Child With HEMA Dis.
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Alterations inHematologic Function
2006 Pearson Education, Inc.
Pearson Prentice HallUpper Saddle River, NJ 07458
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Structure and Function of Blood
ComponentsReview of Hematologic System
Blood formation
Red Blood CellsWhite Blood Cells
Platelets
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Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families 2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458
All rights reserved.
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Hematologic SystemBone marrow contains the essential element
in the hematologic system.
The STEM CELL, is a component that has theability to transform into more than one type ofblood cell.
Remember, every blood cell in the body arisesfrom a stem cell.
Although its fluid, blood is one of the bodysmajor tissues.
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Blood FormationIn utero, the process of blood formation, called
hematopoiesis, occurs in the liver and spleen.These organs retain some hematopoietic abilitythroughout life.
Formation of blood cells begins as early as week 2of intrauterine life.
By month 2 of intrauterine life liver and spleenbegin forming blood components.
After birth, the red bone marrow becomes themain site of hematopoiesis.
Total blood volume upon BIRTH is roughly 85ml/kg.The stem cells contained in the red marrow create
blast cells. These are precursors to
RBCs, WBCs and PLTs
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Blood ComponentsBlood is composed on plasma and cells90% water
10% solutes, such as proteins, electrolytes,albumin, clotting factors, anticoagulants,antibodies and dissolved nutrients.
3 main cell types
RBCs or erythrocytesWBC or leukocytes
Platelets, or thrombocytes
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Red Blood CellsCarry O2 to the tissues, and CO2 away from
tissuesDuring times of hypoxia, a hormone from the
kidneys (erythropoietin) stimulates the bonemarrow to produce more RBCs.Approximately 5 million RBCs per cubic
millimeter of blood at birth.
Life of RBC= 120 daysAn important waste product of RBC death is
bilirubin
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RBC has its components that allows to carry outand transport oxygen, it is called HEMOGLOBIN.
Two Components of Hemoglobin:A.HEME- an iron- containing pigment, it is the portion
that combines with oxygen and carbon dioxide fortransport.
B.GLOBIN- protein dependent on nitrogenmetabolism for its formation.
At birth 40 70 % of the child hemoglobin iscomposed of FETAL HEMOGLOBIN. (hemoglobin F)
Fetal hemoglobin is replaced by adult hemoglobin(hemoglobin A) during the first 6 months of life.
Hemoglobin levels are highest at birth (13.7- 20.1g/100 ml)
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White Blood Cells
Fight different types of infection in ourbody; each type has its own role2 main categories of WBCsGranular leukocytes (granulocytes) Neutrophils- decour invading microorganisms by
phagocytosis Eosinophils- act in allergic rxns, defend against
parasites and lung and skin infections Basophils- release heparin and histamine, involved in
inflammatory and infectious rxns, aka mast cells in
body tissuesNongranular leukocytes (agranulocytes) Lymphocytes- which are the main cells that fight
infections and include B and T cells Monocytes- work with neutrophils to help devour
invading organisms
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.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DGhttp://images.google.com/imgres?imgurl=http://science.uwe.ac.uk/research/uploads/CRIB_blood_cells.jpg&imgrefurl=http://jmgs.wordpress.com/2007/04/11/production-of-universal-red-blood-cells/&h=256&w=340&sz=26&hl=en&start=4&sig2=yFbDr2MVuEx163RTj9fv_w&tbnid=3vSQg4J1u292bM:&tbnh=90&tbnw=119&ei=cpucSIPjE5-gePTwpa8F&prev=/images%3Fq%3DRed%2Bblood%2Bcells%26gbv%3D2%26hl%3Den%26sa%3DG 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Total WBC count in newborns isapproximately
20, 000 per cubic millimeter.
By 14- 30 days of life, the total WBC count
falls to approximately 12, 000 per cubicmillimeter.
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PlateletsIt is a round, non-nucleated bodies formed by
bone marrow which major functions is tomaintain capillary hemostasis and primarycoagulation
Adhere to one another and plug holes invessels or tissues where theres bleeding.
This action is part of a larger coagulationprocess
PLTs also release serotonin at injury sites
Serotonin is a vasoconstrictor, decreases blood
flow to injured areas
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Care for a Child with
Hematologic disorderAssessing the child with a Hematologic
disorder:History
Chief concern: fatigue, easy bruising, epistaxis.Pregnancy Hx.: Low birth weight, blood loss atbirth, lack of vitamin K administration at birth.
Nutrition: Picky eater, or presence of pica.Increased milk intake.
Past illnesses: History of recent illness, history ofrecent medicine ingestion.
Family Hx.: Inherited blood disorders, parentsknown to have sickle- cell trait, thalassemia minor,or hemophilia in family.
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Physical AssessmentGeneral Appearance: Obese infant, fatigueEyes: Retinal hemorrhageFace: Bossing of maxillary bone
Mouth: Pale, mucous membrane, ecchymotic orbleeding gum line.Heart: Increased rate, possible murmurSkin: Petechiae, ecchymosis, blood oozing from
wound or injection point, jaundice, pallor, bronze
color.Abdomen: pain on palpation, increased liver or
spleen sizeGenitourinary: delayed secondary sex
characteristics
Extremities: Spoon nails, joint swelling, pain
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Disorder of Red Blood
CellANEMIA- occurs when there is reduction in the
number or function of erythrocytes.
Also it happens when the rate of RBCproduction falls below that of cell destruction.
POLYCYTHEMIA- over production of RBC in thesystem.
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TYPES OF ANEMIANORMOCHROMIC, NORMOCYTIC ANEMIASACUTE BLOOD- LOSS ANEMIAANEMIA OF ACUTE INFECTIONANEMIA OF RENAL DISEASE
ANEMIA OF NEOPLASTIC DISEASEAPLASTIC ANEMIAHYPOPLASTIC ANEMIAHYPOCHROMIC ANEMIA IRON- DEFICIENCY ANEMIA
MACROCYTIC (MEGALOBLASTIC) ANEMIAANEMIA OF FOLIC ACID DEFICIENCYPERNICIOUS ANEMIA( VITAMIN S2 DEFICIENCY)HEMOLYTIC ANEMIAAUTOIMMUNE ACQUIRED ANEMIA
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NORMOCHROMATIC NORMOCYTICANEMIA- marked by impaired production of
erythrocytes by the bone marrow, or byabnormal or uncompensated loss ofcirculating RBCs such as in acute hemorrhage.
ACUTE BLOOD LOSS ANEMIA- cause from atrauma thus causing blood loss decreasing thenumber of RBC in the circulation, trauma suchas: automobile accident with internalbleeding, acute nephritis with severehematuria, or a newborn born from a
pregnancy disorder such as placenta previa,abruptio placenta , trauma to cord orplacenta.
Tx.: control bleeding by addressing theunderlying cause., place in supine position,keep warm, BT, plasma expanders (plasma or
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ANEMIA OF ACUTE INFECTION
Acute infection or inflammation, especially in
infants may lead to increased destruction oferythrocytes and therefore decreaseserythrocyte level in circulation.
Common causes:
Osteomyelitis
Ulcerative colitis
Advanced renal disease
Mgt.Treating the underlying condition will increase
the number of erythrocytes that leads correctthe anemia.
Antibiotic therapy
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ANEMIA OF RENAL DISEASE
Due to the dysfunction of kidney cells thatdecreases the erythropoietin production thusdecreases also the total number of RBCs inthe system causing anemia.
COMMON CAUSES:
Irritation of nephrons
Autoimmune disorder
Mgt.
Administration of recombinant human
erythropoietin.
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ANEMIA OF NEOPLASTIC DISEASE
It occurs when a neoplastic cells proliferate
inside the bone marrow that causingimpairment of the RBC production, it forms anormochromic normoctic anemia.
Mgt.
Remission of neoplastic process.
Blood transfusion
APLASTIC ANEMIAResults from depression of hematopoietic
activity in the bone marrow thus affecting thedevelopment of WBC, platelets and RBCs.
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A.Congenital Aplastic Anemia (FanconisSyndrome)
Is an inherited autosomal recessive trait.Manifestation:
Children who are having skeletal and renalabnormalities.
Hypogenitalism
And short stature
Usually happens between ages 4- 12 years of
age. The child begins manifesting symptomsofPANCYTOPENIA- reduction of all blood cellcomponents.
Tx:
Bone marrow transplantation
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B. ACQUIRED APLASTIC ANEMIA
Is a decrease in bone marrow production that
occurs during a child has excessive exposureto radiation, drugs, chemicals that are knownto cause bone marrow damage.
CONTRIBUTING DRUGS : chloramphenicol,sulfonamides, arsenic(common in rat poison),hydatoin, benzene or quinine.,chemotherapeutic drugs.
S/Sx: pallor, easy fatigability, anorexia,thrombocytopenia ( bleeding), increase inWBC count (Leukopenia).petechiae, easybruising.
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Treatment:
Administration of Antithymocyte globulin(ATG) and Cyclosporine testosterone thatstimulates RBC growth.
Reminders: ATG should be given cautiously
because it is high risk to cause anaphylaxis.Transfusion of new blood elements. (packed
RBC and platelets)
Erythropoietin administration
Colony stimulating factor- helps improvedbone marrow functioning.
Oral corticosteriods ( Prednisone)
Stem cell transplantation.
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HYPOPLASTIC ANEMIA
Also results from depression of hematopoietic
activity of bone marrow; they can becongenital or acquired.
Unlike APLASTIC anemia, it only affects RBCs.
Types of Hypoplastic anemia:
A. Congenital aka BLACKFAN-DIAMONDsyndrome
Rare disorder revealed in 6-8 months of life
whichTx,: corticosteriod
usually caused by inherited defect in RBCformation.
B. Acquired-usually caused by infection with
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Long term transfusion of PRBCs needed to raiseerythrocyte levels thus necessary to increase also
times of transfusion that causes deposition of irontissue in the body called HEMOSIDEROSIS.
Tx. For Hemosiderosis:
IRON CHELATION PROGRAM
Using a subcutaneous infusion ofHypodermoclysis
Such as DEFEROXAMINE (Desferal)- binds withiron and aids on its excretion from the body in
urine form.Given for 5 to 6 days a weekover an 8 hour
period.
Common site for infusion is on area beside
scapula or on the thigh.
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Iron Deficiency AnemiaA disorder of O2 transport in which the
production of hgb is inadequate.
Without sufficient iron, the body cantproduce the Hgb molecure, b/c the hemecomponent is primarily iron
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Iron Deficiency AnemiaCAUSES:Inadequate intake of iron in the diet,malabsorption of iron through the GI tract, or
chronic blood lossLast trimester of pregnancy, the fetus draws
what iron it needs for the next 6-12 months If mother is deficient in iron or
Baby is more than 4 weeks premature (32 weeks)may not have sufficient iron intake Anemia will usually present in 2nd year of life
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Iron Deficiency AnemiaAbout 80% of iron used in building Hgb isactually reabsorbed in the GI tract from deadRBCs that have broken up.
Therefore, problems w/ GI absorption causesiron deficiency:Cows milk allergy (common in Blacks and
Asians) causes inflammation of GI tract
In adolescents- fad diets
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Iron Deficiency AnemiaCLINICAL MANIFESTATION:Range from mild to severePale appearance and decreased activityToddlers may have h/o prematurity and poor
weight gain
Other Sx include: Fatigue,
inability to concentrate, palpitations, dyspnea on exertion, craving for nonnutritive substances such as ice, tachycardia, dry brittle nails, concave or spoon-shaped fingernails
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Iron Deficiency Anemialab values
Tests:Hgb levels are routinely screened, and a
CBC is
typically done at 9-12 months and 24month wellbaby check-ups and at-risk populationsIron deficiency is a microcytic,
hypochromic anemia, meaning theRBCs are small and pale. RBCs w/decreased iron appear bleached outSerum iron levels are decreased
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Iron deficiency anemia
lab valuesHemoglobin
Hematocrit
Reticulocyte count
Hemoglobin 9.5-11 g/dL= Mild irondeficiency
Hemoglobin 8-9.4 g/dL= Moderate irondeficiency anemia
Hemoglobin less than 8 g/dL= severe irondeficiency anemia
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Iron Deficiency AnemiaSo what is the greatest nutritional risk factor
for developing iron deficiency anemia?
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Iron Deficiency Anemia
ComplicationsUntreated, anemia can cause stress on all
body tissues, w/ decreased oxygenation,especially respiratory and cardiovascular
systems
Decreased ability to concentrate
Poor muscle development
Decreased performance on developmentaltests
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Iron Deficiency AnemiaTreatmentThe Association of American Pediatricsrecommends if Hct less than 34% or Hgb
less than11.3 g/dL begin iron supplementation(4-6
weeks)
Main treatment:Treat underlying problem
GI bleeding, chronic blood loss Lack of iron from diet
Iron Supplementation ORAL ferrous sulfate at 3-6 mg/kg/day for 4-6 weeks,
then repeat Hgb/Hct
Administer through a straw, nipple Administer on empty stomach
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Iron Deficiency AnemiaIron Rich Foods
Iron fortified cereal and formula
Enriched bread
Dark green vegetables
Legumes (kidney and pinto beans)
Figs, raisins
Meats, fish, poultryDried appricots
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Iron Deficiency Anemia
EvaluationWith tx, reticulocyte count increases w/in 3-5
days. Indicates + therapeutic response
Hgb should normalize w/in 4-8 weeks
When lab values are nml, wean from ironsupplements
Repeat labs in 6 months, monitor wt/
development
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Sickle Cell Anemia
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Sickle cell disease
Sickle cell anemia (SS) is an inherited,autosomal recessive genetic disease thataffects the RBCs, which become acutely
sickle-shaped.
Involves RBCs and their ability to carryoxygen
Pathophysiology of the diseaseResults from a single amino acid substitution
(valine for glutamine) in position 6 of the betaglobin chain of hemoglobin
What does this mean?...an unstable RBC w/ a
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Sickle cell diseaseSickle cells only live for about 15 days,while normal hemoglobin can live upto 120 days.
How is the individual affected?Short Hgb life span
Chronically anemic
Sickle cells risk being destroyed by thespleen
Implications
Damage to the spleen
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Sickle cell diseaseAge:
Hematologic changes evident as early as10 weeks, though usually delayed until
age 6-12 months.Why do you think ???
Beta-chain (adult) hemoglobin is not
prominent until the age of 3 months
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Difference in HgbNormal Hgb cellsLive for 120 days
Round
Smooth
Flexible, like a lettero so they can movethrough vessels easily
Sickle Hgb cells
Live for about 15 days
Stiff
Sticky
Form into the shape ofa sicle, or the letterC, when they looseOxygen
Cluster togetherwhatwould this lead to inthe body?
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Jane W. Ball and Ruth C. Bindler
Child Health Nursing: Partnering with Children & Families
2006 by Pearson Education, Inc.
Upper Saddle River, New Jersey 07458All rights reserved.
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Sickle Cell Anemia
SicklingTriggered by fever, emotional stress, physical
stress
States of hypoxia
High altitudes
Hypoventilation
Poorly pressurized aircrafts
DehydrationCold
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Sickle Cell CrisisSS crisis are acute exacerbations of thedisease
Vary in severity and frequency
Three most common types
Vaso-occlusive crisis
Sequestration crisis
Aplastic crisis
Vaso occlusive Crisis
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Vaso-occlusive CrisisPain Crisis
Aka thrombotic crisis
Most common type of crisis
Precipitated by dehydration, exposure tocold, acidosis or localized hypoxemia
Extremely painfulCaused by stasis of blood w/ clumping of
cells in the microciruclation, ischemia andinfarction
Thrombosis and infarction of tissue mayoccur if crisis not reversed
Clinical manifestations include fever, pain,
tissue engorgement, swelling of joints,
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Splenic Sequestration
Life-threatening crisis: death can occur w/inhours; high mortality (up to 50%)
Caused by pooling of blood in the spleenSpleen can hold up to 1/5th of bodys blood
supply at one timeleads to CV collapse
Clinical manifestations include profound
anemia, hypovolemia and shockOccurs b/t 4 months-3 years
Tx: blood transfusions, emergent splenectomy
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Aplastic CrisisDiminished erythropoiesis and increaseddestruction of RBCs
(bone marrow depression resulting from a viral
infection)
Triggered by viral infection or depletion offolic acid
Clinical manifestations include profoundanemia, pallor, fatigue
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Acute Chest SyndromeThis is similar to pneumonia, withsymptoms such as difficulty breathing,chest pain and fever.
It can be caused by an infection or byblocked blood vessels in the lung.This potentially life-threatening disorder
should be treated in the hospital.
Treatments may include antibiotics, bloodtransfusions, pain medications, oxygen andmedicines that help open up blood vesselsand improve breathing.
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Acute chest syndromeThe acute chest syndrome (ACS) in sickle
cell disease (SCD) can be defined as:a new infiltrate on chest x-ray
associated with one or more NEW symptoms:
fever, cough, sputum production, dyspnea, orhypoxia..
A past history of an ACS is associated withearly mortality compared to those who have
never had an episode.The disorder is most common in the 2 to 4
year age group and gradually declines inincidence with age.
:
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:RBCs
Pain can occur in any organ or joint in thebody
Pain can be reversedOxygenation
HydrationPain ManagementRest
Mild pain episodes can be treated w/ OTC
pain meds (tylenol, ibuprofen) and heatingpads
More severe episodes requirehospitalization and IV pain meds
Hydroxyurea
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Nursing Dx: Risk for
InfectionInfants and young children w/ SCD areespecially vulnerable to serious bacterialinfections
Major cause of death in children w/ SCD Dailyprophylactic Pen VK 125 mg BID from 2months- 5 years of age
Erythromycin for children w/ PCN allergies
:
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:Infection
Important to receive regular childhoodvaccinations (Hib and PCV 7)
In addition children w/ SCD should also receive a
yearly flu shot (influenza) beginning at 6 mos ofage
Another type ofpneumoccocal vaccine (PCV23)protects against additional bacteria b/t 2-5
years of ageMeningococcal vaccine (protects against
meningitis at age 5 and beyond)
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Treatment for Sickle Cell
AnemiaTreatment consists of sx management
The primary focus being on prevention of
sickle cell crisisEducation
Blood transfusions
Hydration: Drinking plenty of water daily(8 to 10 glasses) or receiving fluid intravenously
(to prevent and treat pain crises)
Pain Management
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Medications for SS
anemiaHydroxyurea 15-20 mg/kg/day to start andincrease until therapeutic response (not morethan 35 mg/kg)
A chemotherapeutic drug used in CA tx
Shown to decrease the number and severity ofcrises
Increases production of Hemoglobin F
Side effects include bone marrow supression,HAs dizziness, N/V
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Clotting DisordersHemophilia A (Factor VIII deficiency)Von Willerbrand Disease
Disseminated Intravascular Coagulation (DIC)Idiopathic Thrombocytopenic Purpura (ITP)
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Hemophilia AHereditary bleeding disorder, that result from
deficiency of specific clotting factorsHemophilia A aka Factor VIII is most common
type80% of people w/ hemophilia
X-linked recessive traits, which manifests asaffected males, and carrier females
30% of cases are new mutationsRange of manifestations of disease from mild
to severe
Hemophilia A
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Hemophilia AClinical Manifestations
Children usually do not manifest sxs until after 6months of age (begin moving around, loosingteeth)
Spontaneous bleeding
Hemarthrosis (bleeding into joint space)
Deep tissue hemorrhage
Nosebleeds
Easy bruising (ecchymosis)Hematuria
Life-threatening bleeding includes:Head/ intracranialNeck and throatAbdominal/GI
Iliopsoas muscle with decrease hip ROM
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Hemophilia AComplications from bleeding include:Bone changesContractures
Disabling deformities result from immobility andfrom bleeding into joint spacesMuscle contracturesJoint arthritis
Chronic painMuscle atrophyCompartment syndromeNeurologic impairment
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Hemophilia A
Treatment:Goal to control bleeding by replacing the missing
clotting factor and prevent complications
Factor Replacement TherapyOn demand
Prophyllaxis
IV infusions consist of
Fresh frozen plasmaCryoprecipitate
Factor VIII
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Treatment of Hemophilia AProphylaxis:
Scheduled infusions of factor 2-3 X/ weekDDAVP (Desmopressin acetate)An analog of vasopressin, causes a 2-4 fold
increase in factor VIII
Not to be confused w/ DDAVP for nocturnalenuresisSynthetic vasopressinMOA: release of stores from endothelial cells
raising factor VIII.Administered IV, sub-Q or nasally
T t t f H hili A
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Treatment of Hemophilia A
Amicar (epsilon amino caproic acid)Antifibrinolytic
Uses:
Mucocutaneous bleeding
50-100 mg/kg q 6 hours
Contraindications:
hematuria
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Hemophilia AComplications of Treatment:Inhibitors/antibody development IgG antibody to infused factor VIII concentrates which
occurs after exposure to the extraneous VIII protein 20-30% of pts w/ severe hemophilia A
Blood-borne illnessesHep A,B and C
HIV
hili
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Hemophilia ANursing ConsiderationsFactor replacement given on timeLab monitoring as ordered
Increase metabolic states will increase
factor requirementsFactor coverage for invasive procedures
Document- infusion and response to tx
NO NSAIDS
NO HEATNO IM injections
Utilize Hemophilia Center staff .
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Hemophilia A
Nursing ConsiderationsAvoid taking temperatures rectally or giving
suppositoriesCheck Bp by cuff as little as possible
Avoid IM or subcutaneous injectionsUse only paper or silk tape for dressings
Perform mouth care w/ glycerin swab
Limit venipuncturesDo not give aspirin
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Hemophilia A
Psychosocial IssuesGuilt
Challenge of hospitalizations
Control issues
Financial/ insurance challenges
Feeling different/ unable to do certainactivities
Counseling needsRefer for genetic counseling after dx
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Von Willebrand DiseaseA hereditary bleeding disordervWF Involved w/ platelet adhesion
Most common form of disorder is autosomal
dominant traitDisease can occur in both males and females
equallyManifestations:Easy bruisingEpistaxis
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Von Willebrand DiseaseOther clinical manifestations include:Gingival bleeding
Ecchymosis
Increased bleeding w/ lacerations or duringsurgery and dental extractions
Menorrhagia (increased menstrual bleeding)
GI bleeding
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Von Willebrand DiseaseTreatment:Similar to Hemophila A
Restore clotting factor and prevent
complications associated w/ bleeding Infusion of vWB protein concentrate
DDAVP
Amicar for mucous membrane bleeding
Nursing Management:
Similar to Hemophilia A
Disseminated Intravascular
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Disseminated IntravascularCoagulation (DIC)Life-threatening process which occurs as
complication of other serious illnesses ininfants and childrenMost common cause of DIC is infection
An acquired pathologic process in whichthe clotting system is abnormallyactivated, resulting in widespread clotformation in the small vessels throughoutthe body.These changes slow blood circulation,
cause tissue hypoxia and results in tissuenecrosis.The circulating fibrin also interfere w/
clotting process and bleeding and
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DICThe sequence of events for DIC
Clinical Manifestations:
Treatment:Controlling bleeding, identifying and correcting
the primary cause of the disorder, and
preventing further activations of clottingmechanisms
DIC
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DIC
Nursing Assessment and Diagnosis:
Involves all body systems, so frequent thoroughassessment of entire body is criticalObserve for petechiae, ecchymoses, and oozing
every 1-2 hours
Observe for pooling of blood in dependent areasAssess IV site Q 15 minutes for oozingExamine stool for presence of bloodAssess extremities for cap refill, warmth and
pulsesFrequently assess VS and LOCIs and OsMonitor O2 sat and ABGsID familys coping strategies and support
systems
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Idiopathic Thrombocytopenic
Purpura (ITP)Aka autoimmune thrombocytopenicpurpuraMost common bleeding disorder in
childrenOccurs in children 2-10 years-old, peaks b/t 2-5y.o
A disorder characterized by increaseddestruction of platelets in the spleen, even
though plt production in the bone marrowis normalAutoimmunePlts are destroyed as a result of the binding of
autoantibodies to PLT antigens
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ITPClinical Manifestations:Multiple ecchymosesPetechiae
Purpura (purplish areas where blood hascollected d/t bleeding from blood vessels)Bleeding from gumsnosebleeds
Hematuriaheme in stools
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ITPDx is made by Hx and PE and lab findingsTx: depends on PLT counts and clinical
presentation
CorticosteroidsIVIGPLT administration only if hemorrhage occursIf no response to therapy in 6mos-1 year,
splenectomy may be tx of choiceSpontaneous remission in 90% of cases
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Nursing Care of the Child with a
Hematologic DisorderBased on the Disorder
RBCs
Oxygenation
Circulation
Fluid
Nutrition
Pain Management
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Nursing Care of a Child with a
Hematologic DisorderBased on the DisorderWBCsInfectionOxygenationNutrition
Platelets and bleeding disordersBleedingOxygenationCirculationInjury Prevention
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Collaborative Care for a Child
with a Hematologic DisorderTeam Approach
Family Involved
Decisions w/ family and child