End-Stage Dementia Care
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End-Stage Dementia Care

A Basic Guide

C. R. Kovach

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eBook - ePub

End-Stage Dementia Care

A Basic Guide

C. R. Kovach

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About This Book

People with mid-stage dementia are served by special care units in long-term care facilities, although as these residents deteriorate, they are transferred out of the unit and into a general nursing home unit. These nursing homes are not equipped to deal with palliative needs of end-stage dementia care. The book addresses those needs. With this in mind, Part One examines the stages of dementia end-stage in particular. Other chapters in this section provide background on the hospice movement and hospice concepts; the idea of maintaining personhood; and administration of a late-stage care unit. Part Two focuses on treatment approaches for common needs in end-stage dementia - medical and physical care; a supportive environment; the fundamentals of care; psychopharmacology; and therapeutic activities. Part 3 contains chapters on family-centred care; legal and ethical issues; programme evaluation; and future opportunities.

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Information

Year
2013
ISBN
9781135841034
Edition
1
Part One
Foundations and Options for Program Development
Chapter 1
Stages of Dementia: An Overview
Mary Cohan
Caring for a relative or patient with a dementing illness is challenging. A framework for thinking about specific behaviors and symptoms can help caregivers anticipate and deal with new problems. This chapter will briefly review the diagnosis, prognosis, and stages of dementia to help develop that framework. Other chapters will address more detailed strategies targeted to specific medical and behavioral issues.
Fortunately, increased research has been dedicated to Alzheimerā€™s disease and other illnesses associated with dementia. There is an increased awareness of the devastating effects of these illnesses on quality of life, life expectancy, family dynamics, and the cost of health care. There is hope that research will improve the ability to diagnose dementia of the Alzheimer type (DAT) and understand the causal factors that contribute to these illnesses. Research is complicated by heterogeneity in early symptoms and in rate of decline and by difficulties sorting neurobiological changes seen in normal aging from those seen when disease is present. More basic and applied research is needed in virtually all areas under study.
DIAGNOSIS OF DEMENTIA
Diagnosis of DAT often occurs over a period of time when reversible causes of dementia are being eliminated as the factor responsible for manifested changes in memory, behavior, or function. Often, persons with dementia will not present themselves to the physicianā€™s office for diagnosis. Family members, friends, or concerned neighbors often make the initial contact with the health care system when memory impairment is suspected. It is not known if people with early dementia are unaware of the seriousness of their problem, lack the judgment to seek help, or are in a state of denial (Ham, 1992). Older adults who do express concern about their own memory losses usually have benign forgetfulness, depression, or are experiencing one of the reversible causes of dementia. In fact, diagnosis of dementia is often impaired by the plethora of complicating factors that may explain or contribute to cognitive losses. Common reversible causes of dementia include medication side effects, thyroid and other endocrine abnormalities, vitamin B12 deficiency, alcohol ingestion, trauma, depression, and infection.
DSMā€“IV diagnostic criteria for a clinical diagnosis of dementia are listed in Table 1.1. There must be a decline in two or more areas of cognition significant enough to interfere with job or social functioning to establish the diagnosis. Areas of cognitive decline may include memory, language, visual-spatial perception, construction, calculations, judgment, abstraction, and personality changes.
There are a number of causes of dementia, but Alzheimerā€™s disease accounts for 50ā€“60% of cases. Other common causes are vascular problems such as multiinfarct dementia, Parkinsonā€™s disease, and dementia associated with chronic alcoholism. Clinical history, a thorough medical diagnostic workup, and neuropsychological testing are needed to arrive at a probable clinical diagnosis of DAT. Repeated assessments are typically needed to distinguish the persistence or reversibility of the impairments.
Alzheimerā€™s disease continues to be definitively diagnosed only on autopsy. Autopsy studies have confirmed the clinical diagnoses of possible and probable Alzheimerā€™s disease in the majority of cases diagnosed according to the criteria developed by the National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimerā€™s Disease and Related Disorders Association (NINCDSā€“ADRDA).
Table 1.1 DSMā€“IV Criteria for Dementia of the Alzheimerā€™s Type
A. The development of multiple cognitive deficits manifested by both:
1) Memory impairment
2) One or more of the following:
Aphasia
Apraxia
Agnosia
Disturbance in executive function
B. The cognitive deficits in Criteria A1 and A2 each cause significant impairment in social or occupational functioning and represent a significant decline from a previous level of functioning
C. The course is characterized by gradual onset and continuing cognitive decline
D. The cognitive deficits in Criteria A1 and A2 are not due to any of the following:
1) Other central nervous system conditions
2) Systemic conditions known to cause dementia
3) Substance inducted conditions
E. The deficits do not occur exclusively during the course of a delirium
F. The disturbance is not better accounted for by another Axis 1 disorder
Note. From Diagnostic and Statistical Manual of Mental Disorders (4th ed., pp. 142ā€“143). Washington, DC: American Psychiatric Association, 1994. Reprinted by permission.
Computer tomography (CT) and magnetic resonance imaging (MRI) scans are not sensitive enough to confirm a diagnosis of Alzheimerā€™s disease. The degree of atrophy shown in these tests is greater for patients with Alzheimerā€™s disease than for controls, but a large number of patients with Alzheimerā€™s disease show no more atrophy than expected for age alone (Albert & Stafford, 1988; LaRue, 1992). CT and MRI scans are used more successfully to screen for vascular problems associated with dementia. Progress is being made in the development of antemortem diagnostic tests through positive emission tomography (PET) scan procedures, blood testing, and other laboratory analyses.
Some formal cognitive testing is helpful for establishing a probable diagnosis of DAT and following the course of illness. Two brief commonly used screening tools are the Mini-Mental State Exam (MMSE) and the Blessed Dementia Scale. These tools are easily administered in the course of a physical exam, and use of these tools can detect early cognitive problems and improve the objectivity of repeated assessments. Most tools assess orientation, registration, attention and calculation, recall, language, and construction abilities. However, people with dementia can score in the normal range on these tests, and a variety of factors can cause scores to be inaccurately low or reflect more cognitive loss than is true. Factors that may contribute to false low scores are acute illness (e.g., infection), sensoriperceptual deficits (e.g., hearing loss or impaired vision), depression, impaired effort on the part of the person responding to the tool, impaired communication, inability to read or write, and administration conditions.
PATHOLOGY
Brains of people with Alzheimerā€™s disease show atrophy of the cerebral cortex that is usually diffuse but may be more pronounced in the frontal, parietal, and temporal lobes. Atrophy is also seen in normal aging, and the degree of atrophy does not correlate with the degree of cognitive impairment. Microscopic neurofibrillary tangles and senile plaques are seen. The number of senile neuritic plaques per microscopic field correlates with cognitive losses. Biochemically, there is a 50ā€“90% reduction in the activity of choline acetyltransferase, an enzyme found only in cholinergic neurons. It appears that there is a selectively greater loss of cholinergic neurons in the brains of individuals with Alzheimerā€™s disease. Other neurotransmitters in the cholinergic, noradrenergic, and serotonergic systems are reduced. Forty to 60% of large corticoneurons may be destroyed, and there is additional loss of neurons in other portions of the brain (Terry, Peck, DeTeresa, Schecter, & Horoupian, 1981). The fact that pathological changes are distributed selectively in various parts of the brain explains the predominance of cognitive declines in early and mid-stage dementia, with relatively fewer sensory and motor impairments.
STAGES OF ALZHEIMERā€™S DISEASE
Alzheimerā€™s disease is a progressive disorder with an average duration of 9 years (range 1ā€“16 years) from symptom onset to death. The rate of progression is highly variable, and some patients may progress to the late-stage in one year. One study (Walsh, Welch, & Larson 1990) found that a lower MMSE score and the combination of falls and wandering were associated with decreased survival. Comorbid medical conditions were not associated with decreased survival. Particularly early in the illness, there is large variability in symptoms associated with Alzheimerā€™s disease. Authors have classified the stages of Alzheimerā€™s disease in various ways. A common classification system divides the disease into three stages: early, mid, and late.
Early-stage dementia
ā€¢ Memory loss
ā€¢ Time and spatial disorientation
ā€¢ Poor judgment
ā€¢ Personality changes
ā€¢ Withdrawal or depression
ā€¢ Perceptual disturbances
Mid-stage dementia
ā€¢ Recent and remote memory worsens
ā€¢ Increased aphasia (slowed speech and understanding)
ā€¢ Apraxia
ā€¢ Hyperorality
ā€¢ Disorientation to place and time
ā€¢ Restlessness or pacing
ā€¢ Perseveration
ā€¢ Irritability
ā€¢ Loss of impulse control
Late-stage dementia
ā€¢ Incontinence of urine and feces
ā€¢ Loss of motor skills, rigidity
ā€¢ Decreased appetite and dysphagia
ā€¢ Agnosia
ā€¢ Apraxia
ā€¢ Communication severely impaired
ā€¢ May not recognize family members or self in mirror
ā€¢ Loss of most or all self-care abilities
ā€¢ Cognition severely impaired
ā€¢ Immune system depressed
Regardless of how the stages are delineated, there is significant overlap in symptoms between stages. The staging is, in essence, an arbitrary marker of progression through a syndrome notable for extensive variability. Staging has a variety of uses, including assisting in communicating and comparing findings between researchers and health care professionals.
Early-Stage Dementia
Alzheimerā€™s disease has an insidious onset of symptoms, whereas with vascular causes of dementia, cognitive declines may present more abruptly. The initial problem in Alzheimerā€™s disease is the inability to learn new information. During the early stage, memory loss, time and spatial disorientation, and poor judgment become evident. Patients may be unable to reason through problems and may have difficulty functioning outside of established routines. Personality changes, suspiciousness, and depression are common. Depression is present in up to 25% of these patients. Visuospatial skills are affected, and the patient may become lost in familiar surroundings or while driving. Language disturbance starts with poor word list generation and progresses to anomia. Family members may notice personality and mood changes, as well as difficulty with numbers involved in phone use, paying bills, and money handling. Delusions, usually of a persecutory nature, are present in up to half of dementia patients at some point during the illness. Patients commonly think that their belongings are being stolen or that their spouse is unfaithful. Illusions that are misinterpretations of real events are also common. Shadows or television voices may be misinterpreted. The physical exam is usually normal at this stage.
Mid-Stage Dementia
In the middle or moderate stage of dementia, remote and recent memory decline. Patients are disoriented to place and time and may no longer recognize family members. As aphasia progresses, their conversation takes on a vacant quality. Apraxia effects the ability to perform activities of daily living. These are usually lost in descending order from bathing, dressing, mobility, and toileting to eating. Patients may develop increased muscle tone or extrapyramidal symptoms that affect gait and may contribute to falls.
Behaviors are manifested during this stage that may reflect decreased impulse control or responses to fear and frustration. Indifference and irritability increase. Wandering and pacing become evident. Wandering may have different underlying etiologies that need to be addressed: restlessness, stress, delusions about the past, or need for exercise. Aggression, repetition in movement and verbalizations, and socially inappropriate behavior may be present. Hyperorality, placing inappropriate objects in the mouth, may become a problem.
Hallucinations are found in up to one third of patients with Alzheimerā€™s disease, and the majority of these are visual (Lerner, Koss, Patterson, Ownby, Hedera, Fried-land, & Whitehouse 1994). Lerner et al. found that patients with visual hallucinations had more behavioral symptoms such as verbal outbursts, delusions, and paranoia.
Sleep disturbance is present in early dementia and worsens with advancing Alzheimerā€™s disease. Loss or damage to the neuronal pathways responsible for sleep initiation and maintenance lead to impaired sleep. This may be manifested as increased daytime napping and nighttime wakefulness. The daytime napping is mainly Stage 1 and 2 sleep, resulting in a loss of the more restorative REM and Stages 3 and 4 sleep. Sundowning is a clinical term that caregivers and health care professionals use to describe the exacerbation of agitated or disruptive behaviors in the evening. It is seen as a significant burden in caring for patients, but the etiology of this clinical syndrom...

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