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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.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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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
http://www.pathguy.com/lectures/low_iron.jpg


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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
http://images.google.com/imgres?imgurl=http://www.justforparents.com/images/eating.jpg&imgrefurl=http://www.justforparents.com/eating.htm&h=424&w=283&sz=133&hl=en&start=12&sig2=xhhj46hApigDNxWxyIQFcw&um=1&tbnid=p5HvlgSAIHdt8M:&tbnh=126&tbnw=84&ei=Q8acSLq0JqTKesrG9MEF&prev=/images%3Fq%3Dpicture%2Bof%2Bchild%2Beating%26um%3D1%26hl%3Den%26sa%3DN


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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

child with hema dis

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