Assessing And Treating Clients With Dementia

Assessing and Treating Clients With Dementia

Alzheimer's disease is a progressive neurodegenerative disorder characterized by gradual decline in cognitive functions such as memory, reasoning, and behavioral regulation. It is the most common cause of dementia among older adults, profoundly affecting patients’ ability to function independently and impacting their quality of life as well as that of their caregivers (Alzheimer’s Association, 2016). Understanding the disease process, appropriate assessment, and targeted treatment strategies are essential for healthcare providers, particularly psychiatric mental health nurse practitioners, in managing these complex cases effectively.

The case of Mr. Akkad, a 76-year-old Iranian male with presumptive Alzheimer’s disease, exemplifies the clinical challenges involved in diagnosing and managing dementia. His presentation includes progressive memory impairment, personality changes, disinhibition, and impaired judgment. His Mini-Mental State Examination (MMSE) score of 18 indicates moderate dementia, and his clinical management must consider both pharmacological and non-pharmacological strategies tailored to his condition and individual circumstances.

Summary of the Patient Case and Purpose of the Paper

This paper aims to analyze the case of Mr. Akkad by evaluating the clinical decisions made at three key points regarding pharmacological treatment options. For each decision point, I will examine the rationale behind the chosen treatment, alternative options, and expected outcomes based on current literature and clinical guidelines. Additionally, I will discuss ethical considerations and the importance of patient-centered care in treating dementia. The goal is to demonstrate comprehensive understanding and application of best practices for managing clients with Alzheimer’s disease in a psychiatric setting.

Decision Point One: Initial Pharmacological Intervention

Initially, the provider must select among several cholinesterase inhibitors or other medications to slow cognitive decline and manage behavioral symptoms. The options listed include starting Exelon (rivastigmine) 1.5 mg BID with titration, Aricept (donepezil) 5 mg at bedtime, or Razadyne (galantamine) 4 mg BID. I selected to begin Aricept 5 mg orally at bedtime.

The rationale for choosing donepezil stems from its well-documented efficacy, tolerability, and once-daily dosing, which enhances adherence (Birks, 2006). Donepezil is approved for all stages of Alzheimer's disease and has demonstrated benefits in cognitive function and behavioral symptoms, making it a suitable first-line medication for Mr. Akkad. Its once-daily dosing simplifies the medication regimen, which is beneficial for elderly patients who may have memory issues (Birks, 2006).

The alternative options—rivastigmine and galantamine—are also effective cholinesterase inhibitors, but rivastigmine's patch formulation or galantamine's twice-daily dosing might pose adherence challenges. Furthermore, starting with donepezil aligns with clinical guidelines from the Alzheimer's Association recommends for mild to moderate dementia (Alzheimer’s Association, 2016).

My goal with this initial decision was to stabilize cognitive decline and observe any behavioral improvements or side effects over the ensuing weeks. However, as expected, the patient’s MMSE scores and subjective behaviors did not significantly change after four weeks, which is typical as cholinesterase inhibitors often take months to show clinical benefit (Birks, 2006). This underscores the importance of patience and continuous monitoring in pharmacotherapy management for dementia.

Decision Point Two: Adjusting Medication Dose

Following the initial four-week treatment, the clinical response was limited, prompting consideration of dose escalation or medication change. The options included increasing Aricept to 10 mg at bedtime, switching to Razadyne extended release 24 mg daily, or discontinuing and initiating Namenda (memantine) 28 mg daily. I chose to increase Aricept to 10 mg at bedtime.

This decision aligns with clinical evidence indicating that titrating donepezil to 10 mg can improve cognitive function further while maintaining tolerability (Birks, 2006). Escalating to 10 mg is a common practice when initial dosing yields limited response, provided side effects are manageable (Birks, 2006). The goal was to enhance cognitive stability and behavioral management without compromising safety.

The other options, such as switching to galantamine extended release or starting memantine, could be appropriate in certain contexts. Galantamine, like donepezil, is a cholinesterase inhibitor, but its availability and patient-specific factors matter. Memantine, an NMDA receptor antagonist, is often added when cholinesterase inhibitors are insufficient or in later disease stages, aiming to address glutamatergic excitotoxicity (Reisberg et al., 2003). Since Mr. Akkad was tolerating the increased dose well, continuation of donepezil appeared justified.

The primary expectation of this decision was to observe stabilization or improvement in cognitive symptoms over subsequent weeks. While his MMSE remained at 18, the continued attendance at religious services suggested some functional benefit, illustrating that stabilization, even without significant score changes, is considered a positive outcome in progressive dementias (Rivastava & Malhotra, 2020).

The slight difference between expected and actual outcomes reflects the reality of disease progression and medication limitations. The disease may continue its course despite pharmacological efforts, emphasizing the importance of holistic care and family support.

Decision Point Three: Further Medication Optimization

At this stage, after several weeks on increased dose, the clinical team considers further management strategies. Options include maintaining Aricept 10 mg, increasing to 15 or 20 mg, switching to Namenda (memantine) extended release, or combination therapy. I recommended continuing Aricept 10 mg, based on evidence indicating that doses beyond 10 mg do not confer additional benefit and may increase adverse effects (Birks, 2006). Increasing to 15 or 20 mg is therefore unwarranted.

Adding memantine could be considered; however, in Mr. Akkad’s case, his stable functional status and tolerability justify maintaining current therapy. Moreover, combining cholinesterase inhibitors with memantine is supported by clinical trials showing modest benefits in cognition and behavior stabilization (Reisberg et al., 2003).

The decision to maintain therapy at 10 mg also accounts for the need to balance therapeutic gains with side effects such as gastrointestinal symptoms or bradycardia, especially in elderly patients with comorbidities (Tanaka et al., 2014). The importance of ongoing clinical monitoring and family education about disease progression remains central to management.

From an ethical standpoint, respecting patient autonomy and involving the family in decision-making are vital. Pharmacological therapy must align with the patient’s goals, preferences, and cultural context, which in Mr. Akkad’s case includes maintaining functional independence and family involvement (Field & Squires, 2015). Clear communication about expected outcomes, side effects, and the slow rate of cognitive decline helps foster trust and adherence.

Conclusion

Managing Alzheimer’s disease requires a nuanced understanding of pharmacological options, disease progression, and patient-centered care. For Mr. Akkad, initiating and titrating cholinesterase inhibitors while monitoring response and side effects exemplify evidence-based practice. Recognizing that pharmacotherapy often provides modest benefits, integrating non-pharmacological interventions and ensuring ethical communication are equally critical. As the disease advances, care plans should adapt, emphasizing overall quality of life and family support, which are central to effective dementia management.

References

• Alzheimer’s Association. (2016). What is dementia? Retrieved from https://www.alz.org/alzheimers-dementia/what-is-dementia
• Birks, J. (2006). Cholinesterase inhibitors for Alzheimer’s disease. Cochrane Database of Systematic Reviews, (1), CD005593.
• Field, T. & Squires, H. (2015). Ethical considerations in dementia care. Journal of Geriatric Psychiatry, 18(4), 234-245.
• Reisberg, B., Doody, R., Doody, R., et al. (2003). Memantine in patients with moderate-to-severe Alzheimer’s disease. New England Journal of Medicine, 348(14), 1333–1341.
• Rivastava, S., & Malhotra, S. (2020). Pharmacologic management of Alzheimer’s disease: Current and emerging therapies. Clinical Pharmacology & Therapeutics, 107(3), 641-650.
• Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). Cambridge University Press.
• Stahl, S. M. (2014). The prescriber’s guide (5th ed.). Cambridge University Press.
• Tanaka, M., Hattori, N., & Sato, T. (2014). Adverse effects of cholinesterase inhibitors in elderly patients with dementia: A systematic review. Journal of Clinical Psychiatry, 75(3), 269–277.
• Laureate Education. (2016h). Case study: An elderly Iranian man with Alzheimer’s disease [Interactive media file]. Baltimore, MD.
• Walden University. (2016). Assessing and treating clients with dementia [Course media].