13. ICU Deleirum Flashcards

1
Q

Define delirium

A

Acute change in mental status
fluctuating course
characterised:
- Inattention
- disorganised thinking

Acute cerebral insufficiency & considered organ failure

15-80% ICU patients

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2
Q

3 subtypes ICU delirium

A

3 Subtypes

  1. Hyperactive
    - Agitation
    - Relentlessness
    - Emotional lability
  2. Hypoactive / hypokinetic
    Decreased response
    withdrawal
    apathy
    (can be missed / misdiagnosed)
  3. Mixed
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3
Q

Consequences

A

↑ Time ventilated

Delay d/c

↑ unplanned extubation

repeat procedures / removal lines catheters

3x ↑Mortality

↑ Cognitive long term decline

Patient safety/ Staff

Increased medication

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4
Q

Assessment & detection

A

Adequate assessment - sedation optimisation
Ensure pain control
minimal sedation

daily sedation hold sedation

Analgosedation ?agent

Wide variety sedation scores
RASS / Ramsay
0 - -1 to assess

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5
Q

assessment approp screening tool

A

Screening tool
- Consciousness
- inattention
- Disorganised thinking
- fluctuating course
- valid in diverse pop
- completed quick and easy
- not required equipment / psych

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6
Q

EG of Screening tool

A

Commonest - CAM ICU
(confusion assessment method in ICU)

Tool includes asking squeeze fingers
- when letter A mentioned SAVE A HAART

Pass = test four simple questions
eg a stone floats on water true or false

CAM + or -
should be performed @ shift changeover

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7
Q

Management ICU Delirium

A
  1. Adequate pain control
  2. Ensure sepsis Rx & sources infection management
  3. Hypoxia Rx
  4. Biochem abnormalities corrected
  5. Elim predisposing drugs like BZD
  6. Pharmacological
    - haloperidol (QTc)
  • Olanzapine cant use haloperidol
  • quetiapine

Simple measure
day night cycle
glasses / hearing aids
avoid constipation / retention

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8
Q

BJA Article

Key pts

A

• Delirium occurs frequently in critically ill patients and is associated with serious consequences.

• The aetiology of delirium is heterogeneous and multifactorial.

• Non-pharmacological multicomponent interventions seem to be most effective at preventing delirium.

• Treatment of delirium should focus on the treatment of underlying conditions and the symptoms of delirium.

verage incidence rate of 29% during an ICU stay.3

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9
Q

Risk factors of delirium

A
  1. Acute illness-related factors,
  2. Previous coma;
    increased severity of illness,
    mostly expressed in the Acute Physiology and Chronic Health Evaluation (APACHE) score;
    multiple trauma;
    sepsis;
    need for ventilatory support;
    pain;
    and systemic hypoperfusion
    with metabolic acidosis
  3. Medication-related factors:
    benzodiazepines increase the risk in a dose-dependent manner; anticholinergic drugs, opioids, and corticosteroids are probably associated with the development of delirium, although some studies contradict this

Environmental factors, such as increased noise, lack of daylight, and admission to a ward (compared with a personal room) increase the risk of delirium.

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10
Q

Pathophysiology

Clinical presentation

A

Despite homogenous presentation and the possibility of a final common pathway, the pathophysiology of delirium is unclear. Neuroinflammation, an aberrant stress response, imbalance of neurotransmitters, and alterations in neural networks have all been considered as main underlying hypotheses for the pathophysiology of delirium

___________

Changes in consciousness level and inattention, which manifest as difficulty to sustain attention. However, distraction by irrelevant stimuli may occur as well. The sleep–wake rhythm is often disturbed, resulting in sleeplessness. Another frequent sign is disorientation, particularly in time and place

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11
Q

Diagnosis

A

CAM-ICU

  1. Acute onset or fluctuating course
  2. Inattention

Read the following series of 10 letters and let patient squeeze on the letter ‘A’

S A V E A H A A R T† More than two errors

. 3. Altered level of consciousness

Based on the RASS score

  1. Disorganized thinking

Ask the following questions:

  • Will a stone float on water?
  • Are there fish in the sea?
  • Does one pound weigh more than two pounds?
  • Can you use a hammer to pound a nail?

Command

Say to patient: “Hold up this many fingers” (hold two fingers in front of the patient), “Now do the same with the other hand” (without repeating the number of fingers)

Positive CAM-ICU: Criterion 1 plus 2 and either criterion 3 or 4

The CAM-ICU can only be administered when the RASS score < -3.

† If the patient has a neuromuscular disease and squeezing is impossible, eye blinks can be used.

ICDSC other dx

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12
Q

Delirium statement derived from the PADIS guideline

A

Delirium monitoring
(i) Critically ill adults should be regularly assessed for delirium using a valid tool (good practice statement).

(ii) The level of arousal may influence delirium assessments with a validated screening tool (ungraded statement).

Outcomes associated with delirium

(i) Strong association with long-term cognitive impairment and may be with a longer hospital stay

(ii) Not associated with post-traumatic stress disorder or post-ICU distress

(iii) Not associated with ICU length of stay, discharge disposition to a place other than home, depression, functionality/dependence, or mortality

Pharmacological delirium prevention
(i) It is suggested not to use haloperidol, an atypical antipsychotic, dexmedetomidine, an HMG-CoA reductase inhibitor (i.e. statin), or ketamine to prevent delirium in all critically ill adults (conditional recommendation: very low to low quality of evidence).

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13
Q

Delirium treatment

A

(i) Regarding subsyndromal delirium, it is suggested not to use haloperidol or an atypical antipsychotic (conditional recommendation: very low to low quality of evidence).

(ii) Regarding delirium, it is suggested not to routinely use haloperidol, an atypical antipsychotic, or an HMG-CoA reductase inhibitor (i.e. a statin) to treat delirium (conditional recommendation: low quality of evidence).

(iii) It is recommended to use dexmedetomidine for delirium treatment in mechanically ventilated patients, in which agitation is precluding weaning or extubation (conditional recommendation: low quality of evidence).

Non-pharmacological delirium prevention and treatment

(i) It is suggested not to use bright light therapy as single intervention to prevent delirium (conditional recommendation: moderate quality of evidence).

(ii) It is suggested to use a multicomponent, non-pharmacological intervention focusing at (but not limited to) reducing modifiable risk factors; improving cognition; and optimising sleep, mobility, hearing, and vision in critically ill adults (conditional recommendation: low quality of evidence).

rategies to reduce or shorten delirium (e.g. reorientation, cognitive stimulation, and use of clocks), improve sleep (e.g. minimising light and noise), improve wakefulness (i.e. reduced sedation), reduce immobility (e.g. early rehabilitation/mobilisation), and reduce hearing or visual impairment (e.g. enable the use of devices, such as hearing aids or eyeglasses).

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14
Q

Delirium outcome

A

Delirium can be very distressing for the patient and for family members and caregivers.

Delirium may impair outcome because of the increased frequency of self-extubation, removal of catheters, (micro) aspiration, and muscle weakness from immobility.

Delirium is further consistently associated with prolonged durations of mechanical ventilation, ICU and hospital admission, and therefore higher medical costs.

The higher death rate in patients with delirium compared with those without delirium does not appear to result from severity of underlying illness and is thus an indirect effect.26

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15
Q

Patho physiology

A

Pathophysiology

Despite homogenous presentation
and the possibility of a final common pathway, the
pathophysiology of delirium is unclear.

Neuroinflammation,
an aberrant stress response,
imbalance of neurotransmitters,
and alterations in neural networks have all been
considered as main underlying hypotheses for the pathophysiology of delirium.

Critical illness is usually associated with an inflammatory response,
for example, trauma, complicated surgery, or sepsis.

Peripheral pro-inflammatory cytokine signals transmitted to the brain can lead to neuroinflammation that persist for months.

Moreover, the systemic inflammatory response may diminish as a result of sepsis.

Many other factors play a role in delirium in sepsis,
such as reduced cerebral perfusion pressure, i
ischaemia caused by systemic hypotension,
hypoxemia and microcirculatory alterations (including endothelial dysfunction)

These factors contribute to the reduction in cerebral blood flow that has been observed during delirium.

The aberrant stress response hypothesis addresses the adverse effects of acute stress.

Several stressors, such as
surgery, systemic inflammation, and pain, cause the brain to
activate the limbic–hypothalamic–pituitary–adrenal axis with
associated increased concentrations of cortisol.

In healthy individuals, this response is adaptive and has adequate feedback regulation.

Cognitive decline and ageing are associated with impaired feedback regulation
of the stress response pathway,
resulting in sustained high cortisol concentrations that
contribute to the development of delirium.

It is further presumed that delirium is associated with reduced activity of neurones that communicate with the neurotransmitter acetylcholine.

Acetylcholine plays a central role in attention and consciousness;
it is particularly affected in delirium as there are interactions with other pathways such as the dopaminergic system.

In addition, delirium may be associated with the production of a random and loose brain network,
which means that there is reduced concomitant activity of brain regions

As delirium is multifactorial, it is assumed that the interaction of different pathways leads to disruption of large-scale neural networks,
and that this disruption causes attention deficits,
a decreased level of consciousness, and other features of delirium.

Studies with preoperative brain MRIs found cerebral atrophy, white matter hyperintensities, and cortical infarcts were risk factors for postoperative delirium.

These structural changes affect neural network function and may thus predispose to delirium.

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