Anemia - a reduction in red blood cells (erythrocytes) which in turn decreases the oxygen-carrying capacity of blood. It is not a disease itself. Anemia reflects an abnormality in RBC number, structure or function.
Classification of anemias:
Morphologic - more accurate
Etiologic - more practical; according to cause
See Table 29-1; pg 737
I. Anemia caused by decreased erythrocyte production
A. Decreased Hb synthesis
1. Iron deficiency anemia - defined as anemia associated with either
inadequate absorption or
excessive loss of iron; Common in countries where nutrition is poor
& and where blood-
sucking parasites such as hookworm thrive. Pregnant women, young
children
and the
elderly are at risk for iron deficiency anemia. Also occurs with
chronic
blood loss such as
gastrointestinal bleeding. Menstruation is another common cause
Clinical Manifestations-
*Pallor, palpitations, dizziness, sensitivity to cold, *glossitis,
fatigue, stomatitis,
tachycardia, angina, *nails are rigid longitudinally, flattened,
concave.
See Table 29-3 on pg 738.
Management-
1. Treat the underlying disease - alcoholism, poor nutrition,
malabsorption.
2. Replace iron stores- drug therapy
a. Oral iron is inexpensive and convenient; 150-200 mg. elemental iron
daily.
b. Take with Vit C for better absorption.
c. Ingest with meals to reduce gastric irritation.
d. Instruct client that stools will turn black.
e. Constipation may occur necessitating stool softener.
f. Give liquid iron with straw; may stain teeth.
g. Administer IM iron preparation using Z-track method; may stain skin.
Do not massage site.
2. Thalassemia - a group of inherited, chronic blood disorders
characterized
by deficiencies in
the rate of production of the globin protein (part of hemoglobin).
Usually found in clients
of Mediterranean descent. Also called "Cooley's anemia".
Signs & Symptoms -
chronic anemia, splenomegaly/hepatomegaly, pallor, jaundice, Down's
appearance,
mental/physical retardation.
Treatment - usually transfusions.
B. Defective DNA Synthesis
1. Cobalamin (Vit B12) deficiency: Lack of intrinsic factor (a
protein
secreted by parietal
cells of gastric mucosa) necessary for absorption of Vit B12. Clients
who have had
gastrectomy or small bowel resection may have cobalamin deficiency.
Pernicious
anemia is an autoimmune disease. Fatal in 1 to 3 years without Vit
B12 injections.
Assessment - Schilling's test - determines if the client lacks
intrinsic
factor.(See pg
588, Kee).
Clinical Manifestations - like general anemia; see Table 29-3, pg
738
(Lewis). In
addition, tingling of hands & feet is experienced.
Management - Parenteral administration of cobalamin (Vit B12); usual
dose 1000mcg.
daily for 2 weeks; then weekly until Hct normal; then monthly for life.
An intranasal
form of cobalamin (Nascobal) is available. Self-administered weekly.
Nursing management - Evaluate client if positive family history for
pernicious anemia.
See nursing care plan 29-1 on pg 740 (Lewis) for general nursing
measures.
Protect from burns & trauma r/t neurologic impairment.
2. Folic acid deficiency - Folic acid is required for DNA synthesis
leading to RBC formation
and maturation.
Causes of folic acid deficiency include -
1. Poor nutrition - lack of leafy greens, liver, citrus fruits, legumes
and whole grains.
2. Malabsorption syndromes
3. Drugs that impede absorption of folic acid - methotrexate, oral
contraceptives,
anti-seizure drugs.
4. Alcohol abuse
5. Hemodialysis patients.
Clinical Manifestations-
Similar to cobalamin deficiency except absence of neurological symptoms
in folic
acid deficiency anemia.
Management-
Treated with folic acid replacement therapy. Usually 1 mg. per day
by mouth.
C. Decreased number of RBC precursors
1. Aplastic anemia - a life-threatening stem cell disorder resulting
in pancytopenia;
a. Congenital or idiopathic - caused by chromosomal alterations.
b. Acquired - exposure to chemicals (benzene, insecticides, arsenic,
alcohol); viral or
bacterial infections; prescribed medications (alkylating agents,
antiseizure
meds, anti-
microbials, gold)
Clinical Manifestations-
General manifestations of anemia, fatigue & dyspnea, susceptibility
to infections &
bleeding (ecchymosis, petechiae, epistaxsis).
Diagnosis - All bone marrow elements are decreased, WBC's, RBC's, &
platelets. Low
reticulocyte count; prolonged bleeding time. Serum iron & TIBC
elevated r/t erythroid
suppression. Bone marrow aspiration has increased yellow marrow (fat)
Management -
Identify & remove causative agent.
Prevent complications from infections & hemorrhage.
Treatment of choice for adults < 45 yrs. is bone marrow
transplantation.
Immunosuppression for older adults.
II. Anemia Caused by Blood Loss
A. Acute blood loss - caused by hemorrhage > 1000 cc.
Signs & symptoms: early: cool, moist skin, tachycardia,
hypotension,
late : decreased Hb & Hct.
B. Chronic blood loss- GI bleed, malignancy, ulcers, menorrhagia,
bleeding
hemorrhoids.
Signs & symptoms: decreased RBC, Hb, MCV(mean corpucular volume),
and MCHC
(mean corpuscular Hb concentration).
III. Anemia Caused by Increased Erythrocyte Destruction
A. Sickle Cell Disease(SCD) - a family of genetic disorders
collectively
referred to as
hemoglobinopathies, in which normal adult hemoglobin is partly or
completely
replaced
by sickle-shaped hemoglobin. Most often occurs in African-Americans;
occassionally
in those of Mediterranean descent, Hispanic, Caribbean, South &
Central American
peoples. Often fatal by middle-age.
1. Pathophysiology - Abnormal or sickle-shaped RBC's decrease O2
carrying
capacity.
Blood becomes more viscous(thick) which in turn increases hypoxia &
sickling of cells.
Anaerobic metabolism occurs because of hypoxia causing ischemia and
infarction to
organs. VERY PAINFUL. The body recognizes the sickled cell as abnormal
& the cel
is hemolyzed. The sickle cell has a shortened cell life of 7 to 20
days as
compared to the normal cell life of 120 days.
Precipitaing factors - conditions that cause hypoxia such as viral
or
bacterial infections,
high altitudes, emotional or physical stress, surgery, blood loss,
and dehydration (r/t
vomiting, diarrhea, or diaphoresis).
2. Diagnosis - Specially prepared screening tests (see Table 29-11, pg 751, Lewis)
3. Clinical Manifestations - Infants manifest symptoms at 10 - 12
weeks
of age. Failure to
thrive and impaired growth & development is seen in children with
SCD. General
signs & symptoms of anemia such as pallor (mucous membranes),
fatigue
& decreased
exercise tolerance are manifested. See Fig. 29-5 on pg 750 (Lewis).
A. Acute chest syndrome - unknown etiology; characterized by chest
pain,
cough, fever,
pulmonary infiltrates, and dyspnea.
B. Hand and foot syndrome - painful swelling of hands & feet caused
by bone infarction;
Frequently is the first symptom of SCD.
C. Infections - prone to infection r/t failure of spleen to phagocytize
foreign substances.
D. Sickle cell crisis - an acute episode of sickling. * The most common
type of crisis
results from occlusion of blood vessels from sickled cells. Tissue
hypoxia leads
to tissue death and pain. May persist for days to weeks. May lead to
shock &
death. Major causes of mortality is renal or pulmonary complications.
4. Nursing & collaborative management - supportive therapy
a. Client teaching - avoid high altitudes; adequate fluid intake,
prompt
treatment of infections. Pneumovax & flu vaccines; treat leg ulcers
with soaks & antibiotics;
Fanily planning & genetic counseling; support groups activities.
b. Sickle cell crisis - hospitalization; O2; IV fluids; rest;
antibiotics
for acute chest
syndrome; Pain management very important.
c. Droxia(hydroxyurea) - only antisickling agent that has been found
to be beneficial.
d. Bone marrow transplant - can cure SCD but remains rare treatment.
B. Enzyme deficiency anemia - (G6PD) - genetic disorder; deficiency of G6PD. Affects
African-American & Mediterranean population.
Signs & symptoms - back pain, jaundice, hemolysis (self-limiting).
Caused by viral or bacterial infections; drugs such as aspirin,
sulfonamides
& anti-
malarial drugs. Treatment is to discontinue the drug, treat infection.
C. Acquired hemolytic anemia - drug-induced or autoimmune
response.
Transfusion rx;
Hemolytic disease of the newborn (HDN) - formerly called erythroblastosis
fetalis.
Maternal antibodies previously sensitized through blood transfusion
or pregnancy,
destroy the RBC's of the fetus, resulting in a hemolytic anemia.
D. Hereditary spherocytosis - A defective gene causes the
formation
of abnormal RBC
membrane. Because of smaller surface area, inflexible sphere results
making it difficult
to travel through spleen and consequently are destroyed early.
Clinical manifestations - jaundice, splenomegaly, anemia. Newborns
show s & s first
24 hrs. of life.
Treatment - folic acid supplementation; splenectomy.
IV. Polycythemia - refers to abnormal increase in
erythrocytes
(RBC's). *Blood circulation is
impaired as a result of increased blood viscosity and volume.
Two types:
1. Polycythemia vera- bone marrow disorder characterized by
erythrocytosis,
leukicytosis,
& thrombocytosis. Unknown etiology. Clinical manifestations include
hypervolemia,
increased blood viscosity from RBC mass, and platelet destruction.
2. Secondary polycythemia - caused by hypoxia r/t high altitudes,
pulmonary
or cardiac
disease, defective O2 transport or tissue hypoxia.
Signs & Symptoms:
Headaches, hypertension, vertigo, tinnitus, blurred vision, epistaxsis,
ecchymosis,
GI bleed, thromboembolism, intermittent claudication, aangina, CHF,
hepatmegaly,
splenomegaly.
Diagnostics - Hct > 53%, increase in total RBC's, elevated WBC's
with
basophilia,
Elevated platelet, uric acid, alkaline phosphate, and Vit B12.
Medical management - phlebotomy to reduce HCT & Hb, radioactive
phosphorus,
alkylating agent (busulfan) to inhibit bone marrow activity.
Nursing management - client education, phlebotomy, signs of thrombosis
(swelling,
redness, pain), medications (dose, frequency, & side effects),
maintenance of hydration.
V. Defects in Hemostasis
A. Hemophilia - a hereditary bleeding disorder caused by defective
or deficient coagulation
factors; found in males.
Two types:
1. Hemophilia A - most common, 80% of cases, deficiency of Factor VIII.
2. Hemophilia B - also called Christmas Disease, 1 in 100,000 males;
deficiency of
Factor IX.
Von Willebrand's disease is seen in both sexes & is characterized
by a deficiency in
factor VIII and deficiency or absence of von Willebrand factor. Cause
prolonged bleeding
time.
Clinical manifestations - *prolonged bleeding from minor cuts; delayed
bleeding after minor
injuries, uncontrolled hemorrhage after tooth extraction, nose bleeds,
GI bleeds,
hematuria, ecchymosis, hemarthrosis of knees, elbows, ankles.(See Table
35-6, pg 1683,
Whaley & Wong; also Fig. 29-8 & 29-9, pg 760 & 761, Lewis).
Treatment:
1. Cryoprecipitates and Factor VIII concentrates
2. Complications include contamination of concentrates with HIV & hepatitis
3. Goal is to control bleeding
4. Cryoprecipitates contain Factor VIII and fibrinogen and is prepared from plasma. Frozen rapidly and kept frozen until use; thaw slowly and use within 6 hours.
5. Factor VIII concentrates are safer now and are reconstituted prior to use.
6. Factor IX deficiency is treated with Factor IX concentrate.
7. Complications include: infection, reaction to transfusion, HIV & hepatitis
Nursing Care:
1. stop topical bleeding as quickly as possible
2. administer blood component
3. hemarthrosis: immobilize joint and apply ice, as soon as bleeding has stopped begin ROM exercises. Weight bearing should be avoided until all swelling is gone.
4. manage life-threatening emergencies from hemorrhage.
5. Chronic management: teach patient signs & symptoms of bleeding; daily oral hygiene without trauma; understand how to prevent injury; non-contact sports. *Patient should seek immediate medical attention upon experiencing abdominal pain. (intra-abdominal hemorrhage, bleeding ulcers)
B.
Thrombocytopenia – See Lewis page 721
Decrease in the number of circulating platelets (thrombocytes); Normal 150,000-400,000mm cubed.
Etiology:
1. decreased platelet production
2. decreased platelet survival
3. increased platelet destruction (most common)
4. sequestration of blood in the spleen
Acquired thrombocytopenia is caused from defective platelet production. See Lewis, Table 30-12, page 722.
Most common cause of increased platelet destruction is immune thrombocytopenia purpura (ITP). Autoimmune disease.
C.
Immune Thrombocytopenia
Purpura
Most often occurs in women, ages 20-50years. Caused by production of autoantibody (IgG) directed against platelet antigen. It may be caused by some drugs like alcohol, aspirin, chemotherapy, phenobarbital, quinidine, rifampin. After stopping the drug platelet counts return to normal within 1 to 2 weeks.
Clinical
Manifestations
Petechiae, ecchymoses, purpura, menorrhagia, epistaxis, gingival bleeding.
Major complication is hemorrhage.
Diagnosis: reduced platelet count < 150,000. * The bleeding time will be prolonged in any disorder of platelet function such as thrombocytopenia.
Medical management: corticosteroids, splenectomy, platelet transfusions.
Nursing management: tell patient to avoid aspirin and aspirin-containing products because of reduced platelet adhesiveness. See Lewis, page 725,NCP 30-2.
Acute interventions:
Prevent or control hemorrhage
Observe for bleeding into deep tissues, nose bleed
Avoid IM or SQ injections (hold pressure if used)
Menstrual flow is abnormal – count sanitary pads used
Platelet concentrate administration – one unit will increase platelet by 10,000/microl.
DISSEMINATED INTRAVASCULAR COAGULATION (DIC) is a serious disorder where there is an acceleration of clotting, causing small blood vessel occlusion, organ necrosis, depletion of circulating clotting factors and platelets and an activation of the fibrinolytic system. Severe hemorrhage may occur. See Lewis, page 729.
Etiology – See Lewis,
page 729, Table 30-18.
1. infection with gram negative or gram positive septicemia; viral, fungal or rickettsial infection;
2. Obstetrical – abruption placentae, amniotic fluid embolism, retained dead fetus.
3. acute leukemia, metastatic carcinoma
4. burns, transplant rejection
5. heatstroke, shock, snake bites, incompatible blood transfusion
IN DIC THERE IS AN ACCELERATED CLOTTING THAT RESULTS IN GENERALIZED ACTIVATION OF PROTHROMBIN AND CONSEQUENT EXCESS OF THROMBIN. EXCESS THROMBIN CONVERTS FIBRINOGEN TO FIBRIN, PRODUCING CLOTS IN THE MICROCIRCULATION. EXCESS CLOTTING ACTIVATES THE FIBRINOLYTIC SYSTEM TO PRODUCE FIBRIN-SPLIT PRODUCTS WHICH PREVENT CLOTTING OF THE NORMAL BLOOD AND CAUSE ANTICOAGULANT, THUS RESULTING IN HEMORRHAGE.
Clinical
Manifestations – See Lewis, page 730
1. abnormal bleeding in the absence of known hematological disorder
2. lab values: prolonged PTT, PT > 60-80 seconds, decreased fibrinogen levels <150%
3. decreased platelet count of < 100,000
4. increased fibrin split products > 100mcg/ml
Treatment – See
Lewis, page 730
1. *Prompt recognition and treatment of the underlying disease
2. treatment is supportive if patient is not actively bleeding
3. acute bleeding is treated with heparin given IV (controversial); administration of blood, fresh frozen plasma (FFP); platelets, packed RBC’s.
Nursing Care – See
Lewis, page 731
1. recognition of signs of abnormal bleeding
2. recognition of disease which may cause the problem
3. oozing of blood from IV sites, foley catheters
4. pressure to control bleeding on skin
5. protect from injury
6. monitor I & O hourly
7. observe for transfusion reactions
8. observe for fluid overload
9. daily weights of patient
10. hemoccult all stools
11. measure abdominal girth daily
12. monitor lab values