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TEG® Talk: Thromboelastography in Neurocritical Care

By Currents Editor posted 03-21-2019 15:32

  

Pharmacy_BGilbert_TEG_02142019_Currents_rev.jpgBy Brian Gilbert, PharmD, BCPS, BCCCP, Emergency Medicine Clinical Pharmacy Specialist, Wesley Medical Center, Wichita KS

Coagulopathies in neurocritical illness is common. Traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), and acute ischemic stroke (AIS) each pose unique practice dilemmas for identifying optimal regimens for neuroresuscitation. Thromboelastography (TEG), first introduced approximately 70 years ago, is a method to test viscoelastic properties of whole blood and associated coagulopathies. 1 The two commercially available products widely accessible today are TEG® and ROTEM® with the majority of data described in the literature having utilized TEG®. TEG® measures different phases of the coagulation cascade including: formation of clot time (R), enzymatic coagulation factors/anticoagulants/fibrinogen/platelets time (K), fibrinogen and platelet kinetics (α angle), dysfunctional fibrinogen/platelets (maximum amplitude; MA), and lastly fibrinolysis percentage (Lysis 30; Ly 30) (Figure below).

Dysfunction in any or multiple components of the TEG® values can help guide resuscitation efforts.2 Disruption in homeostatic values can help determine if the patient is in a hyper or hypocoaguable state. Patients with prolonged R times benefit from fresh frozen plasma or factor derived blood products. A decreased α angle typically indicates the need for cryoprecipitate. Decreases in maximum amplitude indicate platelet dysfunction and patients may benefit from plateletpheresis or desmopressin (DDAVP). Lastly, if the Ly30% is high, this indicates hyperfibrinolysis, and administration of anti-fibrinolytics like tranexamic acid (TXA) may be warranted. The majority of data on the utility of TEG® comes from the trauma community where it has been shown to help guide resuscitation more effectively in massive transfusion protocols compared to standard 1:1:1 resuscitation.3 However, there remains a paucity of literature on the utility of TEG® in neurocritically ill patients. This article will summarize some of the data behind TEG® utilization in TBI, SAH, ICH, and AIS.

The incidence of coagulopathy in TBI has been reported to occur in up to 50% of patients with tissue factor release, hyperfibrinolysis, disseminated intravascular coagulation, and platelet dysfunction being among some of the most common disturbances noted.3,4 Since the CRASH-2 and MATTERS trials, early administration of TXA has become fairly routine. Recently, there has been data published that has questioned the benefit of routine utilization of TXA.   Utilization of TEG® may serve as a way to stratify those who may benefit from TXA versus another hemostatic agent which could reverse other TBI associated coagulopathies. Platelet dysfunction identified by TEG® was able to predict TBI survivors vs. non-survivors and could aid to stratify mortality risk and potential clinical course.5 Continued efforts to utilize TEG® as a clinical decision tool is ongoing and focused data could be utilized to create a protocolized approach to neuroresuscitation of the TBI patient.

Coagulopathies of ICH and SAH, like TBI, are common. Commonly patients who develop SAH have increased inflammation and platelet dysfunction after acute brain injury. Early platelet dysfunction after SAH identified by TEG® has correlated with increased incidence of delayed cerebral ischemia and worse modified Rankin scores at 3 months after insult.6 Platelet dysfunction is a major contributor of coagulopathy in spontaneous or medication induced ICH and has been accurately identified by TEG®.7,8 Increasing interest is being placed on ways to identify coagulopathies induced by oral anticoagulants specifically from the factor Xa inhibitor class (such as apixaban or rivaroxaban). Calibrated chromogenic assays are expensive and not readily available, and the utility of low molecular weight or unfractionated heparin anti-Xa assays have not yet been validated to identify presence of the oral factor Xa inhibitors. However, there is data to support that TEG® can detect coagulopathies induced by these direct oral anticoagulants and may provide valuable data when determining if a patient is a candidate for anticoagulation reversal or not.9

Lastly, many are attempting to utilize TEG® in the management of AIS. Early hypercoagulability noted on TEG® in AIS has  been associated with acute neurological deterioration which is thought to be secondary to lesion evolution.10 For those with mild stroke or transient ischemic attack, TEG® may be able to predict those at higher risk for recurrent ischemic events which could help providers in their clinical decision making.11 Also, there has been one reported case in which TEG® was used to identify hyperfibrinolysis post alteplase infusion for acute ischemic stroke; this patient suffered from a  hemorrhagic conversion post alteplase therapy. Further work could go into utilizing TEG® as a way to possibly stratify those at high risk for the development of hemorrhagic transformation post alteplase administration.12 Finally, TEG® may be useful at identifying those who may be aspirin or P2Y12 responders which could help individualize individual care to patients.13

Still, there remains a lot of unanswered questions on the utility of TEG® in neurocritically ill patients. Thus far, the data presented is promising with respect to risk stratification, treatment decisions, and prognostication. Larger randomized controlled data are needed to validate the utility of TEG® in this patient population.

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References

  1. Chen A, Teruya J. Global hemostasis testing thromboelastography: old technology, new applications. Clin Lab Med. 2009;29: 391–407.
  2. Bolliger D, Seeberger MD, Tanaka KA. Principles and practice of thromboelastography in clinical coagulation management and transfusion practice. Transfus Med Rev. 2012;26:1–13.
  3. Sun Y, Wang J, Wu X, Xi C, Gai Y, Liu H, Yuan Q, Wang E, Gao L, Hu J, Zhou L. Validating the incidence of coagulopathy and disseminated intravascular coagulation in patients with traumatic brain injury--analysis of 242 cases. Br J Neurosurg. 2011 Jun;25(3):363-8.
  4. Maegele M. Coagulopathy after traumatic brain injury: incidence, pathogenesis, and treatment options. Transfusion. 2013 Jan;53 Suppl 1:28S-37S.
  5. Davis PK, Musunuru H, Walsh M, et al. Platelet dysfunction is an early marker for traumatic brain injury-induced coagulopathy. Neurocrit Care. 2013;18:201–8.
  6. Frontera JA, Provencio JJ, Sehba FA, McIntyre TM, Nowacki AS, Gordon E, Weimer JM, Aledort L. The Role of Platelet Activation and Inflammation in Early Brain Injury Following Subarachnoid Hemorrhage. Neurocrit Care. 2017 Feb;26(1):48-57.
  7. McDonald MM, Almaghrabi TS, Saenz DM, Cai C, Rahbar MH, Choi HA, Lee K, Grotta JC, Chang TR. Dual Antiplatelet Therapy Is Associated With Coagulopathy Detectable by Thrombelastography in Acute Stroke. J Intensive Care Med. 2017 Jan  1:885066617729644. doi: 10.1177/0885066617729644. [Epub ahead of print]
  8. Lauridsen SV, Hvas AM, Sandgaard E, Gyldenholm T, Rahbek C, Hjort N, Tønnesen  EK, Hvas CL. Coagulation Profile after Spontaneous Intracerebral Hemorrhage: A Cohort Study. J Stroke Cerebrovasc Dis. 2018 Nov;27(11):2951-2961.
  9. Dias JD, Norem K, Doorneweerd DD, Thurer RL, Popovsky MA, Omert LA. Use of Thromboelastography (TEG) for Detection of New Oral Anticoagulants. Arch Pathol Lab Med. 2015 May;139(5):665-73.
  10. Shi Z, Zheng WC, Fu XL, Fang XW, Xia PS, Yuan WJ. Hypercoagulation on Thromboelastography Predicts Early Neurological Deterioration in Patients with Acute Ischemic Stroke. Cerebrovasc Dis. 2018;46(3-4):125-131.
  11. Rao Z, Zheng H, Wang F, Wang A, Liu L, Dong K, Zhao X, Cao Y, Wang Y. High On-Treatment Platelet Reactivity to Adenosine Diphosphate Predicts Ischemic Events of Minor Stroke and Transient Ischemic Attack. J Stroke Cerebrovasc Dis. 2017 Oct;26(10):2074-2081.
  12. Rosafio F, Vandelli L, Bigliardi G, Cavallieri F, Dell'Acqua ML, Picchetto L,  Zini A. Usefulness of Thromboelastography in the Detection and Management of Tissue Plasminogen Activator-Associated Hyperfibrinolysis. J Stroke Cerebrovasc Dis. 2017 Feb;26(2):e29-e31.
  13. Sambu N, Radhakrishnan A, Englyst N, Weir N, Curzen N. ‘‘Aspirin resistance’’ in ischemic stroke: insights using short thromboelastography. J Stroke Cerebrovasc Dis. 2013;22: 1412–9.
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