Section of Physical Medicine and Rehabilitation presents GRAND ROUND 5/13/2005 by Anthony Tam Pham, DO - PowerPoint PPT Presentation

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Section of Physical Medicine and Rehabilitation presents GRAND ROUND 5/13/2005 by Anthony Tam Pham, DO

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Title: Section of Physical Medicine and Rehabilitation presents GRAND ROUND 5/13/2005 by Anthony Tam Pham, DO


1
Section of Physical Medicine and
Rehabilitation presents GRAND ROUND
5/13/2005 by Anthony Tam Pham, DO
2
  • Case Report
  • Ms. A, a 74-year old white woman who was
    diagnosed w late-onset bipolar affective disorder
    at the age of 69, came to the hospital after
    sustaining a R hip fracture from fall. In the
    emergency room, she was alert and fully oriented.
    She received 4 mg of IV morphine sulfate for
    pain. She slept well and answered questions
    appropriately the next morning but was drowsy.
  • After hip arthroplasty the following day, she was
    awake but verbally unresponsive. The next day,
    she continued to exhibit a blank expression,
    lethargy, and minimal verbal responses.

3
  • Rehab was consulted for 9G placement for post-op
    rehab.
  • At the consultation, she displayed a fluctuating
    level of consciousness, was disoriented to place
    and time, had poor attention, uttered only a few
    words and short phrases, but was pleasant. She
    did not report feeling depressed, manic, or
    anxious. Her score on the Mini Mental State
    Examination was 10 out of 30. Her performance on
    the clock-drawing task was poor.

4
  • PMH HTN, DM, bipolar disorder, CHF
  • no history of stroke, dementia
  • PSH just hip arthroplasty
  • All none
  • Med Lopressor, Glucotrol, lithium, ASA, Lovenox,
    Percocet prn, dulcolax.

5
  • Her psychiatrist recommended obtaining an EEG and
    Head CT. Results showed diffuse slowing and mild
    small vessel ischemic changes, respectively. EEG
    findings supported the diagnosis of delirium, and
    Ms A was given donepezil, 5 mg/day.
  • The next day, she was better but still confused
    and sleepy.
  • The second day, she was alert and conversant, and
    displayed some insight.
  • The following day, she was alert, fully oriented,
    displayed good eye contact and normal psychomotor
    activity. MMSE was 20/30.
  • She was then transferred to 9G for post-op rehab.

6
DELIRIUM pathogenesis, diagnosis, and treatment
7
Definition and terminology
  • DSM IV
  • Disturbance of consciousness with reduced ability
    to focus, sustain, or shift attention.
  • 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.

8
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.

9
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.

10
Pathogenesis of delirium
  • Poorly understood
  • Difficult to study severely ill patients
  • Hard to separate from that of underlying illness
    and drug treatment

11
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

12
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).

13
  • 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.

14
neurotransmitters
  • 2. Alterations in neuropeptides (eg,
    somatostatin), endorphins, serotonin,
    norepinephrine, and GABA
  • 3. Cytokines, such as interleukins and interferons

15
Pathogenesis (3) risk factors
  • Multifactorial
  • Underlying brain diseases, such as dementia,
    stroke, Parkinsons disease
  • Advanced age and sensory impairment

16
Pathogenesis (4) precipitating factors
  • Polypharmacy (particularly psychoactive drugs)
  • Infections
  • Dehydration
  • Immobility (including restraint use)
  • Malnutrition
  • The use of bladder catheters

17
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.

18
  • 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 uncommon

19
  • 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.

20
  • 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.

21
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.

22
  • 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.

23
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
24
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

25
  • 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

26
Evaluation (4) medication review
27
Differential Diagnosis
  • 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.

28
  • 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.

29
  • 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
    post-ictal state, automatisms (lip smacking,
    chewing, swallowing movements).

30
  • 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

31
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

32
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.

33
  • 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.

34
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)

35
  • 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.

36
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

37
  • 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.

38
Treatment
  • 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)
  • Inouye, Bogardus, Charpentier. A Multicomponent
    intervention to prevent delirium. NEJM 1999.

39
Managing disruptive behaviors
  • 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.

40
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.

41
  • 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.

42
Summary Delirium workup scheme
43
Summary Common causes of Delirium
44
Summary common culprit drugs
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