Nursing Management: Alzheimer’s Disease, Dementia, and Delirium



Nursing Management


Alzheimer’s Disease, Dementia, and Delirium


Sharon L. Lewis





Reviewed by Anna M. Bruch, RN, MSN, Professor of Nursing, Illinois Valley Community College, Oglesby, Illinois.


This chapter discusses the cognitive disorders of dementia and delirium, with a focus on the nursing management of patients with Alzheimer’s disease. The etiology and pathophysiology of dementia and delirium are differentiated, and the collaborative and nursing management of patients with these cognitive disorders are described.


The three most common cognitive problems in adults are dementia, delirium (acute confusion), and depression (Table 60-1). Although this chapter focuses on dementia and delirium, depression is often associated with these conditions.




Dementia


Dementia is a syndrome characterized by dysfunction or loss of memory, orientation, attention, language, judgment, and reasoning. Personality changes and behavioral problems such as agitation, delusions, and hallucinations may occur. Ultimately these problems result in alterations in the individual’s ability to work, fulfill social and family responsibilities, and perform activities of daily living. Dementia is often diagnosed when two or more brain functions, such as memory loss or language skills, are significantly impaired.


Fifteen percent of older Americans have dementia. As the average life span increases, the number of those affected with dementia is growing. There are about 100 causes of dementia, with about 60% to 80% of the patients with dementia having a diagnosis of Alzheimer’s disease (AD) (Fig. 60-1). In the United States, about half of all patients in long-term care facilities have AD or a related dementia.1





image eNursing Care Plan 60-1   Patient With Alzheimer’s Disease




Patient Goal


Functions at highest level of cognitive ability















Outcomes (NOC) Interventions (NIC) and Rationales
Cognition Dementia Management




• Determine type and extent of cognitive deficit(s), using standardized assessment tool, to establish baseline function.


• Include family members in planning, providing, and evaluating care to the extent desired to plan appropriate and consistent interventions.


• Discuss with family members and friends how best to interact with patient to maintain consistency.


• Identify usual patterns of behavior for activities such as sleep, medication use, elimination, food intake, and self-care to maintain familiar routines.


• Give one simple direction at a time to decrease confusion and frustration.


• Use distraction, rather than confrontation, to manage behavior, which will decrease anxiety.


• Avoid unfamiliar situations when possible (e.g., room changes and appointments without familiar people present) to avoid anxiety and confusion.


• Limit number of choices patient has to make so as not to cause anxiety.




image




Patient Goal


Performs basic personal care activities of daily living (ADL)s including bathing, dressing, feeding, and toileting by self or with assistance as needed.















Outcomes (NOC) Interventions (NIC) and Rationales
Self-Care: Activities of Daily Living (ADL) Self-Care Assistance









image




Patient Goals







Patient Goal


Remains in restricted area during ambulation and activity




*Nursing diagnoses listed in order of priority.



image eNursing Care Plan 60-2   Family Caregivers




Patient Goals

















Outcomes (NOC) Interventions (NIC) and Rationales
Caregiver Stressors Caregiver Support




• Monitor for indicators of stress to plan interventions and support.


• Act for caregiver if overburdening becomes apparent.


• Acknowledge difficulties of caregiving role.


• Accept expressions of negative emotion to enable open discussion of needs.


• Encourage the acceptance of interdependency among family members.


• Inform caregiver of health care and community resources to provide support and relief to caregiver as needed.


• Acknowledge dependency of patient on caregiver to demonstrate empathy.


• Teach caregiver strategies to access and maximize health care and community resources to assist caregiver with planning for long-term care.


• Provide support for decisions made by caregiver (e.g., patient placement in long-term care) to allay guilt and reinforce services the patient now requires.




image




Patient Goals







Patient Goals







Patient Goals






*Nursing diagnoses listed in order of priority.






Etiology and Pathophysiology


Dementia is due to both treatable and nontreatable conditions (Table 60-2). The two most common causes of dementia are neurodegenerative conditions (e.g., AD) and vascular disorders. Dementia is sometimes caused by conditions that may initially be reversible (see Table 60-2). However, with prolonged exposure or disease, irreversible changes may occur.



Vascular conditions are the second most common cause of dementia.1 Vascular dementia, also called multiinfarct dementia, is loss of cognitive function resulting from ischemic or hemorrhagic brain lesions caused by cardiovascular disease. This type of dementia is the result of decreased blood supply from narrowing and blocking of arteries that supply the brain. Vascular dementia may be caused by a single stroke (infarct) or by multiple strokes.



Risk Factors.

The greatest risk factor for dementia is aging, although it is not a normal part of aging. Family history is also an important risk factor, since those with a first-degree relative with dementia are more likely to develop the disease. Those who have more than one first-degree relative with dementia are even at higher risk of developing the disease.1


Other risk factors for dementia are diabetes mellitus, obesity, smoking, cardiac dysrhythmias (e.g., atrial fibrillation), hypertension, hypercholesterolemia, and coronary artery disease. Genetic factors (discussed on pp. 1446-1447) also contribute to the risk of dementia.


Diabetes dramatically increases a person’s risk of developing AD or other types of dementia. Diabetes can contribute to dementia in several ways. Insulin resistance, which causes high blood glucose and in some cases leads to type 2 diabetes, may interfere with the body’s ability to break down amyloid, a protein that forms brain plaques in AD. High blood glucose also produces oxygen-containing molecules that can damage cells, in a process known as oxidative stress. In addition, high blood glucose along with high cholesterol has a role in atherosclerosis, which contributes to vascular dementia.2


Diabetes may contribute to poor memory and diminished mental function in various other ways. The disease causes microangiopathy, which damages small blood vessels throughout the body. Ongoing damage to blood vessels in the brain may be one reason why people with diabetes are at a higher risk of cognitive problems as they grow older. 2


Head trauma is also a risk factor for dementia. Professional football players and military veterans who had traumatic brain injury or posttraumatic stress disorder have an increased risk for AD and other types of dementia.3,4



Clinical Manifestations


Depending on the cause of the dementia, the onset of manifestations may be insidious and gradual or more abrupt. Often dementia associated with neurologic degeneration is gradual and progressive over time. Causes of vascular dementia often result in symptoms that appear suddenly or progress in a stepwise pattern. However, it is difficult to distinguish the etiology of dementia (vascular versus neurodegenerative) based on symptom progression alone. An acute (days to weeks) or subacute (weeks to months) pattern of change may be indicative of an infectious or metabolic cause, including encephalitis, meningitis, hypothyroidism, or drug-related dementia. The manifestations of different types of dementia overlap and can be further complicated by coexisting medical conditions.


Depression is often mistaken for dementia in older adults, and, conversely, dementia for depression. Manifestations of depression (especially in the older adult) include sadness, difficulty thinking and concentrating, fatigue, apathy, feelings of despair, and inactivity. When the depression is severe, poor concentration and attention may result, causing memory and functional impairment. When dementia and depression occur together (as happens in many patients with dementia), the intellectual deterioration can be extreme. Depression, alone or in combination with dementia, is treatable. The challenge is to make an accurate and early assessment and diagnosis (see Table 60-1).


Other clinical manifestations of dementia are discussed in the section on clinical manifestations of AD on pp. 1447-1448.




Nursing and Collaborative Management Dementia


In many ways, management of the patient with dementia is similar to management of the patient with AD (described later in this chapter). One form of dementia, vascular dementia, can often be prevented. Preventive measures include treatment of risk factors such as hypertension, diabetes, smoking, hypercholesterolemia, and cardiac dysrhythmias. (Stroke is discussed in Chapter 58.) Drugs that are used for patients with AD are also useful in patients with vascular dementia. Drug therapy is discussed on p. 1452 later in this chapter.



Alzheimer’s Disease


Alzheimer’s disease (AD) is a chronic, progressive, degenerative disease of the brain. It is the most common form of dementia, accounting for 60% to 80% of all cases of dementia.1 AD is named after Alois Alzheimer, a German physician who in 1906 described changes in the brain tissue of a 55-year-old woman who had died of an unusual mental illness.


Approximately 5.2 million Americans suffer from AD. It is estimated that 11% of people age 65 and older, and nearly one third of those over age 85, have AD. Ultimately the disease is fatal, with death typically occurring 4 to 8 years after diagnosis, although some patients live for 20 years. AD is the sixth leading cause of death in the United States.1 It is the only cause of death among the top 10 in United States that cannot be prevented or cured, or its progression even slowed. The burden of care for the patient with AD on the family, caregivers, and society is staggering. AD has often been referred to as the “long good-bye” or “death in slow motion.”


The incidence of AD is slightly higher in African Americans and Hispanic Americans than in whites. AD has been associated with lower socioeconomic status and education level and poor access to health care. Women are more likely than men to develop AD, primarily because they live longer (see the Gender Differences box).




Etiology and Pathophysiology


The exact etiology of AD is unknown, but is likely a combination of genetic and environmental factors. AD is not a normal part of aging, but as with other forms of dementia, age is the most important risk factor for developing AD. Only a small percentage of people younger than 60 years old develop AD. When AD develops in someone younger than 60 years old, it is referred to as early-onset AD. AD that becomes evident in individuals more than 60 years old is called late-onset AD (see the Genetics in Clinical Practice box).



image Genetics in Clinical Practice


Alzheimer’s Disease (AD)







*ApoE testing is useful for studying AD risk in large groups of people, but not for determining an individual’s specific risk.


Individuals with a clear pattern of inheritance within a family have familial Alzheimer’s disease (FAD). Other cases where no familial connection can be made are termed sporadic. FAD is associated with an early onset (before 60 years of age) and a more rapid disease course. In both FAD and sporadic AD, the pathogenesis of AD is similar.


Characteristic findings of AD relate to changes in the brain’s structure and function: (1) amyloid plaques, (2) neurofibrillary tangles, (3) loss of connections between neurons, and (4) neuron death. Fig. 60-2 shows the pathologic changes in AD.



As part of aging, people develop some plaques in their brain tissue, but in AD more plaques appear in certain parts of the brain. These plaques consist of clusters of insoluble deposits of a protein called β-amyloid, other proteins, remnants of neurons, non-nerve cells such as microglia (cells that surround and digest damaged cells or foreign substances), and other cells such as astrocytes.


β-Amyloid is cleaved from amyloid precursor protein (APP), which is associated with the cell membrane (Fig. 60-3). The normal function of APP is unknown. In AD, plaques develop first in areas of the brain used for memory and cognitive function, including the hippocampus (a structure that is important in forming and storing short-term memories). Eventually AD attacks the cerebral cortex, especially the areas responsible for language and reasoning.



Neurofibrillary tangles are abnormal collections of twisted protein threads inside nerve cells. The main component of these structures is a protein called tau. Tau proteins in the central nervous system (CNS) are involved in providing support for intracellular structure through their support of microtubules. Tau proteins hold the microtubules together like railroad ties hold railroad tracks together. In AD the tau protein is altered, and as a result, the microtubules twist together in a helical fashion (see Fig. 60-3). This ultimately forms the neurofibrillary tangles found in the neurons of persons with AD.


Plaques and neurofibrillary tangles are not unique to patients with AD or dementia. They are also found in the brains of individuals without evidence of cognitive impairment. However, they are more abundant in the brains of individuals with AD.


The other feature of AD is the loss of connections between neurons and neuron death. These processes result in structural damage. Affected parts of the brain begin to shrink in a process called brain atrophy. By the final stage of AD, brain tissue has shrunk significantly (Fig. 60-4).


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Nov 17, 2016 | Posted by in NURSING | Comments Off on Nursing Management: Alzheimer’s Disease, Dementia, and Delirium

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