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Module 6: Alterations in Red Blood Cell function and Hemostasis Acute Anemias: Disorders of Inadequate Erythrocytes Anemia: without

t blood; reduction of or dysfunction of erythrocytes. Sign of an underlying disorder. Clinical manifestations: attributable to impaired oxygen transport o Tissue hypoxia: depends on: Rate of onset: Slow: asymptomatic as long as the body is not stressed. Hb 7 or 8 g/dl. Rapid: insufficient time for compensation severe hypoxemia and tissue ischemia Underlying cause: Sickle cell: microvascular occlusion Aplastic anemia: pancytopenia
Anemia Triggering Event

Mechanisms RBC Production RBC Destruction Blood loss

RBC and Hgb O2 carrying capacity (impaired O2 transport) Tissue Hypoxia Compensatory responses General Activity & temp intolerance Heart BP, HR, SV O2 demand on heart angina possible Lungs Kidneys RAAS activity erythropoietin secretion stim of bone marrow bone marrow discomfort

Major Manifestations

Neuro

GI

Integument pale skin & MM

vertigo

Anorexia

RR depth work of breathing dyspnea, orthopnea

irritability

inability to concentrate

Alteration Decreased oxygen affinity

Tissue Hypoxia

Patho Improves oxygen extraction from available hemoglobin to maintain adequate delivery and maintain tissue oxygenation Oxygen supply and demand imbalance

S/S Right shift on oxyhemoglobin-dissociation curve. Decreased PvO2 and SvO2. General Fatigue Pulmonary dyspnea on exertion CV Angina Peripheral intermittent claudication; night muscle cramps Neuro Headache, lightheadedness GI abdominal cramping; nausea

Module 6: Alterations in Red Blood Cell function and Hemostasis Compensatory Mechanism Selective increased tissue perfusion Increased CO (w/out inc BP) Patho Shunts blood from nonvital areas of body to priority organs. The heart works harder to deliver O2. BP does not inc bc blood viscosity is reduced and peripheral vascular resistance becomes lower due to selective vasodilation Develops with severe anemia Production of erythropoietin maintains and inverse relationship with the hemoglobin concentration to maintain a balance of RBC production with RBC loss

2 S/S Pale skin and mm. urine output usually remains normal. Tachycardia, systolic flow murmur, severe anemia; angina, high output heart failure, cardiomegaly (possible), Tachypnea, decreased a-A gradient, exertional dyspnea & orthopnea Stress reticulocytosis increased number and proportion of reticulocytes, increased bone marrow discomfort

Increased Pulmonary Function Increased RBC Production

Grading: o Grade 1 (mild): 10 10.9 o Grade 2 (Moderate): 8.0 9.9 o Grade 3 (Serious/Severe): 6.5-7.9 o Grade 4 (Life threatening): less than 6.5 Classification: o Decreased RBC Production Iron Deficiency Anemia: most common form worldwide. Inadequate dietary intake, increased demand (pregnancy), increased loss of iron (acute or chronic bleeding) problem with iron uptake. Megaloblastic Anemia: large RBCs with large immature nuclei and fragile membranes that are prone to rupture. Vit B12 and folic acid are necessary for RBC development Acquired Aplastic Anemia: decreased production of blood cells from bond marrow failure Peak in young adults (age 15-25) Lesser peak in elderly (age 65-69) Etiology: Benzene, Drugs, infections, ionizing radiation, unknown (idiopathic) Patho: damaged or impaired stem cells inhibit RBC production Treatment: o Supportive: blood transfusion, AB therapy o Immunosuppressive: antithymocyte globulin (ATG), steroids, cyclosporin o Hematopoietic stem cell replacement (HSCT): younger pts. o Increased Destruction of RBCs Hemolytic Anemia: premature destruction of RBCs. Acquired o Drug induced: sulfonamides o Infectious agent: toxins hemolyze cells; malaria o Physical agent: heat/burns o Microangiopathy-induced: fragment as they move through damaged small blood vessels. (DIC, HELLP syndrome, TTP, etc)

Module 6: Alterations in Red Blood Cell function and Hemostasis

Immune mediated: production of AB against own RBCs; ABO blood type incompatibility between mother and baby; Rh incompatibility in newborns o Increased Blood Loss: acute or chronic; gross or occult bleeding. Acute Blood Loss Anemia o Trauma a major cause. Also surgery or acute GI bleeding. o Hgb and Hct do not initially reflect anemia bc plasma and cells are initially lost. Cannot evaluate full extent of the bleed until 48-72 hours later. o Treatment: correct underlying cause; fluid resuscitation and vasopressors; blood transfusion maybe Anemia of Inflammation and Critical Illness o Anemia of inflammation (AI): deficient RBC production in the presence of low serum iron and reduced iron-binding capacity despite adequate bone marrow iron stores. Happens in people with chronic inflammation and infections. Inflammatory bowel diseases, rheumatoid disorders, SIRS, sepsis, chronic abscesses, HIV/AIDS o Critical Illness Develops rapidly, w/in days of illness onset. Over 90% of critically ill pts develop anemia by the third day post admission to ICU. Blood loss through sampling, acute loss, occult loss through stress, chemo related. o Nursing considerations: monitor pts oxygenation status and support tissue oxygenation

Sickle Cell Disease A Disorder of Abnormal RBCs Type Sickle Cell Anemia Sickle Cell Trait Description Hemoglobin is predominantly Hg S (75-95%). Homozygous inheritance. Most severe form of dz. Hemoglobin is Hb A/S. Heterozygous inheritance. Carrier. Rarely develop clinical manifestations

Epidemiology: 20-40% heterozygous prevalence in Africa. In USA prevalence is 8% and primarily found in African Americans. Reduces severity and duration of malaria. Patho: Normally, Hb S functions just fine. But, when PaO2 and SaO2 drop, producing a deoxygenated state, the Hb S polymerizes, forming fibrous polymers, giving it the sickled shape. This shape makes it stiffer and sticky, causing it to obstruct flow in small capillaries and adhere to the endothelium of vessel walls. Abnormal RBCs are destroyed by the spleen but can pool in the spleen and cause tissue ischemia and infarction that destroys the spleen eventually. Manifestations: initially develop between 6 mos to 1 yr. o Intermittent episodes of microvascular occlusion Ischemic pain/tenderness in affected area Organ/tissue dysfunction when the occlusion is Tachycardia Fever o Chronic hemolytic anemia Hgb: 7-10g/dl Hct: 15-30% Elevated reticulocyte count o Sickle Cell Crises Vaso-occlusive (painful) crisis: ischemic pain from sickled cells occluding microcirculation. Usually lasts less than 1 week. Repeated crises result in organ damage.

Module 6: Alterations in Red Blood Cell function and Hemostasis Aplastic crises: erythropoiesis cant meet high demand for new RBCs due to short life span of abnormal RBCs. Global tissue hypoxia results. Morbidity/Mortality: major cause of death is infection o 10% of young children develop sepsis and meningitis by age 5 with a mortality rate of 25%. Diagnosis o Positive family history o Sickle cell screening test o Hemoglobin electrophoresis ordered when screening test is positive. Treatment o Disease related education: avoid crisis o Prevent anemia complications o Psychological support o Genetic counseling o Vaccinations o Hydroxyurea: anti sickling agent

Polycythemia: A Disorder of Excessive RBCs The production and presence of an abnormally high number of RBCs. o Elevated red cell mass and abnormally elevated hematocrit. Primary: polycythemia vera (PV). Excessive production of all three cell types but degree of RBC production is worst. o Risk factors: chemical exposure, unclear genetic influences. o Characteristics: significant increase in RBC mass elevated Hct hypervolemia increased viscosity of the blood splenomegaly from pooling RBCs o Manifestations: thrombosis and acute leukemia Secondary: erythrocytosis occurs as a compensatory response to chronic tissue hypoxia o Manifestations: headache, dizziness, weakness, hypertension, plethora, night sweats, elevated EPO levels Diagnosis: positive HX of chronic conditions that can result in hypoxia (smoking, chronic heart disease, sleep apnea syndrome, COPD), Labs, ABGs Treatment: eliminate/reduce underlying cause Thrombocytopenia: A Problem of Hemostasis A platelet count of less than 150,000 cells/mcL. Major complication is bleeding Manifestations: petechiae and purpura on skin and mm; epistaxis (determine length of time to stop the bleeding an if its 1 or 2 nostrils). Causes: o Decreased platelet production: bone marrow issue chemicals, drugs, irradiation o Increased destruction: immune reaction o Increased utilization: idiopathic thrombocytopenia purpura (ITP) o Problems with distribution: splenomegaly spleen is holding on to them, not letting them into blood. (cirrhosis, leukemia, lymphoma Immune-Mediated Heparin-Induced Thrombocytopenia (HIT type II) o Life threatening complication of heparin therapy.

Module 6: Alterations in Red Blood Cell function and Hemostasis

o Patho: decreased platelet counts plus formation of thrombi. The heparin and platelet factor 4 (PF4) bind, forming a heparin-PF4 complex that the immune system recognizes as foreign and makes antibodies to it, which attach to the complex. This new complex activates other platelets to initiate thrombotic activity, which leads to thrombi. o Treatment: d/c the heparin and initiate alternative anticoagulant therapy, but not warfarin. Disseminated Intravascular Coagulation: A Problem of Hemostasis Systemic activation of the coagulation cascade. A complication of some underlying acute condition, usually sepsis Risk factors: o Sepsis o Severe trauma or burns o Shock o Abruptio placenta o ABO incompatibility, severe liver dz, disseminated cancer or leukemia Patho: excessive systemic clotting followed by excessive bleeding o Platelet activation: massive numbers are activated resulting in microvascular occlusion. Eventually platelet supply is used up, causing thrombocytopenia and bleeding o Clot formation: excessive thrombin is produced and increases clot formation in microcirculation. o Fibrinolysis: blood is coagulating at the same time the clots are being dissolved, resulting in bleeding from the consumption of platelets and coag factors and tissue ischemia Clinical Findings: o Bleeding first and most obvious sign o Ischemic organ dysfunction o Lungs mild to severe problems. o Cerebral vasculature risk for hemorrhage , change in mental status o Shock o Labs platelet count, clotting time, thrombin time, fibrinogen, blood film Treatment: o Treat underlying disease is imperative o Volume replacement and correction of hypotension to improve blood flow o Blood components FFP o Evaluate replacement therapy q 8 hrs. o Heparin therapy only in certain cases Nursing: o Monitor patients at risk o Supportive: anxiety, decreased CO, Fear, fluid volume, pain, skin integrity, tissue perfusion Blood Component Therapy in the Adult Give only the specific constituent that is lacking in the blood. Whole Blood: 1 unit is about 500 ml. treat hypovolemic shock Packed Red Blood Cells: provides the equivalent amount of hemoglobin as whole blood but in half the volume. Used for treating associated with trauma and surgery Platelets: used for severe thrombocytopenia, from any cause, to treat acute bleeding or prevent it. Plasma: o Fresh frozen (FFP): use w/in 24 hrs of thawing. Treats clotting factor deficiencies, not platelet replacement o Cryoprecipitate: derived from FFP, contains coagulation factors. Use w/in 4 hrs. used for hypofibrinogenemia.

Module 6: Alterations in Red Blood Cell function and Hemostasis o Factor concentrates: used for hemophilia A and B. used on a regular prophylactic basis or used during acute bleeding episode. Nursing Implications of Administering Blood o Risks: Transfusion reactions: allergic, febrile, and acute hemolytic Transfusion related complication: infection, acute lung injury, circulatory overload.

Nursing Assessment of the Patient with Problems of Erythrocytes or Hemostasis Neuro: changes related to hypoxia or bleeding. o LOC, pupillary checks, cranial nerve assessment, increased intracranial pressure (headache, weakness) Cardiopulmonary: compensatory vital signs tachycardia, tachypnea, changes in BP. Check for occult blood, vitals, hemodynamic parameters (hypovolemic shock) GI: Hepatomegaly, splenomegaly palpate. Monitor gastric secretions for occult or gross bleeding. Cramping, diarrhea, melena Renal: check urine for occult blood and hemoglobinuria port wine colored urine. Integument: monitor skin, nail beds, and mm for presence and degree of cyanosis. Look for petechiae, purpura, and ecchymosis. Look for a jaundice (hemolytic anemia) and puritis. Plan of Care: o Tissue hypoxia fatigue, activity intolerance, altered perfusion, ineffective breathing pattern, risk for injury, pain r/t hypoxia o Hypertension altered tissue perfusion, pain (headache) o Stasis of blood flow altered tissue perfusion, risk for thrombus and thromboembolism o Bleeding fluid volume deficit, decreased CO