ABSTRACT: The availability of a wide variety of treatments for multiple myeloma    allows healthcare providers to tailor treatments to individual patient needs, and has enabled prolonged survival of patients with the disease. Improved understanding of the disease, its treatment options, and potential side effects of therapy has provided unique opportunities for oncology nurses to employ preventive approaches, care strategies, and patient and family education and support over time. Because therapies have been developed that prolong the survival time, people with multiple myeloma are in the position of living with the disease for many years. Additional challenges are presented as healthcare providers develop wellness and quality of life plans of care in the setting of multiple myeloma survivorship. This article will explore the diagnosis, treatment planning, and clinical management of patients with multiple myeloma.

Multiple myeloma (myeloma) is a malignant disorder of the mature B plasma cell.[1] It can be considered a bone marrow disorder, and like leukemia, it prevents normal hematopoiesis and bone marrow function. This results in anemia, thrombocytopenia, and neutropenia. Unique to myeloma is the ability of the myeloma cell to cause problems such as cavitary bone lesions, hypercalcemia, renal failure, and solid plasmacytomas. Normal plasma cells produce normal immunoglobins. In patients with myeloma, abnormal or fragmented immunoglobin chains are secreted, often causing problems due to deposition in the body, particularly in the kidneys.

Multiple myeloma accounts for only about 1.3% of all malignancies in the United States. The American Cancer Society has estimated that about 20,180 new cases of multiple myeloma were diagnosed in the US in 2010, with an estimated 10,650 deaths.[2] The mean age of affected individuals is 62 years for men and 61 years for women, with less than 2% of cases occurring in patients younger than 40 years old. It is the second most common hematologic malignancy in the United States, second only to non-Hodgkin’s lymphoma if all subtypes are considered.[2,3]

Like many cancers, the exact cause of myeloma is not known. Age is a predominant factor. The incidence is higher in men and twice as high in African Americans. Genetic factors are implicated in familial trends.[4]

Myeloma is considered not curable, but treatment advances have improved the survival. Prior to the introduction of melphalan and prednisone in the 1960s, the survival time was less than a year.[5] Autologous stem cell transplant was introduced in the 1980s, further improving survival. The introduction of therapies such as thalidomide (Thalomid), lenalidomide (Revlimid), and bortezomib (Velcade) has also contributed to improved outcome of patients with myeloma in recent years, both in the relapsed-disease setting and at initial diagnosis. An overall survival time of 44.8  months has been reported,[5] and some patients are living up to 10 years from initial diagnosis.[3]


 Although approximately 20% of all myeloma patients are diagnosed while they are completely asymptomatic, patients with symptomatic active disease will present with bone pain, fatigue, weight loss, and paresthesias.[6] The most common clinical features at presentation are anemia, lytic bone lesions, renal insufficiency, hypercalcemia, and infection.[7]


Initial Diagnostic Workup for Multiple Myeloma 

Initial diagnostic workup includes the items in 

. LDH levels help with assessment of tumor cell burden, and the level of beta-2 microglobulin is now considered a standard measure of the myeloma tumor burden.[8] Blood serum analysis also includes quantitative immunoglobulin testing to determine levels of the different types of abnormal antibodies. Assessing the changes and amounts of the immunoglobins in the serum and urine is often helpful in tracking the progression of myeloma disease, although some patients have myeloma that does not secrete abnormal immunoglobins. For those who do, this is often referred to as the “M-spike,” as the monoclonal myeloma protein shows a spike on the plasma electrophoresis test results. The serum free light chain assay has prognostic value for myeloma as well as other plasma cell disorders, including monoclonal gammopathy of undetermined significance (MGUS), smoldering myeloma, immunoglobulin light chain amyloidosis, and solitary plasmacytoma.[8]


Cytogenetic Abnormalities Associated With “High Risk” Multiple Myeloma              TABLE 3             


Definition of Multiple Myeloma              TABLE 4


Staging Systems for Multiple Myeloma              TABLE 5             


Myeloma Therapy               TABLE 6             


European Bone Marrow Transplant (EBMT) and International Myeloma Working Group (IMWG) Response Criteria  

Along with the diagnostic staging and patient-specific comorbid conditions (such as renal failure, diabetes, heart conditions, etc), cytogenetic markers may be used on an individual basis to determine the best therapy for a given patient. Cytogenetic tests evaluate whole chromosomes from the nucleus of the cell at the time of mitotic metaphase. This helps to determine the changes in number or structure of chromosomes. One drawback of conventional cytogenetic testing (karyotyping) in myeloma is that the myeloma cells have a low proliferative activity, and it may take up to 2 weeks to receive complete results. Fluorescence in situ hybridization (FISH) is more sensitive but also more expensive.[9–11]

A number of these genetic abnormalities, cytokines, and serum tumor markers have been implicated in the pathogenesis and risk-stratification of myeloma. Although some cytogenetic testing may be done at initial diagnosis, the results are not incorporated into response criteria.[11] 

 lists some of the cytogenetic abnormalities that have a negative prognostic implication.

Based on the results of the clinical and laboratory evaluation, patients are initially classified as to whether they have smoldering (asymptomatic) or active (symptomatic) disease. 

 highlights definitions of smoldering and active myeloma that may affect treatment decisions.

The first multiple myeloma classification system was published by Durie and Salmon in 1975.[12] The second classification system, the International Staging System for Multiple Myeloma (ISS) is used more commonly in the clinical setting (see 

Treatment is an induction chemotherapy. This is often a multiagent combination chemotherapy. In selected patients, it is followed by high-dose chemotherapy and autologous hematopoietic stem cell transplant (HSCT). In general, if a patient is a potential HSCT candidate, agents that may later affect stem cell function, such as nitrosoureas or alkylating agents (eg, melphalan or prolonged use of lenalidomide), should be avoided up front. Reduced-intensity or mini-allogeneic transplants have been investigated as therapy following autologous HSCT and as salvage therapy for selected patients.[8] Some patients may be referred to an appropriate clinical trial. In general, different treatment modalities are used over time.

The National Comprehensive Cancer Network (NCCN) has developed clinical guidelines for myeloma treatment.[8] 

 describes the common regimens that are used.

Two different response criteria are used to determine the effectiveness of treatment for multiple myeloma. These are described in 

Myeloma treatment guidelines reflect improvement not only in targeted therapies, but also in supportive care strategies, such as hematopoietic growth factors, blood component support, antibiotics, and antihypercalcemia drugs. Bone disease, renal dysfunction, and other complications such as hypercalcemia, hyperviscosity, and coagulation/thrombosis should be treated with appropriate adjunctive measures.[8]

Nurses have a unique opportunity and challenge to assimilate knowledge about these therapies, disease manifestations, and individual patient comorbidities to collaboratively develop a comprehensive patient care plan with the healthcare team. The section that follows relates to the nursing care of patients with multiple myeloma.


 Skeletal involvement affects nearly 70% of myeloma patients during the course of their disease.[13] Patients with myeloma may have osteolytic or cavitary bone lesions, which may lead to fractures and/or spinal cord compression. Because the myeloma cell produces osteoclast-activating factors (OAFs), there is an upregulation of osteoclast activity. Hypercalcemia is also common.

All patients with documented bone disease should be given a bisphosphonate (pamidronate [Aredia] or zoledronic acid [Zometa]) monthly. It may also be given preventively for patients with osteopenia or osteoporosis.[6,8] The major side effects with prolonged use include renal insufficiency, hypocalcemia, and osteonecrosis of the jaw. Because of the latter, patients should have a comprehensive dental evaluation before receiving any bisphosphonate treatment. They should be instructed to practice good dental hygiene and speak with their oncologists before undergoing any invasive dental procedure.[6] Serum calcium should be routinely monitored; hypercalcemia may be treated with hydration, calcitonin, diuretics, and/or steroids.[8]

Because the osteopenia and lytic lesions place the patient at high risk for fractures, it is crucial that oncology nurses know the number and sites of lytic lesions, to determine whether a patient is at risk for spontaneous pathologic fracture. Orthopedic consultation should be sought for impending or actual long-bone fractures, bony compression of the spinal cord, or any vertebral column instability.

Treatment may include kyphoplasty (vertebroplasty) and/or stabilizing surgery. Percutaneous vertebroplasty is guided by fluoroscopy or CT, with the patient under sedation. An acrylic cement is injected into the malignant bone cavity, thereby strengthening the vertebra(e) and preventing further compression of the myeloma-cavitated body.[14] Prior to the procedure, the patient should have coagulation factors (PT [prothrombin time]/PTT [partial thromboplastin time]) and platelet count checked and corrected if necessary. Nurses need to ensure that the patient and family are informed about any functional limitations that may occur because of pathologic bone lesions. Although even minor movements by the patient alone-such as turning in bed or lifting a shopping bag-can lead to a spontaneous fracture, all healthcare staff need to make sure that the patient is not turned or moved in a way that may contribute to a fracture.

Maintaining and improving physical functioning should be part of the patient’s treatment plan. Exercise training is safe during and after cancer treatment, and it results in improvements in physical functioning, quality of life, and cancer-related fatigue.[15] As with other individuals age 65 years and older, patients with myeloma have particular risk factors related to falls (eg, visual problems, orthostatic hypotension, problems with gait and balance). In 2006, the Centers for Disease Control and Prevention (CDC) estimated that approximately 16% of all US adults in that age group fell at least once, and 31% of those who fell sustained an injury.[16] Assessment of safe mobility should be performed continually, as maximizing balance and strength can reduce the patient’s risk of falls. Exercise prescriptions should be individualized according to the patient’s disease, pretreatment level of aerobic fitness, medical comorbidities, response to treatment, and the immediate or persistent negative effects of treatment that are experienced at any given time.[15]

When recommending activity to patients with myeloma, fracture risk and limitations that may imposed by existing neuropathies, in particular, need to be taken into account. Steroids, a very common component of the treatment plan for myeloma, can cause a wide range of moderate to life-threatening side effects. Those that can affect mobility include proximal myopathy or muscle weakness, weight gain, visual changes, osteoporosis, and osteonecrosis.[17]

At every encounter, nurses should evaluate myeloma patients’ abilities to perform activities of daily living in a safe manner, so that falls and fractures are avoided. The nurse should ensure that appropriate referrals are made to rehabilitation physicians or physical therapists or, minimally, that an activity or exercise program is prescribed.


 Bone pain is the most common presenting symptom in patients with myeloma, and it can occur at any time during the course of the disease. It is often a significant problem. Besides affecting quality of life and function, bone pain can indicate an oncologic emergency, signaling an impending or actual fracture and/or spinal cord compression, or infection. Pain from skeletal lesions occurs in 67% of myeloma patients.[18] Neuropathic pain from the disease alone occurs in up to 13% of patients, with the reported rate as high as 54%, as a result of treatment with novel therapies, especially thalidomide, bortezomib, and lenalidomide.[19,20] Comorbid conditions such as diabetes, HIV infection, alcoholism, and herpes zoster can contribute to neuropathic pain. Patients may report symptoms of burning pain; having a limb “fall asleep”; and various sensations such as burning, stabbing, stinging, squeezing, aching, cramping, shooting pain, and cold.[21]

Nurses are in a unique position to assess and explore pain in a stepwise and ongoing fashion, using verbal and nonverbal pain scales and grading systems. This will help to ensure that the patient receives adequate pain control and ongoing assessment and intervention. Neurophysiologic testing, X-rays, and other diagnostics may be needed to further ascertain or confirm the etiology of the pain. Depending on the type of pain or pain syndromes, one or more therapies may be prescribed. For mild pain (patient report of levels 1–3 on a 0–10 scale), nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen may be prescribed.  However, patients should be cautioned about the renal, gastrointestinal, and bleeding toxicities associated with NSAIDs, and the liver toxicity of acetaminophen. In general, cancer pain is treated with opioids, and additional interventions are meant to complement management. For example, the addition of bisphosphonates, a nerve block, and/or steroids may be helpful for bone pain.[22] Antiepileptic drugs such as gabapentin or pregabalin (Lyrica) and tricyclic antidepressants such as amitryptyline or duloxetine (Cymbalta) may be helpful for neuropathic pain.[21,23] The lidocaine patch 5% (Lidoderm) may also be used. Nonpharmacologic interventions can include supportive braces, physical therapy, massage, acupuncture/acupressure, imagery, application of cold/heat, and others. Side effects from the medications, such as constipation, nausea, pruritus, motor and cognitive impairment, and sedation should be prevented or controlled. For all levels of pain, psychosocial support and patient and family education should be employed, as well as consideration of coanalgesics (antidepressants, topicals, etc) and nonpharmacologic interventions.[22]

Low-dose radiation therapy (10–30 Gy) can be used as palliative treatment for uncontrolled pain, impending pathologic fracture, or impending cord compression.[22] As previously stated, vertebroplasty or kyphoplasty for symptomatic vertebral compression fractures can be helpful to reduce pain and the risk of further injury.


 Patients with myeloma may have pre-existing myelosuppression as a result of the bone marrow being replaced by malignant plasma cells. In addition, most therapies have the potential to cause some degree of myelosuppression.[24,25] The incidence of neutropenia (all grades) is dependent upon the therapy administered, as well as pre-existing myelosuppression from the disease within the bone marrow.

Because myeloma patients may not produce enough normal plasma cells and immunoglobulins, infections can occur from this deficit as well. Renal insufficiency caused by myeloma can also lead to decreased levels of the red blood cell (RBC) growth hormone, erythropoietin, reducing RBC production.[26] 

 proposes nursing care strategies for multiple myeloma patients who have myelosuppression.


 Gastrointestinal side effects of therapy for myeloma may include oral and bowel mucositis, constipation, diarrhea, nausea, and vomiting.[27] Although these effects are fairly predictable and manageable, they can become life-threatening. For example, severe diarrhea due to bowel mucositis from high-dose chemotherapy can lead to electrolyte disorders and intestinal inflammation-and even bowel perforation in extreme cases. Comorbidities can exacerbate these problems. For example, patients taking thalidomide may have up to a 55% risk of constipation.[27] Added to this, if the patient is sedentary because of pain and is taking opioid medications, constipation could become severe. Certainly, even if not physically serious, these symptoms can interfere with quality of life. Intensive therapy, such as during high-dose chemotherapy and autologous stem cell transplant, generally causes a temporary decline in nutritional status and health-related quality of life.[28]

Nursing management of gastrointestinal problems in myeloma is the same as that for other cancer patients with these symptoms. The healthcare team should thoroughly assess a patient’s ability to eat and drink, the presence of nausea and/or vomiting, bowel habits, and any changes that have occurred. Pertinent physical exams and laboratory radiologic examinations need to be done that would indicate fluid and electrolyte or bowel abnormalities. Coexisting factors need to be included in the assessment and plan of care, including dietary patterns, medications taken, and physical activity. Patient and family education is extremely important, as well as medication intervention, such as a bowel regimen to prevent constipation, or antinausea and antidiarrheal medications.


 Steroids are lympholytic and are a main component of most therapy for myeloma. They can affect almost any body system, and side effects from their use are listed in 

.[17] These side effects can be exacerbated by comorbid conditions, such as neuropathy from other myeloma therapies and from the myeloma itself, pre-existing conditions such as diabetes, and others.

Discussion of all interventions for steroid-related side effects is beyond the scope of this manuscript. However, nurses should apply appropriate interventions, including patient and family education, if the side effects occur. For example, the patient should be instructed to have regular eye exams, to screen for vision changes and cataract formation. Patients should be instructed to take the steroid in the morning rather than later in the day if hyperactivity is a problem. The importance of maintaining excellent hygiene should be emphasized, as the immunosuppressive effect of steroids increases the risk of infection. Skin thinning can also lead to easy skin tears and wounds. The patient and family should be instructed to call the patient’s healthcare provider if any signs or symptoms of infection occur. Certain side effects warrant that the patient be referred to a specialist, such as an endocrinologist if the hyperglycemia is not under control, or a psychotherapist if psychological and/or sexual problems occur.


 Thromboembolic events (TE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), can affect the myeloma patient. Patients with cancer are generally at higher risk for a TE, compared with individuals without cancer, and patients with myeloma may incur TEs at an even higher incidence.[29,30] Patients with myeloma are at risk because of individual risk factors, as well as antimyeloma treatment  agents. For example, obesity, immobility, smoking, chronic renal disease, diabetes, and estrogenic agents add to the risk of TEs.[31]

In some patients, the presence of a hyperviscosity syndrome may increase the risk of TEs even further. Up to 5% of patients have a hyperviscosity syndrome; it occurs most commonly in those with the IgM subclass of myelo­ma.[13,32] The blood is so viscous that it starts to inhibit blood flow to vital organs, such as the brain and kidneys. In hyperviscosity syndrome, the myeloma patient may present with neurologic abnormalities, vision changes, and mucosal bleeding; in some cases, the syndrome can lead to seizures and coma. Heart failure symptoms (eg, dyspnea, chest pain, etc) also may be present.[32] Physical findings in combination with serum viscosity levels 45 cp (centipoises) or higher (normal range: 1.4–1.8 cp) are used to confirm suspect hyperviscosity. Serum hyperproteinemia is present, and a peripheral blood smear may reveal rouleaux formation of red cells (resembling a pile of coins). This situation is considered a medical emergency. Aggressive hydration, diuresis, and emergent placement of an apheresis catheter usually are required, followed by plasma exchange to reduce blood viscosity (by decreasing the immunoglobulin concentration).[8,32]

Nurses should ascertain a particular patient’s risk for TEs at any given time throughout the care trajectory. In general, unless the patient is very active physically, hospitalized patients should be prescribed a prophylactic anticoagulation therapy.[31,33] Prophylactic anticoagulation is recommended for all patients who are receiving thalidomide-based therapy or lenalidomide with dexamethasone.[8,33]

Selected Education and Support Resources for Patients With Myeloma, and Their Families 


 Renal insufficiency or failure occurs in up to 25% of patients with myeloma and is a poor prognostic factor of the disease.[13] The cause is multifactoral. It includes hyperuricemia and infiltration of the kidney by plasma cells; deposition of myeloma monoclonal light chains in the kidney; hyperviscosity; poor hydration and volume depletion; urinary tract infection and sepsis; and nephrotoxicity from certain antibiotics, NSAID medications, IV contrast dyes and bisphosphonates, hypercalcemia, and nephrocalcinosis.[13,32] Nursing care goals are to maintain or improve kidney function. The nurse needs to be judicious in making sure that interventions do not compound the problem, by reviewing a patient’s kidney function (laboratory values, intake and output, weight changes, presence of edema, etc.) prior to administration of medications and fluids. Patients need to be coached about the importance of fluid balance and cautioned regarding over-the-counter medications that can contribute to renal dysfunction, such as NSAIDs, as well as effects from IV contrast agents. Renal dialysis may be indicated for patients with chronic renal failure.


 From the moment of diagnosis, myeloma patients face serious life-altering decisions and realize that they are in for a lifelong battle against the disease. Patients with myeloma are living longer, often with pronounced symptoms either from the disease or treatment. These symptoms can substantially reduce their quality of life. Care aims are to treat the disease, prolong survival, and maximize the quality of life. Cancer survivors who are informed about their options and who feel they have more personal control over their decision-making and care generally perceive a higher quality of life than those who feel less informed and less in control.[34] Nurses can help to guide the myeloma patient and family through this long journey.

Unfortunately, few myeloma-specific randomized controlled trials include health-related quality of life as a study end point. However, inference can be made from research that has been done. These results can assist practitioners in developing myeloma-specific evidence-based quality-of-life plans of care.[35]

Articles

The availability of a wide variety of treatments for multiple myeloma   allows healthcare providers to tailor treatments to individual patient needs, and has enabled prolonged survival of patients with the disease. 

Current Diagnosis and Management of Multiple Myeloma

 Denosumab (marketed as Xgeva for this indication)

Drug is indicated for the prevention of skeletal-related events (SREs) in adult patients with bone metastases from solid tumors. SREs include pathological fractures, radiation or surgery to the bone, and spinal cord compression related to cancer. Denosumab is 

 indicated for the prevention of skeletal-related events in patients with multiple myeloma.

Denosumab is an IgG2 monoclonal antibody that inhibits osteoclastic bone resorption (breakdown) via inhibition of RANKL (receptor activator of nuclear factor-kB ligand). It does this by binding to RANKL, thus preventing RANKL from activating its receptor RANK on the surface of osteoclasts and their precursors. It mimics the effect of the RANK modulator osteoprotegerin, and turns off osteoclast formation, function, and survival. The net effect is increased bone mass and strength in both trabecular and cortical bone.

After subcutaneous administration, 62% of the drug is bioavailable. In oncology patients with bone metastases, every-4-week dosing of 120 mg resulted in up to a 2.8-fold increase in serum denosumab concentrations, with steady state achieved by 6 months. The mean elimination half-life is 28 days. In patients with renal impairment, there was no change in pharmacokinetics or pharmacodynamics of the drug. However, no studies have been done on patients with hepatic impairment.

• Correct hypocalcemia prior to starting denosumab. Monitor serum calcium levels prior to treatment, and ensure adequate supplementation with calcium and vitamin D.

• Perform an oral exam and discuss with the provider referral of the patient to a dentist, to complete appropriate preventive dentistry prior to starting the drug, as osteonecrosis of the jaw (ONJ) is a rare complication of therapy.

• Drug is administered subcutaneously, at 120 mg/1.7 mL (70 mg/mL) every 4 weeks (in the upper arm, upper thigh, or abdomen). Store drug in refrigerator, and bring to room temperature prior to administration (15–30 min).

• Administer calcium, vitamin D, and magnesium supplements as necessary to treat or prevent hypocalcemia.

• Monitor serum calcium levels more frequently when patient is receiving other drugs that may cause hypocalcemia, has a creatinine clearance < 30 mL/min, or is receiving dialysis.

• Cancer may spread to your bones. This drug helps to prevent bone damage by stopping bone cells called osteoclasts from breaking down your bone. This helps your bones stay bigger and stronger. Because this drug can lower the amount of calcium in your blood that normally comes from bones, you will need to take calcium and vitamin D supplements.

• Report right away any signs or symptoms of hypocalcemia: pins and needles in your hands, feet, or face (paresthesias), muscle stiffness, twitching, spasms, or cramps.

• The medicine may rarely cause dying of the cells in your jaw bone. This is called osteonecrosis of the jaw (ONJ). To minimize the risk of ONJ, your doctor will examine your mouth before you start your treatment, and if needed, will ask you to see your dentist to complete any dental work before you start therapy. Studies have shown that risk factors for ONJ are tooth extraction right before or during treatment, poor oral hygiene, or use of a dental appliance. Thus, it is important to have any dental work completed prior to starting the drug, and to take good care of your teeth (for example, by brushing your teeth twice daily).

• During treatment, avoid any invasive dental procedures. Report right away any jaw or tooth pain, or changes in your teeth or gums.

• No formal studies have been performed, but there is no apparent effect from concurrent chemotherapy or hormonal therapy.

• Drug may cause fetal harm. If a woman becomes pregnant while receiving the drug, she should be encouraged to enroll in Amgen’s Pregnancy Surveillance Program (1-800-77-AMGEN).

• The drug should be used in a pregnant woman only if the potential benefit is greater than the risk. In studies of laboratory animals that lacked the 

 gene, their offspring had lymph node abnormalities, and impaired dentition and bone growth.

• Mothers should not breastfeed their infants, and a decision should be made regarding whether the patient should discontinue nursing or the drug. It is not known if the drug is excreted in human milk. In laboratory animals, mother mice lacking the 

 gene had impaired mammary gland development and abnormal lactation.

• In clinical trials, although the incidence of ONJ was 2.2% with the drug, 79% of affected patients had a 
 history of tooth extraction, poor oral hygiene, or use of a dental appliance.

– Ensure that patient has had oral dentition problems corrected.

– Assess risk for ONJ: prior tooth extraction, persistent pain or slow healing of the mouth or jaw after dental surgery.

– Assess serum calcium and phosphate levels; correct hypocalcemia.

– Ensure that patient is taking recommended calcium and vitamin D supplements.

– Monitor serum calcium and phosphate levels regularly, and more frequently in patients with creatinine clearance < 30 mL/min or who are receiving dialysis.

– Assess for signs/symptoms of hypocalcemia (paresthesias, muscle stiffness, twitching, spasms, cramps) or hypophosphatemia (weak muscles, muscle dysfunction, dysphagia, altered mental status, irritability).

– Assess for changes in dentition, and presenting signs/symptoms of ONJ: jaw pain, (eg, osteomyelitis, osteitis), bone erosion, tooth or periodontal infection, toothache, gingival ulceration, or gingival erosion.

– If ONJ is suspected, discuss with the physician referral of the patient to a dentist or oral surgeon.

Clinical trials comparing denosumab with zoledronic acid showed denosumab was noninferior to zoledronic acid in first time to SRE; two of the trials showed denosumab was superior in delay to time to first SRE and subsequent SRE, compared with zoledronic acid. There was no difference in overall survival between the two groups. While patients with multiple myeloma were included in one of the trials, a subgroup analysis showed a higher mortality in the denosumab-treated group. Thus, denosumab is not indicated for patients with multiple myeloma at this time. Further investigation of denosumab safety and efficacy in patients with multiple myeloma is planned.

Adverse Reactions to Denosumab by Body System

(boldface type indicates more common events, with 25% or higher incidence)

Endocrine: Hypophosphatemia (severe in 15.4%),

Fetal harm, abnormal breast development and lactation in nursing mothers 

Osteonecrosis of the jaw (ONJ) in 1.8% of patients

The author has no significant financial interest or other relationship with the manufacturers of any products or providers of any service mentioned in this article.

Denosumab is an IgG2 monoclonal antibody that inhibits osteoclastic bone resorption (breakdown) via inhibition of RANKL (receptor activator of nuclear factor-kB ligand).

Denosumab, a RANK Ligand Inhibitor for Prevention of Skeletal-Related Events Due to Bone Metastases From Solid Tumors in Adults

The recent Centers for Disease Control and Prevention (CDC) report carrying good news about cancer sur­vivorship is an urgent “heads up” for all of us in cancer care.[1] The report states that between the years 1971 and 2001, the number of cancer survivors increased by more than three-fold (from 3 million to nearly 10 million). Only 6 years later (between 2001 and 2007), the survivor cohort had increased again, to nearly 12 million. Besides  changing numbers, the report depicts an evolving face of cancer survivorship. Consider the following findings[1]:

•	Nearly 60% of all survivors are over 65 years of age. The majority of cancer survivors are elderly females, as older women with breast cancer (65–84 years of age) represent the largest subset of survivors.
 •	Females account for the largest segment of survivors at 5, 15, and 25 years; more than 75% of survivors at 25 years are female. 
 •	Survival of a solid tumor (ie, breast, prostate, colorectal) accounts for 51% of all survivors.
 •	Approximately one-third (35.2%) of survivors are middle-aged, with most in this age group having survived melanoma, thyroid cancers, and cervical cancers.

Also of note is another recent major report addressing the cost of cancer.[2] In the United States, treatment of the most common cancers-breast, prostate, and colorectal malignancies-represents the largest national expenditure by cancer site. The current cost of cancer is nearly $125 billion (compared with $104 billion in 2006), with a projected cost escalation of 27% anticipated by the year 2020.[2,3]

A caveat is in order. We need to remember that the recent CDC report was based on data up to the year 2007. Researchers estimate that there were 13.8 million cancer survivors in the US in 2010.[2] Based on 2010 US Census Bureau data, this would be equivalent to the populations of Colorado and New Jersey being cancer survivors.[4] With the advent of programs and initiatives directed at prevention and wellness, early screening, and genetic breakthroughs, it could be that our future will require us to care for more cancer survivors than patients undergoing active treatment.

All cancer care professionals must embrace cancer survivorship as a critical element of our specialty. With its escalation in prominence come concerns about detecting second and third primaries in cancer survivors, the potential predominance of new long-term effects, and a dire need for rehabilitation programs and an infusion of geriatric expertise.

How best to ready yourself for a new future of cancer care? Start by becoming attuned to your patients’ needs following the cessation of first-line treatment. Develop a better awareness of the cost of therapies that you are delivering. Keep up with issues in women’s health. Enhance your proficiency in eldercare. All these approaches are a must, as the future is now.

 Centers for Disease Control & Prevention: Cancer survivors-United States, 2007. 

Mariotto AB, Yabroff KR, Shao Y, et al: Projections of the cost of cancer care in the United States: 2010-2020. 

 National Cancer Institute: Cancer Trends Progress Report-2009/2010 Update: Costs of Cancer Care. Available at: 

United States Census Bureau: 2010 Resident Population. Available at: 

The recent Centers for Disease Control and Prevention (CDC) report carrying good news about cancer sur­vivorship is an urgent “heads up” for all of us in cancer care. The report states that between the years 1971 and 2001, the number of cancer survivors increased by more than three-fold (from 3 million to nearly 10 million).

Our New Future

Multiple myeloma (myeloma) is a highly treatable disease, but it remains incurable in the majority of cases. It is a heterogeneous disease with variability in its clinical presentation, treatment options, and prognosis. The majority of patients newly diagnosed with myeloma are over 65 years of age, and most of these patients have one or more comorbid conditions.[1,2] Systemic chemotherapy is the treatment of choice, with local radiotherapy indicated for treatment of skeletal disease or plasmacytomas.

Documented studies in myeloma treatment date back to the early 1960s, when oral melphalan and prednisone were found to be effective in producing remissions in about 30% of treated patients.[3] During the last 15 years, a number of novel agents have been developed based on improved understanding of the pathobiology of the disease and identification of potential targets, offering improvements in response rates, overall survival, and disease control.

Death rates have decreased by 11.3% for women and 7.25% for men between 1991 and 2005.[2,3] Yet there are wide variations in treatment response and survival, ranging from a few months in some cases to more than 10 years. Twenty percent of patients survive longer than 10 years, irrespective of therapy. High-risk attributes are thought to play a primary role in the expected survival of patients with myeloma.[4] Novel agents such as bortezomib (Velcade), lenalidomide (Revlimid), and thalidomide (Thalomid) may neutralize the effects of some high-risk features. Numerous ongoing clinical trials offer promising therapies for their future use, either as single agents or in combination. There were 46 different clinical trials with 6,149 patients enrolled internationally between 1999 and 2009 for induction therapy alone.[5] The present challenges are how to integrate the best combinations of new and old drugs used for initial induction therapy, determine transplant eligibility at the time of diagnosis, and more recently, how best to incorporate maintenance therapy to achieve long-term disease control.

Refinement of the diagnostic evaluation and application of prognostic criteria has led to a risk-adapted treatment approach that introduces the concepts of personalized or precision medicine.

Critical to instituting the most effective therapy early in the course of disease is application of an organized, evidenced based, risk-adapted treatment plan; this plan needs to incorporate key diagnostic elements using a lifespan approach that considers individual patient attributes, including comorbidities. Selection of pretransplant therapies for eligible patients is important, to limit the potential for bone marrow damage and inadequate stem cell collection.

Understanding novel mechanisms of antitumor activity, associated toxicities, and clinical strategies related to myeloma is critical to safe and effective patient management. Many of the emerging therapies may be administered over extended periods of time, and most allow patients to be treated in an outpatient setting. Their toxicities are manageable; an understanding of the unique mechanisms of action and associated side effects of these agents is required.

Effective treatment of the disease-related systemic problems presents another challenge for the patient with myeloma. Supportive care strategies are critical to achieving the best clinical outcome when treating myeloma. However, even supportive care strategies may be associated with adverse events. Elderly patients are particularly at risk of these symptoms and should be monitored carefully while receiving treatment.

Much of the nursing care provided to patients with myeloma is targeted at treating the skeletal, hematological, renal, and infectious complications of the disease. Management of treatment-related adverse events including fatigue, thromboembolism, neuropathy, pain, osteonecrosis, and gastrointestinal toxicities presents additional challenges. The oncology nursing professional is critical to effective management of these disease- and treatment-related adverse events. Oncology nurses also play a central role in coordinating the complex diagnostic process, translating the results for the patient and family, including setting expectations for the immediate treatment plan. Given the chronic nature of this disease, early identification and prompt intervention for disease- or treatment-related adverse events will preserve future treatment options and promote improved quality of life. The article by Sandra Rome provides a clinically relevant and concise overview of the diagnostic staging, risk-adapted treatment selection, and current strategies for supportive care of the patient with multiple myeloma.

 Kurtin S: Laboratory measures for the diagnosis, clinical management, and evaluation of treatment response in multiple myeloma. 

 Jemal A, Siegel R, Ward S, et al: Cancer Statistics 2009. 

 Badros A: In the age of novel therapies, what defines high-risk multiple myeloma? 

 Kurtin S: Risk analysis in the treatment of hematological malignancies in the elderly. 

 Durie BG: Role of new treatment approaches in defining treatment goals in multiple myeloma -the ultimate goal is extended survival. 

Multiple myeloma (myeloma) is a highly treatable disease, but it remains incurable in the majority of cases. It is a heterogeneous disease with variability in its clinical presentation, treatment options, and prognosis.

Advances and New Challenges in Multiple Myeloma

 of the Araliaceae family that is an important part of traditional Chinese medicine (TCM).[1] It is termed an “adaptogen,” as it is believed to have properties that help to restore balance to the body and protect the body from physiologic stress.[1,2] There are two main types of ginseng: Asian (Chinese or Korean) ginseng, called 

.[3] Both Asian and American ginseng have a common mixture of active ingredients, called ginsenosides, although the concentrations of each ginsenoside are slightly different.[4]

Ginsenosides are plant saponins, or steroid-like compounds. More than 150 ginsenosides have been identified from ginseng roots, leaves, stems, berries, and flowers.[5] Based on different ginsenoside compositions, in TCM, Asian ginseng has properties ascribed to it as “yang,” or a ”hot herb,“ whereas American ginseng is thought to be a “yin,” or a ”cooling herb.“[1,2] Siberian ginseng, called 

, is often marketed as a ginseng product with properties similar to Asian and American ginseng, but it is actually from a different plant genus.[1] This article will focus on Asian and American ginseng.

Ginseng is available as an extracted herb or as a dry ground root. The root is considered to be the source of ginsenosides, the active constituents. It is recommended that standardization be achieved through dosing of 0.5–2 grams daily of dry root or equivalent extract, with a 4%–5% ginsenoside content. Extraction can be done with water or alcohol, and the properties of ginseng are affected by the way that it is extracted and processed.[6,7]

American ginseng is native to North America. It was introduced to European settlers by Native Americans in the early 1700s, and harvested in large quantities and exported from the US to Asia beginning in the 1800s. More than 90% of cultivated ginseng grown in the US is grown in Wisconsin, because the state’s climate and mineral-rich soil provide optimal conditions for growing healthy ginseng roots. Wisconsin farmers began cultivating ginseng in the 1900s.[1,8]

A minimum of 3 years, preferably 4 years, is required to grow the roots before they can be harvested. The seed beds must be protected from the sun in the summer and from the cold in the winter. The berries are harvested by hand and de-pulped. The seeds are washed, dried, and buried until the next summer, when they are planted. The roots are also then harvested by hand, refrigerated 10–20 days, and then washed and put on racks for drying. The drying process takes 14 days. How the cooling, washing, and drying are done contribute to the quality of the herb.[8]

 (Asian) ginseng is > 5,000 years old, initially from the Manchurian mountains in China.[1] Currently, Asian ginseng can be from Korea or China. White Asian ginseng is dried, unprocessed root, whereas red ginseng is derived from steam processing. The heat is thought to increase the potency of the ginseng. Asian ginseng also has to grow for at least 5 years in order for the roots to mature.

Because of the long growing time required for mature ginseng, the labor-intensive cultivation process, and changes in the plant’s natural growing habitat, the ginsenoside concentrations and quality of this herb can be quite variable.[9,10]

” means “all-heal” in Greek.[1] With more than 150 identified ginsenosides and other active components such as polysaccharides, all with biologic properties, it is easy to appreciate ginseng’s reputation for widespread use.[2] Ginseng has been used to improve the immune system, cognition, several aspects of fatigue, appetite, physical performance, anemia, glucose regulation, digestion, and sexual performance, and to decrease stress. Various properties of ginseng are being studied as a cancer treatment, particularly for breast and colorectal cancer.

What Is the Evidence Related to Ginseng and the Needs of Cancer patients and Survivors?

Ginseng may be one of the most widely studied herbs. A recent literature search covering the past 6 years yielded 992 references related to ginseng. Most of the published literature falls into the category of basic science, and Asian and American ginseng appear to be equally studied. However, studies in humans, particularly controlled trials, are lacking.

Various in vitro and animal studies have delineated properties of specific ginsenosides. The ginsenoside Rb1 has demonstrated activities consistent with neural and neurocognitive protective effects, such as modulating sodium channels,[11] protecting striatal neurons from 3-nitropropionic acid–induced damage,[12] stimulating neurosecretory cells (eg, dopamine and glutamate),[13] and modulating gaba-aminobutyric acid (GABA) neurotransmission.[14]

Properties that may indicate ginseng has a role in fatigue include both stimulatory and anti-inflammatory effects. The Rg1 and Rb1 ginsenosides have been linked to exercise performance in rats.[15] In MCF-7 human breast cancer cells, a hot-water extract of American ginseng inhibited growth through inhibition of the mitogen-activated protein kinase (MAPK) pathway,[16] a cell-signaling pathway that is upregulated in response to proinflammatory cytokines. Increases in inflammatory cytokines have been associated with fatigue.[17] With regard to anticancer activity, in cell cultures of ER+ breast cancer tissue, American ginseng inhibited cell growth and was synergistc with tamoxifen, Cytoxan (cyclophosphamide), methotrexate, doxorubicin, and 5-fluorouracil.[18] Cell cultures of human colorectal cancer cells were also impacted by steamed American ginseng, which caused apoptosis, likely through mitochondrial damage.[3]

Human clinical trials published in the mid 1990s evaluating effects of ginseng on physical performance in healthy individuals were mixed and suffered from methodological weaknesses.[19–22] More recently, two pilot trials were completed in people with cancer. One study was done in a population of chemonaive patients receiving chemotherapy: during treatment they were randomized to Asian ginseng at a dosage of 250 mg three times per day, or to a placebo. The group that received ginseng reported significantly less fatigue, as measured by the Brief Fatigue Inventory. However, this study was very small (N = 20) and was only reported in abstract form.[23] Another pilot trial evaluated three doses of American ginseng vs a placebo in a heterogeneous group of 290 cancer survivors. Improvements on the Brief Fatigue Inventory and Vitality subscale of the SF-36 were higher for patients who received the two larger ginseng doses (1,000 or 2,000 mg/day) than those on placebo or 750 mg/day of ginseng.[24] A large phase III trial of more than 360 patients is being conducted by the North Central Cancer Treatment Group and will likely be completed this summer, evaluating 2,000 mg of American ginseng vs placebo for fatigue.

Two studies have been published evaluating effects of ginseng on cognition. One small, randomized, double-blind trial assessed its effects on cognitive function in 32 healthy adults. Three doses of American ginseng (100, 200, and 400 mg) were tested and compared with placebo. A battery of neuropsychiatric tests was performed before treatment and at 1, 3, and 6 hours after the study subjects had consumed the ginseng. The most consistent results were an improvement in working memory with 200- and 400-mg doses.There were no adjustments made for multiple endpoints, and several areas of cognition were evaluated.[25] A larger study that was not placebo-controlled evaluated 4.5 grams per day of Asian ginseng in 58 people diagnosed with Alzheimer’s disease. The investigators included a control group of 39 people who were age- and gender-balanced. The primary endpoint was the mini–mental state examination (MMSE) and Alzheimer disease assessment scales (ADAS). The group receiving ginseng improved slightly on the MMSE over a period of 12 weeks, while MMSE scores in the control group declined slightly. A similar improvement in the ginseng group and loss in the control group was demonstrated with scores on the cognitive subscale of the ADAS.[26] Effects of ginseng related to cancer have not been explored.

Finally, an epidemiologic study done in Shanghai with a cohort of 1,455 women with breast cancer suggested that current use of ginseng was associated with better quality of life scores, particularly those related to psychological and social well being. The investigators also found that regular use of ginseng was associated with a reduced disease-free and overall survival rate, compared with nonusers. This study did not report on the dose of ginseng used, but it did include various types of ginseng. The analysis adjusted for age at diagnosis, hormone receptor status, surgery, and several other treatment variables.[27]

American ginseng is categorized as a class I herb using the American Herbal Products Association Safety Rating, which means that it is considered generally safe if used appropriately.[28]

In a journal article evaluating American ginseng for diabetes, doses of up to 3 grams daily did not yield any side effects.[29] In a dose-finding, placebo-controlled trial evaluating 750–2,000 mg of American ginseng as a possible treatment for cancer-related fatigue, there were no differences between the ginseng and placebo arms in terms of any reported adverse event or self-reports of nausea, insomnia, headaches, anxiety, nervousness, or dizziness over 8 weeks of use.[24] Some articles report the possibility of insomnia, but there are no published trial data to support this.

 ginseng performed in men and women with Alzheimer’s disease reported side effects of “heat-sense,” dizziness, nausea, anorexia, headache, and diarrhea in 7 of 58 patients taking 4.5 grams/day of ginseng over a period of 12 weeks.[26]

There have been some reports that ginseng has estrogenic properties and should, therefore, not be used by people who need to avoid estrogen.[1] This property is likely due to two issues. The first relates to an identified fungus on the roots, which in one study did not account for adverse events, but may be associated with possible estrogenic activity.[30] The second relates to the extraction method. Alcohol extraction confers estrogenic properties to the ginseng and should be avoided, especially by those for whom estrogen is contraindicated. Consumers should be aware of the type of ginseng they are purchasing, including whether it is ground root or an extract. Using larger, more established companies and contacting them to obtain this information would be advised.

), a nonprofit organization of Wisconsin ginseng growers, lists companies in the US and overseas that sell USDA-graded Wisconsin ginseng, tested for pesticide residues.

With respect to cytochrome P450 activity, American ginseng has not been found to inhibit any CYP450 pathways.[1,31–33] There is limited evidence that Asian ginseng may activate CYP3A4 or inhibit CYP2D6 in vitro, but at this time, it is not believed that the effects have any clinical relevance.[1] Both pathways are important for drug metabolism.

Safety during pregnancy has not been established. One study using a whole rat embryo culture model found evidence of teratogenicity attributable to the ginsenoside Rb1, a component of both Asian and American ginseng.[34]

Established and emerging data demonstrate some mechanisms of action of ginseng that would be consistent with its having positive effects on cancer as a disease, and on some common symptoms experienced by cancer survivors: namely, cognitive deficits, fatigue, and neuropathies. However, clinical trials in survivors are lacking. There are very limited pilot data and epidemiologic data in cancer survivors supporting the benefits of ginseng in fatigue and overall well being. There are also limited pilot data in Alzheimer’s disease and in healthy adults that support its benefits in cognition. More research is needed to clarify the role of ginseng in cancer, and to definitively determine appropriate dosing, side effects, and drug interactions. Standardization and quality of this herb are also potential concerns.

The author has received American ginseng and placebo from the Ginseng Board of Wisconsin, a nonprofit organization, for two studies of ginseng in cancer patients.

 Natural Standard: Natural Standard Ginseng monograph. Available at: 

Attele AS, Wu JA, Yuan CS: Ginseng pharmacology: multiple constituents and multiple actions. 

 Li B, Wang CZ, He TC, et al: Antioxidants potentiate American ginseng-induced killing of colorectal cancer cells. 

 Wang X, Sakuma T, Asafu-Adjaye E, et al: Determination of ginsenosides in plant extracts from 

 Christensen LP: Ginsenosides chemistry, biosynthesis, analysis, and potential health effects. 

Gafner S, Bergeron C, McCollom MM, et al: Evaluation of the efficiency of three different solvent systems to extract triterpene saponins from roots of 

 quinquefolius using high-performance liquid chromatography. 

 King ML, Adler SR, Murphy LL: Extraction-dependent effects of American ginseng (

 quinquefolium) on human breast cancer cell proliferation and estrogen receptor activation.

 Ginseng Board of Wisconsin: [information about ginseng, its cultivation, and selected research into possible health benefits]. Available at: 

 Harkey MR, Henderson GL, Gershwin ME, et al: Variability in commercial ginseng products: An analysis of 25 preparations. 

 Schlag EM, McIntosh MS: Ginsenoside content and variation among and within American ginseng (

 Liu D, Li B, Liu Y, et al: Voltage-dependent inhibition of brain Na(+) channels by American ginseng. 

 Lian XY, Zhang Z, Stringer JL: Protective effects of ginseng components in a rodent model of neurodegeneration. 

 Lee SD, Lo MJ: Ginsenoside Rb1 promotes PC12 cell cycle kinetics through an adenylate cyclase-dependent protein kinase A pathway.

 Yuan CS, Attele AS, Wu JA, et al: Modulation of American ginseng on brainstem GABAergic effects in rats. 

 Wang LC, Lee TF: Effect of ginseng saponins on exercise performance in non-trained rats. 

 quinquefolius L.) extract alters mitogen-activated protein kinase cell signaling and inhibits proliferation of MCF-7 cells.

 Collado-Hidalgo A, Bower JE, Ganz PA, et al: Inflammatory biomarkers for persistent fatigue in breast cancer survivors. 

 Duda RB, Zhong Y, Navas V, et al: American ginseng and breast cancer therapeutic agents synergistically inhibit MCF-7 breast cancer cell growth. 

 Allen JD, McLung J, Nelson AG, et al: Ginseng supplementation does not enhance healthy young adults’ peak aerobic exercise performance.

 Engels HJ, Wirth JC: No ergogenic effects of ginseng (

 ginseng C.A. Meyer) during graded maximal aerobic exercise. 

 Pieralisi G, Ripari P, Vecchiet L: Effects of a standardized ginseng extract combined with dimethylaminoethanol bitartrate, vitamins, minerals, and trace elements on physical performance during exercise. 

 Ziemba AW, Chmura J, Kaciuba-Uscilko H, et al: Ginseng treatment improves psychomotor performance at rest and during graded exercise in young athletes. 

Ginseng is an herb from the genus Panax of the Araliaceae family that is an important part of traditional Chinese medicine (TCM). It is termed an “adaptogen,” as it is believed to have properties that help to restore balance to the body and protect the body from physiologic stress.

Ginseng

Cognition is a highly sophisticated, multifactorial, interrelated set of neurologic functions responsible for attention, perception, memory, learning, language, and thinking. One’s ability to perceive, recognize, register, store, and use information represents distinct entities of cognition.[1] Illness, medical therapies, and the aging process can negatively affect cognition.

 ADMINISTERING THE 
MINI-COG 
 Instruct the patient to listen carefully and remember three unrelated words. Then ask him or her to repeat the words. Next, ask the patient to draw the face of a clock on a blank piece of paper, adding the numbers and the hands of the clock to reflect a specific time. Then ask the patient to repeat the three words. 

Scoring for the CDT is normal if all numbers are present in the correct sequence and position on the clock, and the hands readably display the requested time. Inability to perform the tasks warrants further evaluation, as does inability to recall all three words. 

Age-related alterations in the brain include morphologic changes in cerebral tissues, reduced blood flow, and neurotransmitter changes.[2] Volumetric reduction in brain size and gray and white matter shrinkage increase with advanced age. Despite degenerative brain changes, however, the adult brain is resilient and able to undergo successful cortical remodeling, resulting in healthy older brains.

In caring for older cancer patients, it is critical to establish the presence of cognitive impairment.


Compromise of cognitive capability can influence treatment tolerance, symptom distress management, and overall quality of life. Older patients with cognitive impairment may have difficulty in articulating their symptoms (some of which may be manifestations of pathological conditions) to the healthcare provider, and in reporting on the effectiveness of treatment interventions. Cognitive impairment may deter patient learning by interfering with information reception, retention, and synthesis, particularly in terms of the patient’s understanding of self-care strategies communicated by the healthcare provider. It also may affect the cancer patient’s capacity to make decisions regarding treatment and care planning, may increase the patient’s feelings of discomfort and distress, and may negatively impact the patient’s relationships with family members.

Healthcare professionals routinely fail to assess patients’ cognitive function. In the absence of obvious pathology, assumptions as to cognitive intactness generally are made that often lead to clinical problems and ethical dilemmas.Routine assessment can detect early signs of cognitive compromise, which in turn can prompt appropriate intervention planning. Given the frequency and intensity of interactions with patients, nurses are instrumental in the determination of cognitive function.[3]

SUGGESTED READINGS FOR A GERIATRIC ONCOLOGY NURSING JOURNAL CLUB
Esbensen BA, Swane CE, Hallberg IR, et al: Being given a cancer diagnosis in old age: A phenomenono-logical study. 

45(3):393–405, 2008.
 
 Jansen J, van Weert J, van Dulmen S, et al: Patient education about treatment in cancer care: An overview of the literature on older patients’ needs. Cancer Nurs 30(4):251–260, 2007.
       
            Klepin HD, Danhauer SC, Tooze JA, et al: Exercise for older adult inpatients with acute myelogenous leukemia: A pilot study. 

 2(1):11–17, 2011.
 
            Mezey M, Mitty E: A bill of rights for hospitalized older adults. 

41(3):115–121, 2011.
 
 Yabroff KR, Lamont EB, Mariotto A, et al: Cost of care for elderly cancer patients in the United States. 


While a decline in cognitive function is a hallmark of aging, pathological variations in human brain anatomy are not.[4] Delirium and dementia represent abnormal neurologic processes. Oncology nurses should be aware of five cardinal characteristics that differentiate dementia from delirium.[5] A comparison of these two conditions is provided in 

Delirium has a sudden onset, and it is characterized by a fluctuating, yet time-limited course of symptoms (including disorientation to time and place) and memory impairment specific to recent events. Dementia is characterized by an insidious, progressive course (over months to years), with symptoms that remain constant over time, and generalized memory impairment (with respect to both recent and remote events).


Tools that oncology nurses can use to assess cognitive function focus on screening, not diagnosis. They are characterized by their brevity and appropriateness of use in clinical practice, and serve to alert practitioners to potential pathology. While the Folstein Mini-Mental Status Exam (MMSE) has been the gold standard, a more contemporary tool has relevance for oncology nurses.

The Mini-Cog is a screening tool comprising a three-item recall test combined with the Clock Drawing Test (CDT). It takes 3 minutes to administer and is not biased by language, education level, culture, and ethnicity (see sidebar, “Administering the Mini-Cog”). Again, this is a screening tool whose results warrant more advanced neuropsychological testing when abnormal findings are identified.

Determination of cognitive status as an element of symptom distress should be a usual corollary of oncology nursing assessment (see box, “Suggested Readings for a Geriatric Oncology Nursing Journal Club,” for additional resources). Alterations in cognition have the potential to significantly interfere with quality of life in the older adult with cancer.

Geriatric Oncology Articles on CancerNetwork.com

Care of the Older Adult With Cancer: The Geriatric Oncology Nursing Imperative 

 February 2011, Deborah A. Boyle, RN, MSN, AOCNS, FAAN              
                               •             

Multiple Myeloma in the Elderly: When to Treat, When to Go to   Transplant

 November 2010, Jean-Luc Harousseau, MD 
                               •             

Geriatric Assessment, Communication Skills Essential for Older Patients 

August 2010, Shalmali Pal
                               •             

Bone Complications of Cancer Treatment in the Elderly

 August 2010, Lodovico Balducci, MD
                               •             

Screening for Emotional Distress in Older Patients With Lung Cancer

 April 2010, Terry Badger, PhD, PMHCNS-BC, FAAN, Virginia T. LeBaron, MS, ACNP-BC, AOCN, ACHPN, Ruth McCorkle, PhD, RN, FAAN 

 Foreman MD, Vermeersch PE: Measuring cognitive status, in Frank-Stromberg M, Olsen SJ (eds): Instruments of Clinical Health Research, ed 3. Boston, Jones and Bartlett, 2004, pp 100â127.
  

 Struble LM, Sullivan BJ: Cognitive health in older adults. 

 Braes T, Milisen K, Foreman MD: Assessing cognitive function, in Capezuti T, Mezey M, Fulmer T (eds): Evidence-Based Geriatric Nursing: Protocols for Best Practice. New York, Springer Publishing, 2008.
  

Cognition is a highly sophisticated, multifactorial, interrelated set of neurologic functions responsible for attention, perception, memory, learning, language, and thinking.

ONCOLOGY Nurse Edition Vol 25 No 4 | Oncology Nurse Edition

Current Diagnosis and Management of Multiple Myeloma

Denosumab, a RANK Ligand Inhibitor for Prevention of Skeletal-Related Events Due to Bone Metastases From Solid Tumors in Adults

Our New Future

Advances and New Challenges in Multiple Myeloma

Ginseng

Cognitive Impairment in Older Adults With Cancer

An Infusion Reaction to Cetuximab