NU 313: Nursing Care of Patients with Coagulation Disorders

Specific Disorders: Too Many Platelets (2)
Essential or Primary Thrombocythemia
Secondary Thrombocytosis

Specific Disorders: Too Few Platelets (4)
Immune Thrombocytopenic Purpura (ITP)
Heparin -Induced Thrombocytopenia (HIT)
Thrombotic Thrombocytopenic Purpura (TTP)

Essential Thrombocythemia: Overview
Stem cell disorder
Platelets > 600,000 mm3
Plts often dysfunctional
More common in adults
Mutation of the Janus kinase 2 (JAK2) gene

Clinical Manifestations: Thrombocythemia
Symptoms from bleeding or thrombosis
If bleeding occurs, it occurs when plt count is > 1.5 million
Vaso-occlusive manifestations:
Erythromelalgia: ↓flow to feet & toes- red, burns, throbs
Neurological manifestations: HA, visual disturbances, etc
Splenomegaly in 50% of patients

Diagnosis: Thrombocythemia
>600,000; may have ↑ in RBCs, WBCs, or both
Bone marrow aspiration or biopsy
R/O other causes of ↑ platelets

Medical Management: Thrombocythemia
Minimize other risk factors
Low dose ASA
Hydroxyurea (Hydrea): myelosuppressive drug
Anagreglide (Agrylin): non-cytotoxic drug: more side effects than Hydrea
Interferon alpha 2b: SQ adm; very expensive; causes liver dysfunction
Platelet Pheresis – immediate reduction; temporary effect; used as a last resort

Nursing Management for Thrombocythemia
Risk for Injury:
Teach about medications that can cause bleeding:
Teach about signs and symptoms of both bleeding and clotting

Secondary Thrombocytosis
“reactive thrombocytosis” – platelet count > normal but does not usually increase to >1 million / mm3; plt function is normal
Other causes: infection, chronic inflammation, iron deficiency anemia, CA, S/P splenectomy
More common than ET
Treatment of underlying cause

Thrombocytopenia causes what 3 effects to platelets?
Decreased production
Increased destruction
Increased consumption

Clinical Manifestations: Thrombocytopenia
Bleeding & petechiae – < 50,000 Mucosal membrane bleeding 20,000 Spontaneous bleeding plt < 5000

Diagnosis: Thrombocytopenia
Bone Marrow Aspiration / biopsy
Platelet counts < 150,000 Bleeding time will be prolonged (> 12 minutes)
PTT, PT and INR are of little value in diagnosing thrombocytopenia- worried about it in HIT and thrombocytopenia

Medical Management: Thrombocytopenia
Determine cause, treat it
Platelet transfusions may be helpful in those situations when production is decreased
Splenectomy may be helpful in those cases where the spleen is destroying plts quicker than normal

Nursing Management: Thrombocytopenia
Early identification of at risk patients
Institute bleeding precautions
Monitor labs
Nurses are the primary advocates for patients!!!

Immune Thrombocytopenic Purpura (ITP)
Autoimmune disease-b/c platelets are being destroyed by antibodies
Acute: affects children & neonates
Chronic: affects adults; women > men
Primary: antibodies attack platelets indiscriminately
Secondary: Antibodies attack offender, then attack platelets
Cause Unknown

Clinical Manifestations of ITP
May be asymptomatic with platelets < 20,000 General manifestations: petechiae on extremities and trunk, easy bruising, heavy menses Classified as: Wet purpura: bleeding from mucosal surfaces Dry purpura: bleeding in the superficial skin Lab findings: ↓plts, may also be anemic

Medical Management for ITP
Remove offending trigger
Treatment depends on platelet count and lifestyle
Steroids: 80% effective; temporary relief
Cyclophosphamide (Cytoxan) & Azathioprine (Imuran) – reduces antibody formation
IV Immune Globulin (IVIG) – binds to receptors on macrophages; expensive, temporary relief
Vincristine (Oncovin) – – binds to receptors on macrophages & inhibits platelet destruction
Anti-D antibody (WinRho)-freeze dried anti-globulin
Surgery: splenectomy- can produce a remission in 60% of patients

Heparin Induced Thrombocytopenia (HIT)
Drug induced, immune mediated thrombocytopenia
8% of heparinized patients will develop the antibody associated with HIT
Immune-mediated: larger drops in plt counts, after 5 days – more severe
Non-immune mediated HIT – plt count decreases within 5 days, less severe drop, benign, self-limiting

Pathophysiology of HIT
Platelet factor 4 (PF4) is released into circulation, binds to platelets
Heparin binds to PF4 molecules; acts as immunogens and leads to antibody formation
Causes platelet activation and aggregation → thrombosis

Medical Management of HIT
Identify patients at risk
Lab test for anti-heparin platelet factor 4 (AHPF4)
Stop heparin
Start with a non-heparin anticoagulant (Argatroban)
Monitor labs
Assess for thrombosis, signs of bleeding

Nursing Management of HIT
Determine risk
Ascertain medication history
Assess for recent viruses, symptoms such as headaches
Bleeding precautions

Thrombotic Thrombocytopenia Purpura (TTP)
Results in formation of small
blood clots which remove
platelets from the circulation, causes clumping of platelets

Manifestations of TTP
Purpura; pale, weak, fever, SOB (hemolytic anemia), jaundice, headache, speech changes, confusion, etc

Diagnostic Tests: of TTP
CBC, Bilirubin, LDH,
Creatinine, ADAMTS13 assay

What are the 2 types of TTP?

Inherited TTP
faulty production of an enzyme needed for clotting, results in clumping of platelets; Affects newborns & children

Acquired TTP
enzyme is not affected but the body makes antibodies that block the enzyme’s production; Affects adults, more common

How do you treat Inherited TTP?
FFP to replace the missing or changed enzyme

How do you treat Acquired TTP?
Plasmapheresis – remove antibodies; Meds to block the antibodies effect (steroids, chemo)

Disseminated Intravascular Coagulation (DIC)
Acquired syndrome that occurs as a result of an underlying condition, which leads to Imbalance in the coagulation system characterized by the simultaneous activation and consumption of clotting factors and platelets, which leads to either bleeding or clotting

Causes of DIC
Infections /Sepsis
Gram – sepsis accounts for 20% of the cases
Bacteria, viruses, fungi
Release of endotoxins activate the tumor necrosis factor
Any type of shock
Trauma / Burns
Cancer – more common with hematologic CA
Pregnancy and OB complications
Toxins from snake bites, spider bites and certain drugs
Injuries to RBC or platelets (hemolytic anemia, transfusion Rxn)

Clinical Manifestations of DIC due to…. (Disease Process)
Expedited clot formation
Consumption of platelets and other clotting factors
Faster clot breakdown
End organ damage / failure

Platelets in DIC: Normal Range & Effects of DIC
Normal: 150,000 – 350,000
DIC: <50,000

PT/INR in DIC: Normal Range & Effects of DIC
Normal: 11 – 12.5
DIC: Any increase

aPTT in DIC: Normal Range & Effects of DIC
Normal: 30-40
DIC: Any increase

Fibrinogen in DIC: Normal Range & Effects of DIC
Normal: 200-400 mg/dl
DIC: <100 mg/dl

Fibrin Degradation Products in DIC: Normal & Effects of DIC
Normal: <10 ng/ml DIC: >40 ng/ml

D-Dimer in DIC: Normal Range & Effects of DIC
Normal: <250 ng/ml DIC: >250 ng/ml

Thrombin time in DIC: Normal Range & Effects of DIC
Normal: 5 seconds of control
DIC: Increased

Medical Treatment of DIC
Remove trigger
Maintain organ perfusion: fluids, oxygen, etc
Restore balance
Replace clotting factors: FFP, cryoprecipitate, vitamin K and folate needed for clotting factors
Slow the coagulation cascade
Heparin (low dose = 5 – 10U/Kg/hour)
Antithrombin III – inactivates thrombin

Nursing Management of DIC
Patient safety is a priority!
Institute bleeding precautions
Monitor vital signs and assess for signs of hypoxia
Review labs
Watch for hypovolemia
Provide support for family

What is the priority nursing diagnosis for a client newly diagnosed with autoimmune thrombocytopenic purpura?

A. Impaired Gas Exchange
B. Impaired Skin Integrity
C. Risk for Injury
D. Acute Pain


While monitoring a patient for the development of disseminated intravascular coagulation (DIC), the nurse should take note of what assessment parameters?

A. Platelet count, prothrombin time (PT), and partial thromboplastin time (PTT)
B. Platelet count, blood glucose level, and white blood cell (WBC) count
C. Thrombin time, calcium level, and potassium level
D. Fibrinogen level, WBC count, and platelet count


During a teaching session with a patient diagnosed with primary thrombocythemia, the nurse correctly instructs the patient to:

A. Decrease cardiac risks by drinking a glass of red wine nightly
B. Take Coumadin daily
C. Administer interferon-alfa-2b subcutaneously
D. Take NSAIDs at the earliest sign of pain


DIC: Syndrome of Disseminated Intravascular Coagulation A syndrome of diffuse clotting and hemorrhage that occurs a complication of another disorder. Triggers for DIC • Massive trauma • Shock • Sepsis or infection • Acute promyelocytic leukemia • Metastatic cancers • …

The nurse is caring for a patient with anemia. Which blood component is deficient in this patient? a. plasma b. platelets c. red blood cells d. white blood cells C red blood cells A patient is diagnosed with anemia and …

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I decided to write my paper about the coagulation system, including clot formation, but mainly about Disseminated Intravascular Coagulation. Disseminated Intravascular Coagulation, also known as DIC, is a pathological activation of blood clotting mechanisms that may happen in response to …

A patient has been diagnosed with thrombocytopenia. What teaching point should the nurse include in the patient’s plan of care? 1.The patient should be instructed to avoid crowds. 2.The patient should be instructed to alternate periods of activity with periods …

Thrombocytopenia • Platelets below 150,000/ μl o Note: platelets normally live about 8-10 days • May be hereditary • Most cases are acquired • ITP- Immune Thrombocytopenia Purpura o Platelets are destroyed by the spleen • Heparin-induced thrombcytopenia Symptoms of …

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