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Additional features
Psychomotor behavioral disturbances such as hypoactivity, hyperactivity w increased sympathetic activity, impairment in sleep duration and architecture
Variable emotional disturbances, such as fear, depression, euphoria, or perplexity.
Epidemiology of delirium
Delirium patients experience prolonged hospitalizations, functional decline, high risk for institutionalization.
DELIRIUM vs DEMENTIA
Delirium and dementia often occur together in older hospitalized patients; the distinguishing signs of delirium are: Acute onset Cognitive fluctuations over hours or days
Hypoactive delirium
less recognized or appropriately treated
Mixed
Pathogenesis of delirium
Poorly understood
Difficult to study severely ill patients
the ascending reticular activating system The nondominant parietal and frontal lobes Intact higher order integrated cortical function
Pathogenesis: 2. Neurotransmitter
1. Acetylcholine
Cause delirium when given to healthy person More likely to lead to confusion in frailty elderly Effects reversed with cholinesterase inhibitors (physostigmine).
Medical conditions precipitating delirium, such as hypoxia, hypoglycemia, thiamine deficiency, decrease acetylcholine synthesis in CNS
Alzheimers disease, characterized by a loss of cholinergic neurons, increases risk of delirium due to anticholinergic medications.
neurotransmitters
2. Alterations in neuropeptides (eg, somatostatin), endorphins, serotonin, norepinephrine, and GABA
3. Cytokines, such as interleukins and interferons
Multifactorial
Underlying brain diseases, such as dementia, stroke, Parkinsons disease Advanced age and sensory impairment
E - Endocrinopathies
A Acute vascular T Toxins and drugs
H Heavy metals
A change in the level of awareness and the ability to focus, sustain, or shift attention.
Often subtle, may precede by one day or more. Patient isnt acting quite right
Distractibility, often evident in conversation. Appearing drowsy, lethargic, or even semi-comatose in advanced cases.
2. Change in cognition
Cognitive problems: memory loss, disorientation, difficulty with language and speech.
Need to ascertain baseline.
3. Temporal course
Develop over hours to days and typically persist for days to months
Acuteness of presentation is the most helpful feature in differentiating from dementia.
Fluctuating: typically most severe in the evening and at night, and relatively lucid during morning.
4. Other features
Not essential diagnostic but common, including psychomotor agitation, sleep-wake reversals, irritability, anxiety, emotional lability, and hypersensitivity to lights and sounds.
Common among older patients includes relatively quiet, withdrawn state that frequently is mistaken for depression.
Two important aspects to the diagnostic evaluation: recognizing that the disorder is present, and uncovering the underlying cause. In some reports, clinicians fail to recognize delirium in 70 percent of cases. Wrongly attributed to the patients age, to dementia, or to other mental disorders such as depression.
Must not normalize lethargy or somnolence by assuming that illness, sleep loss, fatigue, or anxiety cause the change.
Require knowledge of the patients baseline level of functioning.
Evaluation (2):
Evaluation (3)
Withdrawal from barbiturates, benzodiazepines, and SSRI Metabolic disorders (hypoglycemia, hypercalcemia, uremia, liver failure, thyrotoxicosis) Low perfusion states (shock, heart failure)
Differential Diagnosis
1.
Sundowning: a frequently seen but poorly understood; seen in evening hours; typically in demented, institutionalized patients.
Focal syndromes
Temporal-parietal: patients w Wernickes aphasia not comprehend, obey, seem confused; but restricted to language.
2.
Occipital: Antons syndrome of cortical blindness and confabulation Frontal: bifrontal lesions (eg, from tumor or trauma) often show akinetic mutism, lack of spontaneity, lack of judgment, problems w recent or working memory, blunted or labile emotional responses.
4. Dementia
Alzheimers cognitive change is insidious, progressive, without much fluctuation, over a much longer time (months to years). Lewy bodies similar to Alzheimers, but fluctuations and visual hallucinations are more common and prominent.
Laboratory testing
Serum electrolytes, creatinine, glucose, calcium, CBC, and urinalysis Drug levels, when appropriate.
Delirium can occur even w therapeutic levels (digoxin, lithium, or quinidine)
Neuroimaging
Head CT may be used selectively rather than routinely for evaluating delirium. May not be necessary if:
An obvious treatable medical illness or problem No evidence of trauma No new focal neurologic signs are present Patient is arousable and able to follow simple commands.
Lumbar puncture
CSF analysis is the only diagnostic tool for the following mostly treatable conditions in delirium patients:
Bacterial meningitis Encephalitis
Nonbacterial CSF pleocytosis (eg, aseptic meningitis, carcinomatous meningitis, encephalitis, seizures)
EEG
Should be obtained for any patient with altered consciousness of unknown etiology.
Useful to:
Exclude seizures, esp. nonconvulsive or subclinical seizures Confirm the diagnosis of certain metabolic encephalopathies or infectious encephalopatides
Nonconvulsive seizures lack motor manifestations or convulsions, but may impair consciousness. Nonconvulsive status epilepticus may cause continuous or fluctuating impairment of consciousness.
Metabolic encephalopathies may show diffuse bilateral slowing of background rhythm and high wave amplitude. Viral encephalitis may show diffuse background slowing and occasional epileptiform activity.
Treatment
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Multicomponent intervention
Standardized protocols to control six risk factors for delirium: cognitive impairment; sleep deprivation; immobility; visual impairment; hearing impairment; and dehydration. Of 852 hospitalized pts aged 70 or older; resulted in significant reduction in the number of delirium episodes vs usual care ( 62 vs. 90) and in the total number of days w delirium (105 vs 161)
Physical restraints should be used only as a last resort since they frequently increase agitation and create additional morbidity. Hospital environment, characterized by high ambient noise, poor lighting, lack of windows, frequent room changes, and restraint use, often contribute to worsening confusion. Frequent reassurance, touch, and verbal orientation from familiar persons lessen disruptive behaviors.
Psychotropic medication
A review by the Cochrane Collaborative found only one high-quality randomized trial, which compared haloperidol, chlorpromazine, and lorazepam in the treatment of delirium Recommendation: low-dose haloperidol (0.5 to 1.0 mg PO, IV, or IM) be used to control agitation or psychotic symptoms.
Jackson, Lipman. Drug therapy for delirium in terminally ill patients. The Cochrane Library, issue 2, 2004.
Older patients are more likely to experience severe extrapyramidal effects w haloperidol (akathisia, potential fatal neuroleptic malignant syndrome) The newer antipsychotic agents (risperidone, olanzapine) have fewer extrapyramidal side effects. Benzodiazepine (lorazepam 0.5 to 1.0 mg) have a more rapid onset of action (5 min after parenteral), but they commonly worsen confusion and sedation. Drug of choice only in cases of sedative drug and alcohol withdrawal.
E P E C
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