Phys Vivas · geriatric
Delirium — Viva Defence
Structured DCE viva for delirium: long-case defence covering a complex elderly patient with postoperative delirium superimposed on dementia, plus a DCE short-case cognitive assessment and discussion of the CAM, hypoactive delirium, and the differentiation from dementia and depression.
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Target exams
Delirium Viva
Long Case Viva Defence
Candidate's opening statement (model answer)
"Mrs Margaret Chen is an 84-year-old retired nurse presenting with an acute confusional state on day 4 following a cemented hemiarthroplasty for a displaced femoral neck fracture sustained in a fall at home. She has a three-year history of mild-to-moderate Alzheimer disease, with a baseline MoCA of 18 out of 30 six months ago, and was previously functionally independent, living with her husband. [1]
Her past history also includes hypertension and osteoarthritis, and she has overactive bladder. [1]
Her medications are donepezil 10 mg daily, ramipril 5 mg daily, oxybutynin 5 mg twice daily, paracetamol regularly, and codeine as needed for pain. [1]
On the evening of day 4 she became acutely agitated, pulling at her intravenous cannula, calling out for her mother, and trying to climb out of bed. The CAM is positive. She is afebrile with stable observations. [1]
Her main problems are:
- Acute postoperative delirium superimposed on Alzheimer dementia
- High anticholinergic drug burden — oxybutynin directly opposing the donepezil she takes for her dementia
- The recent hip fracture and hemiarthroplasty, with pain control and mobilisation to address
- Risk of falls, pressure injury, and prolonged hospital stay
- Family distress and need for education and involvement [1]
My integrated plan is to run a structured precipitant search using the DELIRIUM mnemonic — I have stopped the oxybutynin and minimised the codeine, I am checking for infection, dehydration, electrolyte disturbance, urinary retention, and constipation, and I have ordered a full septic screen and metabolic panel. I will institute multicomponent non-pharmacological care based on the HELP principles — orientation, environment, sensory aids, mobility, sleep protection, and family involvement. I will avoid benzodiazepines, and reserve low-dose haloperidol only for severe distress or danger, with the lowest effective dose and ECG monitoring, stopping as soon as possible. I will not stop the donepezil. I will explain the delirium to her husband, encourage his presence, and plan a cognitive reassessment after the delirium resolves." [1]
Examiner probing questions and model answers
Q1: "You mentioned stopping the oxybutynin but keeping the donepezil. Explain the pharmacological reasoning." [1]
"The reasoning rests on the cholinergic deficiency hypothesis of delirium. Acetylcholine is the neurotransmitter critical for attention, arousal, and cortical processing — the domains impaired in delirium. Donepezil is a cholinesterase inhibitor that increases acetylcholine and is protective against cognitive decline and, mechanistically, against delirium — I would never stop it in a patient on it for Alzheimer disease, because abrupt withdrawal can precipitate cognitive deterioration. Oxybutynin, in contrast, is a potent antimuscarinic anticholinergic — it directly blocks acetylcholine at muscarinic receptors and opposes the very mechanism the donepezil is supporting. It is among the highest anticholinergic-burden drugs in common use and is a well-established precipitant of delirium, especially in older adults with reduced cholinergic reserve. The combination of donepezil and oxybutynin is pharmacologically irrational — one increases acetylcholine, the other blocks it — and the net effect in this patient is cholinergic deficit contributing to her delirium. So I stop the oxybutynin immediately and keep the donepezil. For her overactive bladder, I would consider mirabegron, a beta-3 adrenergic agonist that relaxes the detrusor without anticholinergic activity, or a timed-voiding regimen, or, if an antimuscarinic is genuinely necessary, tolterodine or solifenacin have a lower anticholinergic burden than oxybutynin but still carry some risk. The principle is to minimise total anticholinergic burden in any older patient, and especially in one with dementia and delirium." [1]
Q2: "The nurses ask you to prescribe something to settle her because she is disturbing the ward. How do you respond?" [1]
"I would resist pressure to prescribe sedation reflexively. My response to the nursing staff is that sedation does not treat the delirium and may prolong it, and that our first priority is the cause search and the non-pharmacological measures. I would ask whether there is a reversible contributor we have not addressed — is she in pain, is she constipated, is she retaining urine, is she hungry or thirsty, is she frightened, has she had her glasses and hearing aids, is the environment contributing? I would ask whether a family member or a familiar aged-care volunteer could sit with her. I would consider one-to-one nursing if she is at risk of falling or removing her surgical drain. Only if her agitation poses a genuine risk of injury to herself or to her surgical repair, and the non-pharmacological measures and the cause treatment have been exhausted, would I consider a single low dose of haloperidol — 0.5 milligrams orally, or intramuscularly if she will not take oral, repeated after 2 to 4 hours if needed, with ECG monitoring for QT prolongation, and stopped as soon as possible. I would explicitly avoid a benzodiazepine — she is not in alcohol or benzodiazepine withdrawal, and benzodiazepines worsen and prolong delirium. I would document the indication, the dose, the monitoring, and the plan to stop, and I would explain the reasoning to the nurses so that we share the same conservative approach." [1]
Q3: "How would you distinguish her current state from progression of her Alzheimer disease?" [1]
"The distinction rests on the temporal pattern and the cognitive domains affected. Alzheimer disease is chronic, insidious, and gradually progressive over months to years, with a stable — though slowly declining — day-to-day course, relatively preserved attention in the early and moderate stages, and a normal level of consciousness until late. Her baseline MoCA of 18 out of 30 six months ago reflects her moderate Alzheimer disease, and her husband reports she had been functioning at that level until this admission. The current picture is an acute change over hours — her husband says she has been 'completely different since this morning' — with fluctuation, inattention on formal testing (she cannot recite the months of the year backwards), disorganised and rambling thinking, and altered behaviour. This acute, fluctuating disturbance of attention and awareness is delirium, not dementia. The key clinical rule is that dementia does not change over hours. An acute deterioration in a patient with known dementia is delirium superimposed on dementia until proven otherwise, and must be investigated and treated as delirium. I would document the baseline from the husband, plan a repeat MoCA after the delirium resolves to check for any step-down in her cognitive baseline — because the Witlox meta-analysis (PMID 20664045) established that delirium accelerates cognitive decline in patients with established dementia — and I would communicate the distinction to the family so they understand that this is a potentially reversible acute deterioration, not an inevitable progression of her dementia." [1]
Q4: "She had a fall at home before admission. Does that change your approach to the delirium workup?" [1]
"Yes, it does, because a fall in an older anticoagulated — or in her case, non-anticoagulated but aspirin-naive at presentation — patient raises the question of a head injury and an intracranial bleed, particularly a subdural haematoma, which can present with acute confusion days to weeks after the injury. I would ask the husband and the patient specifically whether she hit her head, whether there was loss of consciousness, whether she has had headaches, and whether there was any focal weakness or new neurological symptoms. I would examine her for focal neurological signs, papilloedema, and any scalp haematoma. If there is a history of head impact, or if she is anticoagulated or on antiplatelet therapy, or if focal signs emerge, or if the delirium does not begin to resolve with treatment of the identified precipitants over 48 to 72 hours, I would arrange a non-contrast CT brain to exclude a subdural haematoma, an intracerebral haemorrhage, or an infarct. In this patient, she is not on anticoagulants, and the most probable explanation for her delirium is the postoperative state with the anticholinergic drugs — but I would keep the subdural in the differential, particularly if the course is atypical or prolonged. She is not on aspirin currently for this admission, but I would check whether she was taking it before admission as part of her cardiovascular risk management, because even antiplatelet therapy increases the subdural risk." [1]
Q5: "What is the role of the Hospital Elder Life Program, and can it help a patient who already has delirium?" [1]
"The Hospital Elder Life Program, or HELP, developed by Inouye and validated in the landmark 1999 New England Journal trial (PMID 10053175), is the evidence-based multicomponent prevention programme that targets six modifiable risk factors for delirium during hospitalisation — cognitive impairment, sleep deprivation, immobility, visual impairment, hearing impairment, and dehydration — using trained volunteers supervised by an elder life nurse specialist. In the original trial it reduced delirium incidence from 15 percent to 9.9 percent. Its primary role is prevention, in at-risk older inpatients, before delirium develops. However, the same principles apply to a patient who already has delirium — the multicomponent interventions are not only preventive but also part of the management of established delirium. For Mrs Chen, I would apply every HELP component: reorientation and a therapeutic environment (clock, calendar, familiar objects, window view, minimised ward moves, appropriately lit room), sleep protection (clustered overnight nursing tasks, reduced noise), early and frequent mobilisation with the physiotherapist, her glasses and hearing aids at all times, and active hydration and nutrition support. The difference between prevention and treatment in this patient is that she already has the delirium, so I am also running the cause search and treating the precipitants in parallel — but the non-pharmacological supportive care is identical and is the mainstay of her management. The principle generalises to every ward: every older inpatient should have their orientation, hydration, sleep, mobility, vision and hearing actively addressed every day, because these are delirium prevention and delirium treatment." [1]
References5ShowHide
- [1]Inouye SK, van Dyck CH, Alessi CA, et al. Clarifying confusion: the confusion assessment method. A new method for detection of delirium Ann Intern Med, 1990.PMID 2240918
- [2]Inouye SK, Bogardus ST, Charpentier PA, et al. A multicomponent intervention to prevent delirium in hospitalized older patients N Engl J Med, 1999.PMID 10053175
- [3]Inouye SK Delirium in older persons N Engl J Med, 2006.PMID 16540616
- [4]Witlox J, Eurelings LSM, de Jonghe JFM, et al. Delirium in elderly patients and the risk of postdischarge mortality, institutionalization, and dementia: a meta-analysis JAMA, 2010.PMID 20664045
- [5]Inouye SK, Westendorp RGJ, Saczynski JS Delirium in elderly people Lancet, 2014.PMID 23992774