Principles of Care for the Hospitalized Geriatric Patient




INTRODUCTION



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The principles of geriatric assessment focus on function, cognition, and safety. An acute hospitalization is a critical time in which geriatric patients are particularly vulnerable to complications such as delirium, falls, and deconditioning. Using illustrative cases, this chapter focuses on basic skills of geriatric assessment including screening for cognitive and functional impairment. Age-related changes in anatomy and physiology which affect the nervous system are outlined. Changes in pharmacokinetics and pharmacodynamics, which affect medication management in geriatric patients, are reviewed. Included are strategies for identifying potentially inappropriate medications and common medication safety concerns in older adults. The Acute Care of the Elderly unit model incorporates key strategies to minimize the risks of hospitalization and engage an interprofessional team in establishing safe disposition plans for geriatric patients. Key principles of decisional capacity assessment and elder abuse reporting are also included.




CASE 5-1



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Ms. J is a 78-year-old widow with type 2 diabetes mellitus and hypertension who lives alone and was employed as a high school English teacher prior to retiring at age 65. She was admitted to the hospital after being brought to the emergency department (ED) during an episode of right arm weakness, right facial droop, and aphasia. Her symptoms started approximately 1 hour before arrival and completely subsided 2 hours after onset and prior to any intervention. A brain MRI did not show any acute or chronic infarcts. An electrocardiogram showed atrial fibrillation (AF), and a carotid Doppler ultrasound showed 30% stenosis of the right internal carotid artery (ICA). Her blood glucose on arrival was 220 mg/dL. A transient ischemic attack (TIA) caused by a cardioembolic source was suspected and she was started on warfarin and atorvastatin. During her medication reconciliation, it was noted that although the pharmacy had a prescription for insulin glargine 20 units daily on file, Ms. J was not able to recall the dose she takes or explain how she administers her injection. This persisted throughout the stay despite resolution of her aphasia in the emergency room and stable mental status for three days. The primary team placed a consult for diabetes education and it was noted that despite several attempts to teach appropriate insulin administration, Ms. J was not able to draw up the correct dose and administer the injection on her own. This raised concerns for the presence of a cognitive deficit, as well as Ms. J’s ability to return home safely.




What changes in cognition are expected with normal aging?





  • Memory, as measured by immediate recall, declines with normal aging. Therefore, it takes individuals longer to learn new information and this accounts for declines in delayed recall as well.1



  • Cognitive changes that occur with normal aging are different than those seen in the early stages of dementing illnesses such as Alzheimer disease (AD).1




How are the cognitive changes of AD different from that of normal aging?





  • AD patients have even more difficulty with delayed recall compared with individuals of the same age without AD. This deficit is much more dramatic than the age-related decline.2




What changes in the brain are typical of normal aging?1





  • Cerebrospinal fluid (CSF) volume increases.



  • Brain tissue volume decreases.



  • Neuron loss is selective within the hippocampus with loss in the subiculum, but not in CA1, CA2, or CA3.



  • N-methyl-D-aspartate receptor alterations are present despite preserved neuron number in the hippocampus.



  • Positron emission tomography imaging shows differences in regional frontal lobe activation during memory tasks, which is thought to represent differences in retrieval strategies during recall.3



  • Frontal lobe activity changes are most likely mediated by neuron loss in subcortical nuclei that project to the cortex, since cortical neuron numbers are largely preserved with normal aging.



  • Substantial subcortical neuron loss occurs in the basal forebrain, locus coeruleus, and dorsal raphe.4



  • Age-related decreases in dopaminergic neurons projecting to the caudate nucleus and substantia nigraoccur from childhood and throughout normal aging.5



  • Age-related dopamine loss gives rise to several notable neurologic and behavioral symptoms such as decrease in arm swing, increase in rigidity, and changes in “mental flexibility,” but to a lesser degree than with dopamine loss related to Parkinson disease.6




Are Ms. J’s difficulties managing her insulin likely caused by cognitive decline from normal aging?





  • No. Although the exact reason for her inability to administer insulin correctly is still unclear, normal age-related decline in memory does not account for loss of function such as inability to take medications correctly.




What is pathological decline in cognitive function?





  • Mild cognitive impairment (MCI) is defined as mildly impaired cognition in one or more domains with functional activities that have not declined to meet criteria for the diagnosis of dementia (this can be thought of as predementia).7



  • Memory is the most common impaired cognitive domain with a 2 to 1 ratio of amnestic to nonamnestic MCI cases seen.8



  • Very mild problems with high-level functional activities are generally consistent with MCI.9



  • Risk factors for MCI are age, lower level of education, and APOE epsilon 4 allele.9



  • Neuropsychiatric symptoms are common with MCI. In fact, depression is a risk factor for MCI.9



  • Physical, social, and cognitive activities can postpone or prevent MCI.9




In MCI, what changes in the brain are typical of pathological aging due to neurodegenerative disorders?





  • The pathology of MCI is similar to that seen when a patient progresses to dementia and depends on the cause. For example, patients with MCI caused by AD have hippocampal neuronal loss, neurofibrillary tangles, and amyloid plaques primarily in the entorhinal cortex and subiculum. Patients with MCI due to other diseases such as cerebrovascular disease, Lewy body disease (LBD), or frontotemporal degeneration would have disease-specific pathology.9



  • Even prior to dementia, MRI shows medial temporal lobe and posterior cingulate atrophy in MCI caused by AD.9




How common is MCI?





  • In individuals between ages 70 and 89 years without dementia, the prevalence of MCI is about 15%. The prevalence is about 19% in individuals over age 65.10




Is there a pharmacological treatment for MCI?





  • There is no recommended treatment for MCI. However, a study of prescribing habits showed that it is common to see patients on acetylcholinesterase inhibitors and memantine in clinical practice.11




How likely is it for a patient with MCI to progress to Alzheimer dementia?





  • The rate of progression from MCI to Alzheimer dementia is about 5–10% per year.12



  • Although there are no recommended diagnostic tests to predict progression from MCI to AD, APOE epsilon 4 allele positivity, hippocampal atrophy, as well as several other neuroimaging and CSF biomarkers are risk factors for progression.10




How would you evaluate Ms. J to determine whether a cognitive disorder is contributing to her inability to administer insulin correctly?





  • Perform a cognitive screen such as the Mini Mental State Exam (MMSE),3 Mini-Cog,4 Montreal Cognitive Assessment (MoCA),13 or St. Louis Mental Status Exam (SLUMS).14




    • Table 5-1 lists several cognitive screening tools. In general, it is advisable to be familiar with one screening tool that can be used to reliably assess a patient’s cognition.



    • The briefest of these is the Mini-Cog, which consists of asking the patient to draw a clock and recall a three-item word list.15



    • Note that the results of a cognitive screen should not be interpreted without knowledge of a patient’s baseline, since alterations might represent acute changes (delirium). When a baseline is unknown, serial administration of cognitive tests will be required.



    • A functional assessment should be performed by interviewing both the patient and a source of collateral information who has known her well for many years.16,17



    • A functional assessment will explore the patient’s ability to perform various (basic) activities of daily living (ADLs), instrumental activities of daily living (IADLs), and advanced activities of daily living (AADLs), which are outlined in Table 5-2.






Table 5-1.

Comparison of Cognitive Screening Tools





CASE 5-1 (continued)


Collateral is obtained from Ms. J’s daughter who lives nearby and sees her several times a week. She reports that Ms. J has stopped driving after getting lost on multiple occasions, and that Ms. J no longer manages her own finances. Ms. J’s daughter also reports that her memory and functional impairments have progressed gradually over the past 2 years.




How would you use information from the functional assessment to guide your diagnosis at this point?





  • Ms. J has a progressive decline in cognition and function with impairment in her IADLs that is consistent with a diagnosis of dementia. Patients with MCI have deficits in AADLs only or potentially very mild deficits in IADLs. As dementia progresses, IADLs become completely impaired and then deficits in ADLs also become apparent (Table 5-2).9,17





Table 5-2.

Functional Assessment





What risks of hospitalization are known to be increased in geriatric patients?17,18





  • During an acute care hospital stay, geriatric patients have five times the risk of complications including falls, delirium, cognitive decline, functional decline, deconditioning, infection, malnutrition, venous thromboembolism, prolonged hospitalization, and death.



  • Geriatric patients also have an increased risk of institutionalization following a hospital stay and an increased risk of readmission.



  • Frail older adults, defined as those with preexisting risk factors of advanced age, low physical activity, unintentional weight loss, slow walking speed, and easy fatigability, are at an even greater risk of complications related to hospitalization.19



  • Acute Care of the Elderly (ACE) units utilize environmental interventions, interdisciplinary care, and early discharge planning (Table 5-3).



  • Virtual ACE units have been utilized where the team and care model are not on a specific unit, but can be consulted.



  • Stroke units have a similar model of care and improve function at discharge, rates of discharge, and survival.20





Table 5-3.

Features of an ACE Unit





How would you determine a safe discharge plan for Ms. J?





  • The process of safe discharge for geriatric patients should implement early discharge planning and incorporate assessments and recommendations from a team of physicians, nurses, physical therapists, occupational therapists, nutritionists, pharmacists, social workers, and patient educators (Table 5-4).





Table 5-4.

Levels of Care


Dec 26, 2018 | Posted by in NEUROLOGY | Comments Off on Principles of Care for the Hospitalized Geriatric Patient

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