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THROMBOCYTOPENIA (IDIOPATHIC THROMBOCYTOPENIC PURPURA (CLINICAL MANAGEMENT…
THROMBOCYTOPENIA
Heparin-Induced Thrombocytopenia (HIT)
Formation of antibodies against the herparin platelet complex
Risk factors:
type of heparin used, time of heparin use (beyond 4 days), and surgery (especially with cardiopulmonary bypass)
women
Decline in platelet 5-10 days after heparin therapy, usually by 50% of baseline over a period of 1-3 days (counts between 50 and 80)
Increased risk for thrombosis (DVT, ACS, Stroke, ischemic damage to an extremity)
Treatment
The antibodies typically disappear in 2 to 3 months.
Treatment
NO WARFARIN due to initially promoting thrombosis in the microvasculature by depleting protein C, which can lead to ischemia and gangrenous limbs, Avoid platelet transfusion
Prompt cessation of heparin
Blood collection and send to lab
initiation of alternative means of coagulation
Argatroban- inhibitor of thrombin
Nursing Management:
Monitor CBC, PT, INR
Exercise frequently throughout the day
Avoid crossing legs
Anti-embolism stockings
Medications that alter platelet aggregation
If thrombus is formed during HIT, anticoagulation therapy for 3 to 6 months
Monitor for thrombus (DVT, PE, Stroke
IDIOPATHIC THROMBOCYTOPENIC PURPURA
CLINICAL MANAGEMENT:
Platelet count < 30,000/mm3
Easy bruising (dry purpura)
Heavy menses
Fatigue
Petechiae on extremities & trunk (dry purpura)
Wet purpura: MORE complications, which is mucosal surface bleeding (e.g. hemoptysis / GI bleed)
SEVERE
Platelet 20,000/mm3 (life-threatening)
NURSING MANAGEMENT:
Obtain history of lifestyle and medication history (sulfa-drugs & NSAIDs alter plt function)
Complete H&P, especially neurological assessment because there may be intracranial bleeding.
NO injections or rectal medications/temperatures!!!
Education:
Report fatigue, petechiae, ecchymosis.
Medical treatment
Complications of corticosteroids and need to monitor bone mineral density.
AVOID agents that interfere with platelet functions
AVOID straining, vigorous flossing, vigorous sexual intercourse.
USE soft-bristled toothbrushes and electrical razors.
NO contact sports!!!
DIAGNOSTICS:
H&P
Test for Hep. C and HIV (rule out potential causes)
bone marrow aspirate (increase in megakaryocytes)
platelet count
test for H. pylori (found to correlate with ITP). Eradicating infections increases platelet count.
Pathophysiology of ITP is
an autoimmune disorder where the destruction of normal platelets due to an unknown stimulus.
Anti-platelet antibodies develop and bind to the patients platelets
these are then destroyed by the reticuloendothelial system ( RES ) or tissue macrophages
Attempting to compensate the body increases platelet production in the marrow.
platelet production may also be impaired due to the antibodies that may cause
apoptosis of megakaryocytes which inhibits platelet production within bone marrow
TREATMENT
Medical Management
Any medications known to be associated with ITP are stopped immediately
quinine
sulfa-containing medications
Aminocaproic acid (a fibrinolytic enzyme inhibitor) can be used in patients with significant mucosal bleeding
Short term therapy use of immuosuppressive agents - Corticosteroid prednisone 1mg/kg for 21 days then tapper dose until off medication
Administration of IVIG
For chronic ITP involves use of
anti-D (WinRho) in patients whoa re Rh(D) +
Splenectomy as an alternative treatment which results in a sustained normal plt count about 50% of the time.
Pts should receive
pneumococcal vaccine
Haemophilus influenzae Type B vaccine
menigococcal vaccine
2 to 3 weeks before splenectomy
other options include monoclonal antibodies (rituximab) Increases plt count up to 1 not as effective though
Romiplostim (Nplate) weekly Subcutaneous injection
Eltrombopag (Promacta) is given orally
PLT count can fluctuate so treatment needs to be continued indefinitely, however in some situations if plt count can remain at a safe level the medication could be stopped
side effects of eltrombopag - Head ache - Blistering of oral mucosa - ecchymoses