Delirium — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Margaret Chen, 84 years old, retired nurse. [1]

Presenting complaint: Acute confusion and agitation on day 4 after hemiarthroplasty for a femoral neck fracture. [1]

History of the presenting complaint: Mrs Chen fell at home 5 days ago while walking to the bathroom at night, sustaining a displaced left femoral neck fracture. She underwent an uneventful cemented hemiarthroplasty under spinal anaesthetic with sedation on day 2. She was managing on the ward with regular paracetamol and codeine, and was beginning to mobilise with the physiotherapist. On the evening of day 4, the nursing staff noted that she became acutely agitated — she pulled out her intravenous cannula, began calling out for her mother (who died 40 years ago), reported seeing "men in the room" who were not there, and tried to climb out of bed. Her husband, visiting at the time, reported that she had been "completely different since this morning" and "not at all her usual self." She was oriented to her name only. [1]

Past history:

• Mild-to-moderate Alzheimer disease, diagnosed 3 years ago. Baseline MoCA 18/30 six months ago. She was functionally independent, managing her own medications and personal care, living with her husband.
• Hypertension, well-controlled on ramipril.
• Osteoarthritis, affecting her knees and hands.
• Overactive bladder, on oxybutynin for 4 years.
• No history of stroke, cardiac disease, or diabetes.
• No prior psychiatric history.
• No history of alcohol misuse. [1]

Current medications:

• Donepezil 10 mg daily (for Alzheimer disease)
• Ramipril 5 mg daily
• Oxybutynin 5 mg twice daily
• Paracetamol 1 g four times daily (regular, postoperative)
• Codeine 30 mg every 6 hours as needed (postoperative — she has been taking it 3 to 4 times daily) [1]

Social history: Lives with her husband (82, also retired, in good health) in their own single-storey home. Two adult children who live nearby and visit regularly. She was driving until last year and is active in her local church community. She does not smoke and drinks alcohol rarely. [1]

Examination findings (trainee elicits):

• Conscious but drowsy, fluctuating in alertness during the assessment.
• Attention markedly impaired — cannot recite the months of the year backwards (loses the thread after 2 months).
• Disoriented to time (thinks it is 1998), to place (cannot name the hospital), oriented to person only.
• Thinking is rambling, incoherent, and disorganised. She reports visual hallucinations ("there are men standing over there").
• Temperature 37.1 degrees C, pulse 88 and regular, blood pressure 128/74, respiratory rate 16, oxygen saturation 96 percent on room air.
• Cardiovascular: no focal signs. Chest: clear. Abdomen: soft, non-tender. Surgical wound: clean and dry, no haematoma.
• Neurological: no focal signs. GCS 14 (E4 V4 M6 — oriented to name only, inattentive). No meningism. No focal weakness. Reflexes symmetric and normal. Plantars downgoing.
• Bladder scan: 120 mL (not in retention).
• CAM positive: feature 1 (acute onset and fluctuating course — confirmed by husband), feature 2 (inattention on months backwards), feature 3 (disorganised thinking and hallucinations). Feature 4 (altered level of consciousness — drowsy, fluctuating) also present. [1]

Investigations:

• Full blood count: haemoglobin 118 g/L (was 125 pre-operatively), white cell count 9.2, normal differential, platelets 240.
• Urea and electrolytes: sodium 134, potassium 4.1, urea 6.2, creatinine 88 (baseline 82). Calcium normal. Glucose 6.4. Liver function normal.
• CRP 14 (was 8 pre-operatively).
• Urinalysis: trace leucocytes, nitrite negative. Urine culture sent.
• Chest X-ray: clear lung fields, no consolidation.
• ECG: sinus rhythm 88, normal intervals, no acute changes. [1]

Candidate's long-case presentation (SASPOP)

"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. [1]

Her past history includes mild-to-moderate Alzheimer disease diagnosed 3 years ago with a baseline MoCA of 18 out of 30, hypertension, osteoarthritis, and overactive bladder. She was previously functionally independent. [1]

Her medications are donepezil 10 milligrams daily, ramipril 5 milligrams daily, oxybutynin 5 milligrams twice daily, regular paracetamol, and codeine as needed for postoperative pain. [1]

Her main problems are:

1. Acute postoperative delirium superimposed on Alzheimer dementia — confirmed by a positive CAM
2. High anticholinergic drug burden from oxybutynin, directly opposing the cholinergic mechanism of her donepezil — a pharmacologically irrational combination and a key precipitant
3. The recent hip fracture and hemiarthroplasty, with pain control and mobilisation to address
4. Risk of falls, pressure injury, aspiration, and prolonged hospital stay — the complications of delirium
5. Family distress — her husband needs education and involvement [1]

My integrated management plan addresses each problem. For the delirium, I am running a structured precipitant search using the DELIRIUM mnemonic — I have stopped the oxybutynin immediately and minimised the codeine, I am treating pain with regular paracetamol and a fascia iliaca block, I am searching for infection with a septic screen though the initial results are reassuring, I have checked electrolytes which are normal, I have excluded urinary retention on bladder scan, and I will perform a rectal examination for constipation. I am continuing the donepezil — I would never stop a cholinesterase inhibitor in a patient taking it for dementia. I am instituting multicomponent non-pharmacological care based on the HELP principles — orientation, environment, sensory aids, mobility, sleep protection, and family involvement. I will avoid benzodiazepines entirely — she is not in withdrawal. If her agitation poses a genuine risk of injury to herself or her surgical repair and the non-pharmacological measures are insufficient, I would use a single low dose of haloperidol 0.5 milligrams orally, with ECG monitoring for QT prolongation, at the lowest effective dose and stopped as soon as possible — this is acceptable because she does not have Parkinson disease or Lewy body disease, which would be absolute contraindications. I will explain the delirium to her husband, encourage his presence, and plan a cognitive reassessment after the delirium resolves to check for any step-down in her baseline, because delirium accelerates cognitive decline in patients with dementia." [1]

Examiner discussion questions and model answers

Q1: "What is the evidence that her oxybutynin is contributing to the delirium, and what would you use instead for her bladder?" [1]

"The evidence is mechanistic and epidemiological. Mechanistically, the cholinergic deficiency hypothesis is central to delirium — acetylcholine is the neurotransmitter critical for attention and cortical processing, and anticholinergic drugs precipitate delirium by blocking muscarinic receptors. Oxybutynin is among the highest anticholinergic-burden drugs in common clinical use — it crosses the blood-brain barrier and has strong central antimuscarinic activity. The combination of donepezil, which increases acetylcholine, with oxybutynin, which blocks it, is pharmacologically irrational, and in an older patient with dementia and reduced cholinergic reserve, it is a key precipitant. Epidemiologically, multiple observational studies and the Inouye reviews (PMID 16540616, 23992774) identify anticholinergic drug burden as a major, dose-dependent, modifiable risk factor for delirium. For her bladder management, I would stop the oxybutynin immediately. My alternatives would be, first, non-pharmacological measures — timed voiding, prompted voiding by the nursing staff, ensuring easy access to the toilet or a commode, and managing her fluid intake. Second, if pharmacological treatment is needed, I would use mirabegron, a beta-3 adrenergic agonist that relaxes the detrusor muscle via a non-cholinergic mechanism and does not carry the anticholinergic cognitive risk, though it can raise blood pressure and I would monitor that. Third, if an antimuscarinic is genuinely necessary, tolterodine or solifenacin have a lower anticholinergic burden than oxybutynin and are preferable, though they still carry some risk. The principle is to minimise the total anticholinergic burden in any older patient, and especially in one with dementia and delirium." [1]

Q2: "How confident are you that you have found the cause, and what else would you look for over the next 24 hours?" [1]

"I am not confident that the oxybutynin is the sole or even the dominant cause, because delirium is multifactorial and she has several precipitants operating together — the surgery itself (anaesthetic and surgical inflammatory insult, which is a major precipitant, especially in a patient with dementia who has a lowered threshold), the codeine (an opioid), the hospital environment (sleep deprivation, immobility, sensory deprivation), and possibly an as-yet-undetected infection or metabolic disturbance. The oxybutynin is the most clearly modifiable and the most pharmacologically irrational, so I am addressing it first, but I am continuing the full precipitant search. Over the next 24 hours, I would: review the urine culture when it returns — a trace of leucocytes alone does not diagnose a UTI, and asymptomatic bacteriuria is common in older women, so I would treat only if there is a significant culture and a clinical syndrome consistent with UTI. I would repeat the CRP and white cell count to look for a rising trend suggesting occult infection. I would check that she is not constipated — opioids and immobility predispose to this, and faecal impaction is a common, easily missed precipitant that a rectal examination would detect. I would reassess her pain control — uncontrolled pain is a major, under-recognised precipitant. I would ensure she is being mobilised, because immobility itself perpetuates delirium. And I would observe the course — if the delirium is improving with the cause treatment and supportive care, that supports the multifactorial postoperative explanation. If it is not improving at 48 to 72 hours, I would escalate the search — repeat the septic screen, consider a CT brain if there is any concern about a subdural from the fall, check thyroid function, and look harder for occult sources." [1]

Q3: "Her husband is very distressed and asks whether she will recover. What do you tell him?" [1]

"I would have this conversation honestly, with compassion, and without catastrophising or falsely reassuring. I would explain that delirium is a temporary disturbance of the brain caused by the combination of the surgery, the medications, the hospital stay, and possibly a minor infection or dehydration, and that it is very common after surgery in older patients, especially those who already have some memory problems. I would be clear that it is not a permanent loss of her mind, and that it is not her dementia suddenly getting much worse — it is an acute, potentially reversible problem that we are actively treating. I would set out what we are doing — stopping the medication that is contributing, treating any infection or other cause we find, helping her to move around, keeping her hydrated, and ensuring she has her glasses and familiar things around her. I would encourage him to be present as much as possible, to bring a family photograph and a familiar blanket, and to help reorient her, because his presence is one of the most therapeutic things we can offer. I would set realistic expectations: most delirium improves over days to weeks as the underlying problems are treated, but some patients take longer, and a proportion have persistent confusion or a step-down in their thinking afterwards — I would plan to reassess her memory and function once the acute episode has settled. I would acknowledge that this is frightening for him and for her, offer written information about delirium, and arrange for him to speak with the nursing staff and the medical team regularly. I would offer the social work and aged-care team input for discharge planning. I would not give a false guarantee that she will return entirely to her baseline, but I would convey realistic hope and a clear plan." [1]

Q4: "She is on donepezil. Does that affect your choice of sedation if you need it?" [1]

"Donepezil is a cholinesterase inhibitor — it increases acetylcholine. It does not affect my choice of antipsychotic directly, because the sedation decision rests on the dopamine system, not the cholinergic system. Donepezil is mildly protective against delirium, mechanistically, by supporting the cholinergic tone that delirium impairs, and I would continue it — I would never stop a cholinesterase inhibitor abruptly in a patient taking it for Alzheimer disease, because withdrawal can precipitate cognitive deterioration. The interaction I am alert to is the combination of donepezil with the oxybutynin, which I have stopped, because they are pharmacologically opposed. For sedation, the choice of haloperidol or an atypical antipsychotic is governed by her cardiac status (QT prolongation), her Parkinson or Lewy body status (she has neither — confirmed by history — so haloperidol is not contraindicated here, unlike in a patient with Parkinson disease where it would be catastrophic), and her level of consciousness (she is drowsy, so I would be cautious with any sedating drug). There is no specific interaction between donepezil and haloperidol that would change my choice, but I would be aware that donepezil can cause bradycardia and that haloperidol can cause QT prolongation, so I would monitor the ECG if I use it. If I were dealing with a patient with Lewy body dementia, the donepezil (cholinergic) would be continued and the haloperidol (dopaminergic antagonist) would be absolutely contraindicated — a different scenario." [1]

Q5: "What are the longer-term implications of this delirium episode for her?" [1]

"This is an important question because the implications are substantial and often under-appreciated. The Witlox meta-analysis in JAMA in 2010 (PMID 20664045) established that delirium in elderly patients is independently associated with three poor long-term outcomes, even after adjusting for age, comorbidity, illness severity, and baseline dementia: increased mortality, increased institutionalisation, and accelerated cognitive decline toward dementia. For Mrs Chen specifically, the implications are: first, her hospital stay is likely to be prolonged — delirious patients stay roughly twice as long as non-delirious patients with the same admission. Second, she is at increased risk of complications during this admission — falls, pressure injury, aspiration pneumonia, and the need for new residential care if she cannot return to her baseline function. Third, and most importantly for her long-term trajectory, this delirium episode is likely to accelerate her Alzheimer disease — each episode of delirium in a patient with established dementia is associated with a step-down in cognitive baseline that may not fully recover, and the cognitive decline is faster than in matched patients who do not experience delirium. Fourth, she is at high risk of recurrent delirium with any future illness or hospitalisation, because the brain that has had one delirium is more vulnerable. My follow-up plan reflects this: I will reassess her cognition with a MoCA 1 to 3 months after discharge to establish her new baseline and detect any step-down; I will ensure her medications have been reviewed and the anticholinergic drugs removed permanently; I will arrange a comprehensive geriatric assessment and rehabilitation to optimise her function and support her husband; I will address modifiable risk factors for recurrence — her vision and hearing, her comorbidity, her polypharmacy, and her activity and social engagement; and I will educate the husband and her general practitioner about the signs of delirium and the importance of early presentation with any acute illness, so that future episodes are caught and treated early." [1]

DCE Short Case — Cognitive Assessment

Examination instruction

Examiner: "This 82-year-old woman on the general medical ward is said to be confused. Please assess her cognition." [1]

Key signs this patient demonstrates

• Drowsy and fluctuating in alertness — reduced level of consciousness (4AT feature 1 abnormal)
• Attention markedly impaired — cannot recite the months of the year backwards, loses the thread after two months (4AT feature 3, CAM feature 2)
• Disoriented to time (thinks it is 1998) and place (cannot name the hospital), oriented to person only (4AT feature 2 — AMT4 failed: cannot give the correct year)
• Registration of three objects intact, but recall at 3 minutes is zero
• Speech rambling, incoherent, and disorganised — reporting visual hallucinations (CAM feature 3)
• Clock-drawing shows perseveration, crowding of numbers on one side, and misplaced hands — frontal-executive and visuospatial impairment
• CAM positive: features 1, 2, 3, and 4 all present
• No focal neurological signs on motor and sensory examination
• Collateral history from daughter (by telephone) confirms acute change over 24 hours from a baseline of mild cognitive impairment, with fluctuation through the day [1]

Presentation template

"I performed a cognitive assessment on this 82-year-old woman. Her level of consciousness is reduced — she is drowsy and fluctuating in alertness during the assessment, which the nursing staff report has varied through the morning. Attention is markedly impaired — she cannot recite the months of the year backwards and loses the thread after two months. She is disoriented to time, believing it is 1998, and to place, unable to name the hospital. Registration of three objects was intact, but recall at 3 minutes was zero. Her speech is rambling and disorganised, and she describes visual hallucinations of men in the room. Her clock-drawing shows perseveration, crowding of the numbers, and misplaced hands, indicating frontal-executive and visuospatial impairment. A collateral history from her daughter confirms an acute change over the last 24 hours from a baseline of mild cognitive impairment, with fluctuation through the day. There are no focal neurological signs. These findings meet the Confusion Assessment Method criteria for delirium — acute onset and fluctuating course, inattention, disorganised thinking, and altered level of consciousness — consistent with delirium, possibly superimposed on an underlying cognitive impairment given her baseline. I am now investigating the precipitant with a full septic screen, electrolytes, urinalysis, chest X-ray, ECG, and a medication review, and I have instituted multicomponent non-pharmacological management." [1]

Discussion

Q: "How does this picture differ from dementia?" [1]

"The distinguishing features are the acute onset over hours, the fluctuating course, the markedly impaired attention, and the altered level of consciousness. Dementia is chronic and gradual, progressing over months to years, with a stable day-to-day course, relatively preserved attention in the early-to-moderate stages, and a normal level of consciousness until late. This patient's acute change over 24 hours, the drowsiness and fluctuation, the inability to recite the months of the year backwards, and the disorganised thinking are all features of delirium, not dementia. However, the collateral history of a baseline of mild cognitive impairment means this is most likely delirium superimposed on an underlying cognitive impairment or early dementia — the two coexist, and the acute deterioration is the delirium, which must be investigated and treated. The key clinical rule is that an acute change in a patient with known or suspected dementia is delirium until proven otherwise — it must never be dismissed as 'the dementia progressing.'" [1]

Q: "What would you do first to investigate the cause?" [1]

"I would run the DELIRIUM mnemonic at the bedside. First, a medication review — I am looking for anticholinergic drugs (oxybutynin, tricyclics, antihistamines), benzodiazepines, opioids, and any newly added drugs. Second, blood tests — full blood count for infection, urea and electrolytes for dehydration and hyponatraemia (the commonest electrolyte cause), calcium, glucose, liver and thyroid function, and CRP. Third, urinalysis and urine culture — urinary tract infection is the single most common infectious precipitant in older adults, though I would interpret a positive culture cautiously because asymptomatic bacteriuria is common. Fourth, a chest X-ray for pneumonia. Fifth, an ECG for silent myocardial infarction or arrhythmia. Sixth, a focused examination for infection (cellulitis, wound), urinary retention (bladder scan), and constipation (rectal examination). I would only arrange neuroimaging — CT brain — if there were focal neurological signs, head trauma, anticoagulation, deteriorating consciousness, or no cause found on the first-line workup, because the yield is otherwise low." [1]

Q: "What is the single most useful piece of information you have not yet obtained?" [1]

"A collateral history from a family member or carer who knows the patient's baseline cognition, to establish the onset and course of the change. I obtained a telephone collateral history from the daughter, which confirmed an acute change over 24 hours from a baseline of mild cognitive impairment with day-to-day fluctuation — this is the single piece of information that transforms the assessment, because it confirms the acute onset and the fluctuating course (CAM feature 1), distinguishes the delirium from the underlying cognitive impairment, and establishes the baseline against which recovery will be measured. Without the collateral history, I cannot reliably distinguish delirium from dementia at the bedside, because I cannot know whether the current impairment is acute or chronic. This is why every delirium assessment must include, or explicitly plan to obtain, a collateral history." [1]