Interventions for clients with white blood cell disorders

 

Interventions for clients with white blood ncell disorders

 

WHITE BLOOD CELL DISORDERS

As discussed iChapter 20, white blood cells (WBCs), or leukocytes, provide protectiofrom invading non-self cells and cancer cells in several ways. These protective nfunctions depend on maintaining normal numbers and ratios of many specific nmature, circulating leukocytes. When any one type of WBC is present in either nabnormally high or abnormally low amounts, hematopoietic function and immune nfunction may be altered to some degree, placing clients at risk for specific ncomplications. This section covers the pathologic changes and nursing care nrequirements for clients with disorders involving overgrowth of specific types nof WBCs.

LEUKEMIA

OVERVIEW The nleukemias are a group of malignant disorders involving abnormal overproductioof a specific WBC type, usually at an immature stage, in the bone marrow. Leukemia nmay be acute, with a sudden onset and short duration, or chronic, nwith a slow onset and persistent symptoms over a period of years. Leukemias nare categorized by the specific maturational pathway from which the abnormal ncells arise (Dietz, 1999). Leukemias in which the abnormal cells arise from nwithin the committed lymphoid maturational pathways are lymphocytic or lymphoblastic. nLeukemias in which the abnormal cells arise within the committed myeloid nmaturational pathways are myelocytic or myelogenous. Several nsubtypes exist for each of these diseases, which are classified according to nthe degree of maturity of the abnormal cell and the specific cell type involved n(Table 40-4).

Pathophysiology The basic problem in leukemia is a malignant ntransformation of the stem cells or early committed precursor leukocyte cells, ncausing an abnormal proliferation of a specific type of leukocyte. The nfunctionally and structurally abnormal immature leukocytes, produced iexcessive quantities in the bone marrow, essentially shut dowormal bone nmarrow production of erythrocytes, platelets, and other mature leukocytes. This nsituation leads to anemia, thrombocytopenia, and leukopenia of the unaffected nWBC types, even though the number of immature, abnormal WBCs in the circulatiois greatly elevated (Dietz, 1999). Without treatment, the client usually dies nof infection or hemorrhage. For clients with acute leukemias, these pathologic nchanges occur rapidly and, without intervention, progress quickly to death. nChronic leukemia may be present for many years before overt pathologic changes noccur (Pittinger, 1999).

 Etiology nEpidemiologic studies suggest that many different genetic and environmental nfactors may be involved in the development of leukemia. Although only a few of nthese factors have been positively identified, the basic mechanism appears to ninvolve gene damage of cells, changing those cells from a normal to a malignant n(cancer) state. The following conditions or substances are possible risk nfactors: ionizing radiation, chemicals and drugs, marrow hypoplasia (slow nfunctioning with less than the normal production rate of blood cells), nenvironmental interactions, genetic factors, viral factors, immunologic nfactors, and the interaction of these factors (Dietz, 1999). Ionizing nradiation exposure in large quantities appears to be a major risk factor. nExposures ranging from therapeutic irradiation (for such diseases as ankylosing nspondylitis and Hodgkin’s lymphoma) to environmental irradiation (such as the natomic bomb at Hiroshima or the nuclear accident at Chernobyl) have beeassociated with leukemia. Chemicals and drugs have been linked to the ndevelopment of leukemia.

 Marrow hypoplasia caincrease the risk of leukemia. A reduction or alteration in the production of nhematopoietic cells may be responsible. Examples of conditions associated with nthe later development of leukemia include Fanconi’s syndrome, paroxysmal nnocturnal hemoglobinuria during its aplastic phase, and myelodysplastic nsyndromes. Genetic factors are suspected as a cause of leukemia because nof the increased frequency of leukemia in the following populations: identical ntwins of clients with leukemia, as well as people with Down syndrome, Bloom nsyndrome, Fanconi’s syndrome, and Klinefelter’s syndrome. Chromosomal naberration may be an important factor in these syndromes (Dietz, 1999). Immunologic nfactors, especially immune deficiencies, may also favor the development of nleukemia. Leukemia among im- munodeficient people may be a result of nimmunosurveillance failure, or the pathologic mechanisms that cause the immune ndeficiency may also trigger cancer in the WBC population. Interaction of nmultiple host and environmental factors may result in leukemia. Because each nperson tolerates the interaction of these factors differently, it is difficult nto determine the origin of any specific leukemia.

 Incidence/Prevalence The nleukemias account for 2% of all newly diagnosed cases of cancer and for 4% of nall deaths from cancer (American Cancer Society, 2001). The incidence and the nfrequency of leukemia depend on many factors, including the type of WBC naffected, age, gender, race, and geographic locale. In the United States aestimated 28,800 new cases of leukemia were projected for 2001 (American Cancer nSociety, 2000).

In this country, nleukemia is categorized into any one of four basic types based on the cell type naffected and the rate of progression of the leukemia:

• Acute myelogenous leukemia n(AML) occurs with similar frequency in all ages and is the most common form nof leukemia in adults.

• Acute lymphocytic leukemia (ALL) nconstitutes about 10% of adult leukemias but is most common in children.

• Chronic myelogenous leukemia n(CML) constitutes about 20% of adult leukemias, occurring more often ipeople older than 50 years of age.

• Chronic lymphocytic leukemia n(CLL) is the rarest type of leukemia, occurring primarily in people older nthan 50 years of age. Characteristics and risk factors associated with these nfour types of leukemia are presented in Table 40-4.

 COLLABORATIVE nMANAGEMENT

Assessment

 HISTORY The nurse asks nthe client about risk factors and causative factors. Age is important because nthe incidence of adult leukemia increases with age. Occupation and hobbies may nalso reveal specific environmental exposures that increase the risk of nleukemia. Previous illnesses and the medical history may indicate exposure to nionizing radiation or medications that increase risk. Because of nleukemia-related alterations of immune function, the risk for infection is nincreased in the client with leukemia. The nurse asks about the frequency and nseverity of infectious processes (such as colds, influenza, pneumonia, nbronchitis, or unexplained episodes of fever) during the preceding 6 months n(Pittinger, 1999).

Because platelet nfunction may be diminished in people with leukemia, the client is asked about nany overt or hidden excessive bleeding episodes, such as the following:

• A tendency to nbruise easily

• Nosebleeds

• Increased nmenstrual flow

• Bleeding from nthe gums

• Rectal nbleeding

• Hematuria n(blood in the urine)

• Prolonged nbleeding after minor abrasions or lacerations

If the client nhas experienced such an episode, the nurse asks whether this type and extent of nbleeding constitute the usual response to injury or represent a change. The nclient with leukemia often experiences weakness and fatigue resulting from nanemia and increased metabolic and energy demands of the leukemic cells.

The client is nasked whether he or she has experienced any of the following:

Ø     nHeadaches

Ø     nBehavior changes

Ø     nIncreased somnolence

Ø     nDecreased alertness

Ø     nDecreased attention span

Ø     nLethargy, muscle weakness

Ø     nDiminished appetite

Ø     nWeight loss

Ø     nIncreased fatigue

Listing nactivities in the previous 24 hours may disclose additional information about nactivity intolerance, changes in behavior, and unexplained fatigue. The nurse ndetermines how long the client has had any of these debilitating symptoms.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS Because leukemia naffects all blood cells, and blood influences the health and functional ncapacity of all organs and systems, many areas remote from the actual site of norigin of malignant cells may be affected (Chart 40-8).

 

The following nclinical manifestations are associated with the acute leukemias (Cotran, Kumar, n& Robbins, 1999). Some of these findings may also be present in the client nwith chronic leukemia in the blast phase.

CARDIOVASCULAR nMANIFESTATIONS. Cardiovascular manifestations are usually related to nanemia. The heart rate may be increased and blood pressure decreased. Murmurs n(abnormal blood flow sounds through the heart) and bruits (abnormal nblood flow sounds heard over arteries) may be present. Capillary filling time nis increased.

RESPIRATORY nMANIFESTATIONS. Respiratory manifestations are primarily associated nwith anemia and infectious complications. The respiratory rate increases as the ndegree of anemia becomes greater. If respiratory tract infections are present, nthe client may experience signs and symptoms of pneumonia, including cough and nshortness of breath. Abnormal breath sounds are present on auscultation.

INTEGUMENTARY nMANIFESTATIONS. The skin and mucous membranes may manifest nabnormalities. The skin may be pale and cool to the touch as a result of naccompanying anemia. Pallor is especially evident on the face, around the nmouth, and in the nail beds. The conjunctiva of the eye also is pale, as are nthe creases on the palm of the hand (most evident when the skin over the palm nof the hand is stretched). Petechiae (raised red spots) may be present non any area of skin surface, especially the lower extremities (Dietz, 1999). nThe petechiae may be unrelated to any obvious trauma. The nurse carefully ninspects for any skin infections or traumatized areas that have failed to heal. nThe mouth is inspected for evidence of bleeding from the gums and any sore or nlesion of the oral cavity indicating infection.

GASTROINTESTINAL nMANIFESTATIONS. Gastrointestinal manifestations may be related to aincreased tendency toward bleeding and to fatigue. Weight loss, nausea, and nanorexia are common. The nurse examines the rectal area for fissures and tests nthe stool for occult blood. Many clients with leukemia have diminished bowel nsounds and constipation. Enlargement of nthe liver and spleen and abdominal tenderness also may be present from nleukemic infiltration of abdominal viscera (Chielens, 1999).

CENTRAL NERVOUS nSYSTEM MANIFESTATIONS. Cranial nerve disturbances, headache, npapilledema as a result of leukemic infiltration of the meninges or central nervous nsystem (CNS), and in advanced cases, seizure activity and coma may occur. nAlthough clients often have fever, this manifestation may be more a response to ninfection than to malignant changes in the CNS.

MISCELLANEOUS nMANIFESTATIONS. Other manifestations include bone and joint ntenderness as a result of marrow involvement and bone resorption. Leukemic cell ngrowth or infiltration may produce enlarged lymph nodes or masses.

PSYCHOSOCIAL ASSESSMENT The client with newly diagnosed leukemia nis extremely anxious, because the average layperson equates a diagnosis of any ncancer with a death sentence (Dietz, 1999). Current therapies have greatly nimproved the prognoses of most cancers, yet the public is largely unaware of nthese advances. The nurse spends time with the client and family to ascertaiwhat the diagnosis means to them and what they expect from the future. Without nknowing the client’s expectations and feelings, the nurse cannot educate and nprovide support in an individualized manner or develop a meaningful plan of ncare. A diagnosis of leukemia has dramatic implications for a person’s nlifestyle. Hospitalization for initial treatment often lasts several weeks and nmay result in boredom, loneliness, and isolation. The nurse assesses coping npatterns, including activities that the client finds enjoyable and methods that nhelp the client to relax. A plan of care to prevent diversional activity ndeficit is particularly beneficial. After initial therapy, the client may be nable to resume work, depending on his or her occupation. However, he or she noften must make adjustments to accommodate changes in functional status. nRepeated hospitalizations may also be necessary.

 LABORATORY ASSESSMENT The nclient with acute leukemia usually has decreased hemoglobin and hematocrit nlevels, a decreased platelet count, and an altered white blood cell (WBC) ncount. The WBC count may be low, normal, or elevated but usually is quite nelevated; counts of 20,000 to 100,000 are common. The client with a higher WBC ncount on diagnosis has a poorer prognosis (Dietz, 1999). The definitive test nfor leukemia includes various examinations of cells obtained from bone marrow naspiration and biopsy. The bone marrow is full of leukemic blast phase cells n(immature cells that are dividing). The composition of various proteins (antigens) non the surfaces of the leukemic cells helps diagnose the type of leukemia n(Scheinberg, Mazslak, & Weiss, 1997). Such markers include the Til protein, nthe enzyme terminal deoxynucleotidyl transferase (TDT), and the commoacute lymphoblastic leukemia antigen (CALLA). These markers also indicate nthe prognosis. Blood-clotting times and factors are usually abnormal for the nclient with acute leukemia. Reduced levels of fibrinogen and other coagulatiofactors are typical. Whole blood-clotting time (Lee-White clotting test) is nincreased, as is the activated partial thromboplastin time (aPTT). Chromosome nanalysis of the malignant bone marrow cells may identify specific marker nchromosomes to assist in the diagnosis of the type of leukemia, predict the nprognosis, and determine the effectiveness of therapy. An example is the nPhiladelphia chromosome, which is important in the diagnosis of chronic nmyelogenous leukemia (CML) (Chielens, 1999).

RADIOGRAPHIC ASSESSMENT Specific symptoms determine the need for nspecific tests. For example, in a client with dyspnea, a chest x-ray study is nneeded to determine whether leukemic infiltrates are present in the lung. nSkeletal x-ray films may help to determine whether bone resorption (loss nof bone minerals and density) is present.

Analysis

COMMON NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS The nfollowing are commoursing diagnoses for adult clients with acute myelogenous nleukemia (AML), the most common type of adult leukemia:

1. Risk for nInfection related to decreased immune response

2. Risk for nInjury related to thrombocytopenia

3. Fatigue nrelated to decreased tissue oxygenation and increased energy demands

The primary ncollaborative problem is Potential for Antineoplastic Therapy Adverse Effects.

ADDITIONAL NURSING DIAGNOSES AND COLLABORATIVE PROBLEMS Iaddition to the commoursing diagnoses and collaborative problems, clients nwith AML may have one or more of the following:

• Impaired SkiIntegrity related to prolonged immobility

• Impaired Oral nMucous Membrane related to effects of chemotherapy and pancytopenia

• Self-Care nDeficit (Total) related to progressive debilitation and weakness

• Imbalanced nNutrition: Less Than Body Requirements related to anorexia, nausea, and nvomiting

• Anxiety nrelated to fear of death

• Powerlessness nrelated to an inability to control disease progression

• Interrupted nFamily Processes related to acute, life-threatening illness of a family member

• Ineffective nRole Performance related to perceived inability to fulfill parental and other nfamily roles and prolonged hospitalization

• Deficient nDiversional Activity related to prolonged hospitalization.

Planning and Implementation

 RISK FOR INFECTION

PLANNING: nEXPECTED OUTCOMES.

The client with leukemia nis expected to:

• Remain free of ncross-contamination-induced infection

• Remain free of nautocontamination-induced infection

• Not experience nsepsis

INTERVENTIONS. Infectiois a major cause of death in the immunosuppressed client, and septicemia is a ncommon complication (Pittinger, 1999). Infection of the client with leukemia noccurs through both autocontamination (normal flora overgrows and penetrates nthe internal environment) and cross-contamination (microorganisms from another nperson or the environment are transmitted to the client). The three most commosites of infection are the skin, respiratory tract, and gastrointestinal tract. nGram-negative bacteria are most often the cause of infection, although ngram-positive and fungal infections do occur. Interventions aim to interrupt or nhalt the process of infection and control specific infections early. Chart 40-9 nemphasizes the importance of thorough assessment for the client at risk for ninfection.

DRUG THERAPY FOR nLEUKEMIA. Drug therapy for clients with AML is divided into three distinctive nphases: induction, consolidation, and maintenance.

INDUCTION nTHERAPY. Induction therapy is intensive and consists of ncombination chemotherapy initiated at the time of diagnosis. This therapy is naimed at achieving a rapid, complete remission of all manifestations of ndisease. Institutions and physicians differ in agents used and the treatment nschedule, but a typical course of aggressive chemotherapy includes IV nadministration of cytosine arabinoside for 7 days with concomitant nadministration of daunorubicin for the first 3 days (Dietz, 1999). A major side neffect of these agents is severe bone marrow suppression. As a result, the nclient becomes even more vulnerable to infection than before the treatment nstarted. Prolonged hospitalizations are common while the client is nimmunosuppressed. Recovery of bone marrow function requires at least 2 to 3 nweeks, during which time the client must be protected from life-threatening ninfections. Other adverse reactions include nausea, vomiting, diarrhea, nalopecia (hair loss), stomatitis (mouth sores), kidney toxicity, liver ntoxicity, and cardiac toxicity. (See Chapter 25 for information oursing nmanagement of adverse reactions to anticancer agents.)

CONSOLIDATION nTHERAPY. Consolidation therapy usually consists of another course nof either the same agents used for induction at a different dosage or a ndifferent combination of chemotherapeutic agents (Dietz, 1999). This treatment noccurs early in remission, and its intent is to cure. At some institutions, nconsolidation therapy is a single course of chemotherapy; at others, it ninvolves regularly scheduled, repeated courses of chemotherapy for 1 to 2 nyears.

MAINTENANCE nTHERAPY. Maintenance therapy may be prescribed for months to years nafter successful induction and consolidation therapies. It is commonly nindicated for clients with acute lymphocytic leukemia (ALL). The purpose is to nmaintain the remission achieved through induction and consolidation. nMaintenance agents are milder and are often given orally for 2 to 5 years. nThere are conflicting data regarding the effectiveness of maintenance therapy. nMaintenance therapy is not beneficial for clients with AML (Dietz, 1999).

DRUG THERAPY FOR nINFECTION. Drug therapy is the primary defense against infections nthat develop in clients undergoing therapy for AML. Agents used depend on the nsensitivity of the specific organism causing the infection, as well as the nextent of the infection, and are categorized by specificity as antibacterial, nantiviral, or antifungal. Figure 40-2 outlines pharmacologic management of the nfebrile neutropenic client.

ANTIBIOTIC AND nANTIBACTERIAL AGENTS. Antibiotic and antibacterial agents used nfor prophylaxis or treatment of infection in clients with AML usually include nat least one of the aminoglycoside antibiotics (amikacin, gentamicin, and ntobramycin) and a systemic penicillin. Additional, powerful antibiotics used nmay include vancomycin and drugs from the tetracycline and third-generatiocephalosporin classes.

ANTIFUNGAL nAGENTS. Systemic antifungal agents, used when a fungal infectiohas been diagnosed or is strongly suggested, include amphotericin B, nketoconazole (Nizoral), and nystatin (Mycostatin, Nadostine, Nilstat). Ineutropenic clients, antifungal creams (e.g., miconazole nitrate) are nadministered intravaginally to prevent yeast infections.

ANTIVIRAL nAGENTS. Antiviral agents are commonly used in clients with nleukemia to prevent and treat viral infections. Acyclovir is administered neither orally or parenterally before the initiation of antineoplastic agents, nespecially in clients who are cytomegalovirus (CMV) positive. If a viral ninfection is suspected or diagnosed with positive cultures, pharmacologic ntreatments may include ganciclovir, foscarnet, or steroids. The antivirals, nalthough helpful in combating severe infections, are associated with a wide nrange of serious adverse effects, especially ototoxicity (disruption of nhearing and/or balance) and nephrotoxicity (disruption of kidney nfunction). The nurse carefully monitors the client treated with such drugs for nsigns of hearing impairment and renal insufficiency.

 

 

 

INFECTION nPROTECTION. A major objective in caring for the client with leukemia nis protection from infection (Chart 40-10).

Nurses and all assistive nursing npersonnel must use extreme care during all nursing procedures. Frequent, nthorough handwashing is of the utmost importance. Anyone with an upper nrespiratory tract infection who must enter the client’s room must wear a mask. nNurses must also observe strict procedures when performing dressing changes or nwhen helping a physician to insert a central venous catheter. The nurse nmaintains strict aseptic technique in the care of these catheters at all times. nIf possible, the nurse ensures that the client is in a private room to minimize ncross-contamination. Because infection in the immunosuppressed person is most ncommonly caused by normal body microorganisms, protective (reverse) nisolation has been eliminated from the Centers for Disease Control and nPrevention (CDC) guidelines for infection control (see the Evidence-Based nPractice for Nursing box on p. 852). However, other environmental precautions nare heeded, such as allowing no standing collections of water in vases, denture ncups, or humidifiers in the client’s room, because they are excellent breeding ngrounds for microorganisms. Some institutions prescribe a “minimal nbacteria diet” during the neutropenic period. Any uncooked foods, such as nraw fruits and vegetables, and pepper are eliminated from the diet because they ncontain large numbers of microorganisms.

Whether clients benefit from this diet nis controversial. In some institutions, the immunosuppressed client is placed ia room with a high-efficiency particulate air (HEPA) filtration or laminar nairflow system. These systems decrease the number of airborne pathogens. Again, nwhether these restrictions benefit clients is debatable.

The nurse continually assesses the client nfor the presence of infection. This task is difficult because manifestations of ninfection may not be obvious in the client with leukopenia. The development of nfever and the formation of pus (both common indicators of infection) depend othe presence of leukocytes. Therefore the client with leukopenia may have a nsevere infection without pus and with a relatively low fever. The nurse nmonitors the client’s daily complete blood count (CBC) with differential white nblood cell (WBC) count. The oral mucosa is inspected during every nursing shift nfor lesions indicating fungal or viral infection.

The nurse also auscultates the lungs nevery 8 hours for crackles, wheezes, or diminished breath sounds. Each time the nclient voids, the urine is assessed for odor and cloudiness. The client is nasked about any urgency, burning, or pain present on urination. Vital signs are ntaken at least every 4 hours to assess for fever. A temperature elevation of neven 0.5° F (or 0.5° C) above baseline is significant for a client with leukopenia nand indicates infection until it has been proved otherwise. Many hospital units nthat specialize in the care of clients with neutropenia have specific protocols nfor antibiotic therapy if infection is suspected.

Usually, physicians are notified immediately, nand specific specimens are obtained for culture. Blood for bacterial and fungal ncultures is obtained from peripheral sites and from the central venous ncatheter. Urine specimens, sputum specimens, and specimens from open lesions nare taken for culture, and chest x-ray films are taken. After the specimens are nobtained, the client begins a regimen of IV antibiotics.

SKIN CARE. Skin care is nimportant for preventing infection in the client with leukemia. The skin may be nthe only intact defense. The nurse teaches the ambulatory client thorough nhygiene care and encourages daily bathing. If the client is immobile, turning nis necessary every hour and skin lubricants are applied.

RESPIRATORY CARE. Respiratory ncare, including pulmonary hygiene, is performed every 2 to 4 hours. The nurse nauscultates the lungs for crackles, wheezes, or diminished breath sounds. The nclient is encouraged to cough and deep breathe or to perform sustained maximal ninhalations every hour while awake.

BONE MARROW TRANSPLANTATION. Once viewed nas a treatment of last resort, bone marrow transplantation (BMT) is now nconsidered a standard treatment for the client with leukemia. This treatment nmodality began more than 25 years ago (Johns, 1998). BMT is the treatment of nchoice for the client with leukemia who has a closely matched donor and who is nexperiencing temporary remission with induction therapy. Because of the success nof BMT in the client with leukemia, this therapy is now being used for nlymphoma, aplastic anemia, inborn errors of metabolism, and many solid tumors n(Wolf, 1999). The bone marrow is the actual site of production of leukemic ncells. Because it can be difficult to ensure that all leukemic cells have beeeradicated during induction therapy, the goal is for extremely high doses of nchemotherapy to destroy all of the affected marrow. The new, healthy marrow nthen begins the process of hematopoiesis, which results iormal, properly nfunctioning cells and, it is hoped, a permanent cure. For many malignant ndisorders, the dose-limiting toxicity of treatments is bone marrow suppression. n

The aim of bone marrow or stem cell ntransplantation is to rid the client of all leukemic or other malignant cells nthrough high doses of chemotherapy, often in conjunction with whole-body nirradiation. These treatments are lethal to the bone marrow, and without nreplacement of bone marrow function through transplantation of progenitor cells nof the hematopoietic system, the client would die of infection or hemorrhage. nAdvances in the field of transplantation have been remarkable. Even as recently nas the late 1980s, the client undergoing transplantation would have been seeonly in major medical centers. Today, transplant units are becoming ncommonplace, even in community hospital settings. With long-term survival after ntransplantation increasing, nurses can expect to be caring for these people, if nnot during the actual transplantation or recovery period, then during the npost-transplantation period, in a variety of health care settings.

SOURCES OF STEM CELLS. BMT noriginated with the use of allogeneic bone marrow transplantation (transplantatioof identical bone marrow from a sibling) and has advanced to the use of humaleukocyte antigen (HLA)-matched stem cells from the umbilical cords of nunrelated donors (Wolf, 1999). Transplants can be classified based on the nsource of stem cells. In autologous transplants, the clients receive ntheir own stem cells, which were collected before therapy. Syngeneic ntransplants are rare and involve the client’s own identical twin as the ndonor of stem cells. In allogeneic transplants, a closely HLA-matched nsibling or an unrelated donor provides the stem cells. Stem cells for ntransplantation may be obtained by one of the following methods: bone marrow nharvest, peripheral stem cell pheresis, or umbilical cord blood stem cell nbanking. Table 40-5 provides an overview of the types of transplants. nTransplantation procedures have five phases: stem cell procurement, nconditioning regimen, transplantation, engraftment, and post-transplantation recovery. n

 

OBTAINING STEM CELLS. Stem ncells for transplantation are obtained either by harvest of bone marrow, by npheresis for peripheral blood stem cells, or by collection of umbilical cord nstem cells. Bone marrow is harvested either from the client directly n(autologous marrow) or from an HLA-matched person (allogeneic marrow).

For allogeneic marrow, a suitable donor nis selected after family members are tested for HLA type. Preferred transplantations nare those between HLA-identical siblings, but transplantation can also be nsuccessful between those with closely matched HLA types. The chance of matching nwith any given sibling is 25%. Several donor registries have been formed that nkeep records of people willing to donate marrow to provide marrow for clients nwho do not have a family member HLA match. The chance of matching with aunrelated donor is one in 5000 (Alcoser & Burchett, 1999).

After a suitable donor is identified by ntissue typing, the donor is taken to the operating room, where sufficient nmarrow for transplant is harvested through multiple aspirations aspirated; this namount is approximately 5% to 10% of the donor’s marrow supply and will be nreplenished in a few weeks (Poliquin, 1997).

The marrow is then filtered and may be nfurther processed to purge the autologous marrow of any residual cancer cells nor to deplete the allogeneic marrow of T-cells, which may later cause ngraft-versus-host disease (GVHD) (see p. 855). Allogeneic marrow is transfused ninto the recipient immediately; autologous marrow is frozen for later use. The nnurse monitors the donor for signs and symptoms of fluid loss, assesses for ncomplications of anesthesia, and manages postoperative pain. During surgery, ndonors may lose a significant amount of fluid in addition to the volume of nmarrow donated. Donors are often hydrated with saline infusions before and nimmediately after surgery. Occasionally the donor may require an infusion of nautologous salvaged red blood cells (RBCs) (Poliquin, 1997). The nurse assesses nthe harvest sites to ensure that the dressings are dry and intact and that the ndonor is not bleeding excessively. Marrow donation is usually a same-day nsurgical procedure. At home the donors are taught to inspect the harvest sites nfor bleeding and to take analgesics for pain. Pain is often experienced at the nharvest sites (hip) and is usually managed effectively with oral nnon-aspirin-containing analgesics. Individual differences do occur, however. nSome donors refuse pain medication, but others require opioid analgesics.

 There are three phases to obtaining nperipheral blood stem cells (PBSCs): mobilization, collection, and reinfusion. nDuring the mobilization phase, chemotherapy or hematopoietic growth factors are nadministered to the client (Wagner & Quinones, 1998). These agents cause nstem cells to circulate in the peripheral blood and the number of WBCs to nincrease. The stem cells are then collected by pheresis (withdrawing whole nblood, filtering out the cells, and returning the plasma to the client). One to nfive pheresis procedures, each lasting 2 to 4 hours, are usually required to nobtain enough stem cells for PBSC transplantation.

The stem cells are then frozen and nstored for reinfusion after the conditioning regimen (Wolf, 1999). The nurse nmust monitor the client closely during pheresis. Common complications include ncatheter clotting, which may delay pheresis, and hypocalcemia caused by nanticoagulants (Poliquin, 1997). The client with hypocalcemia may experience nchills, paresthesia, abdominal or muscle cramping, or chest pain, and the nurse nmay need to administer oral calcium supplements to manage these symptoms.

The nurse must also monitor vital signs nfrequently. The client may experience hypotension as a result of fluid volume nchanges during the procedure. Stem cells may also be obtained from umbilical ncords. The first cord blood transplant was done in France in 1988 (Wolf, 1999). nUmbilical stem cells are obtained via a simple phlebotomy procedure. After birth, nbefore the placenta detaches, a syringe is used to withdraw 40 to 150 mL of nblood from the umbilical vein. The syringes are placed in a kit, which is nreturned to the Cord Blood Registry for processing and storage (Wolf, 1999). nThe stem cells may be used later for an unrelated recipient or stored in case nthe infant develops a serious illness later in life and needs them. The cost of nbanking and processing umbilical cord stem cells is approximately $1500, with nan additional charge of $100 per year for storage. Umbilical stem cells calast for years when stored properly in liquid nitrogen. The oldest viable nsample is nearly 20 years old (Wolf, 1999).

CONDITIONING nREGIMEN. Figure 40-3 outlines the timing and nsteps typically involved in BMT. The day the client receives the bone marrow is nconsidered day T-0.

 Pretransplantation conditioning days are ncounted in reverse chronologic order from T-0, just like a rocket countdown. nPost-transplantation days are counted in chronologic order from the day of ntransplantation. The client must first undergo a conditioning regimen, which nvaries with the diagnosis and type of transplant to be received. The nconditioning regimen serves two purposes: (1) to obliterate, or “wipe nout,” the client’s own bone marrow, thus preparing the client for optimal ngraft take, and (2) to give higher thaormal doses of chemotherapy and/or nradiotherapy to obliterate, or wipe out, a malignancy, such as breast cancer. nUsually a period of 5 to 10 days is required. The conditioning regimen always includes nintensive chemotherapy and sometimes includes radiotherapy, usually total-body nirradiation (TBI). Each conditioning regimen is individually tailored, with the nclient’s specific disease, overall health, and previous treatment taken into naccount (Poliquin, 1997). A typical conditioning regimen for an adult client nreceiving an allogenic BMT for treatment of acute myelogenous leukemia (AML) is nas follows:

Days T-7 through T-5: High-dose nchemotherapy to obliterate the client’s own bone marrow cells and to eradicate nany remaining leukemic cells. Specific agents include busulfan, carmustine, ncyclophosphamide, cytosine arabinoside, etoposide, and melphalan. The dosages nare many times higher than those used for normal chemotherapy.

 Days T-4 through T-2: Delivery nof fractionated TBI (smaller doses of radiation given over a period of time ninstead of one larger dose). The typical radiation dose for TBI is 1200 rad. nThe client usually receives no cellkilling treatment on day T-l. During nconditioning, bone marrow and normal tissues begin to respond immediately to nthe chemotherapy and radiotherapy. The client experiences all of the expected nside effects associated with both therapies. Because the chemotherapy is nadministered in such high doses, these side effects are much more intense thathose seen with either standard chemotherapy or radiation. These side effects ninclude severe nausea and vomiting, mucositis, capillary leak syndrome, ndiarrhea, and bone marrow suppression (Poliquin, 1997). Late effects from the conditioning nregimen are also common, occurring as late as 3 to 10 years after ntransplantation, and include veno-occlusive disease (VOD), skin toxicities, ncataracts, fibrotic pulmonary disease, secondary malignancies, cardiomyopathy, nendocrine complications, and neurologic complications (Poliquin, 1997).

TRANSPLANTATION. Day T-0, nthe day of transplantation, is separated from the chemotherapy conditioning by nat least 2 days to ensure that the chemotherapeutic agent has cleared and will nnot exert any cytotoxic effects on the transplanted stem cells. The client nshould have few, if any, circulating white blood cells (WBCs) at this point, nindicating successful conditioning. The transplantation itself is very simple. nFrozen marrow, PBSCs, or umbilical cord blood cells are thawed in a ntemperature- controlled warm water bath (D’Andrea et al., 1997). The bone nmarrow is administered through the client’s central catheter like an ordinary nblood transfusion, but not using blood administration tubing. Usually the nmarrow is infused over a 30-minute period, although it may also be administered nby IV push directly into the central catheter with syringes. Side effects of nall types of stem cell transfusions are similar. The client may experience nfever and hypertension as a result of a reaction to the preservative used for nstorage of stem cells (D’Andrea et al., 1997). To prevent these reactions, the nnurse administers acetaminophen (Tylenol), hydrocortisone, and diphenhydramine n(Benadryl) before the transfusion (Johns, 1998). Antihypertensives or diuretics nmay also be required to treat fluid volume changes. The client may experience nred urine secondary to hemolysis of erythrocytes in the infused product.

ENGRAFTMENT. The transfused nPBSCs and marrow cells circulate only briefly in the peripheral blood. Most of nthe cells, especially the stems cells, find their way to the marrowforming nsites of the recipient’s bones and establish residency there. The mechanism by nwhich the donated marrow cells “home in” on the appropriate sites is nnot yet understood. Engraftment, successful “take” of the ntransplanted cells in the recipient’s bone marrow, is key to the whole ntransplantation process. For the donated marrow or stem cells to n”rescue” the client after large doses of chemotherapy and/or radiotherapy nwipe out his or her own bone marrow, the transfused stem cells must survive and ngrow in the clients’ bone marrow sites. The engraftment process takes 8 to 12 ndays for peripheral blood stem cells and 12 to 28 days for bone marrow stem ncells (Poliquin, 1997). To facilitate engraftment, hematopoietic growth nfactors, such as granulocyte colony-stimulating factor or ngranulocyte-macrophage colonystimulating factor, may be administered (Alcoser n& Burchett, 1999). When engraftment is successful, the client’s WBC, nerythrocyte, and platelet counts begin to rise.

PREVENTION OF COMPLICATIONS. The npost-transplantation period is difficult. Because the client remains without nany natural immunity until the transfused stem cells begin to proliferate and nengraftment occurs, infection and severe thrombocytopenia are major problems. nThe nursing care requirements for this client are virtually identical to those nfor the client undergoing aggressive induction therapy for AML. Helping the nclient to maintain hope through this long recovery period is difficult n(Campbell, 1999). Complications are often severe and life threatening.

The nurse should try to encourage the nclient to maintain a positive attitude and be involved in his or her own recovery. nIn addition to the problems related to the period of pancytopenia (too few ncirculating blood cells), other immediate hazards associated with BMT include nfailure to engraft, development of GVHD, and VOD.

Failure nto Engraft. Sometimes the donated marrow or stem ncells fail to engraft. This possibility is discussed in advance with the client nand the donor. Failure to engraft occurs more often among allogeneic stem cell nrecipients than among autologous stem cell recipients. The causes may be nrelated to insufficient numbers of cells transplanted, attack or rejection of ndonor cells by the remaining immunologically competent recipient cells, ninfection of transplanted cells, and unknown biologic factors. If the ntransplanted stem cells fail to engraft, the client will die unless another ntransplantation is successful.

Graft-Versus-Host nDisease. Graft-versus-host disease (GVHD) is aimmunologic event that occurs in allogeneic transplants. The immunocompetent ncells of the donated marrow recognize the client’s (recipient) cells, tissues, nand organs as foreign and mount an immune offense against them. The graft is nactually trying to attack the host (Alcoser & Burchett, 1999). Although all nhost tissues can be attacked and harmed, the tissues most commonly damaged are nthe skin, gastrointestinal tract, and liver. Approximately 25% to 50% of all nallogeneic BMT recipients experience some degree of GVHD, and more than 15% of nthe clients who experience GVHD die of its complications (Johns, 1998). The npresence of GVHD indicates that the transplanted cells are competent and have nsuccessfully engrafted. Management of GVHD is achieved by limiting the nactivation of donor T-lymphocytes through the administration of nimmunosuppressive agents such as cyclosporine, methotrexate, corticosteroids, nand antithymocyte globulin (Alcoser & Burchett, 1999). Care is taken to navoid suppressing the new immune system to the extent that either the client nbecomes more susceptible to infection or the transplanted cells stop nengrafting.

Veno-occlusive nDisease. Veno-occlusive disease (VOD) involves nocclusion of the hepatic blood vessels by clotting and inflammatio(phlebitis). This condition occurs in up to 20% of clients who receive either nan autologous or an allogeneic transplant, and symptoms usually occur withithe first 30 days after transplantation (Johns, 1998). Clients who have nreceived high doses of chemotherapy, especially alkylating agents, are at risk nfor life-threatening hepatic complications. Clinical signs include jaundice, npain in the right upper quadrant, ascites, weight gain, and liver enlargement. nBecause there is no known way of opening the hepatic vessels, treatment is nsupportive. Early detection enhances the chances of survival. Fluid management nis also crucial. The nurse assesses the client daily for weight gain, fluid naccumulation, increases in abdominal girth, and hepatomegaly.

RISK FOR nINJURY

Because normal bone marrow production is nseverely limited with acute myelogenic leukemia (AML), the number of circulating nplatelets is severely diminished, causing thrombocytopenia. This condition puts nthe client with AML at a greatly increased risk for excessive bleeding iresponse to minimal trauma. Thrombocytopenia can also be induced by inductiotherapy for AML or high-dose chemotherapy for transplantation (Rust, Wood, n& Battiato, 1999).

PLANNING: EXPECTED OUTCOMES. The nclient with leukemia is expected to remain free from bleeding. INTERVENTIONS. nAs a result of chemotherapy-induced pancytopenia, the client’s platelet ncount is decreased. During the period of greatest bone marrow suppression (the nnadir), the platelet count may be extremely low (<10,000/mm3). The client is nat great risk for bleeding once the platelet count falls below 50,000/mm3, and nspontaneous bleeding often occurs when the platelet count is lower than 20,000 n(Harrahill & DeLoughery, 1998).

BLEEDING nPRECAUTIONS. The nurse’s major objectives are to protect the client nfrom situations that could lead to bleeding and to closely monitor any bleeding nthat does occur. The nurse assesses the client nfrequently for evidence of bleeding: oozing, confluent ecchymoses, petechiae, nor purpura. All stools, urine, nasogastric drainage, and vomitus are examined nvisually for blood and tested for occult blood. The nurse measures any blood nloss as accurately as possible and measures the client’s abdominal girth daily. nIncreases in abdominal girth can indicate internal hemorrhage. Bleeding nprecautions are instituted (Chart 40-11).

The nurse also monitors laboratory nvalues daily. Complete blood count (CBC) results are reviewed daily to ndetermine the risk for bleeding, as well as actual blood loss. The client with na platelet count below 20,000/mm3 may need a platelet transfusion. Aalternative treatment is the administration of oprelvekin (Neumega), a platelet n(thrombopoietic) growth factor. The recommended dose is 50 xg/kg/day nsubcutaneously starting 6 to 12 hours after the completion of chemotherapy n(Rust, Wood, & Battiato, 1999). For the client with severe blood loss, npacked RBCs may be ordered.

 

FATIGUE

Because normal bone marrow production is nseverely limited in leukemia, the number of circulating erythrocytes is nseverely diminished, creating a condition of anemia, leading in turn to nfatigue. Because leukemic cells tend to have higher rates of metabolism and ngreater utilization of oxygen, the anemic client with leukemia is at risk for nsevere fatigue. Anemia also occurs secondary to chemotherapy treatment n(Richardson, Ream, & Wilson-Barnett, 1998).

PLANNING: EXPECTED OUTCOMES.

The client with leukemia is expected to: n

• Experience no increase in fatigue

• Recognize symptoms of fatigue and nalter activity before fatigue becomes excessive

INTERVENTIONS

ENERGY MANAGEMENT. Energy management naims at decreasing the effects of anemia and conserving energy expenditure (see nChart 40-10).

DIET THERAPY. Diet therapy is nindirectly related to fatigue and subsequent activity intolerance. The client nmust ingest enough calories to meet at least basal energy requirements, but nincreasing dietary intake can be difficult when the client is extremely nfatigued. The nurse thus provides small, frequent meals high in protein and ncarbohydrates. Food items that are liquid or easy to chew also require less neffort to eat.

BLOOD REPLACEMENT THERAPY. Blood ntransfusions are sometimes indicated for the client with fatigue. Transfusions nincrease the blood’s oxygen-carrying capacity and replace missing red blood ncells (RBCs) and some coagulation factors (see Table 40-2). For the client with nleukemia who is experiencing fatigue related to anemia, packed RBCs are usually nthe blood component of choice. (See Transfusion Therapy, p. 862, for a ndiscussion of nursing care during transfusions.)

 DRUG THERAPY. Clients may nreceive subcutaneous injections of epoetin alfa (Epogen or Procrit) 50 to 100 nunits/kg three times per week (Cella & Bron, 1999). This growth factor is nnaturally secreted by the kidney and boosts the production of RBCs. Epoetialfa has previously been used in anemia associated with chronic renal failure nand in clients with human immunodeficiency virus (HIV) who are receiving nzidovudine and is now approved for use in anemia associated with chemotherapy. nThe nurse administers injections three times a week and assesses for side neffects such as hypertension, headaches, fever, myalgia (muscle aches), nand rashes. 

CONSERVATION OF ENERGY. The nnurse examines the hospitalized client’s schedule of prescribed and routine nactivities. Those activities that do not have a direct positive effect on the client’s ncondition are assessed in terms of their usefulness. If the actual or potential nbenefit of an activity is less than its actual or potential worsening of nfatigue, the nurse consults with other members of the health care team about neliminating or postponing it. Candidates for cancellation or postponement ninclude physical therapy and certain invasive diagnostic tests not required for nassessment or treatment of current problems.

 Community-Based nCare The client with leukemia is discharged after inductiochemotherapy and recovery of blood cell-producing function. Follow-up care is nprovided on an outpatient basis. Although the majority of transplant centers ndischarge clients following engraftment, some centers administer high-dose nchemotherapy and stem cell infusion on an outpatient basis. This plan involves ndaily clinic visits and frequent follow-up by nurses in the home care setting n(D’Andrea et al., 1997).

 HOME CARE nMANAGEMENT

Planning for home care for the client nwith leukemia begins as soon as a client achieves remission. He or she will nneed assistance at home until the condition improves. The nurse assesses the navailable support mechanisms. Many clients require the services of a visiting nnurse to assist with dressing changes for central venous catheters, to assist nwith hyperalimentation infusions, to transfuse platelets, and to answer nquestions. Occasionally they may also require home transfusion therapy for one nor more blood components (Bean, 1998). The home care team is critical for the nclient receiving stem cell transplantation in the home setting. Potential ncandidates are evaluated in advance. Criteria include a knowledgeable ncaregiver, a clean home environment, close proximity to the hospital, telephone naccess, and emotional stability on the part of the client and caregiver n(Herrmann et al., 1998). In one sample program, clients receive their daily ndose of chemotherapy in the outpatient clinic in the morning and then receive a nhome visit in the evening. Home care nurses administer chemotherapy and monitor nthe client for complications. Nurses visit the client once or twice a day and nspend between 4 and 8.5 hours per day in the home (D’Andrea et al., 1997). The nclient receives the stem cell transplant infusion in the outpatient clinic. nNursing care is similar to that provided in the hospital. If serious ncomplications such as sepsis or veno-occlusive disease occur, the client is nadmitted to the inpatient facility

HEALTH TEACHING

The client and the family need to be educated nabout the importance of continuing therapy and appropriate medical follow-up, ndespite the unpleasant side effects of therapy. Many clients go home with a ncentral venous catheter in place and require instructions about its care and nmaintenance (Bean, 1998). Chart 40-12 lists general guidelines for central nvenous catheter care at home.

These guidelines may be altered ndepending on the home setting, assistance available, and agency policy. nProtecting the client from infection after discharge from the hospital is just nas important as it was during hospitalization.  nThe nurse urges the client to use proper hygiene and to avoid crowds or nothers with infections. Neither the client nor any household member should receive nlive virus immunization (poliomyelitis, measles, or rubella) for 2 years after ntransplantation (Alcoser & Burchett, 1999). The client should continue nmouth care regimens at home. The nurse emphasizes that the client should nimmediately notify the physician if he or she experiences fever or any other nsign of infection.

Chart 40-13 lists guidelines for clients nfor the prevention of infection.

Because platelet recovery is usually nslower than recovery of white blood cells (WBCs), many clients return home nstill at risk for bleeding. Thrombocytopenia may be present for 6 months nfollowing transplantation (Hurley, 1997). The nurse reinforces the safety and nbleeding precautions initiated in the hospital, emphasizing that the client nmust follow these precautions until the platelet count is above 50,000. The nclient and family are instructed to assess for petechiae, avoid trauma and nsharp objects, apply pressure to wounds for 10 minutes, and report any unusual nsymptoms, including blood in the stool or urine, or headache that does not nrespond to acetaminophen. Chart 40-14 lists guidelines for clients at risk for nbleeding.

PSYCHOSOCIAL nPREPARATION The nurse’s responsibility in psychosocial preparation of nthe client before discharge is very important. A diagnosis of leukemia nthreatens self-esteem and the family role. The client is confronted with the nreality of death, and treatment causes major adjustments in self-image. The nclient and family also experience nchanges in the client’s body image, level of independence, and lifestyle. Some feel nthreatened by their environment, seeing everything as potentially infectious. nClients who are cared for in protective isolation may experience loneliness and nloss of contact with the outside world (Campbell, 1999). The nurse helps the nclient and family redefine priorities, understand the illness and its ntreatment, and find hope. The nurse makes referrals to support groups sponsored nby organizations such as the American Cancer Society (“I Can Cope” nand “Make Today Count”), which can be enormously beneficial to both nthe client and the family.

HEALTH CARE RESOURCES The nclient with limited social support may need assistance at home until strength nand energy return. A home care aide may suffice for some clients, whereas for nothers a visiting nurse may be needed to reinforce teaching. The client may nalso need equipment to facilitate activities of daily living (ADLs) and nambulation. Financial resources are assessed. Treatment of cancer is expensive, nand the nurse works closely with the local social services department to ensure nthat insurance is adequate. If the client is uninsured, other sources, such as ndrug company-sponsored compassionate aid programs, are ex plored. The Leukemia Society of America offers limited financial assistance nfor clients with leukemia, sponsors support groups, and provides publications nfor clients and health care providers. Prolonged outpatient contact and nfollow-up will be necessary, and clients will need transportation to the noutpatient facility. Many local divisions of the American Cancer Society offer nfree transportation to clients with cancer, including leukemia.

Evaluation: nOutcomes

The nurse evaluates the care of the nclient with leukemia on the basis of the identified nursing diagnoses and ncollaborative problems. The expected outcomes include that the client will:

• Remain free of ncross-contamination-induced infection

• Remain free of nautocontamination-induced infection

• Not experience sepsis

• Remain free of episodes of bleeding

• Balance activity and rest

• Use energy conservation techniques

• Adapt lifestyle to energy level

Malignant lymphoma

Malignant lymphomas occur as a result of nabnormal overgrowth of one type of leukocyte (lymphocytes); they differbone nmarrow, and they fall into two major categories among adults: Hodgkin’s nlymphoma and non-Hodgkin’s lymphoma.

Hodgkin’s Lymphoma i nOVERVIEW

Hodgkin’s lymphoma is a cancer that caaffect any age-group, although incidence peaks first in people in their nmid-to-late 20s and then in people older than 50 years of age (Callaghan, n1998). Men and women are affected equally in the first group, but the disease nis more prevalent in men in the older group. Factors implicated as possible ncauses of Hodgkin’s lymphoma include viral infections and previous exposure to nalkylating chemical agents. This cancer usually originates in a single lymph nnode or a single chain of nodes. The lymphoid tissues within the node undergo nmalignant transformation, usually initiating some inflammatory processes. These nnodes contain a specific transformed cell type, the Reed-Sternberg cell, a nmarker for Hodgkin’s lymphoma. The disease first metastasizes (spreads) nto other nearby lymphoid structures and eventually invades nonlymphoid tissues. n»

COLLABORATIVE nMANAGEMENT

Assessment nAssessment most often reveals a greatly enlarged but painless lymph node or nnodes, usually the earliest manifestation of Hodgkin’s lymphoma. The client nalso often experiences fever, malaise, and night sweats (Table 40-6). More nspecific clinical manifestations depend on the site (or sites) of malignancy nand the extent of disease. Diagnosis and grade are established when biopsy of a nnode or mass reveals Reed-Sternberg cells (Callaghan, 1998). The client theundergoes extensive staging procedures to determine the exact extent of disease. nStaging must be detailed and accurate because the treatment regimen is ndetermined by the extent of disease (DeVita, Mauch, & Harris, 1997). nStaging procedures for Hodgkin’s lymphoma include biopsies of distant lymph nnodes, computed tomography (CT) of the thorax and abdomen, staging laparotomy, na complete blood count (CBC), liver function studies, and bilateral bone marrow nbiopsies.

Interventions Such ngreat progress has been made in treatment regimens that Hodgkin’s lymphoma is nnow one of the most curable types of cancer (Callaghan, 1998). Generally, for nstage I and stage II disease without mediastinal node involvement, the ntreatment of choice is extensive external radiation of involved lymph node nregions. With more extensive disease, radiation coupled with an aggressive nmultiagent chemotherapy regimen is most effective in achieving a cure (DeVita, nMauch, & Harris, 1997).

Specific nursing management of the nclient undergoing treatment for Hodgkin’s lymphoma focuses on the side effects nof therapy, especially the following:

Ø     nDrug-induced pancytopenia, which nresults in increased risk for infection, bleeding, and anemia

Ø     n Severe nausea and vomiting

Ø     nSkin irritation and breakdown at nthe site of radiation  from the leukemias nin the degree of maturation of the affected cells and the location of cell nproduction.

Ø     nImpaired hepatic function either nby metastasis to the liver or by multiagent chemotherapy

Ø     nPermanent sterility for male nclients receiving radiation to the abdominopelvic region in the pattern of ainverted Y in combination with specific chemotherapeutic agents (the client nshould be informed of this side effect and given the option to store sperm in a nsperm bank before treatment)

Ø     nSecondary malignancies for nclients receiving radiation alone or chemotherapy (Long-term follow-up should ninclude screening for recurrence, as well as the possible development of a nsecondary cancer.)

Non-Hodgkin’s Lymphoma n

OVERVIEW Non-Hodgkin’s nlymphoma is the classification for all cancers originating from lymphoid ntissues that are not diagnosed as Hodgkin’s lymphoma. There are more than 12 nsubtypes of non-Hodgkin’s lymphoma, including low-grade, intermediate, and nhigh-grade lymphomas.

The low-grade lymphomas usually arise nfrom B-cell lymphocytes and progress slowly. Although clients with lowgrade nlymphomas have longer survival rates, the diseases are less responsive to ntreatment and, consequently, cures are rare (Bilodeau & Fessele, 1998).

At the other end of the spectrum are the nhigh-grade lymphomas, which are aggressive tumors of usually mixed cellularity nwith rapid doubling times. High-grade lymphomas are more responsive to nchemotherapy, and the chances for a longterm cure are greater.

Non-Hodgkin’s lymphoma is ranked as the nsixth most common cause of cancer-related death in the United States. The ndisease is more prevalent in men, Caucasians, and individuals older than 50 nyears of age. The long-term prognosis is better for women and clients younger nthan 65 years of age (Bilodeau & Fessele, 1998). Most non-Hodgkin’s nlymphomas arise from lymph nodes, but they can originate in virtually any ntissue or organ. A low-grade lymphoma also can convert to a highergrade nlymphoma. Definitive causes are unknown, but viral infection, exposure to nionizing radiation, autoimmune disorders, and exposure to toxic chemicals have nall been implicated.

COLLABORATIVE nMANAGEMENT

Because lymphomas may arise from nlymphoid cells in any tissue and because the malignancy can spread to any norgan, assessment reveals no specific clinical manifestations other thalymphadenopathy common to all types of lymphoma. Diagnosis is made from the nhistologic features apparent on biopsy of any suspicious node or mass. nClassification of the specific lymphoma subtype is based on a complex grading nof surface markers, cytogenetic features, cell size, and expression of viral nantigens (Bilodeau & Fessele, 1998). Staging is similar to that for nHodgkin’s lymphoma (see Table 40-6). Treatment consists of radiation therapy nand multiagent chemotherapy. Nursing care needs are similar to those for nclients with Hodgkin’s lymphoma, with additional organspecific problems takeinto account if the disease is widely disseminated.

COAGULATION nDISORDERS

Coagulation disorders are synonymous nwith bleeding disorders and are characterized by abnormal or increased bleeding nresulting from defects in one or more components regulating hemostasis. nBleeding disorders may be spontaneous or traumatic, localized or generalized, nlifelong or acquired. They can originate from a defect in the hemostatic nprocesses at the vascular, platelet, or clotting factor level. Figure 40-4 noutlines blood-clotting cascades and sites where specific defects and drugs ndisrupt the hemostatic processes.

PLATELET DISORDERS Platelets nplay a vital role in hemostasis. For both the intrinsic and the extrinsic npathways, blood clotting starts with platelet adhesion and the formation of a nplatelet plug. Any condition that either reduces the number of platelets or ninterferes with their ability to adhere (to one another, blood vessel walls, ncollagen, or fibrin threads) can be manifested as increased bleeding. Platelet ndisorders can be inherited, acquired, or temporarily induced by the ingestioof substances that limit platelet production or inhibit aggregation. A drop ithe number of platelets below the level needed for normal coagulation is called nthrombocytopenia. Thrombocytopenia may occur as a result of other nconditions or treatments that suppress general bone marrow activity. It also ncan occur through processes that specifically limit platelet formation or nincrease the rate of platelet destruction. The two thrombocytopenic conditions naffecting adults are autoimmune thrombocytopenic purpura and thrombotic nthrombocytopenic purpura.

Autoimmune Thrombocytopenic nPurpura

OVERVIEW Before the underlying cause of nautoimmune thrombocytopenic purpura was identified, this condition was known as nidiopathic thrombocytopenic purpura (ITP). Although the cause is now thought to nbe an autoimmune reaction, the condition is still commonly known as ITP. The ntotal number of circulating platelets is greatly reduced in ITP, even though nplatelet production in the bone marrow is normal. Clients with idiopathic nthrombocytopenic purpura make an antibody directed against the surface of their nown platelets (an antiplatelet antibody). This antibody coats the surface of nthe platelets, making them more susceptible to attraction and destruction by nphagocytic leukocytes, especially macrophages. Because the spleen contains a nlarge concentration of macrophages and because the blood vessels of the spleeare long and twisted, antibody-coated platelets are destroyed primarily in the nspleen. When the rate of platelet destruction exceeds that of production, the nnumber of circulating platelets decreases and blood clotting slows. Although nthe cause of this disorder appears to be autoimmune, the exact mechanism ninitiating the production of autoantibodies is unknown. ITP is most commoamong women between the ages of 20 and 40 and among people with a preexisting nautoimmune condition, such as systemic lupus erythematosus (Cotran, Kumar, n& Robbins, 1999).

COLLABORATIVE nMANAGEMENT

Assessment Clinical manifestations nassociated with ITP are generally limited to the skin and mucous membranes: nlarge ecchymoses (bruises) on the arms, legs, upper chest, and neck or a npetechial rash. Mucosal bleeding occurs easily. If the client has experienced nsignificant blood loss, signs of anemia may also be present. A rare complicatiois an intracranial bleeding-induced stroke. The nurse assesses for neurologic nfunction and mental status. Family members or significant others are asked if nthe client’s behavior and responses to the mental status examination are ntypical or represent a change from usual reactions. Idiopathic thrombocytopenic npurpura is diagnosed by a decreased platelet count and large numbers of nmegakaryocytes in the bone marrow. Antiplatelet antibodies may be present idetectable levels in peripheral blood. If the client experiences any episodes nof bleeding, hematocrit and hemoglobin levels also are low.

Interventions

NONSURGICAL nMANAGEMENT. As a result of the decreased platelet count, the client nis at great risk for bleeding. Interventions include therapy for the underlying ncondition, as well as protection from trauma-induced bleeding episodes.

DRUG THERAPY. Agents used to ncontrol ITP include drugs that suppress immune function to some degree. The npremise for the use of agents such as corticosteroids and azathioprine (Imuran) nis to inhibit immune system synthesis of antiplatelet autoantibodies. More naggressive therapy can include low doses of chemotherapeutic agents, such as nthe antimitotic agents and cyclophosphamide.

BLOOD REPLACEMENT THERAPY. For the client nwith a platelet count of less than 20,000/mm3 who is experiencing an acute nlife-threatening bleeding episode, a platelet transfusion may be required. nPlatelet transfusions are not performed routinely, because the donated nplatelets are just as rapidly destroyed by the spleen as the client’s owplatelets (see later discussion under Platelet Transfusions, p. 865).

MAINTAINING A SAFE ENVIRONMENT. The nnurse’s major objectives are to protect the client from situations that calead to bleeding and to closely monitor the amount of bleeding that is noccurring. (For nursing care actions, see Risk for Injury [Leukemia], p. 856.)

SURGICAL MANAGEMENT. For the client who ndoes not respond to drug therapy, splenectomy may be the treatment of choice. nBecause the leukocytes in the spleen perform many different immunodefensive nfunctions, the client who has undergone a splenectomy is at increased risk for ninfection.

Thrombotic nThrombocytopenic Purpura

OVERVIEW Thrombotic thrombocytopenic npurpura (TTP) is a rare disorder in which platelets clump together ninappropriately in the microcirculation and insufficient platelets remain ithe systemic circulation. The client experiences inappropriate clotting, yet nthe blood fails to clot properly when trauma occurs. The underlying cause of nTTP appears to be an autoimmune reaction in blood vessel cells (endothelial ncells) that makes platelets clump together in very small blood vessels. As a nresult, tissues become ischemic. Common manifestations include renal failure, nmyocardial infarction, and stroke. If left untreated, this condition is fatal nwithin 3 months in 90% of clients (McBrien, 1997).

COLLABORATIVE MANAGEMENT Treatment for nthe client with TTP focuses on inhibiting the inappropriate platelet naggregation and disrupting the underlying autoimmune process. Primary treatment nconsists of plasma pheresis with the infusion of fresh frozen plasma. This ntreatment provides the necessary platelet aggregate inhibitors (McBrien, 1997). nDrugs that inhibit platelet clumping, such as aspirin, alprostadil (Prostin), nand plicamycin, also may be helpful. Immunosuppressive therapy reduces the nintensity of this disorder.

CLOTTING nFACTOR DISORDERS

Coagulation or bleeding disorders caresult from a clotting factor defect, including the inability to produce a nspecific clotting factor, production of insufficient quantities, or a less nactive form of clotting factor. Most clotting factor disorders are congenitally ntransmitted gene abnormalities of one clotting factor. The few acquired nclotting factor disorders are related to an inability to synthesize many nclotting factors at the same time as a result of liver damage or ainsufficiency of clotting cofactors and precursor products. Common congenital ndisorders that result in defects at the clotting factor level include nhemophilias A and B and von Willebrand’s disease. Disseminated intravascular ncoagulation (DIC) may be considered an acquired clotting disorder but is more nclosely associated with septic shock.

Hemophilia

OVERVIEW Hemophilia comprises two nhereditary bleeding disorders resulting from deficiencies of specific clotting nfactors. Hemophilia A (classic hemophilia) results from a deficiency of factor nVIII and accounts for 80% of cases of hemophilia. Hemophilia B (Christmas ndisease) is a deficiency of factor IX and accounts for 20% of cases. The nincidence of both is 1 i10,000. Hemophilia is an Xlinked recessive trait. Female carriers have a 50% nchance of transmitting the gene for hemophilia to their daughters (who then are ncarriers) and to their sons (who will have overt hemophilia). Hemophilia A is, nwith rare exceptions, a disease affecting males, none of whose sons will have nthe gene for hemophilia and all of whose daughters will be carriers (able nto pass on the gene without actually having the disorder). In about 30% of nclients with hemophilia, there is no family history, and it is presumed that ntheir disease is the result of a new mutation (Cotran, Kumar, & Robbins, n1999). The bleeding disorder associated with hemophilia A is so severe that nbefore blood transfusions were available, children with hemophilia rarely nsurvived past age 3 years. With the availability of blood transfusion and nfactor VIII therapy, mean survival time has increased so greatly that hemophilia nnow is commonly seen among adult clients. The clinical pictures of hemophilia A nand B are identical. The client has abnormal bleeding in response to any trauma nbecause of an absence or deficiency of the specific clotting factor. Clients nwith hemophilia do not bleed more frequently or even more rapidly that those nwithout the disease, but they do bleed for a longer period (Ligda, 1998). nHemophiliacs form platelet plugs at the bleeding site, but the clotting factor ndeficiency impairs the hemostatic response and the capacity to form a stable nfibrin clot. This produces abnormal bleeding, which may be mild, moderate, or nsevere, depending on the degree of factor deficiency.

COLLABORATIVE nMANAGEMENT

 Assessment

Assessment of the client with hemophilia nreveals the following:

• Excessive hemorrhage from minor cuts nor abrasions caused by abnormal platelet function

• Joint and muscle hemorrhages that lead nto disabling long-term sequelae

• A tendency to bruise easily

• Prolonged and potentially fatal npostoperative hemorrhage

The laboratory test results for a client nwith hemophilia demonstrate a prolonged npartial thromboplastin time (PTT), a normal bleeding time, and a normal nprothrombin time (PT) (Cotran, Kumar, & Robbins, 1999). The most commohealth problem associated with hemophilia is degenerating joint functioresulting from chronic bleeding into the joints, especially at the hip and nknee.

• Interventions nThe bleeding problems of hemophilia A can be well managed by either regularly nscheduled IV administration of factor VIII cryoprecipitate or intermittent nadministration as needed, depending on the individual’s activity level and ninjury probability (see Cryoprecipitate, p. 865). However, the cost of ncryoprecipitate is prohibitive for many people with hemophilia. In addition, nbecause the precipitated clotting factors are derived from pooled human serum, na risk of viral contamination remains, even with the

use of heat-inactivated serum (Ligda, n1998). Major complications of hemophilia therapy during the 1980s were ninfection with hepatitis B virus, cytomegalovirus, and human immunodeficiency nvirus (HIV). Although heat-inactivated serum and the elimination of nHIV-positive donors have reduced these risks, they have not yet beeeliminated.

TRANSFUSION nTHERAPY

Any blood component may be removed from na donor and transfused to benefit a recipient. Components may be transfused nindividually or collectively, with varying degrees of benefit to the recipient. n

PRETRANSFUSION nRESPONSIBILITIES Nursing actions during transfusions aim largely at nprevention or early recognition of adverse transfusion reactions. Preparatioof the client for transfusion therapy is imperative, and in stitutional blood nproduct administration procedures should be carefully followed. Before administering nany blood product, the nurse reviews the agency’s policies and procedures. nChart 40-15 presents best practices for transfusion therapy.

 Legally, a physician’s order is needed to nadminister blood or its components. The order specifies the type of component nto be delivered, the volume to be transfused, and any special conditions the nphysician judges to be important. The nurse verifies the order for accuracy and ncompleteness. The nurse also evaluates the need for transfusion, considering nboth the client’s clinical condition and the laboratory values. In many nhospitals a separate consent form must be obtained for the administration of nblood products before a transfusion is performed.

A blood specimen is obtained for ncrossmatching (testing of the donor’s blood and the recipient’s blood for ncompatibility). The procedure and responsibility for obtaining this specimeare specified by hospital policy. The laboratory requires at least 45 minutes nto complete the crossmatch testing. In most hospitals a new crossmatching nspecimen is required at least every 48 hours (Dreger & Tremback, 1998).

Because of the viscosity of blood ncomponents, a 19-gauge needle or larger is used, whenever possible, for venous access. nBoth Y-tubing and straight tubing sets are available for blood component nadministration. A blood filter (approximately 170 xm) to remove aggregates nfrom the stored blood products is included with component administratioequipment and must be used to transfuse all blood products. In massive ntransfusion, a microaggregate filter (20 to 40 jam) may be used.

Normal saline is the solution of choice nfor administration. Ringer’s lactate and dextrose in water are contraindicated nfor administration with blood or blood products because they cause clotting or nhemolysis of blood cells.

 Medications nare never added to blood products.

 Before the transfusion is ninitiated, it is essential to determine that the blood component delivered is ncorrect. Two registered nurses simultaneously check the physician’s order, the nclient’s identity, and whether the hospital identification band name and number nare identical to those on the blood component tag. The blood bag label, the nattached tag, and the requisition slip are examined to ensure that the ABO and nRh types are compatible. The expiration date is also checked, and the product nis inspected for discoloration, gas bubbles, or cloudiness—indicators of nbacterial growth or hemolysis.

TRANSFUSION nRESPONSIBILITIES The nurse takes the vital signs, including ntemperature, immediately before initiating the transfusion. Infusion begins nslowly. A nurse remains with the client for the first 15 to 30 minutes. Any nsevere reaction usually occurs with administration of the first 50 mL of blood. nThe nurse assesses vital signs 15 minutes after initiation of the transfusioto detect signs of a reaction. If there are none, the infusion rate can be nincreased to transfuse 1 unit in about 2 hours (depending on the client’s ncardiovascular status). The nurse takes the vital signs every hour throughout nthe transfusion or as specified by agency policy. Blood components without nlarge amounts of red blood cells (RBCs) can be infused more quickly. The nidentification checks are the same as for RBC transfusions. Physiologic changes nin older clients may necessitate that blood products be transfused at a slower nrate. Best practices related to the nursing care needs of older clients nundergoing transfusion therapy are provided in Chart 40-16.

TYPES OF TRANSFUSIONS

 

VIDEO

Red Blood Cell nTransfusions RBCs are administered to replace erythrocytes lost as a nresult of trauma or surgical interventions. Clients with clinical conditions nthat result in the destruction or abnormal maturation of RBCs may also benefit nfrom RBC transfusions. Packed RBCs, supplied in 250-mL bags, are a concentrated nsource of RBCs and are the most common component administered to RBCdeficient nclients (Dreger & Tremback, 1998). Packed RBCs are administered to nindividuals with a hemoglobin concentration less than 6 g/dL (or a hemoglobivalue of 6 to 10 g/dL if clinical symptoms are present) (Kennedy, 1999). Blood ntransfusions are actually transplantations of tissue from one person to nanother. The donor and recipient blood must thus be carefully checked for ncompatibility to prevent potentially lethal reactions (Table 40-7).

Compatibility is determined by two ndifferent types of antigen systems (cell surface proteins): the ABO system nantigens and the Rh antigen, present on the membrane surface of RBCs (Dreger n& Tremback, 1998). RBC antigens are inherited.

For the ABO antigen system, a person inherits none of the following:

• A antigen (type A blood)

• B antigen (type B blood)

• Both A and B antigens (type AB blood)

• No antigens (type O blood)

Within the first few years of a child’s life, ncirculating antibodies develop against the blood type antigens that were not ninherited. For example, a child with type A blood will form antigens against ntype B blood. A child with type O blood has not inherited either A or B nantigens and will form antibodies against RBCs that contain either A or B nantigens. If erythrocytes that contain a foreign antigen are infused into a nrecipient, the donated tissue can be recognized by the immune system of the nrecipient as non-self, and the client may have a reaction to the transfused nproducts. The mechanism of the Rh antigen system is slightly different. ARh-negative person is born without the antigen and does not form antibodies nunless he or she is specifically sensitized to it. Sensitization can occur with nRBC transfusions from an Rh-positive person or from exposure during pregnancy nand birth. Once an Rh-negative person has been sensitized and antibody ndevelopment has occurred, any exposure to Rh-positive blood can cause a ntransfusion reaction. Antibody development can be prevented by administratioof Rh-immune globulin as soon as exposure to the Rh antigen is suspected. nPeople who have Rh-positive blood can receive an RBC transfusion from aRh-negative donor, but Rh-negative people must never receive Rh-positive blood. n

Platelet Transfusions Platelets are administered to clients with platelet counts below 20,000 mm3 nand to clients with thrombocytopenia who are actively bleeding or are scheduled nfor an invasive procedure (Dreger, & Tremback, 1998). Platelet transfusions nare usually pooled from as many as 10 donors and do not have to be of the same nblood type as the client. For clients who are candidates for bone nmarrow transplantation (BMT) or who require multiple platelet transfusions, nsingle-donor platelets may be ordered. Single-donor platelets are obtained from none person and decrease the amount of antigen exposure to the recipient, nhelping prevent the formation of platelet antibodies. The chances of allergic ntransfusion reactions to future platelet transfusions are thus reduced. nPlatelet infusion bags usually contain 300 mL for pooled platelets and 200 mL nfor single-donor platelets. Because the platelet is a fragile cell, platelet ntransfusions are administered rapidly after being brought to the client’s room, nusually over a 15- to 30-minute period. A special transfusion set with a nsmaller filter and shorter tubing is used. Standard transfusion sets are not nused with platelets because the filter traps the platelets, and the longer ntubing increases platelet adherence to the lumen. Additional platelet filters nhelp remove white blood cells (WBCs) in the platelet concentrate. These filters nare connected directly to the platelet transfusion set and are used for clients nwho have a history of febrile reactions or who will require multiple platelet ntransfusions. The nurse takes the vital signs before the infusion, 15 minutes nafter the infusion is initiated, and at its completion. The client may be npremedicated with meperidine (Demerol) or hydrocortisone to minimize the chances nof a reaction. He or she can become febrile and experience rigors (severe nchills) during transfusion, but these symptoms are not considered a true ntransfusion reaction. IV administration of amphotericin B (Amphotec, nFungizone), an antifungal agent given to many clients with leukemia, is ndiscontinued during platelet transfusion and not resumed for at least 1 hour nafter transfusion. Amphotericin B can cause severe allergic reactions that are ndifficult to distinguish from transfusion reactions.

 Plasma Transfusions

 Historically, plasma infusions nhave been administered to replace blood volume, and they are occasionally still nused for this purpose. It is more common for plasma to be frozen immediately nafter donation. Freezing preserves the clotting factors, and the plasma cathen be used for clients with clotting disorders (Kennedy, 1999).

Fresh frozen plasma (FFP) is ninfused immediately after thawing while the clotting factors are still viable. nClients who are actively bleeding with a prothrombin time (PT) or partial nthromboplastin time (FIT) greater than 1.5 times normal are candidates for aFFP infusion (Harrahill & DeLoughery, 1998). ABO compatibility is nrequired for transfusion of plasma products. The volume of the infusion bag nis approximately 200 mL. The infusion takes place as rapidly as the client catolerate, generally over a 30- to 60-minute period, through a regular Y-set or nstraight-filtered tubing.

Cryoprecipitate is a nproduct derived from plasma. Clotting factors VIII and XIII, von Willebrand’s nfactor, fibronectin, and fibrinogen are precipitated from pooled plasma to nproduce cryoprecipitate. Clients with a fibrinogen level less than 100 mg/dL nare candidates for a cryoprecipitate infusion (Harrahill & DeLoughery, n1998). This highly concentrated blood product is administered to clients with nclotting factor disorders at a volume of 10 to 15 mL/unit. Although ncryoprecipitate can be infused, it is usually given by IV push within 3 nminutes. Dosages are individualized, and it is best if the cryoprecipitate is nABO compatible.

Granulocyte nTransfusions At some centers, neutropenic clients with infections nreceive granulocyte transfusions for WBC replacement. However, this practice is nhighly controversial because the potential benefit to the client must be nweighed against the potential severe reactions that often accompany granulocyte ntransfusions. The surfaces of granulocytes contaiumerous antigens that cacause severe antibody-antigen reactions when infused into a recipient whose nimmune system recognizes these antigens as non-self. In addition, transfused ngranulocytes have a very short life span and are probably of minimal benefit to nthe client (see Chapter 20). There is some evidence that treatment with nantibiotics alone results in better survival rates. Granulocytes are suspended nin 400 mL of plasma and should be transfused over a 45- to 60- minute period. nInstitutional policies often require more stringent monitoring of clients nreceiving granulocytes. A physician may need to be present in the hospital nunit, and vital signs may need to be taken every 15 minutes throughout the ntransfusion. Administration of amphotericin B and granulocyte transfusions nshould be separated by 4 to 6 hours.

TRANSFUSION REACTIONS

 

Clients can experience any of the following ntransfusion reactions: hemolytic, allergic, febrile, or bacterial reactions; ncirculatory overload; or transfusion-associated graft-versus-host disease n(GVHD). The nurse is vigilant to prevent serious complications through early ndetection and initiation of appropriate treatment.

Hemolytic TransfusioReactions Hemolytic transfusion reactions are caused by blood type nor Rh incompatibility. When blood containing antibodies against the recipient’s nblood is infused, antigen-antibody complexes are formed and released into the ncirculation. These complexes can destroy the transfused cells and initiate ninflammatory responses in the recipient’s blood vessel walls and organs. The nensuing reaction may be mild, with fever and chills, or life threatening, with ndisseminated intravascular coagulation (DIC) and circulatory collapse (Robb, n1999).

Other clinical signs include the nfollowing:

• Apprehension

• Headache

• Chest pain

• Low back pain

• Tachycardia

• Tachypnea.

• Hypotension

• Hemoglobinuria

• A sense of impending doom

The onset of a hemolytic transfusioreaction may be immediate or may not occur until subsequent units have beetransfused.

Allergic TransfusioReactions Allergic transfusion reactions are most often seen iclients with a history of allergy. They may have urticaria, itching, nbronchospasm, or occasionally anaphylaxis. Onset of this type of reactiousually occurs during or up to 24 hours after the transfusion. Clients with a nhistory of allergy can be given buffy coat-poor or washed red blood cells n(RBCs) in which the white blood cells (WBCs) and plasma have been removed. This nprocedure minimizes the possibility of an allergic reaction.

Febrile TransfusioReactions Febrile transfusion reactions occur most commonly in the nclient with anti-WBC antibodies, a situation seen after multiple transfusions. nThe recipient experiences the following: • Sensations of cold • Tachycardia • nFever • Hypotension • Tachypnea Again, the physician can order buffy coat-poor nRBCs or single-donor HLA-matched platelets. Leukocyte filters may also be used nto trap WBCs and prevent their transfusion into the client.

 Bacterial TransfusioReactions Bacterial transfusion reactions are seen after ntransfusion of contaminated blood products. Usually a gram-negative organism is nthe source because these bacteria grow rapidly in blood stored under nrefrigeration. Symptoms include the following: • Tachycardia • Hypotension • nFever • Chills • Shock The onset of a bacterial transfusion reaction is nrapid. 

Circulatory Overload Circulatory noverload can occur when a blood product is administered too quickly (Goldy, n1998). This complication is most common with whole-blood transfusions or whethe client requires multiple transfusions. Older adults are most at risk for nthis condition (see Chart 40-16). Symptoms include the following: • nHypertension • Bounding pulse • Distended jugular veins • Dyspnea • nRestlessness • Confusion The nurse can both manage and prevent this complicatioby monitoring intake and output, transfusing blood products more slowly, and nadministering diuretics.

Transfusion-Associated nGraft-Versus-Host Disease Transfusion-associated graft-versus-host ndisease (TA-GVHD) is an infrequent but life-threatening complication that caoccur in both immunosuppressed and immunocompetent clients. Its cause iimmunosuppressed clients is similar to that of GVHD associated with allogeneic nbone marrow transplantation (BMT), discussed on p. 855, in which donor T-cell nlymphocytes attack host tissues. The cause of TA-GVHD in immunocompetent hosts nis uncertain. Reactions are more common when the host and donor share similar nhuman leukocyte antigens (HLAs), such as in first-degree relatives or nindividuals with a similar ethnic background. Symptoms typically occur within 1 nto 2 weeks and include thrombocytopenia, anorexia, nausea, vomiting, chronic nhepatitis, weight loss, and recurrent infection. TA-GVHD has a 90% mortality nrate but can be prevented by using irradiated blood products, which destroy nT-cells and their cytokine products (Dreger & Tremback, 1998).

AUTOLOGOUS BLOOD nTRANSFUSIONS Autologous blood transfusions involve collection and ntransfusion of the client’s own blood. Advantages of this type of transfusioare guaranteed compatibility and elimination of the risk of transmitting ndiseases such as hepatitis or HIV. The four types of autologous blood ntransfusions are preoperative autologous blood donation, acute normovolemic nhemodilution, intraoperative autologous transfusion, and postoperative blood nsalvage. Preoperative autologous blood donation, the most common type of nautologous blood transfusion, involves collection of whole blood from the nclient, division into components, and then storage for later use (such as after na scheduled surgical procedure).

As long as hematocrit and hemoglobilevels are within a safe range, the client can donate blood on a weekly basis nuntil the prescribed amount of blood is obtained. Fresh packed RBCs may be nstored for 42 days. For individuals with rare blood types, blood may be frozefor up to 10 years. Platelets and plasma may be collected via pheresis. Some ncardiovascular problems and bacteremia are contraindications for autologous nblood donation. Acute normovolemic hemodilution involves withdrawal of a nclient’s RBCs and volume replacement just before a surgical procedure. The goal nis to decrease RBC loss during surgery. The blood is stored at room temperature nfor up to 6 hours and reinfused after surgery. This type of autologous transfusiois appropriate for healthy clients but is contraindicated for individuals who nare anemic or who have poor renal function. Intraoperative autologous ntransfusion and postoperative blood salvage involve the recovery and reinfusioof a client’s own blood, collected either from an operative field or npostoperatively from a wound.

Several commercial products are navailable that collect, filter, and drain the blood into a transfusion bag. nThis autologous blood is often used for trauma or surgical clients with severe nblood loss and must be reinfused within 6 hours. The nurse transfuses nautologous blood products using the guidelines previously described. Although nthe client receiving autologous blood is not at risk for most types of ntransfusion reactions, the nurse must still assess for circulatory overload or nbacterial transfusion reactions that can occur as a result of contamination