Thrombocytopenia

65 Thrombocytopenia

Overview/pathophysiology

Thrombocytopenia is a relatively common coagulation disorder that results from a decreased number of platelets. It can be congenital or acquired, and it is classified according to cause. Causes include deficient production of thrombocytes, as occurs with bone marrow disease (e.g., leukemia, aplastic anemia) or accelerated platelet destruction occurring from loss or increased use, as in hemolytic anemia, thrombotic thrombocytopenic purpura (TTP), idiopathic (autoimmune) thrombocytopenic purpura (ITP), disseminated intravascular coagulation (DIC), or damage by prosthetic heart valves, as well as hypersplenism and hypothermia. Potential triggers include an autoimmune disorder, severe vascular injury, and spleen malfunction. In addition, thrombocytopenia can occur as a side effect of certain medications, such as heparin. Regardless of cause or trigger, the disorder affects coagulation and hemostasis. With chemical-induced thrombocytopenia, prognosis is good after withdrawal of the offending drug. Prognosis for other types depends on the form of thrombocytopenia and the individual’s baseline health status and response to treatment. Note: Thrombocytopenia may be the first sign of systemic lupus erythematosus (SLE) or infection.

TTP is an acute, often fatal disorder caused by deficiency of a plasma enzyme that normally inactivates the von Willebrand clotting factor (vWF); thus, large and potentially obstructive vWF and platelet complexes occur, resulting in reduced available platelets in circulation. vWF is the most important protein that mediates platelet adhesion to damaged endothelial surfaces.

ITP is thought to be an immune disorder specifically involving antiplatelet immunoglobulin G (IgG), which destroys platelets as well as affecting adequate platelet production. The acute form is most often seen in children (2-6 yr of age) and may be related to a previous viral infection. The chronic form is seen more often in adults (18-50 yr of age) and is of unknown origin.

Heparin-induced thrombocytopenia (HIT) is a disorder in which heparin triggers an antibody response. The heparin-antibody complexes bind to platelet surfaces, causing activated platelets to aggregate, leading to further thrombosis and, because of increased utilization, thrombocytopenia. Because the platelets are activated (although low in number), HIT is uniquely associated with both arterial and venous thrombosis rather than bleeding.

Health care setting

Primary care; hospitalization for complications

Assessment

Chronic indicators:

Long history of mild bleeding or hemorrhagic episodes from the mouth, nose, gastrointestinal (GI) tract, or genitourinary (GU) tract. Increased bruising (ecchymosis) and petechiae also have been noted.

Acute indicators:

Fever, splenomegaly, acute and severe bleeding episodes, weakness, lethargy, malaise, hemorrhage into mucous membranes, gum bleeding, and GU or GI bleeding. Prolonged bleeding can lead to a shock state with tachycardia, shortness of breath, and decreased level of consciousness (LOC). Optic fundal hemorrhage decreases vision and may preclude potentially fatal intracranial hemorrhage. Note: With TTP and HIT, the individual may exhibit signs associated with platelet thrombus formation, such as skin necrosis, and ischemic organ failure (decreased renal function or neurologic changes).

History of:

Recent infection, myeloproliferative disease, or aplastic anemia; recent vaccination; binge alcohol consumption; positive family history of thrombocytopenia; or use of chlorothiazide, digitalis, quinidine, rifampin, sulfisoxazole, chloramphenicol, phenytoin, chemotherapy, or heparin.

Diagnostic tests

Platelet count:

Can vary from only slightly decreased to nearly absent. Less than 100,000/mm³ is significantly decreased; less than 20,000/mm³ results in a serious risk of hemorrhage.

Peripheral blood smear:

May reveal megathrombocytes (large platelets), which are present during premature destruction of platelets, as well as reticulocytosis and fragmented red cells.

Lactate dehydrogenase:

May be elevated.

Bilirubin:

Complete blood count:

Low hemoglobin (Hb) and hematocrit (Hct) levels because of blood loss or aggregates with clotting; white blood cell (WBC) count usually within normal range.

Bone marrow aspiration:

Reveals increased number of megakaryocytes (platelet precursors) in the presence of ITP and HIT but may be decreased in other causes of thrombocytopenia.

Antibody screen:

May be positive because of the presence of IgG platelet antibodies or positive HIT antibody tests.

Nursing diagnosis:

Risk for bleeding

related to decreased platelet count

Desired Outcome: Patient is free of the signs of bleeding as evidenced by secretions and excretions negative for blood, blood pressure (BP) 90/60 mm Hg or greater or within patient’s baseline range, heart rate (HR) 100 bpm or less, respiratory rate (RR) 12-20 breaths/min with normal depth and pattern (eupnea), and absence of bruising or active bleeding.

ASSESSMENT/INTERVENTIONS	RATIONALES
Assess patient for hematuria, melena, epistaxis, hematemesis, hemoptysis, menometrorrhagia, bleeding gums, petechiae, or severe ecchymosis. Teach patient to be alert to and report these indicators promptly as well as any headache or changes in vision.	These are signs of bleeding that could occur as a result of thrombocytopenia. These signs should be reported promptly for timely intervention.
Monitor platelet count daily and coagulation studies at least weekly or as prescribed.	Optimal range is 150,000-400,000/mm³. Less than 100,000/mm³ is significantly decreased; less than 20,000/mm³ results in a serious risk of hemorrhage.
Ensure that there is a current type and crossmatch in the blood bank for red blood cells (RBCs).	RBC transfusions would be necessary to help maintain intravascular volume in the event acute bleeding occurs.
Prevent or promptly control symptoms that can trigger bleeding, such as retching, vomiting, coughing, and straining with bowel movements.	Straining and similar actions increase intracranial pressure and can result in intracranial hemorrhage.
When possible, avoid venipuncture. If performed, apply pressure on site for 5-10 min or until bleeding stops. Do not give intramuscular (IM) injections. If injections are necessary, use subcutaneous route with a small-gauge needle.	Patient is at risk for prolonged bleeding because of the decreased platelet count.
Advise patient to avoid straining at stool.	Straining increases intracranial pressure and can result in intracranial hemorrhage.
Obtain prescription for stool softeners, if indicated. Teach patient anticonstipation routine as described in “Prolonged Bedrest” for Constipation, p. 64.	These measures help prevent constipation, thereby minimizing need to strain at stool and risk for bleeding.
Administer corticosteroids as prescribed.	Corticosteroids enhance vascular integrity and diminish platelet destruction.
Teach patient to use electric razor and soft-bristle toothbrush.	These items minimize risk of injury and hence bleeding.
Instruct patient about the association of alcohol consumption, smoking, and use of aspirin or nonsteroidal antiinflammatory drugs (NSAIDs) with increased risk of bleeding.	Alcohol may suppress bone marrow production of blood cells, smoking affects circulation, and aspirin and NSAIDs reduce platelet adhesion.
Administer platelet-increasing agents as prescribed.	Intravenous immunoglobulin (IV IgG) increases platelet count by impeding the antibody production that destroys platelets. Romiplastim stimulates thrombopoiesis in ITP. < div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Psychosocial support Care of the renal transplant recipient Polycythemia Bronchiolitis Stay updated, free articles. Join our Telegram channel Tags: All-In-One Care Planning Resource Jul 18, 2016 \| Posted by admin in NURSING \| Comments Off on Thrombocytopenia Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access