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33 Cards in this Set
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Delirium |
Common life-threatening preventable clinical syndrome induced by a variety of physical causes. Often defined as an acute decline in the cognitive processess of the brain. Strongly associated with hospitalized patients who are 65 years old or older.
May exhibit periods of inattention, disorganized thinking changes in level of consciousness, disorientation, delusions, perceptual disturbances, impaired memory, speech, sleep and psychomotor activity.
It is often under-recognized and under-treated. Delirium complicated the hospital stays in North America by 20%. Changes in cognitive function can fluctuate in severity throughout the day.
Only 40% of clinicians screen for delirium in hospital elderly patients. |
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Diagnostic Criteria |
A. Disturbances of consciousness (e.g., reduced clarity of awareness of the environment) with reduced ability to focus, sustain or shift attention
B. A change in cognition (such as memory deficit, disorientation, language disturbances) or the development of a perceptual disturbance that is not better accounted for by a preexisting, established or evolving dementia.
C. The disturbance develop over a short period of time (usually hours to days) and tends to fluctuate during the course of the day
D. There is evidence from the history, physical examination or laboratory findings that the disturbance is caused by the direct physiological consequences of a general medical condition. |
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Clinical Features |
1. Acute onset = occurs abruptly
2. Fluctuating course = symptoms tend to come and go or increase and decrease in severity over 24 hour period
3. Inattention = difficulty focusing, sustaining and shifting attention, maintaining conversations or following commands
4. Disorganized thinking = manifested by disorganized or incoherent speech, rmabling or irrelevant conversation or following commands.
5. Altered level of consciousness = clouding of consciousness, reduced clarity of awareness
6. Cognitive Deficits = global or multiple deficits in cognition, including disorientation, memory deficits, language impairment
7. Perceptual Disturbances = illusions or hallucinations
8. Psychomotor disturbances = hyperactive (agitation and vigilance), hypoactive (lethargy, markedly decrease level of motor activity), mixed.
9. Altered Sleep-wake cycle = daytime drowsiness, nightime insomnia, fragmented sleep, anxiety, depression, irritability, apathy anger, or euphoria.
10. Emotional disturbance = common, manifested by intermittent and labile symptoms of fear, paranoia, anxiety, depression, irritability, apathy, anger, or euphoria. |
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Delirium, Dementia & Depression |
Many of the symptoms observed in patients with delirium are also observed in patients with other neuropsychiatric diseases or medical illnesses.
In cases of delirium, the onset of altered consciousness, cognitive disturbances or hallucinations is typically acute, and presents in the context of medical illness, surgery or medication change.
Schizophrenia tends to have a gradual onset, and appears in late adolescence/early adulthood. Phase of isolation that lasts weeks to months.
May be mistaken for dementia, patients rarely exhibit fluctuations in their cognitive function, level of consciousness is typically intact and inattention is either absent or mild when compared to other cognitive function.
Mistaken for depression - when patient's symptoms are hypoactive in nature. Depression has a more gradual onset of psychomotor slowing and cognitive deficits tends to reflect disinterest. |
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Hyperactive Delirium |
Often characterized by symptoms of restlessness, constant movement and agitation.
Insomnia, hyper-vigilance, irritability, distractibility, rapid speech, uncooperativeness and wandering behaviour also observed.
Often mistaken for schizophrenia, bipolar disorder or agitated disease. |
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Hypoactive Delirium |
Slowing or lack of movement, a paucity of speech with or without prompting, and unresponsiveness characterize hypoactive delirium. Apathy and decreased alertness are also typical in patients with the hypoactive subtype of delirium.
Mistaken for depression. More common in elderly. Due to its almost silent nature, this form of delirium is the most difficult for clinicians to identify. |
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Mixed Delirium |
Characterized by alternating hyperactive and hypoactive states.
Hyperactive delirium are more likely to be referred to psychiatrists and receive appropriate therapy or interventions due to the more disruptive and potentially self-harming nature of the subtype. In contrast, hypoactive delirium may be mistaken for compliance, fatigue, or simply behaviors incorrectly ascribed to old age.
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Screening |
Given that unmanaged delirium is associated with a significant risk of mortality in the first year, the use of effective screening tools for the diagnosis of delirium is critical.
The Confusion Assessment Method Instrument or CAM has been widely accepted as the most useful scale for diagnosing delirium. This screening tool diagnoses the delirious state by a yes or no answer to a four-point algorithm based on the DSM-IV-TR criteria.
Proper use of this instrument has the potential to enhance the detection of delirium in hospital settings, and reduce the number of delirious patients who go undiagnosed and untreated.
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Confusion Assessment Method Instrument |
1. Acute onset = mental change
2. Inattention = easily distracted
3. Disorganized thinking = incoherent
4. Altered level of consciousness = coma, alert
5. Disorientation = thinking they were somewhere else
6.Memory Impairment = memory problems
7. Perceptual Disturbances = hallucination, illusions
8. Psychomotor = part 1 agitation ( tapping fingers, restlessness), part 2 retardation (decreased level of motor activity)
9. Altered sleep - wake cycle = excessive daytime sleepiness with insomnia. |
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Scoring |
To have a positive CAM result, the client must have:
1) Presence of acute onset and fluctuating course
AND
2) Inattention
AND EITHER
3) Disorganized thinking
OR
4) Altered level of consciousness
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Causes |
Delirium is rarely caused by a single factor. Rather, it is multi-factorial, and involves a complex interaction between the vulnerable patient and their exposure to precipitating factors.
Consequently, all factors – predisposing, and precipitating should be addressed. Fortunately, most of the risk factors outlined in these two tables are modifiable and amendable to intervention.
Patients who are highly vulnerable to delirium, such as those with dementia, will develop delirium after exposure to a minor insult, such as a single dose of a sedative drug.
In contrast, in patients who are not vulnerable or predisposed to delirium, the condition will only manifest after exposure to a number of noxious insults, such as general anesthesia, major surgery, and multiple psychoactive medications.
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Predisposing Factors |
Baseline characteristics present at time of admission (patient dependent)
1) Demographic Characteristics
a. Age of 65 years or older
b. Male sex
2) Cognitive Status
a. Dementia
b. Cognitive impairment – related to a 2.82 times increased risk for delirium
c. History of delirium
d. Depression
3) Functional Status
a. Functional dependence
b. Immobility
c. Low level of activity
d. History of falls
4) Sensory Impairment
a. Visual impairment – related to a 3.51 times increased risk for delirium
b. Hearing impairment
5) Decreased Oral Intake
a. Dehydration – related to a 2.02 times increased risk for delirium
b. Malnutrition
6) Drugs
a. Treatment with multiple psychoactive drugs
b. Treatment with many drugs
c. Alcohol abuse
7) Coexisting Medical Conditions
a. Severe illness – related to a 3.49 times increased risk for delirium
b. Multiple coexisting conditions
c. Chronic renal or hepatic disease
d. History of stroke
e. Neurologic disease
f. Metabolic derangements
g. Fracture or trauma
h. Terminal illness
i. Infection with human immunodeficiency virus
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Precipitating Factors |
Noxious insults or factors related to hospitalization (environment/illness dependent)
1) Drugs
a. Sedative hypnotics
b. Narcotics
c. Anticholinergic drugs
d. Treatment with multiple drugs related to a 2.9 times increased risk for delirium
e. Alcohol or drug withdrawal
2) Primary Neurologic Disease
a. Stroke, particularly nondominant hemisphere
b. Intracranial bleeding
c. Meningitis or encephalitis
3) Incurrent illness
a. Infections
b. Latrogenic complications
c. Severe acute illness
d. Hypoxia
e. Shock
f. Fever or hypothermia
g. Anemia
h. Dehydration
i. Poor nutritional status
j. Low serum albumin levels – related to a 4 times increased risk for delirium
k. Metabolic derangements (e.g. electrolyte, glucose, acid-base)
4) Surgery
a. Orthopedic surgery
b. Cardiac surgery
c. Prolonged cardiopulmonary bypass
d. Noncardiac surgery
5) Environmental
a. Admission to an intensive care unit
b. Use of physical restraints – related to 4.4 times increased risk for delirium
c. Use of bladder catheter – related to a 2.4 times increased risk for delirium
d. Use of multiple procedures
e. Pain
f. Emotional stress
6) Prolonged Sleep Deprivation
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Multi-factorial Model |
A wide variety of factors, or noxious insults, can precipitate delirium. Similarly, a wide variety of factors can influence a patient’s vulnerability to developing delirium in response to a noxious stimulus. For example, in elderly patients, age is a predisposing factor. However, for young to middle aged adults, age is a protective factor.
Similarly, poor cognitive function, even full blow dementia is a predisposing factor for delirium, whereas healthy cognitive function or “cognitive reserve” reduced a patient’s risk for delirium by exerting a protective effect. The same can be said for sensation. Good vision and hearing are protective factors against delirium, while hearing or visual impairments increase a patients risk for developing delirium. |
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Pathophysiology |
Remains poorly understood.
First, the core features of delirium – inattention and impaired cognition are difficult to define.
Second, the fluctuating course of the syndrome and its diverse clinical symptoms make delirium difficult to recognize.
Third, delirium can be caused by a multitude of risk factors, reflecting a complex interaction between environmental and individual factors.
And finally, the overall inaccessibility of the central nervous system limits scientific investigation into the possible neurological correlates of delirium.
This syndrome manifests from a strong link between the brain and the body. Delirium occurs when physical stressors affect a vulnerable patient. As such, there must be a link between physiological changes in the body, and the cognitive changes that constitute delirium. |
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Neuroinflammatory Hypothesis |
Systemic inflammation is a predominant feature of many surgical and medical conditions associated with delirium, especially when tissue destruction and/or infection are involved.
Delirium is a presenting clinical feature of sepsis, urinary tract infections, pneumonia, myocardial infarctions, fractures, hepatitis, burns, and also commonly appears with complications following major surgical procedures. All of these medical or surgical conditions share a common thread; the release and production of pro-inflammatory mediators into the systemic circulation.
Cells within the brain – neurons, glia, and astrocytes react to the presence of peripheral immune cells in the systemic circulation. Activation of the brain by peripheral immune cells leads to the production of cytokines, neuronal cell proliferation, and activation of the hypothalamus-pituitary-adrenal axis. These changes allow the central nervous system to help combat acute infections in the body.
Peripheral immune cells are able to gain access to the brain by altering the expression of tight-junction proteins that help from the blood-brain-barrier, and allow for the recruitment and infiltration of blood-derived leukocytes and other inflammatory agents into brain tissue.
Once inside the brain, these pro-inflammatory agents activate endothelial cells, microglia and astrocytes. Activation of the microglia induces morphological changes and initiates the production of pro-inflammatory cytokines such as interleukin-1, interleukin-2, and tumor necrosis factor – alpha. Changes within the microglia in turn modulate the activity of adjacent endothelial cells, astrocytes and neurons, impacting cerebral blood flow, signal propagation and neuronal excitability.
It is hypothesized that these changes in neurotransmission and cerebral blood flow contribute to the pathogenesis of delirium.
The symptoms of inattention and decreased cognitive functioning observed in patients with delirium may be associated with decreased cerebral blood flow. Reduced blood supply to the brain impairs the supply of oxygen and glucose – both of which are essential to proper cognitive functioning. |
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Acetylcholine |
Neuroinflammation has been shown to induce a cholinergic deficit in the brain. Acetylcholine plays an important role in memory and cognition.
A decrease in acetylcholine levels within the brain would be somewhat expected in patients presenting with delirium.
The finding that anticholinergic drugs cause delirium in healthy adults, and are even more likely to cause delirium in the elderly population supports this hypothesis. In fact, most drug-induced episodes of delirium are associated with a medication that possesses anticholinergic activity.
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Dopamine |
Opiate drugs, such as morphine, are common cause of drug-induced delirium.
Opiate administration induces an increase in dopamine levels which leads to a corresponding decrease in acetylcholine levels within the brain.
Commonly observed with dopaminergic drugs because dopamine has an inhibitory effect on acetylcholine release. As such, dopamine antagonists have been shown to effectively treat some of the symptoms associated with delirium.
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Cholinergic Hypothesis |
Medical conditions that precipitate delirium, such as hypoxia and hypoglycemia decrease acetylcholine synthesis in the central nervous system.
Higher levels of serum anticholinergic activity are associated with an increased risk of delirium in both medical and surgical inpatients.
While both neuroinflammatory and cholinergic hypothesis of delirium provide insight into the biological mechanisms that underlie delirium, it is evident that neither hypothesis can full explain all of the characteristic features of delirium.
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Delirium Prevention |
Most common preventable adverse event. Adverse effects to medication, complication of invasive procedures, immobilization, dehydration, the use of bladder catheters & sleep deprivation.
Targeted Risk Factor Intervention Protocols Description Cognitive Impairment Orientation Protocol
Therapeutic Activities Protocol Board with names of care-team members and day’s schedule; communication to reorient to surroundings.
Cognitive stimulating activities three times daily (e.g. discussion of current events, structured reminiscence, or work games) Sleep deprivation Non-pharmacological Sleep Protocol
Sleep Enhancement Protocol At bedtime, warm drink (milk or herbal tea), relaxation tapes or music, and back massage.
Unit-wide noise-reduction strategies (e.g. silent pill crushers, vibrating beepers, and quiet hallways) and schedule adjustments to allow sleep (e.g. rescheduling of medications and procedures) Immobility Early Mobilization Protocol Ambulation or active range-of-motion exercises three times daily; minimal use of immobilizing equipment (e.g. bladder catheters or physical restraints)
Visual Impairment Vision Protocol Visual aids (e.g. glasses or magnifying lenses) and adaptive equipment (e.g. large illuminated telephone key pads, large-print books, and fluorescent tape on call bell), with daily reinforcement of their use. Hearing impairment Hearing Protocol Portable amplifying devices, earwax disimpaction, and special communication techniques, with daily reinforcements of these adaptations. Dehydration Dehydration Protocol Early recognition of dehydration and volume repletion (i.e. encouragement of oral intake of fluids)
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Delirium Management
Monitor Cognitions Function |
Formal cognitive testing with CAMI should be preformed to establish baseline cognitive performance in elderly patients and identify cases of hypoactive delirium.
Coordinating schedules for drug administration, obtaining vital signs, and performing procedures during the night will provide patients with an uninterrupted period for sleep. Opening blinds and promoting wakefulness and mobility during the daytime can also encourage normal sleep-wake cycles.
All preadmission and current medications should be reviewed. Even long-term medications can contribute to delirium and should be reevaluated.
Non-pharmacological approached to managing symptoms should always be instituted. Creating a calm, comfortable environment with the use of orienting influences such as calendars, clocks, and familiar objects from home are important. Regular reorienting communications with staff, involving the family and supportive care and limiting and staff changes can also make a difference.
Pharmacological therapy should be reserved for patients whose symptoms threaten their own safety or the safety of other persons or would result in the interruption of essential therapy such as mechanical ventilation and central venous catheters.
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Delirium Management ACUTE |
Acute onset is hallmark feature of delirium, if the patient’s mental status has decreased over time and the change is more chronic in nature then possibility of dementia should be explored. |
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Prevention Steps |
1. 1. Address risk factors for delirium
2. 2. Provide orienting communication
3. 3.Encourage early mobilization
4. 4. Usual visual and hearing aids
5. 5. Prevent dehydration
6. 6. Provide uninterrupted sleep time
7. 7. Avoid psychoactive drugs
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Identify & address predisposing and precipitating factor |
Health care team should be aware of atypical presentations of many diseases in the elderly, including myocardial infarction, infection and respiratory failure. Delirium is often a sole manifestation for serious underlying disease in this population.
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Initial Evaluation |
1. Obtain history (including alcohol and benzodiazepine use)
2. Obtain vital signs
3. Perform physical and neurological examination
4. Order selected laboratory tests
5. Search for occult infection
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Review Medication |
1. Review the use of prescription drugs, as-needed drugs, over-the-counter drugs, herbal remedies
2. Identify psychoactive effects and drug interactions
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Remove or Alter potentially harmful drugs |
1. Change to less noxious alternative
2. Lower doses
3. Non-pharmacological approaches
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Potential Contributing Factor Identified |
· YES – Evaluate and treat as appropriate for each contributing factor
· NO – Further Options o Order laboratory tests: thyroid-function tests, measurements of drug levels, toxicology screen, measurement of ammonia or cortisol levels, test for vitamin B12 deficiency and arterial blood gas levels
o Electrocardiography
o Neuroimaging
o Lumbar puncture, electroencephalography
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Provide Supportive & Prevent Complications |
1. Protect airway, prevent aspiration
2. Maintain volume status
3. Provide nutritional support
4. Provide skin care, prevent pressure sores
5. Use mobilization, prevent deep venous thrombosis, pulmonary embolus
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Non-Pharmacological Treatment |
1. Continue delirium prevention
2. Reorient patient, encourage family involvement
3. Use sitters
4. Avoids use of physical restraints and Foley catheters
5. Use of non-pharmacological approaches for agitation: music, massage, relaxation techniques
6. Use of eyeglasses, hearing aids, interpreters
7. Maintain patient’s mobility and self-care ability
8. Normalize sleep-wake cycle, discourage naps, aim for uninterrupted period of sleep at night
9. At night, have patient sleep in quiet room with low-level lighting
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Pharmicological Treatment |
1. Reserve this approach for patients with severe agitation at risk for interruption of essential medical care (e.g. intubation) or for patients who pose safety hazard to themselves or staff
2. Start low doses and adjust until effect achieved
3. Maintain effective dose for 2-3 days
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Antipsychotic Drugs |
Antipsychotic are the drug class of choice for the treatment of delirium. Both low dose haloperidol treatment and atypical antipsychotic therapy are effective in managing the symptoms of delirium. High dose haloperidol therapy should be avoided due to the increased risk of extrapyramidal side effects.
As such, clinicians need to use careful judgment when prescribing for delirium, as the majority of patients in their care are elderly and medically compromised the dose and duration of neurological therapy should always be minimized for this patient population.
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Delirium & Dementia |
While delirium and dementia are two distinct conditions, there is significant evidence to suggest that delirium and dementia are highly interrelated.
First, dementia is the leading risk factor for delirium. Two-thirds of delirium cases occur in patients with dementia. This finding suggests that dementia is a significant predisposing factor for delirium, and is also highly vulnerable to mino insults.
Second, both conditions are associated with decreased cerebral blood flow, acetylcholine deficiency and inflammation, suggesting overlapping neurobiological mechanisms.
Third, in some patients, delirium can last for months to years, blurring the boundaries between delirium and dementia. In fact, 50% of delirium cases persistent after discharge. Persistent delirium is associated with worse long-term cognitive and functional outcomes and is 2.3 more likely to occur in patients with underlying dementia.
Most significant risk factor for persistent delirium is the use of physical restraints. The use of restraints leads to increased agitation, immobility, functional decline, incontinence, pressure ulcers, asphyxiation, and in some cases, cardiac arrest. As such, physical restraints should not be used for older persons with delirium, especially those with agitated dementia.
In those with dementia, delirium worsens functional status, accelerates the patient’s loss of independence and is associated with poorer outcomes. Patients with dementia never return to their baseline mental state after an episode of delirium, and are more likely to experience delirium in the future.
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