tissue perfusion.pptx

7/29/2019 tissue perfusion.pptx

1/23

Module 10.3: Children Who Have

Alterations in Tissue Perfusion

Stephanie Talbot


2/23

EO 1.1: Terms

Haemophilia

X-linked, autosomal

recessive bleedingdisorder occurs as

result of deficienciesin coagulation

proteins

Classic Haemophilia most

common

Also called

haemophilia typeA in which there isa deficiency incoagulation factorVIII(AntihemophilicfactorAHF)

produced in liver


3/23

EO 1.1: Terms

Christmas Disease

Also called

haemophilia type BCharacterized bydeficiency in

coagulation factor IX(Plasma

thromboplastin

componentPTC)

Hemoarthrosis

Bleeding into

the jointsMainly knee, hip

& elbow

disabling


4/23

EO 1.1: Terms

Hydrops fetalis

Accumulation of

fluid in two ormore body areas

in the fetus

Serious condition

Breast Milk Jaundice

Occurs breast fed

babies @ 5-7dys oldProducts (fatty acids,

b- glucuronidase &

pregnanediol) in

breast milk inhibitbilirubin conjugation


5/23

EO 1.1: Terms

Icterus neonatorum (Physiologic

jaundice)

Yellowing of the skin inthe newborn due to

increased bilirubin inblood

Why?

Newborns immature liver

cannot excrete bile @

same rate destruction

RBCs occurs.

Kernicterus

Neurologic condition inwhich high levels of

bilirubin result in thedeposition of bilirubin intothe brain & spinal cord.

Produces convulsions ininfants.


6/23

EO-1.2:Describe w/ rationale, each of the

following for the child w/ HAEMOPHILIA

Etiology & Pathophysiology

Deficiency in factor VIIIinability to from

thromboplastin duringphase I of blood-clottingprocess = prolongedbleeding anywhere from

or in the body.

Bleeding into the mouth,neck or thorax seriouscause can lead to

obstruction

EO 1.3 Signs & Symptoms

1. SQ & IM hemorrhages

2. Hemoarthrosis s/s:stiffness, tingling, achyjoint

3. Bony changes as resultrepeated bleeding

episodes4. Prolonged bleeding

5. Spontaneous hematuria

6. Epistaxis-nose bleed

7. Ecchymoses & SQhematomas


7/23



Diagnostics Evaluation:

1.Hx bleeding episodes

2.X-linked inheritance

3.Laboratory findingsa)Factor VII & IX assay (deficiency)

b)Clotting times

c)PT=N, aPTT prolonged, INR=N


8/23

EO-1.2:Describe w/ rationale,

each of the following for the

child w/ HAEMOPHILIA

Therapeutic Management:

1. Replacement of clottingfactor

Factor VIII concentrates &

CryoprecipitateAHF

(antihaemophilic factor) (not

for VII deficiency though, )-for

acute bleeding when factorconcentrates not available

ex. Aafact (Alphonate)from

human plasma, Advate-

recombinant antihaemophilicfactor synthetic)

DDAVP (1-deamino-8-

arginine vasopressin)-

synthetic vasopressin, results

3-4 fold increase factor VIII

2. Corticosteroids txhematuria, Hemoarthrosis,

synovitis

3. NSAIDS for pain-

ibuprofen...NO ASPIRIN

increases bleeding

4. E-aminocaproic acid

(EAC, Amicar) to prevent

clot destruction

5. Exercise & physicaltherapyactive ROM so pt

can detect own level of

painNO CONCTACT

SPORTS

6. Teach family: venipunctureif


9/23



Nursing Management:1. Recognize s/s internal

bleeding: headache, slurredspeech, loss consciousness,

black tarry stools2. Prevent bleeding-encourage

appropriate exercise, safetyequipment, no contact sports,soft tooth brush or sponge-tipped toothbrush & waterpic, electric shaver

3. Use SQ injections whenpossible & venipuncture forblood samples

4. Wear medical bracelet

5. No aspirin or aspirincontaining products

6. Recognize & control

bleeding: RICE (Rest, Ice,

Compression, Elevate)

7. Prevent crippling effects

bleeding- elevate &immobilize joint during

bleeding episodes, AROM,

physical therapy- admin

analgesics before exercise

8. Adequate diet

9. Teach: child & family

preventative measures,

administration factor

replacements

10.Genetic counselling as soon

as poss. After diagnosis


10/23

EO 1.4 & 1.5 expected outcomes: NSG DX

Haemophila

NSG DX

1. Bleeding, Risk for

2. Impaired mobility3. Acute pain

4. Deficient fluid vole r/tloss blood

5. Ineffective healthmaintenance

6. Fear r/t high risk HIV

7. Fatigue r/t loss bloodvolume

Expected outcomes

1.Goal = Prevent or treatbleeding

Outcome: maintain stable VS w/minimal blood loss

2. Goal= prevent contractures

&joint deformities

Outcome/intervention:maintain mobility/RICE, bedrest, ambulation, AROM,positioning

3. Goal = treat pain

Outcome/interventions: be freeof pain/admin analgesics


11/23

EO 1.6 Describe the classification, actions,

& NSG implications of the following:

1. Antihemophilic factor (AHF)-( Alphonate, - from pooledhuman plasma DDAVPsynthetic vasopressin &

cryoprecipitate AHF-)prevent & control bleedingthose w/ Haemophilia A byincreasing factor VIII levels inblood

2. Anti-inhibitor coagulantcomplex- (Amicar, EACA,Autoplex T)- prevents clotdestruction (fibrinolysis),used if mouth trauma,

surgery (dose factorconcentrate must be givenfirst)

3. Factor IX complex-

(Alphanine SD,

Proplex, ProplexT-

from pooled human

plasma)-to prevent &

control bleeding in

those w/ haemophiliaB by increasing factor

IX levels in blood

NSG implications: from

plasma increased risktransmission of

viruses & allergic rxs


12/23

EO 1.7: Describe each of the following for

Rh & ABO incompatibility

Hemolytic Disease of the newborn is an

abnormally rapid rate of RBC destruction

hyperbilirubinemia in 1st 24hrs cardinal sign

Two main causes:

Isoimmunization (RhD)- a sensitivity rx to Rh

antigens in which Rh-antibodies form

ABO incompatibility

Blood contains agglutinogens which produce

immune response. In ABO & Rh (recessive)

blood group, antigens occur naturally.


13/23

EO 1.7: Describe etiology &

pathophysiology for Rh incompatibility

Problem arises when mother is Rh- & fetus is Rh+ --

sometimes fetal blood enters mothers circulation causing

mothers defence system to produce anti-Rh antibodies

enter fetal circulation where they destroy fetalerythrocytes fetus compensates by increases

haematopoiesis--> immature RBCs (erythroblasts)-

Erythroblastosis fetalis.

Most severe form erythroblastosis fetalis = hydropsfetalis hypoxia, heart failure, generalized

Generalized edema(anasarca), hydrops, &

effusions into pericardial,

pleural, & peritoneal space

Doesnt affect first pregnancy, next pregnancy


14/23

EO 1.7: Describe etiology &

pathophysiology for ABO incompatibility

Main blood groups are A, B, AB, O & allcontain anti-bodies except AB, so when mixone blood group w/ another = agglutination

(clumping)

Most common blood type = O, most commonblood incompatibility is between a mother w/

O blood and an infant w/ A or B blood becausethe anti-A&B antibodies of O type crossplacenta & attach to fetal RBC hemolysis.

Can occur 1st pregnancy


15/23

EO 1.7/1.8: Describe Clinical Manifestations for


1. Jaundice w/in 24hrs birth

NB: most newborns not jaundiced @ birth due to non-fxning liver

2. Increased serum Unconjugated bilirubin3. Anemia-from hemolysis lg amts RBCs

4. Hyperbilirubinemia-cause liver unable conjugate &excrete excess bilirubin

5. Hepatomegaly & varying degrees Hydrops

6. Anemia

7. Hypovolemic shock

8. Hypoglycemiadue to pancreatic cell hyperplasia


16/23

EO 1.7: Describe Diagnostic evaluations for


1. Indirect Combs test (maternal body titre drawn1st prenatal visit)

2. Amniocentesis- if test positive for antibodies

Delta OD 450 test- tests optical density of amnioticfluid

3. Ultrasonography- adjunctivecheck foralterations placenta, umbilical cord, amnioticfluid volume & hydrops

4. Timing & appearance jaundice

Confirm w/ Direct Combs test or Direct antiglobulin

test5. Genetic testing- early ID of paternal zygosity


17/23

EO 1.7: Describe Therapeutic Management

for Rh & ABO incompatibility

Goal therapeutic

management is PREVENTIONInvolves phototherapy,

exchange transfusion,

pericardial & pleural fluidaspiration, mechanicalventilation & inotrope

therapy


18/23


for Rh incompatibility

Prevention Rh Isoimmunization

1. Administration RhIg (RhoGAM) to all mothers @ 26 &

28wks gestation as well as after delivery, abortion &

miscarriage- prevents ant-D antibodies & memory cellsfrom forming

2. Admin tin mesoporphyrin IM tx Hyperbilirubinemia

3. Admin IV immunoglobulin (IVIG)- decrease severity RBC

destruction & development of jaundice

4. Intrauterine transfusion of Rh O neg. RBCs via umbilical

vein when mom already sensitized, raises fetal HCT levels

5. Exchange transfusions- tx choice severe

Hyperbilirubinemia & Hydrops caused by Rh-

incompatibility


19/23



Exchange transfusions: sterile procedure

Indication= Hyperbilirubinemia unresponsive

to phototherapySm. Amts infants blood removed (5-10mL)&

replaced w/ compatible Rh- blood in order to

remove sensitized RBCs, lower serum bilirubin

levels (prevents bilirubin encephalopathy),

corrects anemia, prevents cardiac failure

Must be @ least 35wks gestation


20/23



Signs blood exchange transfusionrx:

Tachycardia or bradycardiaRespiratory distress

Dramatic change blood pressureTemperature instability

rash


21/23


for ABO incompatibility

Goal= early detection &implementation phototherapy

for reductionHyperbilirubinemia

IVIG transfusions are used incombination w/ phototherapyin some centers.


22/23

EO 1.7: Describe Nursing Management for


1. Recognize jaundice: anticipate from prenatal

& Perinatal hx

2. If transfusion exchange needed: NPO during procedure, IV dextrose & e-lytes

Document blood volumes exchanged

Monitor VS, cardiac & respiratory fxn ,transfusion rxs

Maintain adequate thermoregulation, blood

levels & fluid balance

3. Support family, encourage express feelings


23/23

EO 1.9: Select the appropriate NSG Dx for

infants w/ hemolytic dx

1.Risk for injury

2.Neonatal jaundice r/t Rh orABO incompatibility

3.Deficient knowledge r/t txregime

4.anxiety

tissue perfusion.pptx

Documents

Transcript of tissue perfusion.pptx