONLY ONE CAUSE!
It is important to note that delirium is not likely to have one single cause and that not one etiological pathway has been linked to a specific subset of delirium. Therefore, a thorough assessment of a patient's potential multi-factorial causes of delirium is essential.