Management of Patient with Nonmalignant Hematologic Disorders

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Bleeding Disorders

Failure of normal hemostatic mechanisms results in bleeding

Can occur anywhere in the body

Trauma

Platelet factor abnormality

Liver & spleen

Coagulation factor abnormality

Tiny vessels usually affected

Deeper bleed

Vascular abnormality

Skin surface

General clinical manifestations

Vary according to the type of defect

Careful H & P

Bleeding may be superficial or deeper within the body

Petechiae

With platelet factor abnormality

Risk factors for bleeding (Chart 33-6)

Severity/duration of thrombocytopenia

Sepsis (­ high platelet consumption)

Increased intracranial pressure (rupture vessels; causes bleeding)

Liver (coagulation factors) /renal dysfunction (erythropoietin)

Dysproteinemia – low platelet function

Alcohol abuse – low platelet production

Splenomegaly – ­ high platelet destruction

Medications

Medical management

Treat underlying cause

Anemia, blood loss

Transfusions of blood products

Hemostatic agents if fibrinolysis excessive (aminocaproic acid)

Nursing Management

Patient education

Bleeding precautions, if Pt knows they are on bleeding precautions (keep body away from risk of falls, hurting, brushing teeth, if they bleed what will happen? It will not stop)

Avoiding activities that increase the risk of bleeding

Examination for bleeding

Testing of all drainage and excreta

Thrombocytopenia

Low platelet level

low production of platelets within bone marrow

­high destruction of platelets

­high consumption of platelets

See table 33-3 for causes and treatments

Clinical manifestations

< 50,000: possible bleeding

< 20,000: Petechiae, nasal/gingival bleeding, excessive menstrual bleeding, excessive bleeding after surgery/dental extractions

<5,000: spontaneous, fatal CNS bleeding or GI hemorrhage

Assessment & Diagnostic

Bone marrow biopsy

Genetic testing

CBC

Hepatitis screening

Medical Management

Treat underlying cause

Platelet transfusion

Splenectomy

Nursing Management

Education

Measures to minimize bleeding (see Chart 15-7 in Chapter 15)

Immune Thrombocytopenic Purpura (ITP)

Affects all ages but more common in children & young women

Primary ITP occurs in isolation

Secondary ITP occurs from autoimmune disease, viral infections, and medications

Pathophysiology

Destruction of platelet by unknown stimulus

Anti-platelet antibodies develop >>>

antibodies bind to platelets >>>

platelets ingested/destroyed >>>

bone marrow increases platelet production to compensate >>>

compensation becomes not as effective as thrombopoietin levels are not elevated in patients with ITP >>>>

platelet production becomes diminished

Clinical Manifestations

May have no symptoms

Easy bruising

Heavy menses

Petechiae

Dry purpura

Mucosal bleeding (wet purpura)

­ risk for intracranial bleeding

Assessment & Diagnostics

History & physical

HIV/Hepatitis C testing

Bone marrow biopsy

Helicobacter pylori

Medical Management

Goal: “safe” platelet level

Stop medication immediately if cause

Pharmacological measures

Immunosuppressive agents

Corticosteroids

Monoclonal antibodies

Chemotherapeutic agents

Thrombopoietin receptor agonist

IVIG

Splenectomy

Nursing Management

Determine risk of bleeding

Medication history

Sulfa-containing drugs

STOP medication is PT has sulfa allergy present

ASA based and NSAIDs

Chart 33-9

Neurological assessments

Avoid injections and rectal procedures

Patient education

Platelet Defects

Qualitative defects; number of platelets normal but the platelets do not function normally

Causes

Aspirin and NSAIDs Use

ESRD

MDS

Multiple myeloma

Cardiopulmonary bypass

Herbal therapy (Chart 33-9)

Acquired Coagulation Disorders

Liver Disease

Diminished coagulation factors produced

Prolonged PT

Risk for bleeding

Transfusion with FFP (in severe cases PRBCs and platelets)

Vitamin K Deficiency

Synthesis of many coagulation factors depends on vitamin K

Common in malnourished patients

Prolonged use of antibiotics decreases intestinal flora that produce vitamin K à depleting vitamin K stores

Vitamin k administration (PO or SQ)

Adequate synthesis of coagulation factors is reflected by normalization of the PT

Vitamin K is the antidote for warfarin toxicity

Monitor INR

Anticoagulant Therapy Complications

Most common in those taking warfarin

INR monitoring

Vitamin K antidote for warfarin toxicity

Transfusion with fresh frozen plasma