Delirium is an acute disturbance in attention and awareness that develops over a short period of time and fluctuates in severity. It is common in older adults due to age-related physiological changes and multiple medical conditions or medications. Delirium is diagnosed based on impairment in attention, cognition, and perception, as well as changes in psychomotor behavior. It requires identification and treatment of underlying causes, along with non-pharmacological and pharmacological interventions as needed to manage symptoms. Delirium is associated with poor outcomes, so prevention through risk factor modification is important.

1. Delirium
By
Asmaa fathy abd ellah
lecturer of geriatrics and gerontology medicine

2. Key notes
•Introduction
•EPIDEMIOLOGY
•PATHOPHYSIOLOGY
•Causes
•Clinical picture
•Differential diagnosis of delirium
•DIAGNOSIS
•Prevention
•Treatment
•Prognosis
•Post operative delirium

3. • Delirium is an acute transient disturbance in consciousness
that is characterized by a change in cognition manifest
primarily by an impairment of attention.
• The patient's inability to focus, sustain, or shift attention can
result in the impairment of other neurobehavioral tasks (e.g.,
memory).
• Language and visual spatial skills also can be affected.
• Changes in cognition seen in delirium are not explained by
an underlying dementia.
• These changes fluctuate considerably during a 24-hour
period and tend to be more pronounced at night.
INTRODUCTION

4. Other names:
• Intensive care unit psychosis
• Acute confusional state
• Acute brain failure
• Encephalitis
• Encephalopathy
• Toxic metabolic state
• Central nervous system toxicity
• Paraneoplastic limbic encephalitis
• Cerebral insufficiency
• Organic brain syndrom

5. 1. Physiological, anatomical, neurochemical age related
changes in the brain increase its susceptibility to further
insults
2. Reduced capacity of homeostasis and sensory
impairment
3. Multiple chronic pathologies superimposed upon age
related decline of functions of nearly all organs.
4. Polypharmacy
Delirium is common in old age due to:

6. • The overall prevalence of delirium varies widely, between 9% and
80% by setting, with lower levels among outpatient and residential
care homes.
• The lowest incidence occurs in the outpatient office setting, at only
2%, but this is expected to increase with population aging and age-
associated increases in multimorbidity and dementia.
• Among elderly patients presenting to emergency departments, up
to 17%of all community-dwelling seniors and 40%of nursing home
residents present with this diagnosis.
EPIDEMIOLOGY

7. • Patients requiring hospital admission, between 18% and 35% of
patients had a diagnosis of delirium on admission.
• Once hospitalized, elderly patients have a high risk of developing
delirium, especially if they have an underlying dementia disorder.
• Those in postoperative wards, intensive care units (ICUs), geriatric
wards, and hospice wards had the highest prevalence of delirium
50% to 80%.
EPIDEMIOLOGY

8. • Patients who develop delirium are at increased risk for a variety of
poor outcomes, including
 falls,
catheter-associated infections,
debility,
prolonged hospital stay, and
increased likelihood of physical restraints and antipsychotic
medication administration.
• Patients who develop delirium in the ICU are at 2 to 4 times
increased risk for death both during and after hospitalization; those
on general medicine or surgical wards have a 1.5-fold increased risk
of death in the year after hospitalization.
EPIDEMIOLOGY

9. • The interplay between a patient’s existing pathophysiology and the
changes occurring with an acute illness result in an imbalance of
brain chemistry.
• Factors involved in delirium pathophysiology can be separated into
preexisting risk factors and predisposing factors.
• Anatomical areas
• Prefrontal cortex,
• Right cerebral hemisphere (esp. parietal), and
• Sub cortical nuclei (esp. right sided thalamus & caudate).
• (Trzepacz, 1994)
PATHOPHYSIOLOGY

11. • Infection leads to inflammatory cascade that cause cytokine
activation, which in turn leads to impaired blood flow and neuronal
death causing delirium.
• Neurotransmitters such as acetylcholine, serotonin, gamma-
aminobutyric acid, and dopamine become imbalanced in delirium,
which results in the inability of delirious patients to process
information and respond appropriately.
PATHOPHYSIOLOGY

12. 1. ACETYLCHOLINE - decreased
• Anti cholinergic medications
• B1 deficiency
• Hypoxia
• Hypoglycemia
2. DA:
Increased Dopamine activity
Administration of anti DA-ergic drugs treat delirium
Delirium from intoxication with DA ergic drug (L-dopa,
dopamine, bupropion).
Opiates, common cause of delirium, increase activity of DA and
glutamate, whereas they decrease that of Ach.
Hypoxia

13. 3- GABA
Delirium in conditions that either increase (e.g. hepatic
encephalopathy) or decrease (e.g. hypnosedative withdrawal).
4-5HT
Postulated as either increase or decrease in different types of
delirium:
Increase in hepatic encephalopathy and serotonin syndrome
Decreased in post cardiotomy patients with delirium and
withdrawal from serotonergic drugs .

14. 5-Histamine
• Antihistamines (H1 antagonists) are associated with delirium
esp. in the elderly. They also increase catechols and serotonin
as possible mechanisms for delirium. (Tejera, 1994)
• H2 blockers – associated with delirium, mechanism is
uncertain, probably anticholinergic action.
6- Glutamate
• Glutamate excitatory neurotoxicity via NMDA receptor
apoptosis and neuronal death associated with alcohol
intoxication and withdrawal, delirium.
• NMDA antagonists, such as phencyclidine (PCP) and
ketamine, are also associated with delirium

15. 7- Cytokines
• Delirium from inflammatory or infectious causes.
• Therapeutic administration of some cytokines, such as
interferons and interleukins has been reported to cause
delirium, perhaps related to increase b-b-b permeability.
• Cytokines may influence activity of neurotransmitter
systems, such as catecholamines, GABA and acetylcholine
8- Oxidative Metabolism
Disturbance in brain oxygen supply versus demand has been
one of the theories proposed for delirium.
Impaired oxidative metabolism appears to be a predisposing
factor for later development of delirium.

17. • Most cases of delirium result from a complex multifactorial process.
• It is important to determine underlying causes contributing to this
syndrome.
Causes

20. D=  Drugs (use new drug, or ↑ the dose, esp.anticholinergics), dehydration
E=  Electrolytes & physiological causes (eg: ↓ Na, hypoxia)
L=  lack of drug (withdrawal esp. sedatives, hypnotics)
I=  Infection (eg: chest infection, urinary tract infection)
R=  Reduced sensations (eg: deafness, blindness)
I=  Intra-cranial problem (eg: stroke, trauma, infection, epilepsy, ….etc)
U=  Urinary retention (cystocerebralsynd) – Fecal impaction
M=  Myocardial causes: (eg: MI, arrhythmia, heart failure) AND
 Metabolic & Endocrinal: hypoglycemia-hyperglycemia-hypothyroidism-
hyperthyroidism.
Causes of delirium:Remember D.E.L.E.R.I.U.M.

21. • acute onset with fluctuation with;
•
• 1-Disorders of attention;
• Attention= ability to maintain focus and selectively shift
mental activities
•
• 2-Arousal;
 Increased; irritability and excitability
 Decreased; cloudiness of consciousness and decreased
response to stimuli
•
• 3-cognitive impairment
 Disorientation
 Poor memory, short and long term
 Incoherent thinking/ speak
Clinical picture:

22. • 4-Neuropsychiatric findings;
 Hallucinations
 Illusions
 Delusions
 Emotional distress
 sleep disturbances:
Disturbance of sleep or the sleep-wake cycle, manifest by at
least one of the following:
1. insomnia, which in severe cases may involve total sleep
loss, with or without daytime drowsiness, or reversal of the
sleep-wake cycle;
2. nocturnal worsening of symptoms;
3. disturbing dreams and nightmares which may continue as
hallucinations or illusions after awakening.

23. • 5-Vegitative function abnormality;
 autonomic arousal; e.g. dilated pupil, rapid pulse, sweating,
incontinence
• Types (classification) of delirium:
 Hyperactive delirium: Characterized by increased
psychomotor activity & agitation.
 Hypoactive delirium: Characterized by decreased
psychomotor activity. It resembles depression.
 Mixed delirium: Has both hypoactive and hyperactive
features.
 Normal psychomotor state.

24. • Dementia
• Depression
• Nonconvulsive status epilepticus
• Schizophrenia
• Adjustment disorders,
• Anxiety disorders,
• Agitated depression
• Mania
Differential diagnosis of delirium:

25. Delirium Dementia
Onset Acute Insidious
Duration Hours/days/weeks Months/years
Course Fluctuates Stable and progressive
Alertness Fluctuates Normal
Orientation Always impaired May be normal
Thoughts Often paranoid and grandiose Slowed/reduced interests
Perception Visual and auditory hallucinations
common
Normal/hallucinations in 30-
40%(often visual)
Emotions Irritable-aggressive-fearful Shallow-apathetic-labile-Irritable
Sleep Nocturnal confusion Often disturbed-nocturnal wandering
common

26. • It is important, and at times difficult, to discern dementia behaviors
from delirium, especially Lewy body dementia.
• The key to differentiating whether a patient is experiencing
dementia-related behaviors or acute brain failure is in a combination
of history taking and determination of attention.
• Many patients with dementia have behavioral disturbances, also
often referred to as psychosis, and may have hallucinations and other
cognitive disturbances. However, with the exception of some patients
with Lewy body dementia, patients with dementia should not have a
disturbance of attention.
• In effect, unless the dementia is end stage, patients should be able to
have a conversation and perform some tests of attention such as
counting backward from 20 or naming the months of the year or days
of the week in reverse.
Differentiation from Dementia

27. • Patients’ abilities to perform these tests vary based on the level of
cognitive decline, but each patient should be able to show some level
of attention.
• This observation is important, along with documenting a change from
the patient’s normal baseline status (obtained from collateral history
obtained from family or caregivers), in determining whether an acute
change indicates that delirium has occurred. This finding helps
clinicians differentiate dementia from delirium.
Differentiation from Dementia

28. • CLASSIFICATION
• Delirium is classified in DSM 5 in chapter of neurocognitive
disorders, which consist of delirium, major NCD, mild NCD
and their etiological subtypes.
• In ICD 10- F00-F09 Organic, including symptomatic, mental
disorders.. F05
• F10-F19 Mental and behavioural disorders due to
psychoactive substance use with individual substance
DIAGNOSIS

29. • Diagnostic Criteria:
• A. A disturbance in attention (i.e., reduced ability to direct,
focus, sustain, and shift attention) and awareness (reduced
orientation to the environment).
• B. The disturbance develops over a short period of time
(usually hours to a few days), represents a change from
baseline attention and awareness, and tends to fluctuate in
severity during the course of a day.
• C. An additional disturbance in cognition (e.g., memory
deficit, disorientation, language, visuospatial ability, or
perception).
DSM 5

30. • D. The disturbances in Criteria A and C are not better
explained by another preexisting, established, or evolving
neurocognitive disorder and do not occur in the context of a
severely reduced level of arousal, such as coma.
• E. There is evidence from the history, physical examination,
or laboratory findings that the disturbance is a direct
physiological consequence of another medical condition,
substance intoxication or withdrawal (i.e., due to a drug of
abuse or to a medication), or exposure to a toxin, or is due to
multiple etiologies

31. • Specify whether
(1) substance intoxication delirium
(2) substance withdrawal delirium
(3) medication induced delirium
(4) delirium due to another medical condition
(5) delirium due to multiple etiologies
Specify if
1. Acute – lasting a few hours or day
2. Persistent- lasting weeks or months
Specify if
1. Hyperactive
2. Hypoactive
3. Mixed level of activity

32. Associated feature supporting diagnosis :
• Disturbance in sleep wake cycle
• Emotional disturbance like anxiety, fear, depression,
euphoria, anger, irritability and apathy. There may be rapid and
unpredictable shift from one state to another.
• OTHERS - Other specified delirium, Unspecified delirium

33. • Confusion Assessment Method (CAM)
• CAM-ICU for critically ill patients
• Severity of delirium –
• 1. Delirium Rating Scale (DRS),
• 2. Memorial Delirium Assessment Scale (MDAS
SCALES

34. ASSESSMENT

37. • HELP (hospital elder life program) included interventions
for cognitive impairment, sleep deprivation, immobility,
sensory impairment, dehydration
• Primary prevention
Minimization of polypharmacy.
Anti cholinergic, hypnosedative and opioid medications
should be used sparingly in the elderly.
Maintain hydration and nourishment and ensure sufficient
sleep.
Caregivers and nursing staff must be trained to recognize
delirium.
PREVENTION

38. • Secondary prevention
Early diagnosis and treatment
Improved recognition of the condition.
It is recommended that all acutely ill elderly patients should
have a brief mental test on admission to increase the rate of
detection of delirium.
Environment modifications, close monitoring to prevent
further morbidity and mortality
For sleep depriviation :
Non pharmacological measures
0.5 mg melatonin or 8 mg ramelteon may prevent delirium in
acute care.

39. Basic algorithm for initial delirium management:
• 1. Identify and remove or treat underlying cause
• 2. Taper or discontinue non-essential medications.
• 3. Close observation.
• 4. Monitor vital signs and fluid intake and outputs.
• 5. Complete history and perform initial laboratory studies
• 6. Implement environment and psychosocial interventions.
• 7. Pharmacological treatment as indicated.
• 8. Physical restraints are used only as a last resort.
MANAGEMENT

40. In the future, a measure of total serum
anticholinergic activity may prove
helpful in deciding whether to
discontinue some or all medications.
This is a radioreceptor assay that
has been validated at several centers;
however, it is not yet available
commercially.

41. • Ensure effective communication & reorientation (e.g.
explaining where the person is, who they are, and what your
role is)
• Promoting day activity
• Maintaining quite, well-lit environment
• Staff continuity
• Avoiding room and bed changes
• Providing hearing and visual aids
• Encouraging personal items
• Limiting visits especially for hyperactive delirium patients,
• Remove noxious stimuli (e.g., catheters, pumps, etc.)
NON PHARMACOLOGICAL
INTERVENTION

42. • Normal sleep–wake cycles can be promoted by the use of
day time activity and environmental cues (such as windows
and clocks).
• Interruptions of sleep should be minimized when possible.
• Adequate nutrition.
NON PHARMACOLOGICAL
INTERVENTION

43. • General principles
• • Keep the use of sedatives and antipsychotics to a minimum , use
it after non pharmacological measures failed
• • Use one drug at a time.
• • Titrate doses to effect.
• • Review at least every 24 hours. Once an effective has been
established, a regular dose should be prescribed.
• • Maintain at an effective dose and discontinue 7–10 days after
symptoms resolve.
 Use lorazepam in sedative and alcohol withdrawal( also
thiamine 100mg), and history of neuroleptic malignant
syndrome
PHARMACOLOGICAL INTERVENTION
BEHAVIORAL PROBLEMS

44. Haloperidol use:
• 0.5 -1 mg po evaluate effect in 1-2 h
• 0.5 -1mg IM peak effect 20-40 min
• Reevaluate q30-60min for agitation
• Double dose if initial dose ineffective
• Administer additional doses (aim q30 min or oral q 60
min ) until agitation is controlled
• Calculate total dose and give half the equivalent oral dose
the next day divided for q 12
• Hold dose if sedation occur
• Maintain effective dose for 2-3 d

45. • Slowly taper and D/C over 3-5 d and monitor recurrence of
symptoms
• If necessary continue the minimal dose necessary to contral
symptoms
• Assess for akathisia and extrapyramidal effects
• Avoid in older people with parkinsonism
• Monitor for QT interval prolongation, torsade de pointes,
neuroleptic malignant syndrome, withdrawal dyskinesias
• If use exceed 1 wk switch to 2 nd generation antipsychotic
• Obtain ECG before the first dose or as soon as the patient is calm
• If QTC exceed 500 ms do not administer any antipsychotic
• If QTC exceed 460 ms correct any deficiency of Mg and K and
recheck

46. • Quetiapine is drug of choice for patients with LBD, Parkinson disease
,AIDS related dementia or EPS
• Initial dose 12.5-25 mg po daily or q12h
• Increase q2d to max of 100mg /d (50 mg if frail elderly)
• Once symptoms are controlled , administer half the dose needed to
control symptoms for 2-3 d then taper as before.

48. • By the third hospital day, approximately one-half the
patients who are diagnosed with delirium have been
diagnosed.
• Symptoms of delirium usually last 3 to 5 days, but there is
slow resolution of symptoms contributing to persistent
symptoms of delirium at 6 to 8 weeks for severely ill
patients.
• Symptom resolution is frequently incomplete by hospital
discharge, with as many as 15 percent of patients remaining
symptomatic of delirium at 6 months.
COURSE AND PROGNOSIS

49. • In general, studies suggest that the increased mortality risk
associated with delirium was maintained at 12, 24, and 36 months
with a risk ratio of at least 2 at all time points.
• Additionally, at 24 months, the increased risk of cognitive and
functional impairment remained.
• Sequels of delirium:
1. Iatrogenic complications (eg: drugs, mechanical constraints)
2. Incontinence
3. complications of bed ridden (eg: pressure ulcers, aspiration)
4. malnutrition
5. hospitalization
6. long-term care admission
7. In general, there is an increased mortality in hospitalized
patients who had delirium.

50. •Preoperative risk factors :
•Age 70 and older
•Cognitive impairment
•Physical functional impairment
•History of alcohol abuse
•Abnormal serum chemistries
•Intrathoracic and aortic aneurysm surgery
POSTOPERATIVE DELIRIUM

51. • Peak onset is on 2nd postoperative day
• Associated with postoperative pain, postoperative
anemia, use of benzodiazepines and opioids (esp.
meperidine)
• Recommended:
 Limit sedation
 Provide adequate analgesia
KEYS TO PREVENTING
POSTOPERATIVE DELIRIUM

52. THANK YOU