Heparin-induced thrombocytopenia
Introduction
Heparin induced thrombocytopenia is a complication that develops in heparin therapy and occurs in two types. The first type of Heparin induced thrombocytopenia is type 1 HIT which develops two days after the patient has been exposed to heparin. During this period, the platelet count reverts to normal as the patient continues with the heparin therapy. Type 1 HIT is therefore a disorder that is as a result of the effect that heparin causes to the body when the platelets are being activated. The second type of Heparin induced thrombocytopenia is type 2 HIT which is an immune mediated disorder that occurs between 4 to 10 days following exposure to heparin (Crowther et al, 2012). The second type of Heparin induced thrombocytopenia has far reaching consequences as can result in the patient losing their limbs or even dying.
Heparin induced thrombocytopenia is one of the most important immune mediated type of thrombocytopenia and requires to be frequently administered to the body. If left unchecked or goes unrecognised, it often results to morbidity or death to the victims (Crowther et al, 2012). The drug Heparin is commonly used for thromboprophylaxis and other treatments such as acute coronary syndrome, atrial fibrillation, dialysis, venous thromboembolism, cardiovascular surgery, invasive procedures and during extracorporeal circulation. Despite its advantages however, there are serious side effects, some of which cause serious medical conditions and could even cause death, an example being Heparin induced thrombocytopenia (Francini, 2005). Patients are at further risks because there are various factors that could result to patients admitted in hospital getting thrombocytopenia which results to Heparin induced thrombocytopenia occurring but remaining unrecognised until adverse effects appear.
It is estimated that about eight percent of heparinised patients also develop the antibodies that are associated with Heparin induced thrombocytopenia and that about five percent of those on heparin will also develop Heparin induced thrombocytopenia with thrombocytopenia. The patients are also likely to suffer from venous and arterial thrombosis
Description of the HIT currently used in the practice.
Heparin induced thrombocytopenia is associated with a decrease in the number of platelets during the period when the patient is exposed to heparin or shortly after exposure. Although the mechanisms of the first type of Heparin induced thrombocytopenia (type 1 HIT) are still unknown, type 1 HIT affects the immune system as it has a pro-aggregating effect on the platelets (Arepally, 2017). Type 1 HIT affects about 10 percent of patients who receive heparin treatments and causes mild and transient asymptomatic thrombocytopenia. The effects occur within 2 days after heparin is first administered but disappear quickly after the heparin treatments stop. Type 2 HIT on the other hand is immune mediated and poses great risk to the thrombosis. Since type 2 HIT is more serious than type 1 HIT, proposals have been made to change the definition for type 1 HIT to non-immune heparin associated thrombocytopenia and type 2 HIT be recognised as HIT so as to resolve the confusion surrounding the two syndromes (Francini, 2005). The definitions are intended to help differentiate the two so as to easily identify which preventive measures to take according to the type of syndrome being resolved.
Patients that are undergoing cardiovascular surgery have been identified as being more likely to develop more antibodies compared to those undergoing orthopaedic surgery. Post-surgical patients are also at a higher risk of developing antibodies compared to patients undergoing treatments that do not require surgery (Cucker, 2016). Patients that receive unfractionated heparin are also at a higher risk of developing antibodies compared to those that receive treatments containing low molecular weight heparin. It is however important to note that antibodies that develop in patients that get UFH often have a high likelihood of cross reacting with LMWH. According to a study involving 665 patients undergoing elective hip arthroplasty, it was discovered that LMWH has a higher chance of preventing the occurrence of Heparin induced thrombocytopenia (Francini, 2005). In the study, the patients had been randomly selected and given either LMWH or UFH. The results revealed that 9 out of the 332 patients who were given UFH developed Heparin induced thrombocytopenia while none of the patients who received LMWH developed Heparin induced thrombocytopenia (Francini, 2005). Patients who received UFH were also more likely to develop antibodies that depended on the presence of heparin compared to patients who received LMWH.
Description of HIT change for the practice.
Danaparoid can be an ideal substitute for heparin when treating patients with Heparin induced thrombocytopenia. Danaparoid is an anticoagulant that is made up of three glycosaminoglycans and through antithrombin, help to prevent anti-FXa activity. The three glycosaminoglycans include dermatan sulfate, heparin sulfate and chondroitin sulfate (Weigelt, 2012). According to research conducted to assess the effectiveness of alternatives like danaparoid, results from the 460 patients involved in the study revealed that patients with Heparin induced thrombocytopenia associated thrombosis had a success rate of 90 percent when danaparoid was used as a substitute for heparin (Francini, 2005). The research further revealed that danaparoid is 70 times more successful than dextran in relation to the treatment of Heparin induced thrombocytopenia associated venous and arterial thrombosis.
Description of how it will improve the HIT of the practice
The treatment of Heparin induced thrombocytopenia involves stopping all formulations of heparin immediately after Heparin induced thrombocytopenia has been identified in the patient. Stopping the formulations of heparin however do little to prevent the severe consequences as thrombin continues to be generated which causes thrombotic events that take plays days, and even weeks after Heparin induced thrombocytopenia has been identified (Askari & Linkolf, 2010). Even in cases where heparin cessation is done early, the chances of reducing mortality and morbidity thus proving that caseation is not an ideal treatment method. This is especially because successful treatment is dependent on successful removal of the triggers and also full control of the thrombin storm of Heparin induced thrombocytopenia which can be achieved by the use of an alternative anticoagulation agent such as danaparoid (Kaushansky & Levi, 2018). Since Danaparoid does not cross-react with HIT antibodies, it acts as a suitable alternative and is immediately active and is able to stop the thrombin directly or inhibit its generation process.
Description of the implementation process or roll-out and how the change would be evaluated.
The treatment of Heparin induced thrombocytopenia will involve giving patients an intravenous bolus dose of 2500 that is followed by 400 U/hour for 4 hours. This is followed by another dose of 300 U/hour for 4 hours another subsequent 200 U/hour which is done until anticoagulation is no longer necessary (Abrams et al, 2013). The dose should be adjusted accordingly to ensure that the plasma anti-Xa levels are maintained between 0.5 to 0.8 U/mL. The use of danaparoid is likely to prevent the generation of thrombin and any reduction should be seen as a n indication that the approach is working.
Conclusion
The importance of Heparin induced thrombocytopenia as an immune mediated type of thrombocytopenia has made it difficult to manage the condition due to the health risks the patient is exposed to. Even when the condition has been identified, managing it is made difficult by the lack of appropriate substitutes for heparin. There are however other alternatives like danaparoid that have made it easier to manage the condition without exposing the patient to the adverse effects of Heparin induced thrombocytopenia.
References
Arepally M, (2017) “Heparin-induced thrombocytopenia” Blood, retrieved from, https://ashpublications.org/blood/article/129/21/2864/36268/Heparin-induced- thrombocytopenia
Askari, A. T., & Lincoff, A. M. (2010). Antithrombotic drug therapy in cardiovascular disease. Dordrecht: Springer.
Crowther M, Dans A, and Linkins L, (2012) “Treatment and prevention of Heparin-induced thrombocytopenia” CHEST, retrieved from, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278058/#
Cucker A, (2016) “HIT syndrome (heparin-induced thrombocytopenia with thrombosis)” Cancer Therapy, retrieved from, https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/critical- care-medicine/hit-syndrome-heparin-induced-thrombocytopenia-with-thrombosis/
Franchini, M. Heparin-induced thrombocytopenia: an update. Thrombosis J 3, 14 (2005). https://doi.org/10.1186/1477-9560-3-14
Kaushanky K and Levi M, (2018) “Williams haematology haemostasis and thrombosis” McGraw-Hill Education
Shaz, B., Hillyer, C. D., In Abrams, C. S., & Roshal, M. (2013). Transfusion medicine and haemostasis: Clinical and laboratory aspects. London: Elseiver
Weigelt, J. A. (2012). Surgical Critical Care, An Issue of Surgical Clinics - E-Book. Saunders
