platelet disasters heather a. knouff, msn, rn. learning objectives the learner will be able to...
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Platelet DisastersHEATHER A. KNOUFF, MSN, RN
Learning Objectives
The learner will be able to explain how DIC, HIT, and ITP develop in the body
The learner will be able to describe manifestations, complications, and diagnostic criteria for DIC, HIT, and ITP
The learner will be able to discuss current guidelines for treatment and management of patients with DIC, HIT, and ITP.
So what is DIC?
A widely accepted definition is…
“ DIC is an acquired syndrome characterized by the intravascular activation of coagulation with loss of localization arising from different causes. It can originate from and cause damage to the microvasculature, which if sufficiently sever, can produce organ dysfunction” (Venugopal, 2014).
“ DIC is an acquired clinical syndrome characterized by widespread activation of coagulation, resulting in formation of fibrin clots in medium and small vessels throughout the body” (Huether & McCance, )
Causes of DIC
Sepsis – 30-50%
Trauma and Burns
Obstetric Emergencies
Malignancy
Vascular disorders
Toxic reactions or snake bites
(Levi & van der Poll, 2013)
The coagulation cascade – Normal circumstances
http://openi.nlm.nih.gov/detailedresult.php?img=3222266_hr-2010-1-e2-g008&req=4
The Fibrinolytic System – Normal circumstances
http://ocw.tufts.edu/Content/51/lecturenotes/561424/561457
Pathogenesis of DIC
http://medicinembbs.blogspot.com/2013/04/pathogenesis-of-disseminated.html
Pathogenesis of DIC, cont.
1. Precipitating event/tissue damage/endothelial damage
2. Release of excess amounts of tissue factor/tissue thromboplastin
3. Activation of the coagulation cascade through the extrinsic pathway
4. Platelet activation and intravascular fibrin form blood clots which get deposited intravascularly
5. Because of the multiple blood clots being formed, thrombocytopenia and a depletion of coagulation factors occurs
6. At the same time, secondary fibrinolysis is occurring causing a build-up of FDP.
7. Damage from DIC occurs either due to the bleeding from the secondary fibrinolysis or tissue ischemia due to thromboembolus.
http://www.nejm.org/doi/story/10.1056/feature.2014.02.11.23
How is DIC diagnosed?
Common laboratory abnormalities used to diagnose DIC:
Rapid thrombocytopenia – important hallmark!
Prolonged aPTT and PT
Fibrinogen level – can be low, but not a useful lab value to evaluate
Elevated FDP (Fibrin Degradation Products) (D-Dimer)
Low levels of natural anti-coagulants: Protein C or antithrombin
Thromboelastography (TEG) or Rotational Thromboelastography (ROTEM) – not well evaluated
TEG/ROTEM
Scoring System for DIC
Assessment findings/Clinical Signs of a patient with DIC
Obvious indications: Unusual bleeding, hemorrhage, or oozing of blood from new or old sites of
trauma
Ecchymosis, hematoma formation, petechiae, purpura
Excessive bleeding from surgical sites or excess blood loss in surgical drains
Signs of hypovolemia from the blood loss Poor tissue perfusion and signs of circulatory shock
Tachycardia, tachypnea, hypotension, oliguria, change in LOC
Bleeding may also be more subtle Restlessness, anxiety, unstable BP, increase in abdominal or limb girth, pain.
Signs of organ failure due to thromboembolism lodging in organs such as the kidneys or lungs.
Manifestations of DIC
http://www.skinsight.com/info/for_professionals/10-serious-rash-causes-every-medical-student-should-know
https://www.nhlbi.nih.gov/health/health-topics/topics/dic/signs
Manifestations of DIC, cont.
http://www.myvmc.com/diseases/disseminated-intravascular-coagulation/
http://www.emsworld.com/article/10951842/diagnosing-disseminated-intravascular-coagulation-dic
Complications of DIC
Stroke
Heart Attack
Hemorrhage
Shock
Organ Failure
Death
Support organ perfusion and function as organ failure and death are the biggest complications associated with DIC
How do we treat DIC?
Treat the underlying cause*
Transfusions RBC, Cryo, Platelets, Plasma
Anticoagulants Remains controversial
Recombinant human soluble thrombomodulin (rTM) A newer treatment for DIC that is reported to be superior to heparin
Other supportive care while patient remains in the ICU Ventilator, fluids, vasopressors, dialysis
Support Organ perfusion and function
How do we treat DIC?, cont.
According to Yamakawa, et al (2013), “Therapy with rTM may be associated with reduced in-hospital mortality in adult mechanically ventilated patients with sepsis induced DIC.”
Nursing Management for patients with DIC
Be aware of and assess for manifestations of DIC Signs of clotting from micro-emboli, the signs of bleeding
Close monitoring of patients various organ systems Looking for neuro changes
Changes in urine output
Increased bleeding
Provide adequate pain relief
Administration of blood products or other therapies
Education!!
Mortality Rate for patients with DIC
One study indicated: The mortality rate for sepsis is high; that despite intensive care
mortality is 30-50%.
More than half of the patients with sepsis present with some type of coagulation factor abnormality and an incidence of DIC in greater than 20% of those patients
In the case of DIC, mortality rate is almost 63%.
Remember…..
Prevention of DIC may be possible for some patients. So early recognition and intervention in conditions associated with DIC may help prevent DIC from occurring.
What is HIT and how is it diagnosed?
Heparin induced thrombocytopenia (HIT) is an immunologic adverse reaction to heparin therapy
Your body forms antibodies to the heparin that cause platelet aggregation
Estimated in 2011 that 12 million or 1/3 of all hospitalized patients will receive heparin, and 0.5% - 5% of patients will develop HIT
Diagnosis of HIT is based on both laboratory values and clinical findings Platelet levels
Assay’s to confirm the detection of HIT antibodies
Clinical findings
Manifestations/Complications of HIT
Patient dependent factors play a role in the location of the thrombosis, although venous thrombosis occurs more often
Common manifestations/complications of DIC: DVT
PE
Skin lesions
Limb Ischemia
Acute stroke or MI
Treatment for HIT
Eliminate all forms of heparin exposure However just stopping the heparin is not enough
Postpone the introduction of warfarin for patients requiring long term anticoagulation
Administration of direct thrombin inhibitors (DTI) Argatroban
Lepirudin (Refludan)
Bivalirudin (Angiomax)
Fondaparinux (Arixtra) Not labeled for HIT, but may be used for HIT treatment
Nursing Management for HIT
Monitor for signs of bleeding or thromboembolism deposit in tissue and organs
Monitor lab values
Optimize skin integrity and proper skin care May include use of specialty beds or pressure reducing measures
Signage alerting staff about heparin allergy
Patient and family education
What is ITP?
Immune (Ideopathic) thrombocytopenia purpura is an autoimmune disease that causes your platelets to be destroyed by the spleen.
Approximately 66 new cases per 1 millions are diagnosed May be low because many patients with the disease have no
symptoms
Manifestations may not be evident until platelet count is <30,000 Frequent, easy bruising and petechiae
Prolonged bleeding from cuts
Nosebleeds, blood in the urine, or in the gums
Diagnosis and Treatment of ITP
Diagnosis for ITP is usually done by excluding all other diseases and conditions that could cause thrombocytopenia
If ITP is suspected blood tests, physical exam, and a complete medical history are completed
Treatment for ITP will depend on the patient and how low the platelet count drops The initial drug of choice is Corticosteroids
Other treatments can include intravenous immune globulin or splenectomy if the pharmacological treatment is not successful
Nursing management includes thorough assessment, preventing or controlling hemorrhage, and patient education
References
Chinen, Y., Kuroda, J., Ohshiro, M., Shimura, Y., Mizutani, S., Nagoshi, H., Sasaki, N., Nakayama, R., Kiyota, M., Yamamoto-Sugitani, M., Kobayashi, T., Matsumoto, Y., Horiike, S., & Taniwaki, M. (2013). Low ADAMTS-13 activity during hemorrhagic events with disseminated intravascular coagulation. International Journal of Hematology, 97, 511-519.
Dressler, D.K. (2012). Coagulopathy in the intensive care unit. Critical Care Nurse, 32(5), 48-60.
Fennessy-Cooney, M. (2011). HIT: Heparin induced thrombocytopenia. The Nurse Practitioner, 36(6), 31-37.
Fisher, V.R., Scott, M.K., Tremblay, C.A., Beaulieu, G.P., Ward, D.C., & Byrne, K.M. (2013). Disseminated intravascular coagulation: Laboratory support for management and treatment. Lab Medicine, 44(3), 205-209.
References
Huether, S.E. & McCance, K.L. (2012). Understanding Pathophysiology (5th edition). St. Louis, Missouri, Elsevier Mosby.
Hunt, C.W. (2010). Immune thrombocytopenia Purpura. Clinical Practice, 19(4), 237-239.
Kusuma, B. & Schulz, T.K. (2009). Acute disseminated intravascular coagulation. Hospital Physician, March/April 2009, 35-40.
Levi, M. (2014). Diagnosis and treatment of disseminated intravascular coagulation. International Journal of Laboratory Hematology, 36, 228-236.
References
Levi, M. & van der Poll, T. (2013). Disseminated intravascular coagulation: A review for the internist. Internal and Emergency Medicine, 8, 23-32.
Lewis, S.L., Dirksen, S.R., Heitkemper, M.M., Bucher, L., & Camera, I.M. (2011). Medical-Surgical Nursing: Assessment and Management of Clinical Problems (8th edition). St. Louis, Missouri: Elsevier Mosby
Liu, X., Wang, X., Liu, X., Hao, D., Jaladat, Y., Lu, F., Sun, T., & Lv C. (2014). Low-Dose heparin as treatment for early disseminated intravascular coagulation during sepsis: A prospective clinical study. Experimental and Therapeutic Medicine, 7, 604-608.
References
Overbey, D.M., Jones, E.L., & Robinson, T.N. (2014). How hemostatic agents interact with the coagulation cascade. AORN, 100(2), 149-156.
Perrin, K.O. (2009). Understanding the essentials of critical care nursing. New Jersey: Pearson Prentice Hall.
Venugopal, A. (2014). Disseminated intravascular coagulation. Indian Journal of Anaesthesia, 58(5), 603-608.
Winkeljohn, D. (2013). Diagnosis, treatment, and management of immune thrombocytopenia. Clinical Journal of Oncology Nursing, 17(6), 664-666.
Yamakawa, K., Ogura, H., Fujimi, S., Morikawa, M., Ogawa, Y., Mohri, T., Nakamori, Y., Inoue, Y., Kuwagata, Y., Tanaka, H., Hamasaki, T., & Shimazu. (2013). Intensive Care Medicine, 39, 644-652.