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ANEMIA & COAGULATION

DISORDERS
By Tonie Metheny, MS, RN

TYPES OF BLOOD CELLS


Erythrocytes
Leukocytes
Platelets

ERYTHROPOIESIS

Erythrocyte= red blood cell (RBC)

ERYTHROPOIESIS
Nutrient

Function in erythropoiesis

Cobalamin (B12)

RBC maturation

Folic Acid

RBC maturation

Iron

Hemoglobin synthesis

OVERVIEW OF ANEMIA

Anemia = Decreased RBC, decreased H/H


RBC

erythrocyte

Most abundant blood cell

Hemoglobin

Oxygen carrying protein


Oxygen receptors
Sp02%

Hematocrit

RBC/whole blood

OVERVIEW OF ANEMIA

RBC production

RBC destruction

http://www.youtube.com/watch?v=_ZV5140OykE

OVERVIEW OF ANEMIA

Common causes
Dietary

intake, hemolysis, blood loss, cancer

Anemia causes problems with O2 delivery


Decreased RBC= Decreased O2 carrying capacity\

Lab findings vs. Diagnostics


CBC
Iron

Bilirubin

Erythropoetin
Biopsy

CT/MRI

OVERVIEW OF ANEMIA

Clinical manifestations
Vague

Secondary

to decreased O2 carrying capacity

Fatigue
Pallor or jaundice
Increased HR and SV
SHOB
Palpitations

OVERVIEW OF ANEMIA

Nursing Management
Blood
Epo

transfusion

Vitamins

Iron supplement

O2

therapy
Volume replacement
Dietary teaching

IRON-DEFICIENCY ANEMIA
Look to your left and right
Chronic condition

Decreased

Causes

hemoglobin synthesis

Inadequate

intake
Malabsorption
Blood loss
Hemolysis
Alcoholism
Malnutrition

IRON-DEFICIENCY ANEMIA

Clinical Manifestations
Low

RBC

Pallor
Sensitivity to cold
Headache

Low

Iron

Glossitis
Cheilitis
Parethesia

IRON-DEFICIENCY ANEMIA

Diagnostics

Determine

the cause of iron deficiency

Guaiac test
http://www.youtube.com/watch?v=W4NCWt0hQJM

Endoscopy
Colonoscopy

IRON-DEFICIENCY ANEMIA

Collaborative Care & Nursing Management


Target

and treat cause


Iron rich foods
Iron supplement

Enteral vs. parenteral

Monitor

effectiveness of therapy

THALASSEMIA

Decreased, malformed hemoglobin production


Increased

hemolysis of RBCs

Autosomal, recessive gene


Thalassemia

minor vs thalassemia major

THALASSEMIA

Clinical Manifestations of thalassemia major


Symptoms

of anemia
Physical and mental retardation
Splenomegaly and hepatomegaly
Jaundice
Bone marrow expansion and hyperplasia
Cranial & maxillary thickening

THALASSEMIA

Clinical Manifestations of thalassemia minor


Typically

asymptomatic
Microcytosis
Hypochromia

THALASSEMIA

Collaborative Care and Nursing Management


Thalassemia

major

No drug or dietary treatment options


Manage anemia
Transfusions to maintain Hb of 10g/dL
Chelation therapy
Binds to excess serum iron
Reduces iron overloading secondary to transfusions
No iron supplements
Splenectomy
Monitor for complications
Hep C, cardiac issues, etc

COBALAMIN (B12) DEFICIENCY

Decreased intrinsic factor secretion by the


parietal cells of the gastric mucosa
Functions

in B12 uptake
Decreased intrinsic factor= decreased cobalamin
uptake

Decreased RBC maturation


Decreased erythropoiesis

Causes

Anemia!

Pernicious

anemia

Atrophy and autoimmune destruction of gastric mucosa

GI

surgery, gastritis, alcoholism

PERNICIOUS ANEMIA

Clinical Manifestations
Secondary

to tissue hypoxia

Beefy, red tongue


n/v, abdominal pain, anorexia
Weakness, peripheral paresthesias, confusion

Diagnositics
Macrocytic

RBC
Low serum cobalamin
Endoscopy
Shilling test

PERNICIOUS ANEMIA

Collaborative Care and Nursing Management


Maintain

good nutrition
Lifelong B12 injections

1000mg IM QD x 2 weeks
Weekly until H/H is normalized
Monthly for life

http://
www.youtube.com/watch?v=VkgE6X_NErM

APLASTIC ANEMIA

AKA pancytopenia
Decrease

Causes

in RBC, WBC, and platelets

Congential

vs Acquired

Clinical Manifestations
Minor

to severe
Secondary to pathophysiology
Anemia
Neutropenia
Thrombocytopenia

APLASTIC ANEMIA

AKA pancytopenia
Decrease

Causes

in RBC, WBC, and platelets

Congential

vs Acquired

Clinical Manifestations
Minor

to severe
Secondary to pathophysiology
Anemia
Neutropenia
Thrombocytopenia

APLASTIC ANEMIA

Diagnostics
Bone

marrow biopsy & aspiration

Hypocellular bone marrow with increased yellow marrow

Collaborative Care and Nursing Management


Protect

patient from infection, bleeding, and


complications of anemia
Immunosuppresive therapy
Stem cell transplant
Blood and platelet transfusions

http://www.youtube.com/watch?v=w8-jx1dtg0U

SICKLE CELL ANEMIA

Inherited, autosomal recessive disorder


Abnormal

hemoglobin that cause abnormal RBCs

Prone to sickling

SICKLE CELL ANEMIA

Sickle Cell crisis


Sudden

onset, persists for days or weeks


Triggered by low serum O2 and hypoxia

Dehydration, infection, stress, exertion

Cells

sickle and clump together in the small vascular


pathways

Occlusion occurs

Spleen

destroys sickled cells causing anemia

SICKLE CELL ANEMIA

Sickle Cell crisis

SICKLE CELL ANEMIA

Sickle Cell crisis


Clinical

Manifestations

Extremely painful
Fever
Swelling
Tenderness
Hypertension
n/v

SICKLE CELL ANEMIA

Collaborative Care and Nursing Management


Prevent

complications
Avoid triggers

High altitudes
Stay hydrated
Treat infection promptly
Immunizations

COAGULATION DISORDERS

Hemorrhagic disorders
Hemophilia
Deep

Vein Thrombosis
Pulmonary Embolism
Thrombocytopenia
Disseminated Intravascular Coagulation

PLATELET

BLOOD CLOTS

Factors that affect normal


coagulation
Hemostasis=

blood clotting process

Four components
Vascular response

Vasoconstriction restricts blood flow


and presses tissue together so blood
cant escape

Platelet plug

Congregate at site of damage to


plug blood loss
Originate from stem cells in the bone
marrow

Fibrin clot
Clot Lysis

BLOOD CLOTS

Factors that affect normal


coagulation
Hemostasis=

process

blood clotting

Four components
Vascular response
Platelet plug
Fibrin clot

Clot forms over the platelet


plug

Clot Lysis

Natural anticoagulants
Heparin, Protein S, Protein
C
Keeps blood in a fluid state

CLOTTING STUDIES

ACT

Activated

Clotting Time
70-120 seconds

PTT

Activated

Partial Thromboplastin Time


25-35 seconds

INR

International

PT

Prothrombin

Normalized Ratio

Time
11-16 seconds

THROMBOCYTOPENIA

Low platelet count


Reduction

of platelets below 150,000

Causes abnormal hemostasis


Prolonged bleeding

Inherited

vs acquired thrombocytopenia

IMMUNE THROMBOCYTOPENIC
PURPURA
Most common type of thrombocytopenia
Autoimmune disease

Lysis

of the platelets by the spleen

Clinical Manifestations
Mucosal

or cutaneous bleeding
Petechiae, purpura, superficial ecchymoses
Prolonged bleeding after routine procedures
Manifestations of internal hemorrhage

IMMUNE THROMBOCYTOPENIC
PURPURA

Diagnostic Studies
CBC

H/H
Platelet count

PT/PTT

Antigen

assay
Bone Marrow Analysis
Flow Cytometry

Analyzes antiplatelet antibodies

IMMUNE THROMBOCYTOPENIC
PURPURA

Collaborative Care
Corticosteroids

(phagocytosis)

suppress autoimmune response

Prednisone
Solu-medrol

Splenectomy

Increases number of circulating platelets

Platelet

transfusions

THROMBOCYTOPENIA

Nursing Management
Teach

patients to avoid acquired thrombocytopenia


Medically prevent and control bleeding
Procedures
Menstruation

Monitor

for signs of internal bleeding


Teach patient to prevent and control bleeding
How to avoid bleeding
How to manage bleeding

HEMOPHILIA

X-linked recessive genetic


disorder
Defective

factors

or deficient clotting

Three types

Hemophilia

A (Factor VIII)
Hemophilia B (Factor IX)
Von Willebrand disease (vWF,
VIII, and platelets)

HEMOPHILIA

Clinical Manifestations- Could lead to life


threatening blood loss
Slow,

persistant, prolonged bleeding


Delayed bleeding
Uncontrollable hemorrhage
Occult blood, hematuria
s/s of hematoma
Nerve compression- pain, paralysis
Subcutaneous hemotoma

Limited

ROM- Bleeding in the joints

HEMOPHILIA

Diagnostic studies
Platelet

PT/PTT
Factor

count

assays

Collaborative care
Prevent

and treat bleeding


Replace volume loss
Replacement deficient clotting factors
Antifibrinolytics

Enhances clotting stability

Treatment

of complications

HEMOPHILA

Nursing Management
Stop

bleeding quickly

Compression, ice, gelfoam, fibrin foam, hemostatic agents

Joint

bleeds

Rest, ice, mobilization, treat pain

Manage

life-threats

DISSEMINATED INTRAVASCULAR
COAGULATION
Thrombotic disorder
Abnormally initiated and accelerated clotting

Causes

a decrease in available clotting factors


Leads to uncontrollable hemorrhage

Occurs in response to a disease/disorder


Example

Shock
Septicemia
Cardiac arrest
Snakebites

DIC

Clinical manifestations
Bleeding
Bleeding

with no history or obvious cause

hematoma, petchiae, purpura


Respiratory tachypnea, hemoptysis
CV-tachycardia, hyptotension
GI/GU-abdominal distension, bloody stools
Neuro-headache, changes in neuro status
MS- bone and joint pain

Thrombotic

PE, ARDS, ischemic tissue, paralytic ileus

DIC

Diagnostic studies
PT/PTT,

Thrombin time
Fibrinogen & platelet counts
Factor assays

Collaborative Care
Stabilize

patient

O2
Volume replacement
Treat cause
Provide supportive care of manifestations

DIC

Nursing care
Early

detection of bleeding
Astute assessment

Internal vs. external bleeding


Indications of microthrombi

Administer

medications and blood products

http://
www.npr.org/2011/06/28/137454415/the-child-cases-guilt
y-until-proven-innocent

DEEP VEIN THROMBOSIS

Thrombus is a deep vein


Femoral
Iliacs

Popliteal

Virchows triad
Venous

stasis
Endothelial damage
Hypercoagulation

DEEP VEIN THROMBOSIS

Pathophysiology
Platelet

aggregation creates
entrapment of RBC, WBCs and
more platelets
Thrombus occurs usually at valve
because of stasis
Thrombus can resolve or may
eventually break off

What is the difference in a thrombus


and embolus?
Where would an emboli caused by
DVT travel to?

DEEP VEIN THROMBOSIS

Clinical Manifestations
Unilateral
Pain

Sensation

LE edema

of fullness of the area


Parethesia
Warmth
Erythema

DEEP VEIN THROMBOSIS

Diagnostic studies
CBC,

clotting studies
Venous compression ultrasound
Duplex ultrasound

Most commonly used

DEEP VEIN THROMBOSIS

Collaborative care
Anticoagulation

treatment

therapy- DVT prophylaxis or

Coumadin
Heparin
Unfractionated heparin

Heparin Sodium

LMWH

Lovenox

Thrombolytic

therapy- TPA (clot busting drug)


Surgical intervention
Greenfield filter
thrombectomy

DEEP VEIN THROMBOSIS

Nursing interventions for anticoagulation


therapy
Minimize

bleeding
Monitor CBC and coagulation test
Use electric razors- not straight
Soft toothbrushes
Administer stool softeners
Assess for mental status changes

PERIPHERAL BLOOD FLOW

Venous blood flow vs


arterial blood flow
If

a clot broke off where


would it go?

PULMONARY EMBOLISM

Blockage of the pulmonary arteries by thrombus,


fat or air embolus, or tumor tissue.
Embolus

plug

Emboli- mobile plugs looking for a landing spot

Clinical manifestations
Dyspnea
Chest

pain
Hemopytsis
May be sudden or develop slowly

PULMONARY EMBOLISM

Complications
Pulmonary

infarction

Embolus cuts off collateral circulation of lung


Decreased lung tissue=decreased oxygen perfusion

Pulmonary

hypertension

Emboli lodged in pulmonary circulation causes blood flow to


lungs to back up
Eventually the right ventricle is involved and we see right
sided heart failure

Dx Studies
X-ray,

CT scan, Pulmonary angiogram, D-Dimer,


ABG analysis

PULMONARY EMBOLISM

Collaborative Care
Prevent

DVT!

Compression devices, ambulation, anticoagulants


prophylactically

Early

treatment of PE

Prevent growth and spread, cardiopulmonary support as


needed
Administer O2
Intubation/mechanical ventilation if necessary
Treat symptoms
Fibrinolytic therapy (tPA or activase)

Long

term therapy with heparin and coumadin


Surgical embolectomy for severe obstruction

PULMONARY EMBOLISM

Nursing interventions
Semi-fowlers

position
Administer 02, fluids and medications as ordered
Monitor for complications
Emotional support
Education for long term anticoagulation therapy

COUMADIN
Used to prevent thrombosis
Has a delayed onset
Inhibits Vitamin K

Lots

of clotting factors are dependent on vitamin K to


be active

Decreased Vitamin K, decreased clotting

Vitamin K is the antidote


Monitor INR and PT
Vitamin K rich foods

Green

leafy veggies
Dried herbs
Broccoli, brussel sprouts

HEPARIN

Activation of antithrombin
Inactivates

clotting factors
Immediate effects
Protamine Sulfate is the antidote
Monitor PTT

HERE ARE SOME EXTRA MEMORY


SLIDES!