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.