Polypharmacy and Deprescribing — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mrs Eleanor Davies, 84 years old, retired schoolteacher. [1]

Presenting complaint: A fall at home, resulting in a minor head laceration but no fracture. [1]

History of the presenting complaint: Mrs Davies got up to go to the bathroom at 3 am, felt dizzy and light-headed on standing, grabbed for the door frame, missed, and fell, striking her head on the bedside table. Her husband heard the fall and found her on the floor, conscious but shaken, with a bleeding laceration on her forehead. She did not lose consciousness. She had not eaten since dinner at 6 pm. She describes that she has been feeling generally unsteady and "woozy" for the last few weeks, particularly in the mornings and on standing, and she has had two near-falls in the last month. [1]

Past history:

• Atrial fibrillation (diagnosed 12 years ago)
• Ischaemic heart disease (prior non-ST-elevation myocardial infarction 8 years ago; no recent symptoms; no recent stent)
• Heart failure with reduced ejection fraction (ejection fraction 35 percent 3 years ago)
• Hypertension (long-standing)
• Type 2 diabetes (diagnosed 15 years ago)
• Osteoporosis (diagnosed after a distal radial fracture 5 years ago)
• Overactive bladder (symptoms for several years)
• Insomnia (long-standing)
• Depression (diagnosed 4 years ago after the death of her son) [1]

Current medications (the list the patient and the GP letter provide):

1. Warfarin 3 mg daily (atrial fibrillation)
2. Bisoprolol 5 mg daily (heart failure, rate control)
3. Frusemide 40 mg daily (heart failure)
4. Ramipril 5 mg daily (heart failure, hypertension)
5. Spironolactone 12.5 mg daily (heart failure)
6. Metformin 500 mg twice daily (diabetes)
7. Glibenclamide 5 mg daily (diabetes)
8. Atorvastatin 40 mg at night (secondary prevention)
9. Alendronate 70 mg weekly (osteoporosis)
10. Oxybutynin 5 mg twice daily (overactive bladder)
11. Diazepam 5 mg at night (insomnia, for approximately 10 years)
12. Amitriptyline 25 mg at night (sleep and depression)
13. Omeprazole 20 mg daily (reflux, duration unclear)
14. Aspirin 100 mg daily (secondary prevention) [1]

That is 14 regular medications. She also takes paracetamol occasionally for joint pain and has been buying ibuprofen 200 mg over the counter for knee pain, taking it two to three times a week for the last month, which is not on the GP list. [1]

Social history: She lives with her husband (86, also frail, with early dementia) in their own single-storey home. They have two adult children who visit weekly. She was managing at home with some difficulty, using a walking stick for longer distances, until the fall. She does not smoke and drinks alcohol rarely. She is independent in personal care but her husband helps with meal preparation and medication management. [1]

Examination findings (trainee elicits):

• Conscious, alert, orientated to person and place but not to the exact date.
• Blood pressure 104/58 mmHg lying, 88/52 mmHg standing (significant orthostatic drop).
• Pulse 54 beats per minute, irregularly irregular (atrial fibrillation).
• Weight 46 kilograms, height 158 centimetres (BMI 18.4).
• Minor laceration to the right forehead, no haematoma, no focal neurological signs.
• Cardiovascular: jugular venous pressure not elevated, no peripheral oedema, heart sounds dual with an irregular rhythm.
• Respiratory, abdominal, and neurological examinations unremarkable. [1]

Investigations:

• Full blood count: haemoglobin 112 g/L, white cell count 6.2, platelets 220.
• Urea and electrolytes: sodium 134, potassium 5.2, urea 12, creatinine 78 micromol per litre (reported as "within normal range").
• eGFR (2021 CKD-EPI creatinine): 29 mL per minute per 1.73 metres squared.
• Liver function tests and TSH: normal.
• HbA1c: 6.3 percent.
• INR: 3.8 (target range 2.0 to 3.0).
• CT brain (performed because of the head injury and the anticoagulation): no intracranial haemorrhage, no fracture, mild chronic small-vessel changes.
• ECG: atrial fibrillation at 54 beats per minute, no acute ischaemia.
• Clinical Frailty Scale: 5 (mild frailty). [1]

Candidate's long-case presentation (SASPOP)

"Mrs Eleanor Davies is an 84-year-old retired schoolteacher presenting after a fall at home, sustained on standing to go to the bathroom, with dizziness and light-headedness, resulting in a minor head laceration but no fracture and no intracranial bleed on CT. She has been feeling unsteady for several weeks. [1]

Her past history includes atrial fibrillation, ischaemic heart disease with a prior myocardial infarction 8 years ago, heart failure with reduced ejection fraction, hypertension, type 2 diabetes, osteoporosis, overactive bladder, insomnia, and depression. Her Clinical Frailty Scale is 5. [1]

She is taking 14 regular medications plus over-the-counter ibuprofen, which is not on her GP list — a total of 15 agents, constituting polypharmacy approaching hyperpolypharmacy. [1]

Her main problems are:

1. A multifactorial fall with the medications as the most modifiable contributors — orthostatic hypotension from her antihypertensives and diuretics, bradycardia from the bisoprolol, sedation and ataxia from the diazepam and the amitriptyline, and the over-anticoagulated INR of 3.8 with dual antiplatelet-anticoagulant therapy (aspirin plus warfarin) increasing her bleeding risk.
2. Polypharmacy with multiple potentially inappropriate medications — the glibenclamide (Beers list, prolonged hypoglycaemia in renal impairment), the diazepam (long-acting benzodiazepine, falls risk), the oxybutynin (high anticholinergic burden), the amitriptyline (anticholinergic and sedating), the aspirin combined with warfarin (bleeding), the over-the-counter ibuprofen (NSAID in CKD, worsening blood pressure and renal function), the omeprazole (long-term without a current specialist indication), and the spironolactone in renal impairment with an ACE inhibitor (hyperkalaemia — her potassium is 5.2).
3. Renal impairment with a falsely reassuring creatinine of 78 — her eGFR is 29, and given her low weight and muscle mass, even this may overestimate her true function. Her renally-cleared drugs (metformin, glibenclamide) need dose adjustment or cessation, and I would request a cystatin C-based eGFR to refine the estimate.
4. Possible prescribing omissions — I would assess whether she is missing guideline-directed heart failure therapy such as an SGLT2 inhibitor (balancing this against her blood pressure and renal function), and ensure her vaccinations are up to date. [1]

My integrated management plan addresses each problem. For the medications, I am using the five-step deprescribing process. Immediately, in hospital, I will stop the glibenclamide and the aspirin, reduce the warfarin dose to bring the INR into range, hold or reduce the spironolactone (her potassium is 5.2 and she is at risk of hyperkalaemia), reduce the frusemide and the ramipril to correct the orthostatic hypotension, and stop the over-the-counter ibuprofen. I will plan a supervised taper of the diazepam over several months combined with cognitive behavioural therapy for insomnia, a step-down of the omeprazole, and a switch from the oxybutynin to mirabegron or non-pharmacological bladder management. I will review the amitriptyline and consider stopping it or switching to sertraline. I will request the cystatin C-based eGFR and dose-adjust the metformin. I will apply the START criteria to identify any missing indicated therapy. Every decision is anchored to her goals — maintaining her independence, preventing further falls, and avoiding hospital readmission — and to her frailty and her renal function. I will conduct a formal discharge medication reconciliation, provide her and her GP with a reconciled list and the deprescribing plan, and arrange a follow-up review with the GP, the pharmacist, and the geriatric clinic at 4 to 6 weeks." [1]

Examiner discussion questions and model answers

Q1: "Which single medication change would have the greatest immediate impact on her risk of another fall?" [1]

"The single most impactful change is to address her orthostatic hypotension by reducing her cardiovascular medication load — the combination of frusemide, ramipril, and spironolactone, with the bisoprolol contributing to the bradycardia. Her lying-to-standing blood pressure drop of 16 mmHg systolic is clinically significant and is the direct mechanism of her fall (she was dizzy on standing). Reducing the frusemide and holding or reducing the ramipril and the spironolactone would raise her standing blood pressure and directly reduce her fall risk. This is more immediately impactful than the benzodiazepine taper, which is important but slower. If I could only make one change, it would be to reduce the diuretic and the afterload/hyperkalaemia agents, but in practice I would make several changes in parallel because the fall is multifactorial — the orthostatic hypotension, the bradycardia, the sedation from the diazepam and the amitriptyline, and the anticholinergic burden are all contributing, and addressing only one leaves the others to cause the next fall." [1]

Q2: "Her creatinine is 78 and is reported as normal. Why is her renal function still a concern?" [1]

"Because her serum creatinine is generated by muscle, and she is a frail, 46-kilogram, 84-year-old woman with very low muscle mass — she produces less creatinine for any given level of GFR, so her creatinine of 78 micromol per litre, which would be reassuring in a 70-kilogram younger adult, is a red flag in her. Her creatinine-based eGFR is 29, which is stage 4 chronic kidney disease, and even this may overestimate her true function because the equation is creatinine-derived and muscle-mass-dependent. The clinical consequence is that her renally-cleared drugs — the metformin (risk of lactic acidosis), the glibenclamide (accumulation and prolonged hypoglycaemia), and, if she were on them, the gabapentinoids, the DOACs, and digoxin — will accumulate and cause harm at standard doses. I would request a cystatin C-based eGFR to refine the estimate, dose-adjust or stop the renally-cleared drugs, and monitor her renal function and electrolytes closely during the admission and after any change. The principle, as Inker and colleagues established with the 2021 CKD-EPI equation (PMID 34554658), is that the eGFR is an estimate with important limitations in the frail, low-muscle patient, and a normal creatinine in such a patient never excludes significant renal impairment." [1]

Q3: "She is on aspirin and warfarin. What is your reasoning for stopping the aspirin?" [1]

"The combination of aspirin and an oral anticoagulant is flagged by the STOPP criteria unless there is a clear indication for dual therapy — typically a recent coronary stent, a mechanical heart valve, or a recent acute coronary syndrome. Mrs Davies had a myocardial infarction 8 years ago with no recent event and no stent, and her atrial fibrillation is the indication for the anticoagulation. In this setting, the warfarin alone provides adequate stroke prevention for the atrial fibrillation and reasonable ischaemic protection for the coronary disease, and adding aspirin increases the bleeding risk — particularly intracranial and gastrointestinal bleeding — without a meaningful incremental ischaemic benefit. Her INR of 3.8 is above the therapeutic range, compounding the bleeding risk. The current guidelines (and the STOPP criteria) support stopping the aspirin in a patient like this, and her recent fall with a head laceration (and the CT performed to exclude a bleed) underscores the importance of reducing the bleeding burden. I would stop the aspirin, reduce the warfarin to bring the INR into the 2.0 to 3.0 range, and at her follow-up discuss whether she should transition from warfarin to a DOAC (lower intracranial bleeding risk, no INR monitoring, advantageous in a patient with falls and labile INRs), dose-adjusted for her renal function and weight." [1]

Q4: "How would you approach the diazepam — she has been on it for 10 years?" [1]

"I would not stop it abruptly, because long-term benzodiazepine use causes physiological dependence, and abrupt cessation can precipitate a severe withdrawal syndrome — anxiety, insomnia, tremor, perceptual disturbance, and, at the extreme, seizures. The correct approach is a slow, supervised taper, reducing the dose by 10 to 25 percent every 1 to 2 weeks, which takes 3 to 6 months for a 10-year user. Because diazepam is long-acting (with active metabolites and a half-life that exceeds 80 hours in an older adult), a direct taper of the diazepam itself is feasible and smoother than switching to another agent. I would combine the taper with cognitive behavioural therapy for insomnia (CBT-I), which is the most effective single intervention for chronic insomnia and reduces both the withdrawal symptoms and the likelihood of relapse. I would warn her and her family about the withdrawal symptoms and set the expectation that the taper is a process, not an event, and that the goal is to improve her clarity, her steadiness, and her safety, not to deprive her of something she needs. I would involve her GP and her pharmacist in the follow-up so that the taper is sustained. The evidence consistently shows that most long-term benzodiazepine users can successfully taper and stop with a supervised program — the fear of withdrawal is greater than the reality." [1]

Q5: "What are the longer-term implications of this admission for her medication management?" [1]

"This admission is a critical opportunity to reset her entire medication regimen and her follow-up, because the current polypharmacy is causing her active harm. Beyond the acute changes, the longer-term plan is: first, a formal discharge medication reconciliation with a written, reconciled list provided to her, her family, her GP, and her pharmacist, so that the changes are not reversed at the next GP visit. Second, a structured GP and pharmacist medication review within 1 to 2 weeks of discharge, with a deprescribing plan and review dates. Third, a geriatric clinic review at 4 to 6 weeks to assess the blood pressure, the renal function, the INR or the transition to a DOAC, the glycaemic control, the success of the benzodiazepine taper, and her cognitive function. Fourth, a comprehensive geriatric assessment to address her frailty, her function, her home environment, her sensory aids, and her social support, including a falls assessment (strength and balance training, home hazard reduction, and a vision and hearing check). Fifth, a goals-of-care conversation with her and her family to ensure that every future prescribing decision is anchored to her priorities — maintaining her independence, preventing falls, and avoiding hospital readmission — rather than to a list of single-disease targets. The admission is the trigger, but the sustained change happens in the community, which is why the communication and the follow-up plan are as important as the in-hospital changes." [1]

DCE Short Case — The Bedside Medication Review

Examination instruction

Examiner: "This 82-year-old man on the general medical ward has been admitted with a fall. Please review his medications at the bedside and present your plan." [1]

Key findings this patient demonstrates

• The verified medication list comprises 12 regular medications and 2 over-the-counter preparations (ibuprofen and a nighttime antihistamine) that he had not previously reported to his doctors.
• Potentially inappropriate medications identified by STOPP/START and Beers: diazepam 5 mg at night (10-year duration, long-acting benzodiazepine), oxybutynin 5 mg twice daily (highest anticholinergic burden), diclofenac 50 mg three times daily bought over the counter (NSAID in CKD), and amitriptyline 25 mg at night (anticholinergic and sedating).
• Renal function: eGFR 32 by creatinine, but he is frail and low-muscle; the gabapentin 300 mg three times daily (for neuropathic pain) and the metformin 500 mg twice daily are not dose-adjusted for his renal function.
• Falls risk medications present: diazepam, amitriptyline, diclofenac, and two antihypertensives (amlodipine and ramipril).
• Anticholinergic burden score: 3 (oxybutynin 3, amitriptyline 2, diclofenac 0, diazepam 0 — cumulative 3 by the Anticholinergic Burden Scale).
• Prescribing omission: he has atrial fibrillation at high stroke risk (CHA2DS2-VASc 4) and is not anticoagulated. [1]

Presentation template

"I performed a bedside medication review on this 82-year-old man admitted with a fall. His verified medication list comprises 12 regular medications and 2 over-the-counter preparations — ibuprofen and a nighttime antihistamine — that he had not previously reported, which I identified by explicitly asking about over-the-counter and complementary medicines. Using the STOPP/START version 3 criteria and the 2023 AGS Beers Criteria, I identified four potentially inappropriate medications to address: the diazepam, a long-acting benzodiazepine he has taken for 10 years, which I will taper by 10 to 25 percent every 1 to 2 weeks combined with cognitive behavioural therapy for insomnia; the oxybutynin, the highest anticholinergic burden agent, which I will stop and replace with mirabegron or non-pharmacological bladder management; the diclofenac he has been buying over the counter, an NSAID contributing to his elevated blood pressure and his falling eGFR, which I will stop, managing his pain with paracetamol and a topical agent; and the amitriptyline, which I will stop or switch. I identified one prescribing omission — he has atrial fibrillation at high stroke risk and is not anticoagulated, and after discussing the bleeding risk with him, I will start an anticoagulant dose-adjusted for his renal function. His renal function requires a dose reduction of his gabapentin and his metformin, and I have requested a cystatin C-based eGFR to refine the estimate given his low muscle mass. His anticholinergic burden score is 3, which I will reduce to 1 by stopping the oxybutynin. I have communicated the plan to him and his family, and I will reconcile the medication list at discharge and arrange a GP and pharmacist review within 2 weeks." [1]

Discussion

Q: "How do you prioritise which medication changes to make first?" [1]

"I prioritise by the balance of current harm against the feasibility and safety of the change. The highest-priority changes are those that are causing the presenting problem (his fall) and that can be made safely and immediately — in this case, stopping the over-the-counter diclofenac (which is worsening his blood pressure and his renal function, both contributors to the fall), and beginning the process of reducing the benzodiazepine and the anticholinergic burden. The benzodiazepine requires a supervised taper, so I begin it now but complete it over months in the community. The anticoagulation omission is important but is not an emergency and requires a shared decision about the bleeding risk versus the stroke risk, so I address it at the follow-up after I have stabilised the acute picture. The principle is to make the changes that reduce the immediate harm first, then to build the longer-term plan with the patient, the GP, and the pharmacist." [1]

Q: "What is the role of medication reconciliation at discharge, and how do you do it?" [1]

"Medication reconciliation at discharge is the formal process of ensuring that the medications the patient is sent home on are correct, intentional, and communicated. It is a patient-safety standard under the ACSQHC Medication Safety Standard and NICE NG56, because transition errors are the source of a large proportion of preventable drug harm. I do it in three steps: first, I compare the pre-admission best possible medication history against the discharge medication list, identifying every change — every stop, every start, every dose change, every continuation — and I document the reason for each. Second, I ensure that every transient inpatient medication (a PPI started for prophylaxis, a hypnotic started on the ward, an antiemetic) is either explicitly continued with an indication or stopped. Third, I communicate — I provide the patient and the family with a written, reconciled medication list, I send the list and the deprescribing plan to the GP and the pharmacist, and I set the review dates. The goal is that the GP, the pharmacist, the patient, and the family all have the same, accurate, up-to-date list and the same plan — because a list that is changed in hospital but not communicated will simply be reversed at the first GP visit, undoing the deprescribing and recreating the harm." [1]

Q: "What single principle underpins safe deprescribing?" [1]

"The single principle is that deprescribing is a patient-centred, supervised process, not a drug-stopping reflex. Every decision must be anchored to the patient's current goals, life expectancy, and frailty, and to the current balance of benefit and harm of each drug; it must be done with the patient's understanding and agreement; it must use a taper where withdrawal or rebound is possible; and it must include a monitoring plan. The five-step framework — ascertain, identify, assess, taper or stop, monitor — operationalises this. The evidence shows that most deprescribing succeeds when it is supervised and the patient is engaged, and that the fear of relapse is greater than the reality. A medication list changed unilaterally without the patient's agreement and a follow-up plan will be reversed." [1]