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- 1. Delirium in Critically Ill Patients Gemma Wilson Junior Presentation
- 2. Patients Perspectives â The time I spent seems like it was in a huge, empty grey space, sort of like a monstrous underground parking garage with no cars, only me, floating or seeming to float, on something. Every once in a while I would get to an edge of something horrible and I thought, âif I just let go, then this horror will be overâ SB âI was in a tunnel knee-deep in mud. It was pitch black, but I could see light in the end. I felt a cold chill on my back. I thought it was the grim reaper, I knew i had to get to the lightâ 2
- 3. Learning Outcomes ⢠Overview of Delirium ⢠Detection of Delirium ⢠Prevention of Delirium ⢠Treatment of Delirium
- 4. Delirium Delirium has been defined as: âan acute, reversible organic mental syndrome with disorders of attention and cognitive function, increased or decreased psychomotor activity and a disordered sleep- wake cycleâ. It is commonly found in the critically ill (i.e. not always in ICU) with a reported incidence of 15-80%. The term ICU psychosis is old fashioned, inaccurate and not appropriate.
- 5. ICU Delirium is a predictor of ⢠Increased ICU length of stay (8 vs 5 days) ⢠Increased hospital length of stay (21 vs 11 days) ⢠Increased time on ventilator (9 vs 4 days) ⢠Higher ICU costs (£15,700 vs £9,200) ⢠Higher ICU mortality (19.7% vs 10.3%) ⢠Higher hospital mortality (26.7% vs 21.4%) ⢠3-fold increased risk of death at 6 months
- 6. Delirium Three delirium subtypes have been characterised: 1. Hyperactive - Agitated, paranoid. 2. Hypoactive - Withdrawn, quiet, paranoid. 3. Mixed - Combination of hyperactive and hypoactive
- 7. Delirium Subtypes Combative Hyperactive Delirium Agitated Restless Mixed Delirium Lethargic Sedated Stupor Hypoactive Delirium
- 8. Risk Factors
- 10. Diagnosis Traditionally ICU Delirium was diagnosed by a psychiatrist using: â DSM IV criteria The assessment tool most commonly used in the UK: â Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)
- 11. What is CAM-ICU? ⢠An adaptation of The Confusion Assessment Method (CAM). ⢠Bedside assessment tool usable by non- psychiatrists to assess for delirium. ⢠Delirium is defined in terms of 4 diagnostic features: 1. Acute Onset or Fluctuating Course 2. Inattention 3. Altered Level of Consciousness 4. Disorganised Thinking Feature 1 plus 2 and either 3 or 4 present = CAM- ICU positive (Delirium Present)
- 12. CAM-ICU Feature 1: Acute change or fluctuating course of mental status And Feature 2: Inattention And Feature 3: Altered level of Or Feature 4: Disorganized consciousness thinking
- 13. CAM-ICU Worksheet and Video http://www.youtube.com/watch?v=fyaQuYnnoZ4
- 14. Who can be assessed? ⢠Any patient, sedated or not, who can open their eyes when you say their name and can keep their eyes open for the duration of the test. 14
- 15. What are the elements of the test? 1. Acute Onset or Fluctuating Course 2. Inattention 3. Altered Level of Consciousness 4. Disorganised Thinking 15
- 16. 1. Acute onset of mental status changes/fluctuation in the last 24 hours Essentially the patient is not their self, e.g. ⢠Reduced/fluctuation in GCS/AVPU ⢠Reduced/fluctuation in sedation score (not dose related) ⢠Agitated, hyper-active, combative, restless, confused, withdrawn, lethargic, stuporous. 16
- 17. 2. Inattentive The patient cannot concentrate during a simple test or makes mistakes. ⢠Ask the patient to squeeze your hand or nod their head, to indicate when you have said the letter âAâ in a 10 letter sequence of: SAVE A HAART OR HAVE A HAART ⢠Failure to indicate or indicating when a different letter is said it is a mistake More that 2 mistakes = inattention 17
- 18. Key Point If they are NOT inattentive they are not delirious so at this point you can stop the test at this point if it is negative for inattention. 18
- 19. 3. Altered level of consciousness Is the patient anything other than Alert? Present if the RASS score is anything other than alert and calm (zero) 19
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- 21. 4. Disorganised thinking This includes answering 4 logical questions and obeying a simple command, e.g. 1.Will a stone float on water? 2.Are there fish in the sea? 3.Does on pound weigh more than two pounds 4.Can you use a hammer to pound nail. Errors are counted when the patient incorrectly answers the question Command: Hold up 2 fingers with one hand - then do the same with the other hand. An error is counted if the patient is unable to complete the entire command 21
- 22. Wakey Wakey!!! Itâs Case Study Time!!!
- 23. The POSITIVE CAM-ICU ⢠We should THINK first about: Toxic situations ⢠reversal and aggressive treatment of underlying cause(s) such as CHF and shock ⢠stopping unnecessary deliriogenic agents that may be impairing brain function Hypoxemia, or consider giving Haloperidol or other antipsychotics Infection/sepsis, or Immobilization Nonpharmacological interventions such as eyeglasses, hearing aids, reorientation, and sleep hygiene K+ medical management other than new drugs (e.g., correction of electrolyte disorders) ONLY after the above considerations should we add new agents that the patient is not on, such as antipsychotics 23
- 24. Pathophysiology ⢠Currently no comprehensive explanation for the mechanism by which delirium occurs. ⢠Numerous hypothesis likely to be multifactorial. ⢠A review by Girard et al covers several of the leading suggestions.
- 25. Abnormal+tryptophan+metabolism+ Decreased!tryptophan! Increased!tryptophan! Glutamate! Histamine! Decreased!serotonin! Increased!serotonin! Endorphins! GABA! Mechanism!of!action!unknown! Decreased!melatonin! Increased!melatonin! Hyperactive+delirium+ Hypoactive+delirium+ Cerebral!ischaemia!leading! Endothelial!damage! to!diffuse!brain!injury! DELIRIUM+ Thrombin!formation! Microvascular!compromise! Neuronal!excitability!increased! Neurotransmitters+ Increased! Increased! Reduced! noradrenaline! dopamine! acetylcholine! Increased:! IL1! IL2! TNF! ! Increased!phenylalanine! Inflammatory+response+ 25 (precursor!of!dopamine!&!NA)!
- 26. PREVENTION Prevention A recent paper by Morandi et al introduces the concept of an âABCDE bundleâ which uses an evidence-based approach in the prevention of -based in the prevention of delirium. 22 This is summarised in Figure 2. delirium. !
- 27. Treatment: NonâPharmacological 1. Recognise the presence of delirium by use of assessment tool. 2. Review delirium risk factors, looking for precipitant causes that may be correctable.
- 28. Treatment: NonâPharmacological Cont General factors Medications ⢠Avoid deliriogenic drugs where possible ⢠Correct visual impairment with glasses Environmental factors ⢠Correct hearing impairment with hearing aids ⢠Orientate the patient regularly Medical factors ⢠Reduce noise ⢠Reduce sleep disturbance ⢠Correct metabolic derangement ⢠Mobilise where possible ⢠Diagnose and treat sources of infection ⢠Achieve adequate tissue oxygen delivery ⢠Administer adequate analgesia ⢠Remove lines and catheters promptly ⢠Do not use physical restraints routinely but only use acutely to prevent harm
- 29. Treatment: Pharmacological ⢠Haloperidol ⢠Atypical anti-psychotics ⢠olanzapine ⢠quetiapine ⢠Benzodiazepines
- 31. Summary ⢠Delirium = Organ dysfunction ⢠Recognising delirium is like a âburglar alarmâ or the âcanary in the coal mineâ ⢠There are many potential causes of this organ disfunction therefore many routes to correct treatment for a given patient. ⢠Do NOT automatically link delirium with a specific drug treatment
- 32. Summary Cont BRAIN ROAD MAP FOR INTERDISCIPLINARY COMMUNICATION Investigate the following: Where is the patient going? (i.e., sedation targets/goals) Where is the patient now? (i.e., current RASS/CAM-ICU) How did they get there? (i.e., sepsis, drug exposures) State the following (only takes 10 seconds!): 1.!Target RASS 2.!Actual RASS 3. CAM-ICU 4. Drugs Skipping any of these steps will leave the clinical team wanting more information! 32
Editor's Notes
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- Delirium is a common complication of critical illness. It has conventionally been regarded as an unavoidable and benign side effect of long-term sedation on an intensive care unit (ICU). \n
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- The clinical classification system of delirium was first described in elderly patients by Lipowskiin in 1983.2 \n\nThree sub-types of delirium were described\n\nThe hyperactive form is usually well recognised and the patient may be labelled as being “agitated”.\nSuch patients exhibit some or all of the following features: -\n\nContinual movement (fidgeting, pulling at clothes, catheters or tubes, moving from side to side)\nDisorientated (in at least one aspect such as who they are or where they are)\nCommands may not be followed (complex commands followed less than simple ones)\nPatients who can communicate verbally may be unintelligible, or make inappropriate responses.\nThe patient may shout or call out\nPain is exaggerated\nAbnormal vital signs\n\nThe hypoactive form is often not well recognised and inappropriate therapy may be started if the\npatient is misdiagnosed as being depressed\n\nPsychomotor lethargy & sedation\nAppears quiet \nCo-operative BUT with inattention and disorganised thinking \n\nMixed\nPatients fluctuate between hypo and hyperactive subtypes \n
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- \nAPACHE II score \n\nAPACHE II ("Acute Physiology and Chronic Health Evaluation II") is a severity-of-disease classification system (Knaus et al., 1985),[1] one of several ICU scoring systems. It is applied within 24 hours of admission of a patient to an intensive care unit (ICU): an integer score from 0 to 71 is computed based on several measurements; higher scores correspond to more severe disease and a higher risk of death.\n
- Delirium can be mistaken for, or found in combination with other forms of mental illness. \n\nThis table.\nsummarises the features of various forms of mental illness.\n
- Delirium was traditionally diagnosed by a psychiatrist using DSM IV criteria.\n \nDiagnostic and Statistical Manual of Mental Disorders is a manual published by the American Psychiatric Association (APA) that includes all currently recognized mental health disorders.\n\nWhilst psychiatric referral can still be helpful, the development of specific delirium assessment tools for use by the multi-disciplinary team has greatly improved its recognition on intensive care. However delirium is probably still under-diagnosed, particularly in the hypoactive sub-type, where the more subtle features may be overlooked. \n
- The Confusion Assessment Method (CAM) was created in 1990, and it was intended to be a bedside assessment tool usable by non-psychiatrists by Dr. Sharon Inouye to assess for delirium.\n\n The CAM-ICU is an adaptation of this tool for use in ICU patients (e.g., critically ill patients on and off the ventilator who are largely unable to talk). \n\nDelirium is defined in terms of four diagnostic features, and is deemed present when a patient has positive Feature 1 and Feature 2 and either Feature 3 or 4 (see CAM-ICU schematic on next page). \n
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- Delirium assessment is actually part of the overall consciousness assessment. \n\nConsciousness is defined in two parts—arousal level plus content (see next page). \n\nThe first step to assessing consciousness is to assess level of consciousness. This is best done using a validated sedation/arousal scale. \n\nThe Richmond Agitation-Sedation Scale (RASS) is used in this training manual, though other tools are fine to use with the CAM-ICU. For more information on other sedation scales see question #15 on page 19 in the “Putting it into Practice” section. \n\nThe next step is assessment of content of consciousness. At deeper levels of consciousness (i.e., RASS -4 & -5), it is difficult to ascertain content because the patient is not responsive. These levels are referred to as coma or stupor, and in those situations we do not conduct the CAM-ICU, thus referring to the patient as ‘unable to assess’. However, at the lighter levels of consciousness (i.e., RASS -3 & above), patients are able to display at least the beginnings of meaningful responsiveness (i.e., response to voice). At these levels you are able to assess for clarity of thought, specifically delirium. The following pages include the CAM-ICU in a worksheet format (page 7) and in a flowsheet format (page 8) – same material, different layout. Then starting at page 9 are detailed instructions for assessing the four CAM-ICU features. \n
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- Prevent in more effective than treatment \n\nA study by Morandi et al introduces the concept of an ‘ABCDE bundle’ which uses an evidence-based approach in the prevention of delirium. \n\nAwake and Breathing \nThe Awakening and Breathing Controlled Trial found that daily sedation breaks paired with trials of spontaneous breathing significantly improved outcome at 1 year.23 These findings have led to the adoption of this practice in many intensive care units, although in a survey of clinical practice, the majority of practitioners admit that sedation breaks are not performed as frequently as intended.24 \nChoice of sedation \nThe mainstay of sedation on ICU has traditionally been propofol, benzodiazepines and opiates, all of which have been implicated in altering sleep patterns.25 Trials involving α2 receptor agonists (clonidine and shorter-acting dexmedetomidine) have reported a lower incidence of delirium and shorter time to extubation.26,27Remifentanil is a short-acting pure μ receptor agonist. Its use as a sedative agent in intensive care has been shown to reduce the time to extubation28 but further work is needed to assess its impact on the incidence of delirium. Interestingly, a Danish study randomised 140 mechanically ventilated patients to receive either ‘no sedation’ or propofol sedation with daily sedation breaks. 29 It reported shorter times to extubation and a lower incidence of delirium without an increase in self-extubation in the group randomised to no sedation, but it is unlikely that this practice will become widely adopted. \nDaily delirium monitoring \nDaily screening for delirium is important as delirium is under-diagnosed without the use of assessment tools.30 \nEarly mobility and exercise \nSchweickert et al demonstrated that if physical and occupational therapy was provided at the same time as a sedation break and trial of spontaneous breathing then patients had shorter episodes of delirium and improved function at hospital discharge.31 \nSleep \nIt is unclear whether sleep disruption on intensive care is a cause or a consequence of delirium. Studies have shown that the total sleep time is unaffected by sedation but that altered REM patterns are observed, suggesting an impact on the quality of sleep.32 High levels of noise or ambient light, drugs, mechanical ventilation and routine patient care at inappropriate times of the day have all been associated with sleep disruption\n
- The first stage in the management of delirium is to recognise its presence by use of an appropriate assessment tool. The next stage is to review the delirium risk factors,looking for precipitant causes that may be correctable. Some of the risk factors listed are clearly more amenable to modification than others. \n
- The importance of using non-pharmacological interventions that encourage orientation of the patient to their surroundings cannot be over stated. \n\nMaintaining normal physiological function is also important.\n
- Haloperidol \nHaloperidol is a dopamine receptor (D2) antagonist and acts centrally to reduce hallucinations and delusions. It is hepatically metabolised with an elimination half-life of 10-36 hours secondary to active metabolites. Recognised adverse side effects include extra-pyramidal side effects, prolonged QT interval (which can precipitate torsades de point) and neuroleptic malignant syndrome. The optimum dosing schedule has not yet been established by trial evidence but a commonly used schedule is 2.5-5mg intravenously every 6 hours. Doses may need to be reduced in the elderly. It has also been used as a continuous infusion in severe cases but this does not represent routine practice.36 \nA retrospective study of 989 mechanically ventilated patients identified a significant reduction in hospital mortality in those patients who had received haloperidol during their intensive care stay.However, the study design meant that it was not possible to identify if the indication for commencing the haloperidol was delirium.37 \nAtypical anti-psychotics \nAtypical anti-psychotics (such as olanzapine, quetiapine) are also dopamine receptor (D2) antagonists but have additional antagonistic effects on serotonin receptors (5-HT2A). Enteral administration is required as there are no intravenous preparations available. They are generally metabolised in the liver and have active metabolites. Their half-lives vary according to the preparation with quetiapine having the shortest half-life of 6 hours. The adverse effects that are most likely to be encountered include sedation and anti-cholinergic symptoms. \nA randomised but un-blinded trial of enteral olanzapine versus haloperidol in 103 patients demonstrated improvement in daily Delirium Index scores and reduced benzodiazepine administration in both trial groups without a significant difference between them.\n\nA randomised, double blinded trial of quetiapine against placebo with rescue haloperidol if required found that the quetiapine group had a faster resolution of delirium.39 \nThe recently published MIND study randomly assigned 101 patients to haloperidol, ziprasidone (atypical anti-psychotic) or placebo. Doses were adjusted according to the level of delirium as assessed by CAM-ICU. There was no significant difference in the number of days patients survived without delirium or coma in any of the 3 groups in this small pilot study. A further multi-centre placebo trial is planned.40 \nBenzodiazepines \nBenzodiazepines have a role in the management of delirium caused by alcohol withdrawal. However, their administration in other patient sub-groups has been identified as an independent risk factor for delirium development. Their use should therefore be avoided where possible in critically ill patients \n
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