Polypharmacy and Deprescribing Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Eleanor Davies is an 84-year-old retired schoolteacher who has been admitted after a fall at home in which she sustained a minor head laceration but no fracture. She has atrial fibrillation, ischaemic heart disease, heart failure with reduced ejection fraction, hypertension, type 2 diabetes, osteoporosis, overactive bladder, insomnia, and depression. Her Clinical Frailty Scale is 5, indicating mild frailty. ^[1]

She is taking 14 regular medications: warfarin, bisoprolol, frusemide, ramipril, spironolactone, metformin, glibenclamide, atorvastatin, alendronate, oxybutynin, diazepam, amitriptyline, omeprazole, and aspirin. This is polypharmacy, with at least 7 of these drugs flagged as potentially inappropriate by the STOPP/START or Beers criteria. ^[1]

Her admission observations show orthostatic hypotension (104/58 lying, 88/52 standing), bradycardia at 54 in atrial fibrillation, a low body weight of 46 kilograms, an eGFR of 29, an HbA1c of 6.3 percent, and an INR of 3.8. She is on both aspirin and warfarin. ^[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 with dual antiplatelet-anticoagulant therapy increasing her bleeding risk.
2. Polypharmacy with multiple potentially inappropriate medications — the glibenclamide (prolonged hypoglycaemia in renal impairment, on the Beers list), the diazepam (long-acting benzodiazepine, falls risk), the oxybutynin (high anticholinergic burden), the amitriptyline (anticholinergic and sedating), the aspirin combined with warfarin (bleeding), the omeprazole (long-term without a current specialist indication), and the spironolactone in renal impairment with an ACE inhibitor (hyperkalaemia risk).
3. Renal impairment with a falsely reassuring creatinine-based eGFR, given her low weight and muscle mass — her drugs need renal dose adjustment and I would request a cystatin C-based eGFR.
4. Possible prescribing omissions — I would assess whether she is missing guideline-directed heart failure therapy such as an SGLT2 inhibitor, and ensure her vaccinations and osteoporosis management are optimised. ^[1]

My integrated plan is a structured medication review using the five-step deprescribing process of Scott and colleagues. I will immediately stop the glibenclamide and the aspirin, reduce the warfarin, hold or reduce the spironolactone, and reduce the frusemide and the antihypertensives to correct the orthostatic hypotension and the bradycardia. I will plan a supervised taper of the diazepam combined with cognitive behavioural therapy for insomnia, a step-down of the omeprazole, a switch from the oxybutynin to mirabegron, and a review of the amitriptyline. I will request a cystatin C-based eGFR and dose-adjust her renally-cleared drugs. I will apply the START criteria to identify any missing indicated therapy. I will anchor every decision to her goals of care, her frailty, and her renal function, and I will communicate the reconciled and deprescribed medication list to her, her family, and her GP at discharge, with a follow-up review in 4 to 6 weeks." ^[1]

Examiner probing questions and model answers

Q1: "You plan to stop the glibenclamide. Walk me through the pharmacological reasoning and what you will use instead." ^[1]

"Glibenclamide, also known as glyburide, is a long-acting sulfonylurea that is on the 2023 AGS Beers Criteria (PMID 37139824) as potentially inappropriate in older adults because of its prolonged and unpredictable hypoglycaemia, which is mediated by its active metabolites that accumulate in renal impairment. Mrs Davies has an eGFR of 29, so the metabolites will accumulate, and her HbA1c of 6.3 percent indicates that her diabetes is over-treated — the risk of a severe hypoglycaemic event, which can cause falls, confusion, arrhythmia, and death in an older adult, far exceeds any microvascular benefit of pushing the HbA1c lower. The STOPP criteria also flag long-acting sulfonylureas in this context. So stopping the glibenclamide is both evidence-based and patient-specific. For her ongoing diabetes management, in a frail 84-year-old with an HbA1c already at 6.3 percent, I would relax the glycaemic target — a target HbA1c of 7.5 to 8.5 percent is appropriate in frailty, prioritising the avoidance of hypoglycaemia over tight control. I would continue the metformin at a renal-appropriate dose (the eGFR of 29 is at the threshold where metformin is still permitted with caution and dose reduction, though I would consider holding it acutely while her renal function is assessed and during the admission). If a second agent is needed, I would add a DPP-4 inhibitor such as linagliptin or vildagliptin (linagliptin is hepatically cleared and does not need renal dose adjustment), or consider an SGLT2 inhibitor if her heart failure and renal function make it appropriate. I would explicitly avoid a thiazolidinedione (fluid retention, heart failure) and avoid initiating insulin unless there is a clear symptomatic hyperglycaemia. The principle is that the glycaemic target must match the patient's frailty, life expectancy, and goals — and in this patient, the current regimen is causing harm." ^[1]

Q2: "Her INR is 3.8 and she is on both aspirin and warfarin. How do you reconcile her antithrombotic therapy?" ^[1]

"The combination of aspirin and warfarin 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 has atrial fibrillation and ischaemic heart disease, but without a recent coronary event or stent, the aspirin adds bleeding risk without a meaningful reduction in ischaemic events on top of the anticoagulation. Her INR of 3.8 is above the therapeutic range for atrial fibrillation (2.0 to 3.0), which reflects her age (older adults are more sensitive to warfarin, pharmacodynamically), her low weight (46 kilograms, reducing the volume of distribution), and her reduced warfarin clearance. The combination of an above-target INR with aspirin is a high-risk situation for a major bleed, and it is likely a significant contributor to her fall (an intracranial bleed must be excluded given her head laceration — I would arrange a CT brain on admission). My plan is to stop the aspirin immediately (the anticoagulant alone provides adequate stroke prevention for the atrial fibrillation and reasonable ischaemic protection for the coronary disease), to withhold the warfarin until the INR is in range, and to reduce her maintenance warfarin dose (a frail, low-weight older adult typically needs a lower maintenance dose — perhaps 1.5 to 2.5 mg daily). I would monitor the INR daily until it is stable, and I would review her for interactions (amiodarone, antibiotics, and the recently stopped drugs all interact with warfarin). I would also address whether she should be on a DOAC instead of warfarin — a DOAC has a lower intracranial bleeding risk than warfarin and does not require INR monitoring, which is an advantage in a patient with falls and labile INRs, though the dose must be carefully chosen for her renal function and weight. This is a decision I would make with her and her GP after the acute admission." ^[1]

Q3: "How would you assess her renal function, given her weight and frailty?" ^[1]

"Her creatinine-based eGFR of 29 by the 2021 CKD-EPI equation (Inker et al, NEJM 2021, PMID 34554658) is a starting point, but I am concerned that it may overestimate her true renal function because the equation derives the GFR from the serum creatinine, and creatinine is generated by muscle — a frail, 46-kilogram, 84-year-old woman has very low muscle mass, so she produces less creatinine for any given GFR, and the creatinine-based estimate can be falsely reassuring. For drugs with a narrow therapeutic index that are renally cleared — and several of her drugs fall into this category (metformin, the DOACs if she switches, gabapentin or pregabalin if she were on them) — I would refine the estimate with a cystatin C-based eGFR. Cystatin C is produced by all nucleated cells at a relatively constant rate and is much less dependent on muscle mass, so it provides a more accurate estimate in the low-muscle patient. Alternatively, a measured creatinine clearance from a 24-hour urine collection, though logistically harder in a frail patient, would provide a direct measurement. For drug dosing, many references still use the Cockcroft-Gault creatinine clearance in mL per minute, which I would calculate using her actual (or an estimated) weight. The clinical principle is that in a frail, low-muscle older patient, you must not trust the serum creatinine or the creatinine-based eGFR alone for a high-stakes dosing decision — you verify with cystatin C or a measured clearance, and you dose conservatively with close monitoring of the drug effect and the renal function." ^[1]

Q4: "She is on oxybutynin and amitriptyline. Why are these a particular concern in this patient, and what would you do?" ^[1]

"Both oxybutynin and amitriptyline have high anticholinergic (antimuscarinic) activity, and together they create a significant anticholinergic burden — the cumulative central antimuscarinic effect that is associated with cognitive impairment, delirium, falls, dry mouth, constipation, and urinary retention. Oxybutynin is the highest-burden agent on the Anticholinergic Burden Scale and is on the Beers list; amitriptyline, a tricyclic antidepressant, is also on the Beers list for its anticholinergic, sedating, and orthostatic-hypotension effects. In a patient who has had a fall and who is on a benzodiazepine as well, the combined CNS depression and the anticholinergic burden are a major, modifiable contributor to her presentation. My plan is to stop the oxybutynin — she is on it for an overactive bladder, and I would offer mirabegron, a beta-3 adrenergic agonist that relaxes the detrusor without anticholinergic activity, though I would monitor her blood pressure as mirabegron can raise it. If pharmacological treatment of the bladder is not essential, I would prioritise non-pharmacological measures — timed voiding, prompted voiding by the family or the carers, fluid management, and ensuring easy access to a toilet or a commode. For the amitriptyline, she is taking it for sleep and possibly for depression — I would stop it, and if there is a genuine current depressive episode, I would switch to sertraline, an SSRI with a lower anticholinergic burden, while being alert to the hyponatraemia risk (she is on diuretics, which compounds this). For the sleep, I would use sleep hygiene and CBT-I principles. The overarching principle is to calculate and actively reduce the anticholinergic burden in every older patient with cognitive symptoms or falls — it is one of the highest-yield deprescribing targets." ^[1]

Q5: "How would you explain the deprescribing plan to Mrs Davies and her family?" ^[1]

"I would frame the conversation around her goals and her safety, not around a list of drug names. I would start by asking her and her family what matters most to her — and in a woman who has just been admitted with a fall, the answer is likely to be staying independent, avoiding another fall, and not coming back to hospital. I would then explain that several of her medications, which were all started with good intentions at different times, are now working against those goals — that the sleeping tablet is making her unsteady, that the bladder tablet and the antidepressant are clouding her thinking and contributing to the fall, that the diabetes tablet is lowering her blood sugar too much, and that the combination of the aspirin and the warfarin is making her prone to bleeding. I would explain that stopping or reducing these is an active, positive step to make her safer and clearer-headed, not a withdrawal of care — and that we will do it carefully, one change at a time, with a plan and a follow-up, so that she is in control. I would acknowledge that some of these medications have been part of her life for years and that she may have strong feelings about them — she may believe the sleeping tablet is essential, or that stopping a heart medication is dangerous — and I would address each concern with evidence and patience. I would provide a written, reconciled medication list and a deprescribing plan with the timeline, and I would involve her GP and her pharmacist in the follow-up so that the changes are sustained after discharge. The conversation is the intervention — a medication list changed without the patient's understanding and agreement will simply be reversed at the next GP visit." ^[1]