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CHAPTER 40 Care of Patients with Hematologic Problems

Terms in this set (110)

Sickle cell disease (SCD) is a genetic disorder that results in chronic anemia, pain, disability, organ damage, increased risk for INFECTION, and early death. Normal hemoglobin (hemoglobin A [HbA]) molecule has two alpha chains and two beta chains of amino acids. Normal adult red blood cells usually contain 98% to 99% HbA, with a small percentage of a fetal form of hemoglobin (HbF).
SCD, at least 40% (and often much more) of the total hemoglobin is composed of an abnormal beta chain (hemoglobin S [(HbS]). HbS is sensitive to low oxygen content.
HbS are exposed to decreased oxygen conditions, the abnormal beta chains contract and pile together within the cell, distorting the cell into a sickle shape. Sickled cells become rigid and clump together, causing the RBCs to become "sticky" and fragile. The clumped masses of sickled RBCs block blood flow (Fig. 40-1), known as a vaso-occlusive event (VOE). VOE leads to further tissue hypoxia (reduced oxygen supply) and more sickle-shaped cells, which then leads to more blood vessel obstruction and ischemia. Cause progressive organ damage from anoxia and infarction. Conditions that cause sickling include hypoxia, dehydration, INFECTION, venous stasis, pregnancy, alcohol consumption, high altitudes, low or high environmental or body temperatures, acidosis, strenuous exercise, emotional stress, and anesthesia. Usually sickled cells go back to normal shape when the precipitating condition is removed, the blood oxygen level is normalized, and proper tissue PERFUSION resumes. Some of the hemoglobin remains twisted.
The average life span of an RBC containing 40% or more of HbS is about 10 to 20 days compared to 120. Reduced RBC life span causes hemolytic (blood cell-destroying) anemia.
CRISES have a sudden onset, which are periodic episodes of extensive cellular sickling. Damage results from tissue hypoxia, anoxia, ischemia, and cell death. Organs begin to have small infarcted areas and scar tissue formation, and eventually organ failure results. Tissues most often affected are the spleen, liver, heart, kidney, brain, joints, bones, and retina.
Pain is the most common manifestation of SCD crisis.
Cardiovascular changes, including the risk for high-output heart failure, occur because of the anemia. Assess the patient for shortness of breath and general fatigue or weakness. Other problems may include murmurs, the presence of an S3 heart sound, and increased jugular-venous pulsation or distention. Compare peripheral pulses, temperature, and capillary refill in all extremities. Extremities distal to blood vessel occlusion are cool to the touch with slow capillary refill and may have reduced or absent pulses. Heart rate may be rapid and blood pressure may be low to average.
Priapism is a prolonged erection that can occur in men who have SCD. The cause is excessive vascular engorgement in erectile tissue. Urinary retention!
Skin changes include pallor or cyanosis because of poor GAS EXCHANGE from decreased PERFUSION. Examine the lips, tongue, nail beds, conjunctivae, palms, and soles of the feet for color. With cyanosis, the lips and tongue are gray and the palms, soles, conjunctivae, and nail beds have a bluish tinge. Jaundice results from RBC destruction and release of bilirubin. To assess for jaundice in patients with darker skin, inspect the roof of the mouth for a yellow appearance. Examine the sclera closest to the cornea. Jaundice equals itching. Inspect the legs and feet for ulcers or darkened areas that may indicate necrotic tissue.
Abdominal changes include damage to the spleen and liver. In crisis, abdominal pain is diffuse and steady, involving the back and legs. The liver or spleen may feel firm and enlarged with a nodular or "lumpy" texture in late stage.
Kidney and urinary changes are common. Chronic kidney disease occurs as a result of anoxic damage to the kidney nephrons. The urine contains protein, and the patient may not concentrate urine. Eventually, the kidneys fail, resulting in little or no urine.
Musculoskeletal changes occur because arms and legs are often sites of blood vessel occlusion. Joints may be damaged from hypoxic episodes and have necrotic degeneration. Inspect the arms and legs, and record any areas of swelling, temperature, or color difference. Ask patients to move all joints. Record the range of motion and any pain.
Central nervous system (CNS) changes may occur. With crises, patients may have a low-grade fever. If the CNS has infarcts or repeated episodes of hypoxia, patients may have seizures or manifestations of a stroke. Assess for the presence of "pronator drift," bilateral hand grasp strength, gait, and coordination.
A deficiency of circulating red blood cells (RBCs) because of failure of the bone marrow to produce these cells. It is caused by an injury to the immature precursor cell for red blood cells. Although aplastic anemia sometimes occurs alone, it usually occurs with leukopenia (a reduction in white blood cells [WBCs]) and thrombocytopenia (a reduction in platelets), a condition known as pancytopenia.
The most common type of the disease is caused by long-term exposure to toxic agents, drugs, ionizing radiation, infection, or idiopathic.
Common hereditary form of the disease is Fanconi's anemia.
The patient has manifestations of severe anemia. A complete blood count (CBC) shows severe macrocytic anemia, leukopenia, and thrombocytopenia. A bone marrow biopsy may show replacement of cell-forming marrow with fat. Infection is common.
Blood transfusions are used only when the anemia causes disability or when bleeding is life threatening. Unnecessary transfusion increases the chances for developing immune reactions to platelets. Discontinued as soon as the bone marrow begins to produce RBCs.
Hematopoietic stem cell transplantation with donor cells is the most successful method of treatment for aplastic anemia that does not respond to other therapies.
Immunosuppressive therapy helps patients who have the types of aplastic anemia with a disease course similar to that of autoimmune problems. Drugs such as prednisone, antithymocyte globulin (ATG), and cyclosporine A (Sandimmune) have resulted in partial or complete remissions. For moderate aplastic anemia, daclizumab (Zenapax) has improved both blood counts and transfusion requirements. Splenectomy may be needed for patients with an enlarged spleen that is either destroying normal RBCs or suppressing their development.
In polycythemia, the number of red blood cells (RBCs) in the blood is greater than normal. The blood of a patient with polycythemia is hyperviscous (thicker than normal blood).
Polycythemia vera (PV) is a disease with a sustained increase in blood hemoglobin levels to 18 g/dL, an RBC count of 6 million/mm3, or a hematocrit of 55% or greater. PV is a cancer of the RBCs with three major hallmarks: massive production of RBCs, excessive leukocyte production, and excessive production of platelets. More than 90% of patients with PV show a mutation of the JAK2 kinase gene. Extreme hypercellularity (cell excess) of the peripheral blood occurs.
Facial skin and mucous membranes have a dark, purple or cyanotic, flushed (plethoric) appearance with distended veins. Intense itching caused by dilated blood vessels, and poor PERFUSION. Thick blood moves more slowly and places increased demands on the heart, resulting in hypertension. Vascular stasis causes thrombosis (CLOTTING) within the smaller vessels, occluding them, which leads to tissue hypoxia, anoxia and, later, to infarction and necrosis. Tissues most at risk for this problem are the heart, spleen, and kidneys.
Cell life spans are shorter. The shorter life spans and increased cell production cause a rapid turnover of circulating blood cells. This rapid turnover increases the amount of cell debris (released when cells die) in the blood, adding to the general "sludging" of the blood. This debris includes uric acid and potassium, which cause the manifestations of gout and hyperkalemia (elevated serum potassium level).
Oxygen-carrying capacity is impaired from abnormal RBCs, and patients have poor GAS EXCHANGE with severe hypoxia. Bleeding problems are common because of platelet impairment.
Cardiovascular changes often are related to adjustments needed when PERFUSION and GAS EXCHANGE are reduced. The heart rate is increased, and blood pressure is decreased. Murmurs (abnormal blood flow sounds in the heart) and bruits (abnormal blood flow sounds over arteries) may be heard. Capillary refill is slow. When the WBC count is greatly elevated and blood is highly viscous, blood pressure is elevated with a bounding pulse.
Respiratory changes are related to reduced GAS EXCHANGE from anemia and to INFECTION. Respiratory rate increases as anemia becomes more severe. If a respiratory infection is present, the patient may have coughing and dyspnea. Abnormal breath sounds are heard.
Skin changes include pallor and coolness to the touch as a result of reduced PERFUSION from anemia. Pallor is most evident on the face, around the mouth, and in the nail beds. The conjunctiva of the eye also is pale, as are the creases on the palm. Petechiae may be present on any area of skin surface, especially the legs and feet. Inspect for skin infections or injured areas that have failed to heal. Inspect the mouth for gum bleeding and any sore or lesion.
Intestinal changes may be related to an increased bleeding tendency and to fatigue. Weight loss, nausea, and anorexia are common. Examine the rectal area for fissures, and test stool for occult blood. Many patients with leukemia have reduced bowel sounds and are constipated because reduced perfusion. Enlargement of the liver and spleen and abdominal tenderness also may be present.
Central nervous system (CNS) changes include cranial nerve problems, headache, and papilledema from leukemic invasion of the CNS. Seizures and coma also may occur.
Miscellaneous changes can include bone and joint tenderness as the marrow is damaged and the bone reabsorbs. Leukemic cells invade lymph nodes, causing enlargement.
General Condition
• Age
• History of allergies
• History of chemotherapy, radiation therapy, or other immunosuppressive therapies, such as steroid use
• Chronic diseases
• History of febrile neutropenia and associated symptoms
• Nutrition status
• Functional status—problems with immobility
• Tobacco use—cigarettes, pipe, cigars, oral
• Recreational drug use
• Alcohol use
• Prescribed and over-the-counter drug use
• Baseline and ongoing vital signs—blood pressure, heart rate, respiratory rate, and temperature
Skin and Mucous Membranes
• Thorough inspection of all skin surfaces with attention to axillae, anorectal area, and under breasts; inspection of skin for color, vascularity, bleeding, lesions, edema, moist areas, excoriation, irritation, erythema; general condition of hair and nails, pressure areas, swelling, pain, tenderness, biopsy or surgical sites, wounds, enlarged lymph nodes, catheters, or other devices
• Inspection of oral cavity, including lips, tongue, mucous membranes, gingiva, teeth, and throat—color, moisture, bleeding, ulcerations, lesions, exudate, mucositis, stomatitis, plaque, swelling, pain, tenderness, taste changes, amount and character of saliva, ability to swallow, changes in voice, dental caries, patient's oral hygiene routine
• History of current skin or mucous membrane problems
Head, Eyes, Ears, Nose
• Pain, tenderness, exudate, crusting, enlarged lymph nodes
• Respiratory rate and pattern, breath sounds (presence/absence, adventitious sounds), quantity and characteristics of sputum, shortness of breath, use of accessory muscles, dysphagia, diminished gag reflex, tachycardia, blood pressure
• Pain, diarrhea, bowel sounds, character and frequency of bowel movements, constipation, rectal bleeding, hemorrhoids, change in bowel habits, sexual practices, erythema, ulceration
• Dysuria, frequency, urgency, hematuria, pruritus, pain, vaginal or penile discharge, vaginal bleeding, burning, lesions, ulcerations, characteristics of urine
Central Nervous System
• Cognition, level of consciousness, personality, behavior
• Tenderness, pain, loss of function
All personnel must use extreme care during all nursing procedures. Frequent, thorough handwashing is of the utmost importance. Anyone with an upper respiratory tract infection who enters the patient's room must wear a mask. Observe strict asepsis.
Ensure that the patient is in a private room to reduce cross-contamination. Do not allow standing water in vases, denture cups, or humidifiers in the patient's room, because they are breed grounds.
Some facilities place a high-efficiency particulate air (HEPA) filtration or laminar airflow system.
The patient with leukopenia may have a severe infection without pus and with only a low-grade fever.
Monitor the patient's daily CBC with differential WBC count and absolute neutrophil count (ANC). Inspect the mouth during every shift. Assess the lungs every 8 hours for crackles, wheezes, and reduced breath sounds. Assess urine for odor and cloudiness. Ask about any urgency, burning, or pain. Assess VS for fever.
Obtain blood for bacterial and fungal cultures from IV sites. After the specimens are obtained, the patient begins IV antibiotics.
Skin care is important for preventing INFECTION in the patient with leukemia because the skin may be the only intact defense. Teach him or her about hygiene, and urge daily bathing. If the patient is immobile, turn him or her every hour and apply skin lubricants.
Perform pulmonary hygiene every 2 to 4 hours. Listen to the lungs for crackles, wheezes, and reduced breath sounds. Urge the patient to cough and deep breathe or to perform sustained maximal inhalations every hour.
Taken either from the patient directly (autologous stem cells), an HLA-identical twin (syngeneic stem cells), or from an HLA-matched person (allogeneic stem cells).
Bone marrow harvesting occurs after a suitable donor is identified. Marrow is removed through multiple aspirations from the iliac crests. About 500 to 1000 mL of marrow is aspirated, and the donor's marrow regrows. The marrow is then filtered and, if autologous, is treated to rid the marrow of any remaining cancer cells. Allogeneic marrow is transfused into the recipient immediately. Autologous marrow is frozen for later use.
Monitor the donor for fluid loss, assess for complications of anesthesia, and manage pain. Donors are hydrated with saline infusions before and immediately after. Assess the harvest site/dressing.
Peripheral blood stem cell (PBSC) harvesting requires three phases: mobilization, collection by apheresis, and reinfusion. PBSCs are stem cells that have been released from the bone marrow and circulate within the blood. During the mobilization phase, chemotherapy or hematopoietic growth factors are given to the patient for an autologous collection, and hematopoietic growth factors alone are given to the donor for an allogeneic or syngeneic collection. These agents increase the numbers of stem cells and WBCs in the peripheral blood. Drug used is plerixafor (Mozobil).
Stem cells are then collected by apheresis (withdrawing whole blood, filtering out the cells, and returning the plasma to the patient).
During apheresis, complications include catheter clotting and hypocalcemia (caused by anticoagulants). Low calcium levels may cause numbness or tingling in the fingers and toes, abdominal or muscle cramping, or chest pain.
Cord blood harvesting involves obtaining stem cells from umbilical cord blood of newborns.
The conditioning regimen serves two purposes: (1) to "wipe out" the patient's own bone marrow, thus preparing him or her for optimal graft take; and (2) to give higher-than-normal doses of chemotherapy and/or radiotherapy to rid the person of cancer cells (myeloablation). Regimen usually includes high-dose chemotherapy and, less commonly, total-body irradiation (TBI).
A non-myeloablative approach may be used instead. Non-myeloablative regimens use lower doses of chemotherapy and/or lower dose of TBI that allow for recovery of a recipient's own immune system. The use of non-myeloablative conditioning regimens decreases the chemotherapy side effects but relies on the development of graft-versus-host disease (GVHD) for the control of the cancer.
Myeloablative conditioning regimens use high doses of chemotherapy with or without radiation therapy to completely destroy a recipient's bone marrow, allowing for replacement by a new immune system.
During conditioning, bone marrow and normal tissues respond immediately to the chemotherapy and radiation. The patient has all of the expected side effects associated with both therapies. When chemotherapy is given in high doses, these side effects are more intense than those seen with standard doses.
Late effects from the conditioning regimen may occur as late as 3 to 10 years after transplantation. These problems include veno-occlusive disease (VOD), skin toxicities, cataracts, lung fibrosis, second cancers, cardiomyopathy, endocrine complications, and neurologic complications.
INFECTION and poor CLOTTING with bleeding are severe problems because recovery period. Care for this patient is the same as for the patient during induction therapy.
In addition to the problems related to the period of pancytopenia (too few circulating blood cells), other complications of HSCT include failure to engraft, development of graft-versus-host disease (GVHD), and veno-occlusive disease (VOD).
Failure to engraft occurs when the donated stem cells fail to grow in the bone marrow and function properly. The causes include too few cells transplanted, attack or rejection of donor cells by the recipient's remaining immune system cells, infection of transplanted cells, and unknown biologic factors. If the transplanted cells fail to engraft, the patient will die unless another transplant with stem cells is successful.
Graft-versus-host disease (GVHD) is when immunocompetent cells of the donated marrow recognize the patient's (recipient) cells, tissues, and organs as foreign and start an immunologic attack against them. The graft is actually trying to attack the host tissues and cells. The tissues usually damaged are the skin, eyes, intestinal tract, liver, female genitalia, lungs, immune system, and musculoskeletal system. Fig. 40-6 shows the typical skin appearance of GVHD. GVHD indicates successful engraftment.
Management of GVHD involves limiting the activity of donor T-cells by using drugs to suppress IMMUNITY such as cyclosporine, tacrolimus, methotrexate, corticosteroids, mycophenolate mofetil (Cellcept, MMF), and antithymocyte globulin (ATG).
Veno-occlusive disease (VOD) is the blockage of liver blood vessels by CLOTTING and inflammation (phlebitis). Patients who received high-dose chemotherapy, especially with alkylating agents, are at risk for life-threatening liver complications. Manifestations include jaundice, pain in the right upper quadrant, ascites, weight gain, and liver enlargement.
Because there is no way of opening the liver vessels, treatment is supportive. Early detection improves the chance for survival. Fluid management is also crucial. Assess the patient 814daily for weight gain, fluid retention, increases in abdominal girth, and hepatomegaly.
• Reassure the patient that fatigue is temporary and energy levels will improve over a period of weeks to months. Stress that a return to previous energy levels may take as long as a year.
• Teach the patient that shortness of breath and palpitations are symptoms of over-activity.
• Instruct the patient to stop activity when shortness of breath or palpitations are present.
• Space care activities at least an hour apart, and avoid the time right before or right after meals.
• Schedule care activities at times when the patient has more energy (e.g., immediately after naps).
• Perform complete bed bath only every other day. In between complete baths, ensure cleansing of face, hands, axillae, and perineum.
• In collaboration with other members of the health care team, cancel or reschedule non-essential tests and activities.
• Provide four to six small, easy-to-eat meals instead of three larger ones.
• Urge the patient to drink small amounts of protein shakes or other nutritional supplements.
• During periods of extreme fatigue, encourage the patient to allow others to perform personal care.
• Help the patient identify one or two lead visitors (those designated as allowed to visit at any time and who do not disturb the patient).
• Selectively limit non-lead visitors when the patient is resting or sleeping.
• Remind families that, although independence is important, independence in ADLs during extreme fatigue can be detrimental to the patient's health.
• Monitor oxygen saturation and respiratory rate during any activity to determine patient responses and activity tolerance.
• Avoid crowds and other gatherings of people who might be ill.
• Do not share personal toilet articles, such as toothbrushes, toothpaste, washcloths, or deodorant sticks, with others.
• If possible, bathe daily.
• Wash the armpits, groin, genitals, and anal area at least twice a day with an antimicrobial soap.
• Clean your toothbrush daily by either running it through the dishwasher or rinsing it in liquid laundry bleach and then rinsing it with running water.
• Wash your hands thoroughly with an antimicrobial soap before you eat or drink, after touching a pet, after shaking hands with anyone, as soon as you come home from any outing, and after using the toilet.
• Eat a low-bacteria diet, and avoid salads, raw fruits and vegetables, and undercooked meat.
• Wash dishes between uses with hot, sudsy water, or use a dishwasher.
• Do not drink water that has been standing for longer than 15 minutes.
• Do not reuse cups and glasses without washing.
• Avoid changing pet litter boxes. If unavoidable, use gloves or wash hands immediately.
• Avoid keeping turtles and reptiles as pets.
• Do not feed pets raw or undercooked meat.
• Take your temperature at least twice a day.
• Report any of these manifestations of infection to your physician immediately:
▪ Temperature greater than 100° F (38° C)
▪ Persistent cough (with or without sputum)
▪ Pus or foul-smelling drainage from any open skin area or normal body opening
▪ Presence of a boil or abscess
▪ Urine that is cloudy or foul smelling, or burning on urination
• Take all drugs as prescribed.
• Do not dig in the garden or work with houseplants.
• Avoid travel to areas of the world with poor sanitation or inadequate health care facilities.
Non-Hodgkin's lymphoma (NHL) includes all lymphoid cancers that do not have the Reed-Sternberg cell. NHL generally spreads through the lymphatic system in a less orderly fashion than HL.
Incidence is higher among patients with solid organ transplantation, immunosuppressive drug therapy, and HIV disease. Chronic infection from Helicobacter pylori is associated with a type of lymphoma called mucosa-associated lymphoid tissue (MALT) lymphoma, and Epstein-Barr viral infection has been associated with Burkitt's lymphoma. There is an increased incidence of NHL among people exposed to pesticides, insecticides, and dust.
Patients usually have swollen lymph nodes (lymphadenopathy) or tumor spread to other organs (e.g., GI tract, skin, bone marrow, sinuses, thyroid, central nervous system). Enlarged lymph nodes may be the only manifestation of lymphoma. Painless swelling of the cervical, axillary, inguinal, and femoral nodes is most often seen. The diagnosis of NHL is made only after the biopsy of an involved lymph node. NHLs are broadly classified as B-cell or T-cell lymphomas, depending on the lymphocyte type that gave rise to the cancer.
Lactate dehydrogenase (LDH) levels and beta-2 microglobulin levels are also evaluated to measure tumor growth rates and calculate prognosis. (High LDH levels and high beta-2 microglobulin levels are associated with a poorer prognosis.) Cerebrospinal fluid is evaluated when lymphoma is present in the CNS, around the spinal column, brain, or testes, and when HIV-related lymphoma is diagnosed.
Patients with indolent (slow-growing) lymphomas usually have painless lymph node swelling at diagnosis. Those with more aggressive B-cell lymphomas may have large masses at diagnosis and manifestations. Constitutional manifestations ("B symptoms"), as seen in Hodgkin's lymphoma, occur in about one third of patients with aggressive lymphomas and rarely in indolent lymphomas. Bone marrow involvement in indolent lymphomas is common.
An elevation of serum total protein or a detection of a monoclonal protein (also known as paraprotein) in the blood or urine may be the only finding. Other common manifestations include fatigue, anemia, bone pain, pathologic fractures, recurrent bacterial INFECTIONS, and kidney dysfunction. A positive finding of a serum monoclonal protein is not sufficient to make a diagnosis. Multiple myeloma is distinguished from MGUS by having more than 10% of the bone marrow infiltrated with plasma cells, the presence of a monoclonal protein in the serum or urine, and the presence of osteolytic bone lesions.
Stages and prognostic groups based on the serum beta-2 microglobulin and albumin levels. Other factors that help determine prognosis include age, performance status, serum creatinine, serum albumin, serum calcium, lactate dehydrogenase (LDH) level, C-reactive protein, hemoglobin level, platelet count, quantitative immunoglobulins, beta-2 microglobulin, serum free light chains, serum protein electrophoresis (SPEP) with immunofixation, 24-hour urine for SPEP, and cytogenetic abnormalities found in the bone marrow biopsy.
The patient usually first notices fatigue, easy bruising, and bone pain. Bone fractures, hypertension, INFECTION, hypercalcemia, and fluid imbalance may occur as the disease progresses. Diagnosis is made by x-ray findings of bone thinning with areas of bone loss that resemble Swiss cheese, high immunoglobulin and plasma protein levels, and the presence of Bence-Jones protein (protein composed of incomplete antibodies) in the urine. A bone marrow biopsy is performed to diagnose the disease
Watchful waiting may be an option instead of chemotherapy. Standard treatment for multiple myeloma is the use of proteasome inhibitors, such as bortezomib (Velcade) or carfilzomib (Kyprolis), and immunomodulating drugs, such as thalidomide (Thalomid) or lenalidomide (Revlimid). All these agents, which are types of targeted cancer therapy, may be used alone or in combination with steroids, such as dexamethasone (Decadron).
Drug therapy is used to reduce tumor burden before transplantation. For patients who are not eligible for an autologous stem cell transplantation, standard chemotherapy drugs such as melphalan, prednisone, vincristine, cyclophosphamide, doxorubicin, and carmustine are usually effective in controlling but not curing the disease.
Myelosuppression is an expected side effect of many myeloma therapies. A nursing priority is to teach the patient about the manifestations. The risk for thromboembolic events is increased with the use of thalidomide and lenalidomide. Peripheral neuropathy can be challenging, causing pain and poor quality of life. GI side effects, such as nausea, vomiting, diarrhea, and constipation, are severe and can be life threatening.
Despite therapy, multiple myeloma remains largely incurable. Best outcomes are seen with autologous hematopoietic stem cell transplantation.
Most patients with multiple myeloma have bone pain, analgesics and alternative approaches for pain management.
The bone disease of multiple myeloma is treated with bisphosphonates (pamidronate [Aredia], zoledronic acid [Zometa], denosumab [Xgeva]), which inhibit bone resorption and can help reduce the skeletal complications.
Chart 40-12 lists best practices for transfusion therapy.
A health care provider's prescription is needed to administer blood components. The prescription specifies the type of component, the volume, and any special conditions. Verify the prescription for accuracy and completeness.
A separate consent form obtained from the patient before a transfusion according to agency.
A blood specimen is obtained for type and crossmatch. Usually a new type-and-crossmatch specimen is required at least every 72 hours.
Both Y-tubing and straight tubing sets are used for blood component infusion (Fig. 40-7). A blood filter (about 170 µm) to remove sediment from the stored blood products is included with blood administration sets and must be used to transfuse most, but not all, blood products.
Use normal saline ONLY as the solution to administer with blood products.
Priority action is to determine that the blood component delivered is correct and that identification of the patient is correct. Check the physician's prescription together with another registered nurse to determine the patient's identity and whether the hospital identification band name and number are identical to those on the blood component tag.
Examine the blood bag label, the attached tag, and the requisition slip to ensure that the ABO and Rh types are compatible with those of the patient. Check the expiration date, and inspect the product for discoloration, gas bubbles, or cloudiness, which are all indicators of bacterial growth or hemolysis.
RBCs are given to replace cells lost from trauma or surgery. Patients with problems that destroy RBCs or impair RBC maturation also may receive RBC transfusions. Packed RBCs, supplied in 250-mL bags, are a concentrated source of RBCs.
Blood transfusions are transplantations of tissue!! Donor and recipient blood must be carefully checked for compatibility. Compatibility is determined by two different antigen systems (cell surface proteins): the ABO system antigens and the Rh antigen.
RBC ANTIGENS are inherited. For the ABO system, a person inherits one of these:
• A antigen (type A blood)
• B antigen (type B blood)
• Both A and B antigens (type AB blood)
• Neither A nor B antigens (type O blood)
A person with type A blood forms antibodies against type B blood. A person with type O blood has not inherited either A or B antigens and will form antibodies against RBCs with either A or B antigens. If RBCs that have an antigen are infused into a recipient who does not share that antigen, the infused blood is recognized by the recipient's antibodies as non-self and the recipient then has a reaction to the transfused products.
An Rh-negative person is born without the Rh-antigen on his or her RBCs and does not form antibodies unless specifically sensitized to it. Sensitization can occur with RBC transfusions from an Rh-positive person or from exposure during pregnancy and birth. Once an Rh-negative person has been sensitized and antibodies develop, any exposure to Rh-positive blood can cause a transfusion reaction. Antibody development can be prevented by giving anti-Rh-immunoglobulin (RHoGAM) as soon as exposure to the Rh antigen is suspected. People who have Rh-positive blood can receive an RBC transfusion from an Rh-negative donor, but Rh-negative people should not receive Rh-positive blood.
Autologous blood transfusions involve collection and infusion of the patient's own blood. Four types of autologous blood transfusions are preoperative autologous blood donation, acute normovolemic hemodilution, intraoperative autologous transfusion, and postoperative blood salvage.
Autologous blood donation before surgery is the most common type of autologous blood transfusion. It involves collecting whole blood from the patient (who must meet certain criteria), dividing it into components, and storing it for later use. As long as hematocrit and hemoglobin levels are within a safe range, the patient can donate blood on a weekly basis until the prescribed amount of blood is obtained. Fresh packed RBCs 826may be stored for 40 days.
Acute normovolemic hemodilution involves withdrawal of a patient's RBCs and volume replacement just before a surgical procedure. The goal is to decrease RBC loss during surgery. The blood is stored at room temperature for up to 6 hours and reinfused after surgery. This type of autologous transfusion is not used with anemic patients or those with poor kidney function.
Intraoperative autologous transfusion and blood salvage after surgery are the recovery and reinfusion of a patient's own blood from an operative field or from a bleeding wound. Special devices collect, filter, and drain the blood into a transfusion bag. This blood is used for trauma or surgical patients with severe blood loss. The salvaged blood must be reinfused within 6 hours.
Transfuse autologous blood products using the guidelines previously described.