M

Macular degeneration

Description

Age-related macular degeneration (AMD) is a degeneration of the retina involving the macula that results in varying degrees of central vision loss. It is the most common cause of irreversible central vision loss in people over 60 years old in the United States. AMD is divided into two classic forms: dry (atrophic), which is more common, and wet (exudative), which is more severe. Wet AMD accounts for 90% of the cases of AMD-related blindness.

Pathophysiology

■ In dry AMD, people notice that reading and other close-vision tasks become more difficult. This form starts with the abnormal accumulation of yellowish extracellular deposits called drusen in the retinal pigment epithelium. Atrophy and degeneration of macular cells then result, leading to a slowly progressive and painless vision loss.

■ Wet AMD is characterized by the growth of new blood vessels from their normal location in the choroids to an abnormal location in the retinal epithelium. As the new blood vessels leak, scar tissue gradually forms. Acute vision loss may occur in some cases from bleeding.

Clinical manifestations

The patient may experience blurred and darkened vision, scotomas (blind spots in the visual fields), and metamorphopsia (distortion of vision).

Diagnostic studies

■ Visual acuity measurement

■ Ophthalmoscopic examination to look for drusen and other changes in the fundus

■ Amsler grid test to define the involved area and provide a baseline for future comparison

■ Fundus photography and IV fluorescein angiography to further define the extent and type of AMD

Nursing and collaborative management

Vision does not improve for most people with AMD. Limited treatment options for patients with wet AMD include several medications (i.e., ranibizumab [Lucentis], bevacizumab [Avastin], and pegaptanib [Macugen]) injected directly into the vitreous cavity. These drugs are selective inhibitors of endothelial growth factor and help to slow vision loss.

■ Photodynamic therapy is used in wet AMD to destroy abnormal blood vessels without permanent damage to the retinal pigment epithelium and photoreceptor cells.

■ Patients at risk for AMD (in consultation with their health care provider) should consider supplements of vitamins and minerals.

■ Many patients with low-vision assistive devices can continue reading and retain a license to drive during the daytime and at lowered speeds.

The permanent loss of central vision associated with AMD has significant psychosocial implications for nursing care. Nursing management of the patient with uncorrectable visual impairment is discussed in Lewis et al.: Medical-Surgical Nursing, ed. 9, pp. 388 to 389, and is appropriate for the patient with AMD. It is especially important when caring for patients to avoid giving them the impression that “nothing can be done” about their problem. Although therapy will not recover lost vision, much can be done to augment the remaining vision.

Malignant melanoma

Description

Malignant melanoma is a tumor arising in cells producing melanin, which are usually the melanocytes of the skin. Melanoma has the ability to metastasize to any organ, including the brain and heart. This is the deadliest form of skin cancer.

The exact cause of melanoma is unknown. Risk factors include long-term UV exposure or overexposure to artificial light, such as a tanning booth. People with fair skin and eyes and those with a prior diagnosis of melanoma or having a first-degree relative diagnosed with melanoma have an increased risk. Immunosuppression and dysplastic nevi also increase a person’s risk.

Clinical manifestations

About 25% of melanomas occur in existing nevi or moles; about 20% occur in dysplastic nevi. Melanoma frequently occurs on the lower legs in women and on the trunk, head, and neck in men. Because most melanoma cells continue to produce melanin, melanoma tumors are often brown or black.

■ Individuals should consult their health care provider immediately if their moles or lesions show any of the clinical signs (ABCDEs) of melanoma (see Fig. 24-4, Lewis et al.: Medical-Surgical Nursing, ed. 9, p. 433). These signs include Asymmetry, Border irregularity, Color varied from one area of the lesion to another, Diameter greater than 6 mm, and Evolving, changing appearance.

■ Any sudden or progressive increase in the size, color, or shape of a mole should be checked. When melanoma begins in the skin, it is called cutaneous melanoma. Melanoma can also occur in the eyes, meninges, lymph nodes, digestive tract, and anywhere else in the body where melanocytes are found.

Collaborative care

All suspicious pigmented lesions should be biopsied using an excisional biopsy technique. The most important prognostic factor is tumor thickness at the time of diagnosis.

■ Two methods are used to determine tumor thickness: the Breslow measurement, which indicates tumor depth in millimeters, and the Clark level, which indicates the depth of invasion of the tumor. The higher the number, the deeper the melanoma.

Treatment depends on the site of the original tumor, stage of the cancer, and patient’s age and general health. Initial treatment of malignant melanoma is surgical excision. Melanoma that has spread to the lymph nodes or nearby sites usually requires additional therapy, such as chemotherapy, biologic therapy (e.g., α-interferon, interleukin-2), and/or radiation therapy. Chemotherapy may include dacarbazine (DTIC), temozolomide (TMZ), procarbazine (Matulane), carmustine (BCNU), and lomustine (CCNU). Two newer options for patients with metastatic melanoma are ipilimumab (Yervoy) and vemurafenib (Zelboraf).

Cutaneous melanoma is nearly 100% curable by excision if diagnosed at stage 0. The 5-year survival rate depends on sentinel node biopsy results, which indicate if metastasis has occurred. If metastasis to other organs is found (stage IV), treatment then becomes palliative.

Patient and caregiver teaching

Emphasize the importance of protection from the damaging effects of the sun, such as wearing a large-brimmed hat, sunglasses, and a long-sleeved shirt of a lightly woven fabric.

■ Inform patients that the rays of the sun are most dangerous between 10 AM and 2 PM standard time and 11 AM and 3 PM daylight savings time. Recommend patients use a sunscreen with a minimum SPF of 15 on a daily basis. Sunscreen should be reapplied every 2 hours.

■ Teach patients to self-examine their skin at least monthly to detect new or persistent skin lesions.

Malnutrition

Description

Malnutrition is an excess, deficit, or imbalance of the essential components of a balanced diet. Malnutrition is also described as undernutrition or overnutrition. Undernutrition describes a state of poor nourishment as a result of inadequate diet or diseases that interfere with normal appetite and assimilation of ingested food. Overnutrition refers to the ingestion of more food than is required for body needs, as in obesity.

■ The incidence of hospitalized patients who are malnourished or at nutritional risk is 20% to 70%. The prevalence of malnutrition in older adults ranges from 6% (community-dwelling older adults) to 50% (rehabilitation settings).

The following etiology-based terminology indicates the interaction and importance of inflammation on nutritional status:

■ Chronic disease–related malnutrition, or secondary PCM, is associated with conditions that impose sustained inflammation of a mild to moderate degree. This occurs when tissue needs are not met even though the dietary intake would be satisfactory under normal conditions. Conditions associated with this type of malnutrition include organ failure, cancer, rheumatoid arthritis, obesity, and metabolic syndrome.

■ Acute disease- or injury-related malnutrition is associated with acute disease or injury states with marked inflammatory response (e.g., major infection, burns, trauma, closed head injury).

Many factors contribute to the development of malnutrition, including socioeconomic factors, physical illnesses, incomplete diets, and food-drug interactions.

Pathophysiology of starvation

Initially, the body selectively uses carbohydrates (glycogen) rather than fat and protein to meet metabolic needs. This depletes glycogen stores in the liver and muscles within 18 hours.

■ When carbohydrate stores are depleted, skeletal protein begins to be converted to glucose for energy, resulting in a negative nitrogen balance. Within 5 to 9 days, body fat is fully mobilized to supply much of the needed energy.

■ In prolonged starvation up to 97% of calories are provided by fat, and protein is conserved. Depletion of fat stores depends on the amount available, but fat stores are generally used up in 4 to 6 weeks. Once fat stores are used, body proteins, including those in internal organs and plasma, can no longer be spared and rapidly decrease because they are the only remaining body source of available energy.

■ When the diet is extremely deficient in calories and essential proteins, the sodium-potassium exchange pump fails, leaving sodium inside the cell (along with water, causing cell expansion), and potassium levels in extracellular fluid rise.

The liver is the body organ that loses the most mass during protein deprivation. It gradually becomes infiltrated with fat secondary to decreased synthesis of lipoproteins. If dietary protein and other necessary constituents are not given, death will rapidly ensue.

Clinical manifestations

Manifestations of malnutrition range from mild to emaciation and death. The most obvious clinical manifestations on physical examination are apparent in the skin (dry and scaly skin, brittle nails, rashes, hair loss), mouth (crusting and ulceration, changes in tongue), muscles (decreased mass and weakness), and CNS (mental changes such as confusion, irritability).

■ The person is susceptible to infection. Both humoral and cell-mediated immunity are deficient. There is a decrease in leukocytes in the peripheral blood. Phagocytosis is altered as a result of the lack of energy necessary to drive the process. Many malnourished people are also anemic.

Diagnostic studies

■ Serum albumin, prealbumin, and transferrin levels are decreased.

■ C-reactive protein (CRP) and serum potassium are often elevated.

■ RBC count and hemoglobin (Hgb) levels indicate the presence and degree of anemia.

■ WBC count and total lymphocyte count are decreased.

■ Liver enzyme studies may be elevated.

■ Waist circumference and hip-to-waist ratio help evaluate the response to therapy.

Nursing and collaborative care

Nutritional screening identifies individuals who are malnourished or at risk for malnutrition and to determine if a more detailed nutritional assessment is necessary. Hospital-specific screening tools based on common admission assessment criteria include history of weight loss, prior intake before admission, use of nutritional support, chewing or swallowing issues, and skin breakdown.

Across all care settings, be aware of the patient’s nutritional status. Obtaining an accurate measure of body weight and height and recording this information are critical components of this assessment. Body mass index (BMI) is a measure of weight for height (see Fig. 41-2, Lewis et al.: Medical-Surgical Nursing, ed. 9, p. 907). BMIs outside the normal weight range are associated with increased morbidity and mortality.

Goals

The patient with malnutrition will gain weight (particularly muscle mass), consume a specified number of calories per day (with a diet individualized for the patient), and have no adverse consequences related to malnutrition or nutritional therapies.

Ménière’s disease

Description

Ménière’s disease is an inner ear disease characterized by episodic vertigo, tinnitus, aural fullness, and fluctuating sensorineural hearing loss. Symptoms are incapacitating as a result of sudden, severe attacks of vertigo with nausea and vomiting. Symptoms usually begin between ages 30 and 60 years.

Pathophysiology

The cause of the disease is unknown, but it results in an excessive accumulation of endolymph in the membranous labyrinth. The volume of endolymph increases until the membranous labyrinth ruptures, mixing high-potassium endolymph with low-potassium perilymph.

Clinical manifestations

■ Attacks may occur without warning or be preceded by an aura consisting of a sense of fullness in the ear, increasing tinnitus, and muffled hearing.

■ The patient may report a whirling sensation and experience the feeling of being pulled to the ground (“drop attack”).

■ Autonomic symptoms include pallor, sweating, nausea, and vomiting.

■ Duration of an attack may be hours or days, and attacks may occur several times per year. The clinical course is highly variable.

■ Low-pitched tinnitus may be present continuously in the affected ear or it may be intensified during an attack.

■ Hearing loss fluctuates, decreasing with each vertigo attack and eventually leading to permanent hearing loss.

Diagnostic studies

■ Audiogram results demonstrate mild, low-frequency hearing loss.

■ Vestibular tests

■ Glycerol test supports the diagnosis if hearing improvement occurs.

Nursing and collaborative care

During an acute attack, antihistamines, anticholinergics, and benzodiazepines can be used to decrease the abnormal sensation and lessen symptoms such as nausea and vomiting. Acute vertigo is treated symptomatically with bed rest, sedation, and antiemetics or antivertigo drugs for motion sickness. Diazepam (Valium), meclizine (Antivert), and fentanyl with droperidol (Innovar) may be used to reduce the vertigo. Most patients respond to the prescribed medications but must learn to live with the unpredictability of the attacks and the loss of hearing.

■ During an acute attack, a patient needs reassurance that the condition is not life threatening.

■ Focus on providing only essential care because movement aggravates vertigo.

■ Side rails should be up and the bed in low position if the patient is in bed. Avoid the use of lights and television, which exacerbate symptoms. Have an emesis basin available because vomiting is common. Assist with ambulation because unsteadiness remains after an attack.

Management between attacks may include calcium channel blockers, diuretics, antihistamines, and a low-sodium diet.

With frequent incapacitating attacks and reduced quality of life, surgical therapy is indicated. Surgical options include endolymphatic shunt, vestibular nerve resection, and labyrinth ablation. Careful management can decrease the possibility of progressive sensorineural loss in many patients.

Meningitis, bacterial

Description

Meningitis is an acute inflammation of the meningeal tissues surrounding the brain and spinal cord. Older adults and people who are debilitated are more often affected than is the general population. College students living in dormitories and individuals living in institutions (e.g., prisoners) are also at a high risk for contracting meningitis.

Bacterial meningitis is considered a medical emergency. If it is left untreated, the mortality rate approaches 100%. See Table 36, p. 214, for a comparison of meningitis and encephalitis.

Pathophysiology

Meningitis usually occurs in the fall, winter, or early spring and is often secondary to viral respiratory disease. Streptococcus pneumoniae and Neisseria meningitidis are the leading causes of bacterial meningitis. Organisms usually gain entry to the central nervous system (CNS) through the upper respiratory tract or bloodstream, but they may enter by direct extension from penetrating wounds of the skull or through fractured sinuses in basal skull fractures.

The inflammatory response to the infection tends to increase cerebrospinal fluid (CSF) production with a moderate increase in intracranial pressure (ICP). The purulent secretion produced by bacteria quickly spreads to other areas of the brain through the CSF.