Kristen Mauk

Background

Hypothyroidism results from lack of sufficient thyroid hormone being produced by the thyroid gland. Older adults may have subclinical hypothyroidism, in which the TSH (thyroid-stimulating hormone) is elevated and the T4 (thyroxine or thyroid hormone) is normal; 4.3–9.5% of the general population has this problem (Woolever & Beutler, 2007). In this condition, the body is trying to stimulate production of more thyroid hormone. Some older adults with this condition will progress to have primary or overt hypothyroidism. This is when the TSH is elevated and T4 is decreased. Hashimoto’s disease is the most common cause and represents 90% of all patients with hypothyroidism (American Association of Clinical Endocrinologists [AACE], 2005; Woolever & Beutler, 2007), though certain pituitary disorders, medications, and other hormonal imbalances may be causal factors.

Warning Signs

Older adults may present an atypical picture, but the most common presenting complaints are fatigue and weakness.

Diagnosis

Diagnosis should include a thorough history and physical. Bradycardia and heart failure are often associated factors. Lab tests should include thyroid and thyroid antibody levels (common to Hashimoto’s), and lipids, because hyperlipidemia is also associated with this disorder.

Treatment

Treatment centers on returning the thyroid ¬hormone level to normal. This is done through oral thyroid replacement medication, usually L-thyroxine. In older adults with coexisting cardiovascular disease, starting with the usual doses may exacerbate angina and worsen the underlying heart disease, so it is important to start low and go slow. Titration should be done cautiously, with close monitoring of the older adult’s response to the medication. The does should be adjusted on 6- week intervals until normal levels of thyroid hormone are achieved. Once the TSH is within normal limits, then checking the TSH should be done every 6 to 12 months to monitor effectiveness and blood levels, because hyperthyroidism is a side effect of this therapy and can have serious implications on the older person’s health.

Patients need to learn the importance of taking thyroid medication at the same time each day without missing doses. Sometimes older adults have other problems associated with hypothyroidism, such as bowel dysfunction and depression. Any signs of complicating factors should be reported to the physician, and doctors’ appointments for monitoring should be religiously kept. Strategies for managing fatigue and weakness should also be addressed, because some lifestyle modifications may need to be made as treatment is initiated.

Adapted from Mauk, K. L., Hanson, P., & Hain, D. (2014). Review of the management of common illnesses, diseases, or health conditions. In K. L.
Mauk’s (Ed.) Gerontological Nursing: Competencies for Care. Sudbury, MA: Jones and Bartlett Publishers. Used with permission.

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Background

Parkinson’s disease (PD) is one of the most common neurological diseases, affecting at least 1.5 million people in the United States (American Parkinson Disease Association {APDA}, 2010). The average age of onset is about 59 years of age (APDA, 2010), and the likelihood of developing PD increases with age (National Institute of Neurological Disorders, 2008). It affects both men and women, particularly those over the age of 60 years (American Parkinson Disease Foundation, 2012). Parkinson’s disease was first described by Dr. James Parkinson as the “shaking palsy,” so named to describe the motor tremors witnessed in those experiencing this condition.

Parkinson’s disease is a degenerative, chronic disorder of the central nervous system in which nerve cells in the basal ganglia degenerate. A loss of neurons in the substantia nigra of the brainstem causes a decrease in the production of the neurotransmitter dopamine, which is responsible for fine motor movement. Dopamine is needed for smooth movement and also plays a role in feelings and emotions. One specific pathological marker is called the Lewy body, which under a microscope appears as a round, dying neuron.

Signs and Symptoms

Parkinson’s disease has no known etiology, though several causes are suspected. There is a family history in 15% of cases. Some believe a virus or environmental factors play a significant role in the development of the disease. A higher risk of PD has been noted in teachers, medical workers, loggers, and miners, suggesting the possibility of a respiratory virus being to blame. More recent theories blame herbicides or pesticides. An emerging theory discusses PD as an injury related to an event or exposure to a toxin versus a disease. Interestingly, coffee drinking and cigarettes are thought to have a protective effect in the development of PD (Films for the Humanities and Sciences, 2004).

The signs and symptoms of PD are many; however, there are four cardinal signs: bradykinesia (slowness of movement), rigidity, tremor, and gait changes such as imbalance or incoordination. A typical patient with PD symptoms will have some distinctive movement characteristics with the components of stiffness, shuffling gait, arms at the side when walking, incoordination, and a tendency to fall backward. Not all patients exhibit resting tremor, but most have problems with movement, such as difficulty starting movement, increased stiffness with passive resistance, and rigidity, as well as freezing during motion (NINDS, 2012). Advanced PD may result in Parkinson’s dementia.

Diagnosis

Diagnosis of PD is made primarily on the clinician’s physical examination and thorough history taken from the patient and/or family. Several other conditions may cause symptoms similar to PD, such as the neurological effects of tremor and movement disorders. These may be attributed to the effects of drugs or toxins, Alzheimer’s disease, vascular diseases, or normal pressure hydrocephalus, and not be true PD. There is no one specific test to diagnose PD, and labs or X-rays rarely help with diagnosis.

Treatment

Management of PD is generally done through medications. Levodopa, a synthetic dopamine, is an amino acid that converts to dopamine when it crosses the blood–brain barrier. Levodopa helps lessen most of the serious signs and symptoms of PD. The drug helps at least 75% of persons with PD, mainly with the symptoms of bradykinesia and rigidity (NINDS, 2008). One important side effect to note is hallucinations. A more common treatment, and generally the drug of choice, involves a medication that combines levodopa and carbidopa (Sinemet), resulting in a decrease in the side effect of nausea seen with levodopa therapy alone, but with the same positive control of symptoms, particularly with relation to movement. Patients should not be taken off of Sinemet precipitously, so it is important to report all of a patient’s medications if they are admitted to either acute or long-term care. Dopamine agnoists trick the brain into thinking it is getting dopamine. This class of medications is less effective than Sinemet, but may be beneficial for certain patients. The most commonly prescribed dopamine agonists are pramipexole (Mirapex) and ropinirole (Requip) (Parkinson’s Disease Foundation, 2012). Medications such as Sinemet show a wearing-off effect, generally over a 2-year period. During this time, the person must take larger doses of the medication to achieve the same relief of symptoms that a smaller dose used to bring. For an unknown reason, if the medication is stopped for about a week to 10 days, the body will reset itself and the person will be able to restart the medication at the lower dose again until tolerance is again reached. This time off from the medication is called a “drug holiday” and is a time when the person and family need extra support, because the person’s symptoms will be greatly exacerbated without the medication. The earliest drugs used for PD symptom management were anticholinergics such as Artane and Cogentin, and these medications are still used for tremors and dystonias associated with wearing-off and peak dose effects (Parkinson’s Disease Foundation, 2012).

There are many other treatments for Parkinson’s disease being explored. These include deep brain stimulation (DBS), with electrode-like implants that act much like a pacemaker to control PD tremors and other movement problems. The person using this therapy will still have the disease and generally uses medications in combination with this treatment, but may require lower doses of medication (NINDS, 2012). Thalamotomy, or surgical removal of a group of cells in the thalamus, is used in severe cases of tremor. This will manage the tremors for a period of time, but is a symptomatic treatment, not a cure. Similarly, pallidotomy involves destruction of a group of cells in the internal globus pallidus, an area where information leaves the basal ganglia. In this procedure, nerve cells in the brain are permanently destroyed.

Fetal tissue transplants have been done experimentally in Sweden with mild success in older adults and more success among patients whose PD symptoms were a result of toxins. Stem cell transplant uses primitive nerve cells harvested from a surplus of embryos and fetuses from fertility clinics. This practice, of course, poses an ethical dilemma and has been the source of much controversy and political discussion.

A more recent development includes the use of adult stem cells, a theory that is promising but not yet well researched. Cells may be taken from the back of the eyes of organ donors. These epithelial cells from the retina are micro-carriers of gelatin that may have enough cells in a single retina to treat 10,000 patients (Films for the Humanities and Sciences, 2004). In addition, cells modified from the skin of patients with PD can be engineered to behave like stem cells (NINDS, 2012). Both of these alternatives present a more practical and ethically pleasing source of stem cells than embryos.
Other research includes areas include those related to alternative therapies. For example, Tai Chi has been shown to be effective in improving balance and reducing falls for PD patients (NINDS, 2012). Rehabilitation units have been using Tai Chi for similar benefits in other patients with neurological deficits. Simple interventions such as using Wii games to promote activity and exercise may be explored. The role of caffeine in PD is also being examined. In a small randomized control study of 61 patients with PD, caffeine equivalent to 2–3 cups of coffee per day was given to subjects and compared with a control group of those taking a placebo. Those patients receiving the caffeine intervention showed little improvement in daytime sleepiness, but modest improvement in PD severity scores related to speed of movement and stiffness (Postuma et al., 2012). Further study with larger groups was recommended by the researchers.

Much of the nursing care in PD is related to education. Because PD is a generally chronic and slowly progressing disorder, patients and family members will need much instruction regarding the course of the disease and what to anticipate. Instruction in the areas of medications, safety promotion, prevention of falls, disease progression, mobility, bowel and bladder, potential swallowing problems, sleep promotion, and communication is important. Most of the problems seen as compli¬cations of PD are handled via the physician as an outpatient, but certainly complications such as swal¬lowing disorders as the disease progresses may require periods of hospitalization. When persons suffer related dementia in the final phases of the disease, they are often cared for in long-term care facilities that are equipped to handle the challenges and safety issues related to PD dementia. In ¬addition, access to resources and support groups is essential.

Adapted from Mauk, K. L., Hanson, P., & Hain, D. (2014). Review of the management of common illnesses, diseases, or health conditions. In K. L. Mauk’s (Ed.) Gerontological Nursing: Competencies for Care. Burlington, MA: Jones and Bartlett Publishers. Used with permission.

Background

Once thought to be mainly a disorder of children, recurrent seizures or epilepsy is thought to be present in about 7% of older adults (Spitz, 2005) and is usually related to one of the common comorbidities found in older adults (Bergey, 2004; Rowan & Tuchman, 2003). Epilepsy affects up to 3 million Americans of all ages (Velez & Selwa, 2003). Davidson & Davidson (2012) summarized findings of most studies on epilepsy in older adults with these main points:
Seizures can be caused by a variety of conditions in older persons, but “the most common cause of new-onset epilepsy in an elderly person is arteriosclerosis and the associated cerebrovascular disease” (Spitz, 2005, p. 1), accounting for 40–50% of seizures in this age group (Rowan & Tuchman, 2003). Seizures are associated with stroke in 5–14% of survivors (Spitz, 2005; Velez & Selwa, 2003). Other common causes of epilepsy in the elderly include Alzheimer’s disease and brain tumor.
There are three major classifications of epilepsies, although there are many additional types. Generalized types are more common in young people and associated with grand mal or tonic-clonic seizures. A number of cases have an un¬determined origin and may be associated with certain situations such as high fever, exposure to toxins, or rare metabolic events. In older adults, localized (partial or focal) epilepsies are more common, particularly complex partial seizures (Luggen, 2009). In contrast to young adults, Rowan and Tuchman (2003) cite other differences in seizures in the elderly: low frequency of seizure activity, easier to control, high potential for injury, a prolonged postictal period, and better tolerance with newer antiepileptic drugs (AEDs). Additionally, older adults may have coexisting medical problems and take many medications to treat these problems.

Risk Factors/Warning Signs

Risk factors for seizures in older adults include cerebrovascular disease (especially stroke), age, and head trauma. The most obvious signs and symptoms of epilepsy are seizures, although changes in behavior, cognition, and level of consciousness may be other signs. Also, note that exposure to toxins can cause seizures that are not epilepsy. Complex partial seizures in older adults may include symptoms such as “confusion, memory loss, dizziness, and shortness of breath” (Davidson & Davidson, 2012, p. 16). Automatism (repetitive movements), facial twitching with following confusion, and coughing are also signs of the more-common complex partial seizure (Luggen, 2009).

Diagnosis

Diagnosis is made by careful description of the seizure event, a thorough history, and physical. Eyewitness accounts of the seizure incident can be quite helpful, although many community-dwelling older adults go undiagnosed because their seizures are never witnessed. In addition, complete blood work, neuroimaging, chest X-ray, electrocardiogram (ECG), and electroencephalogram (EEG) help determine the cause and type of seizure (National Institute for Health and Clinical Excellence {NICE}, 2012).

Treatment

Treatment for epilepsy is aimed at the causal factor. The standard treatment for recurrent seizures is antiepilepsy drugs (AEDs). The rule of thumb, “start low and go slow,” for medication dosing in older adults particularly applies to AEDs. The elderly tend to have more side effects, adverse drug interactions, and problems with toxicity levels than younger people.
Research has suggested that older adults may have better results with fewer side effects with the newer AEDs than the traditional ones, though about 10% of nursing home residents are still medicated with the first-generation AEDs (Mauk, 2004). The most common older medications used to treat seizures include barbiturates (such as phenobarbital), benzodiazepines (such as diazepam/Valium), hydantoins (such as phenytoin/Dilantin), and valproates (such as valproic acid/Depakene) (Deglin & Vallerand, 2005; Resnick, 2008).
Several newer drugs are also used, depending on the type of seizure. Second-generation AEDs, including gabapentin (Neurontin), lamotrigine (Lamictal), oxcarbazepine (Trileptal), levetiracetam (Keppra), pregabalin (Lyrica), tiagabine (Gabitril), and topiramate (Topamax), are generally recommended over the older AEDs; however, older AEDS such as phenytoin (Dilantin), valproate (Depakote), and carbamazepine (Tegretol) are the most commonly prescribed treatment options (Resnick, 2008). Each of these medications has specific precautions for use in patients with certain types of medical problems or for those taking certain other medications. Regarding side effects in older patients, watch for potential stomach, kidney, neurological (especially poor balance or incoordination), and liver problems. Additionally, some newer extended-release AEDs are thought to be better tolerated and have a lower incidence of systemic side effects (such as tremors) (Uthman, 2004).

Adapted from Mauk, K. L., Hanson, P., & Hain, D. (2014). Review of the management of common illnesses, diseases, or health conditions. In K. L. Mauk’s (Ed.) Gerontological Nursing: Competencies for Care.Burlington, MA: Jones and Bartlett Publishers. Used with permission.

According to the CDC, nearly 800,000 persons in the United States have a stroke each year. This is about one every 4 minutes, resulting in over 130,000 deaths annually. Stroke is simply defined as an interruption to the blood supply to the brain and is caused by a clot or hemorrhage. It can be a devastating problem for survivors, resulting in changes in mobility, cognition, speech, swallowing, bowel and bladder, self-care, and general functioning to varying degrees.  Some people recover completely after a stroke, but others experience lifelong challenges.

The good news is that there is hope and quality of life after stroke. In my research with stroke survivors, I discovered 6 phases that survivors reported as they made the journey through rehabilitation towards recovery. These steps can be used to see where a person is in the recovery process, help us understand how they may be feeling, and help guide the way we interact with them.

Agonizing:  In this first phase of the process, stroke survivors are in shock over what has happened to them. They can’t believe it, and may even deny the warning signs of stroke. The important task during this time is survival from the stroke itself.  Call 911 if you see the warning signs of facial droop, arm weakness, or speech difficulties.

Fantasizing:  In the second phase of the stroke process, the survivor may believe that the symptoms will all go away. Life will return to normal, and there is a sense of the problem being unreal. Time takes on a different meaning. The way to help is to gently help them recognize reality, and without taking away hope for recovery.

Realizing: This is the most important phase that signals a turn in the recovery process. This is when the survivor realizes that he/she may not fully recover from the effects of the stroke and that there is work to be done to rehabilitate and reclaim life. Common feelings during this phase of realizing are anger and depression. The way to help is to encourage the person to actively engage in rehabilitation. The real work of recovery is just beginning.

Blending: These last 3 phases in the process of stroke recovery may be occurring at much the same time. This is where the real work of adaptation to life after stroke begins. The survivor begins to blend his “old life” before stroke with his new life as a stroke survivor. He/she may start to engage in former activities even if it requires adaptations to be made. He/she will be actively engaged in therapy and finding new ways to do things. The way to help is to promote education. This is a time when survivors are most ready to learn how to adjust to life after stroke. Listen to your rehab nurses, therapists, and physician. Be active in the recovery process.

Framing: During this phase, the individual wants to know what caused the stroke. Whereas in the Agonizing phase they were asking “why me?”, now they need to the answer to “what was the cause?”  Stroke can be a recurring disorder, so to stop a subsequent stroke, it is important to know the cause. Interestingly, if the physician has not given the survivor a cause for the first stroke, patients often make up a cause that may not be accurate. Help the survivor to learn from the health care provider what the cause of his/her own stroke was. Then steps can be taken to control those risk factors.

Owning:  In this final phase of stroke recovery, the survivor has achieved positive adaptation to the stroke event and aftermath. The survivor has accomplished the needed grief work over the losses resulting from the stroke. He/she has realized that the effects may not go away and has made positive adjustments to his/her life in order to go on. Survivors in this phase have blended their old life with the new life after stroke and feel better about their quality of life. While they still may revisit the emotions of the prior phases at times, they have accepted life as a survivor of stroke and made good adjustments to any changes that resulted. They feel that they have a more positive outlook on life. At this point, survivors can use their experience to help others cope with life after stroke.

For more information about stroke recovery, visit www.seniorcarecentral.net and view Dr. Mauk’s model for stroke recovery.