DELIRIUM BY MOHAMED HAMDY

Definition and terminology

DSM IV
1.

Disturbance of consciousness with reduced ability to focus, sustain, or shift attention.

2.

not better accounted for by a preexisting, established, or evolving dementia.

Over a short period of time (usually hours to days), fluctuating during the course of the day Evidence that it is caused by a medical condition, substance intoxication, or medication side effect.

3.

4.

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

30% - older medical patients

10-50% - older surgical patients 70% - ICU 42% - Hospice units 16% - postacute care settings

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

Impaired consciousness and attention

Altered sleep cycles

DELIRIUM TAKES VARIOUS FORMS

Hyperactive or agitated delirium

25% of all cases

Hypoactive delirium
less recognized or appropriately treated

Mixed

Additional features include emotional symptoms, psychotic symptoms, sundowning

NEUROPATHOPHYSIOLOG Y Cholinergic deficiency

Delirium is associated with serum anticholinergic activity Physostigmine and cholinesterase inhibitors are beneficial

Serotonin excess or deficiency

Dopamine excess (regulates release of acetylcholine) Cytokines (interleukin-1,and 2, tumor necrosis factor)

As seen in patients with cancer or infections Increases permeability of the BBB

Chronic stress and hypercorticolism Other neurotransmitters: GABA, glutamate, melatonin

Pathogenesis of delirium

Poorly understood
Difficult to study severely ill patients

Hard to separate from that of underlying illness and drug treatment

Pathogenesis: 1.Neurobiology of attention

Arousal and attention are governed by:

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

Pathogenesis: (3) risk factors

Multifactorial
Underlying brain diseases, such as dementia, stroke, Parkinsons disease Advanced age and sensory impairment

Pathogenesis: (4) precipitating factors

Polypharmacy (particularly psychoactive drugs)

Infections Dehydration Immobility (including restraint use) Malnutrition The use of bladder catheters

Differential Diagnosis for Etiology of Delirium I Infection

W - Withdrawal A Acute metabolic T - Trauma C CNS pathology H - Hypoxia D Deficiencies

E - Endocrinopathies
A Acute vascular T Toxins and drugs

H Heavy metals

Delirium in the Elderly Predisposing Factors

Visual impairment (< 20/70)

Severe illness (APACHE > 16) Cognitive impairment (MMSE < 24) SUN/Cr > 18 LOW RISK 0 factors INTERMEDIATE RISK 1 to 2 factors

HIGH RISK 3 to 4 factors

Delirium in the Elderly Precipitating Factors

Use of physical restraint

Malnutrition (loss of 5.6 kg) > 3 medications added Use of bladder catheter Any iatrogenic event
LOW RISK 0 factors INTERMEDIATE RISK 1 to 2 factors HIGH RISK 3 to 4 factors

Clinical presentation of delirium

1. Disturbance of consciousness

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.

Perceptual problems: misidentify the clinician, vague delusions of harm.

Visual and tactile hallucinations are not uncommon

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.

Evaluation of delirium (1)

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):

Confusion Assessment Method (CAM):

- sensitivity of 94 to 100 percent; - specificity of 90 to 95 percent - a standard screening device in clinical studies of delirium

Evaluation (3)

Investigating medical etiologies:

Fluid and electrolyte disturbances (dehydration, hyponatremia and hypernatremia) Infections (urinary, respiratory, skin and soft tissue) Drug or alcohol toxicity Withdrawal from alcohol

Withdrawal from barbiturates, benzodiazepines, and SSRI Metabolic disorders (hypoglycemia, hypercalcemia, uremia, liver failure, thyrotoxicosis) Low perfusion states (shock, heart failure)

Postoperative states, especially in the elderly

Evaluation (4): medication review

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.

3. Nonconvulsive Status Epilepticus (NCSE):

Requires EEG for detection Show no classical ictal features Features: prominent bilateral facial twitching, unexplained nystagmoid eye movements during obtunded periods, spontaneous hippus, prolonged postictal state, automatisms (lip smacking, chewing, swallowing movements).

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.

5. Primary psychiatric illnesses:

Depression (poor sleep, difficulty w attention or concentration) Mania

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)

Toxic screen of blood and urine

Blood gas: Respiratory alkalosis is due to early sepsis, hepatic failure, early salicylate intoxication. Metabolic acidosis reflects uremia, diabetic ketoacidosis, lactic acidosis, late phases of sepsis or salicylate intoxication, methanol, ethylene glycol

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.

Head CT may be required if:

Delirium does not improve despite appropriate treatment of underlying medical condition The neurologic examination is confounded by diminished patient responsiveness or cooperation.

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)

Elevated CSF glutamine concentration in hepatic encephalopathy

Elevated opening pressure due to increased ICP

LP is mandatory when the cause of delirium is not obvious.

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
1.

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.

Managing 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.

Summary: Delirium workup scheme

Summary: Common causes of Delirium

E P E C

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