ASSESSMENT
HISTORY. Approximately one to two out of four patients with allergic purpura have GU symp- toms such as dysuria and hematuria. Other symptoms include headaches; fever; peripheral edema; and skin lesions accompanied by pruritus, paresthesia, and angioedema (swelling of the skin, mucous membranes, or organs). Other patients describe severe GI symptoms (spasm, colic, constipation, bloody vomitus, bloody stools) and joint pain.
PHYSICAL EXAMINATION. Inspect the patient’s skin for the typical skin lesions—patches of purple macular lesions of various sizes that result from vascular leakage into the skin and mucous membranes. These lesions most commonly occur on the hands and arms. Note that, in children, the lesions more commonly start as urticarial areas that then expand into hemorrhagic lesions. Determine if the patient has any peripheral swelling, particularly in the hands and face.
Perform gentle range of motion of the extremities to determine the presence and location of joint pain. Assess the color of the patient’s urine and stool, and note any bleeding.
PSYCHOSOCIAL. The patient may experience a disturbance in body image because of the disfigurement caused by the rash and swelling. Determine the patient’s response to her or his appearance, and identify whether the changes interfere with implementing various roles such as parenting or work.
DRG Category: 012 Mean LOS: 6.3 days
Description: MEDICAL: Degenerative Nervous System Disorders
Independent
Protect open or irritated skin lesions from further tissue trauma and infection. Apply unguents and soothing creams, if appropriate, to manage discomfort. Assist the patient with colloidal baths and activities of daily living if joint pain and the lesions give the patient limited activity tolerance. Reas- sure the patient that the lesions are of short duration prior to healing. Explore possible sources of the allergy. Allow the patient time to discuss concerns about the disease. If the patient or significant other appears to be coping ineffectively, provide a referral to a clinical nurse specialist or counselor.
DOCUMENTATION GUIDELINES
• Extent, location, and description of erythema; degree of discomfort; signs of wound infection;
presence and description of edema
• Response to allergy testing and withdrawal of the provocative agent if identified
• Response to treatments: Medications, creams, and colloidal baths
• Emotional response to the condition; problems coping; body image disturbance
DISCHARGE AND HOME HEALTHCARE GUIDELINES
PREVENTION. Teach the patient about the disease and its cause. If the allergen is identified, assist the patient in eliminating the allergen if possible. Teach the patient to protect lesions from additional trauma by wearing long-sleeved blouses or shirts. Teach the patient to pay particular attention to edematous areas where skin breaks down easily if injured. Encourage the patient to prevent secondary infections by avoiding contact with others and by using good hand-washing techniques. Encourage the patient to report recurrent signs and symptoms, which are most likely to occur 6 weeks after the initial onset of symptoms.
MEDICATIONS. Provide the patient with information about the medications, including dosage, route, action, and side effects. Provide the patient with written information so that the patient can refer to it for questions at home.
58 Alzheimer’s Disease
Alzheimer’s Disease
A
lzheimer’s disease (AD) is a degenerative disorder of the brain that is manifested by demen- tia and progressive physiological impairment. It is the most common cause of dementia in the elderly but is not a normal part of aging. More than 4 million Americans suffer from AD.Dementia involves progressive decline in two or more of the following areas of cognition:
memory, language, calculation, visual-spatial perception, judgment, abstraction, and behavior.
Dementia of the Alzheimer’s type (DAT) accounts for approximately half of all dementias. The average time from onset of symptoms to death is 8 to 10 years. The pathophysiological changes that occur in DAT include the following:
1. Presence of neurofibrillary tangles, neuritic plaques, and amyloid angiopathy
2. Accumulation of lipofuscin granules and granulovacuolar organelles in the cytoplasm of the neurons
3. Structural changes in the dendrites of the neurons and in the cell bodies
4. Predominant neuronal degeneration in the cortical association areas of the basal ganglia 5. Gross cortical atrophy and widening of the sulci
6. Enlargement of the ventricles
7. Decrease in neurotransmitters (acetylcholine, dopamine, norepinephrine, serotonin), somato- statin, and neuropeptide substance P
CAUSES
The cause of AD is unknown but knowledge about the hereditary links is growing (see Genetic Considerations, below). Patients with Down syndrome eventually develop DAT if they live long enough. There is a higher-than-normal concentration of aluminum in the brain of a person with DAT, but the effect is unknown. A distinct protein, AZ-50, has been identified at autopsy in the brains of DAT patients. This protein has been isolated from neurons that were not yet damaged, suggesting that its presence early in the degenerative process might cause the neuronal damage.
The life expectancy of a DAT patient is reduced 30% to 60%.
GENETIC CONSIDERATIONS
AD is not caused by a single gene. The genetic contributions to the disease are complex because more than one gene mutation can cause AD, and genes on multiple chromosomes are involved.
There are two basic types of AD from a genetic standpoint: familial and sporadic (associated with late-onset disease). Familial AD (FAD) is a rare form of AD that has an early onset before age 65 and affects less than 10% of AD patients. FAD is caused by gene mutations on chromosomes 1, 14, and 21 and has an autosomal dominant inheritance pattern. Therefore, if one of these mutated genes is inherited from a parent, the person will almost always develop early-onset AD.
The majority of AD cases are late-onset (developing after age 65), have no known cause, and show no clear inheritance pattern. Late onset AD is linked with the apolipoprotein E (ApoE) gene on chromosome 19. It is involved with making ApoE, a substance that transports cholesterol in the bloodstream. The ApoE e4 gene is considered a risk-factor gene for AD and appears to influ- ence the age of onset of the disease. The ApoE gene comes in several different alleles, but the three alleles that occur most frequently are ApoE e2, ApoE e3, and ApoE e4. No one really under- stands the degree of risk of AD based on ApoE status. Scientists continue to search for genetic risk factors for late-onset AD on regions of chromosomes 9, 10, and 12 as well as chromosome 19.
GENDER, ETHNIC/RACIAL, AND LIFE SPAN CONSIDERATIONS
The onset of DAT may occur at any age but is rare before age 50; the average onset occurs after age 65. Approximately 3% of men and women ages 65 to 74 have AD, and some scientists note that about 50% of those age 85 and older may have AD. The prevalence of AD doubles every 5 years beyond age 65. More females than males have the disease. It is difficult to determine if there are racial and ethnic differences in the prevalence of AD. However, a unique issue for older black/African Americans is that, contrasted with other ethnic/racial groups, they are dispropor- tionately affected by stroke, high blood pressure, and diabetes. These diseases can increase the risk of developing AD.
ASSESSMENT
HISTORY. DAT is a slowly progressing disease, and secondary sources are used for diagnosis because the patient is often unaware of a thought-processing problem. Past medical history should be evaluated for previous head injury, surgery, recent falls, headache, and family history of DAT.
PHYSICAL EXAMINATION. The history will help determine which stage the disease process has reached at the time of patient assessment. The following four-stage scale reflects the progressive symptoms of DAT:
Stage 1is characterized by recent memory loss, increased irritability, impaired judgment, loss of interest in life, decline of problem-solving ability, and reduction in abstract thinking.
Remote memory and neurological exam remain unchanged from baseline.
Alzheimer’s Disease 59
Stage 2lasts 2 to 4 years and reveals a decline in the patient’s ability to manage personal and business affairs, an inability to remember shapes of objects, continued repetition of a mean- ingless word or phrase (perseveration), wandering or circular speech patterns (circumlocu- tion dysphasia), wandering at night, restlessness, depression, anxiety, and intensification of cognitive and emotional changes of stage 1.
Stage 3is characterized by impaired ability to speak (aphasia), inability to recognize familiar objects (agnosia), inability to use objects properly (apraxia), inattention, distractibility, involuntary emotional outbursts, urinary or fecal incontinence, lint-picking motion, and chewing movements. Progression through stages 2 and 3 varies from 2 to 12 years.
Stage 4,which lasts approximately 1 year, reveals a patient with a masklike facial expression, no communication, apathy, withdrawal, eventual immobility, assumed fetal position, no appetite, and emaciation.
The neurological examination remains almost normal except for increased deep tendon reflexes and the presence of snout, root, and grasp reflexes that appear in stage 3. In stage 4, there may be generalized seizures and immobility, which precipitate flexion contractures.
Appearance may range from manifesting normal patient hygiene in the early stage to a total lack of interest in hygiene in the later stages. Some patients also demonstrate abusive language, inappropriate sexual behaviors, and paranoia. The Folstein-mini-mental exam is a quick evalua- tion tool that can assist in diagnosis and monitoring of the disease’s progression.
PSYCHOSOCIAL. The nurse needs to assess the family for its ability to cope with this pro- gressive disease, to provide physical and emotional care for the patient, and to meet financial responsibilities. A multidisciplinary team assessment approach is recommended for the patient and family.
60 Alzheimer’s Disease
Diagnostic tests need to rule out a treatable condition that could be causing demen- tia; these conditions include thyroid disease, stroke, vitamin deficiency, brain tumor, drug and medication effects, infection, anemia, and depression.
Abnormality with
Test Normal Result Condition Explanation
Diagnostic Highlights
Brain biopsy upon
autopsy Negative Positive for cellular changes that are associated with the disease
No diagnostic test is definitive for AD.
Clinical criteria for diagnosis of DAT:
(1) presence of at least two cognitive deficits; (2) onset occurring between ages 40 and 90; (3) progressive deteri- oration; (4) all other causes ruled out.
Other Tests: Supporting tests include computed tomography (CT) scan; magnetic reso- nance imaging (MRI); positron emission tomography (PET). During the early stages of dementia, CT and MRI may be normal, but in later stages, an MRI may show a decrease in the size of the cerebral cortex or of the area of the brain responsible for memory, particularly the hippocampus. Genetic testing for the ApoE gene is available and the presence of the gene is a risk factor for AD. Genetic tests may be helpful in diagnosis, but further studies are needed to confirm their reliability.
PRIMARY NURSING DIAGNOSIS
Self-care deficit related to impaired cognitive and motor function
OUTCOMES. Self-care: Activities of daily living—Bathing, Hygiene, Eating, Toileting;
Cognitive ability; Comfort level; Role performance; Social interaction skills; Hope
INTERVENTIONS. Self-care assistance: Bathing and Hygiene; Oral health management;
Behavior management; Body image enhancement; Emotional support; Mutual goal setting;
Exercise therapy; Discharge planning
PLANNING AND IMPLEMENTATION Collaborative
The initial management of the patient begins with education of the family and caregivers regard- ing the disease, the prognosis, and changes in lifestyle that are necessary as the disease pro- gresses. Basic collaborative principles include:
• Keep requests for the patient simple
• Avoid confrontation and requests that might lead to frustration
• Remain calm and supportive if the patient becomes upset
• Maintain a consistent environment
• Provide frequent cues and reminders to reorient the patient
• Adjust expectations for the patient as he or she declines in capacity
Alzheimer’s Disease 61
Generally, therapy is focused on symptoms with an attempt to maintain cognition.
Medication or
Drug Class Dosage Description Rationale
Pharmacologic Highlights
Donepezil
Antidepressants
5–10 mg PO qd
Varies with drug
Cholinesterase inhibitor;
elevates acetylcholine con- centration in cerebral cortex by slowing degradation of acetylcholine released by intact neurons
Selective serotonin reuptake inhibitors; increases activity of serotonin in the brain
Improves cognitive symptoms;
improves cognitive function in the early stages of the disease only;
drug effects diminish as the dis- ease progresses
Treats depression, anxiety, and irritability
Other Therapies: Secondary treatments are aimed at treating depression, psychosis, and agitation. To control night wandering and behavioral outbursts, physicians pre- scribe mild sedatives such as diphenhydramine. Barbiturates are avoided because they can precipitate confusion. Depression is treated with antidepressants (trazodone), and agitation is controlled by anxiolytics (oxazepam or diazepam). Psychotic behaviors are treated with antipsychotics (chlorpromazine or haloperidol).
Independent
Promote patient activities of daily living to the fullest, considering the patient’s functional ability.
Give the patient variable assistance or simple directions to perform those activities. Anticipate and assess the patient’s needs mainly through nonverbal communication because of the patient’s inability to communicate meaningfully through speech. Many times emotional outbursts or changes in behavior are a signal of the patient’s toileting needs, discomfort, hunger, or infection.
To maximize orientation and memory, provide a calendar and clock for the patient. Encour- age the patient to reminisce, since loss of short-term memory triggers anxiety in the patient.
Emotional outbursts usually occur when the patient is fatigued, so it is best to plan for frequent rest periods throughout the day.
Maintain physical safety of the patient by securing loose rugs, supervising electrical devices, and locking doors and windows. Lock up toxic substances and medications. Supervise cooking, bathing, and outdoor recreation. Be sure that the patient wears appropriate identification in case he or she gets lost. Terminate driving by removing the car keys or the car. Provide a safe area for
DRG Category: 113 Mean LOS: 12.7 days
Description: SURGICAL: Amputation for Circula- tion System Disorders, Except Upper Limb and Toe DRG Category: 442
Mean LOS: 5.8 days
Description: SURGICAL: Other Operating Room Procedures for Injuries with CC wandering. Encourage and anticipate toileting at 2- to 3-hour intervals. Change incontinence pads as needed, but use them only as a last resort. Bowel and bladder programs can be beneficial in the early stage of the disease.
Provide structured activity during the day to prevent night wandering. If confusion and agi- tated wandering occur at night, provide toileting, fluids, orientation, nightlights, and familiar objects within a patient’s view. Some patients respond calmly when given the security of a stuffed animal or a familiar blanket.
Encourage family members to verbalize their emotional concerns, coping strategies, and other aspects of caregiver role strain. Discuss appropriate referrals to local support groups, clergy, social workers, respite care, day care, and attorneys. Provide information about advanced directives (living wills and durable power of attorney for healthcare).
DOCUMENTATION GUIDELINES
• Any changes in cognitive function: Confused orientation (time, place, person), emotional out- bursts, forgetfulness, paranoia, decreased short-term memory, impaired judgment, loss of speech, disturbed affect, decline of problem-solving ability, and reduction in abstract thinking
• Response to medications (anxiolytics, antipsychotics, cholinesterase inhibitors, antidepres- sants, sedatives)
• Verbal and nonverbal methods that effectively meet or communicate the patient’s needs
• Caregiver response to patient behaviors and information about DAT
• Ability to perform the activities of daily living
DISCHARGE AND HOME HEALTHCARE GUIDELINES
MEDICATIONS. Be sure the caregiver understands all medications, including the dosage, route, action, and adverse effects.
SAFETY. Explain the need to supervise outdoor activity, cooking, and bathing. Lock doors and windows, and lock up medications and toxic chemicals. Make sure the patient wears identifica- tion to provide a safe return if she or he becomes lost. Commercially made products are avail- able that trigger an alarm if the patient wanders out of safe territory.
62 Amputation
Amputation
A
mputation is the surgical severing of any body part. Amputations can be surgical (therapeu- tic) or traumatic (emergencies resulting from injury). The type of amputation performed in the Civil War era by a surgeon called a “sawbones” was straight across the leg, with all bone and soft tissue severed at the same level. That procedure, known as a guillotine (or open) amputation, is still seen today.A traumatic amputation is usually the result of an industrial accident, in which blades of heavy machinery sever part of a limb. A healthy young person who suffers a traumatic amputation with- out other injuries is often a good candidate for limb salvage. Reattachment of a limb will take place as soon as possible following the injury. The chief problems are hemorrhage and nerve damage. A closed amputation is the most common surgical procedure today. The bone is severed somewhat higher than the surrounding tissue, with a skin flap pulled over the bone end, usually from the pos- terior surface. This procedure provides more even pressure for a weight-bearing surface, promot- ing healing and more successful use of a prosthesis. (See Table 7 for levels of amputations.)
Amputation 63
•TABLE 7 Levels of Amputation
TYPE DESCRIPTION
Below the knee
Syme procedure
Transmetatarsal/toe amputation Hip disarticulation/
extensive hemipelvectomy Upper extremity
Most common surgical site, performed rather than above-the-knee amputation whenever possible because the higher the amputation performed, the greater the energy required for mobility
Partial amputation with salvage of the ankle; has advantages over loss of the limb higher up because it does not require a prosthesis and produces less weight-bearing pain
Involves removal of limited amount of limb; requires little rehabilitation; often followed by additional surgery at a higher level because of inadequate heal- ing when used for patients with peripheral vascular disease
Usually performed for malignancies; because of the surgery involved and the extremely bulky prosthesis required for ambulation, these procedures are used either as life-saving measures in young patients or as a surgery of last resort for pain control
Performed with salvage of as much normal tissue as possible. Function of the upper extremity is vital to normal activities of daily living. Much research is being conducted at the current time to manufacture and refine prostheses that can substitute for the patient’s arm and hand, providing both gross and fine movement. Cosmetic considerations are extremely important in the loss of the upper extremity for many patients.
Note:The terms “below the knee amputation,” or BKA, and “above the knee amputation,” or AKA, are also commonly used.
CAUSES
Peripheral vascular disease is much more frequently the cause of amputation than are traumatic injuries. Poor foot care, impaired circulation, and peripheral neuropathy lead to serious ulcerations, which may be undetected until it is too late to salvage the foot or even the entire limb. Congenital deformity, severe burns, and crushing injuries that render a limb permanently unsightly, painful, or nonfunctional may be treated with surgical amputation. Tumors (usually malignant) and chronic osteomyelitis that does not respond to other treatment may also necessitate amputation.
GENETIC CONSIDERATIONS
No clear genetic contributions to susceptibility have been defined.