Case 144 – Summary

The case this week focused on the use of Viscoelastic Haemostatic assays (VHA). The patient had a ruptured AAA. Initial TEG testing was normal but she continued to bleed. Repeat TEG showed she had developed shortened R time and increased MA that responded to product replacement with FFP and platelets. She had an increased Ly 30 % but the team were uncertain about the use of TXA. Eventually a repeat TEG showed Ly 30 % > 70% and TXA was given to good effect and haemostasis was achieved.

VHA are uniquely placed to diagnose hyperfibrinolysis and there is no equivalent conventional lab test to detect this. In TEG studies 10-34% of patients having a major haemorrhage have Hyperfibrinolysis and this can lead to unnecessary mortality and morbidity for patients.

VHA Background:

The ideas behind Viscoelastic Haemostatic Assays (VHA) are old and in fact “whole blood assays” as they were known were first described by Prof Hartert in 1948. These were mainly research tools due to long sample processing times and the susceptibility to external vibration. These issues started to be overcome and over the past few years these have gradually made there way into clinical use. It should be acknowledged that the evidence base is limited. A 2014 NICE DG13 only recommends the use of TEG and ROTEM post cardiac surgery and states there is insufficient evidence to recommend the routine adoption of ROTEM and TEG in trauma and post partum haemorrhage. The research has continued and in 2018 a BSH guideline was published on their use as an adjunct to usual care. Many hospitals in the UK have access to VHA and these are being used in settings other than the accepted role post cardiac surgery.

BENEFITS VHA:

  • SPEED – Traditional coagulation tests are slow and can lag behind in rapidly evolving clinical situations like haemorrhage. Viscoelastic assays are quick taking 30 mins but a rapid TEG is available in 15 minutes.
  • HYPERFIBRINOLYSIS DIAGNOSIS- uniquely placed to diagnose this issue and allow correction with TXA like in case 144.
  • LIVER DISEASE ? Recognised for some time that PT/APTT prolongation in liver disease for example don’t correlate with bleeding risk due to fall in protein C or S levels. Viscoelastic assays may help in this setting.
  • PLATELET FUNCTION – Useful for platelet inhibition testing for anti platelet agents – may yield important information regarding drug resistance.
  • PATIENT BLOOD MANAGEMENT – Good evidence to show can reduce blood product use in a variety of settings.

Difficulties VHA:

  • STANDARDISATION – Poorly standardised no generalised reference ranges.
  • TRAINING ISSUES – Older Viscoelastic assays rely on pipetting rather than cartridges so issues with user were common.
  • REPLACING TRIED AND TESTED TESTS – Temptation this is used as replacement for tried and tested lab tests rather than adjunct to care.
  • INCREASES COST OF CARE – Additional costs to testing with unclear benefit in some settings such as trauma.
  • INTERPRETATION/ COMPLEXITY – Specialised test needs someone who understands to interpret and apply to clinical situation and this may be difficult in stressful situations like Major haemorrhage.
  • ONLY INFORMATION ON SECONDARY HAEMOSTASIS- No use in assessing vascular issues or primary haemostasis as evidenced by the normal traces seen in VWD, Lupus, HITT or Protein C or S deficiencies.
  • ACTING ON SINGLE RESULT – Generally trends helpful in these assays rather than a one off result often tempting to over interpret one abnormal trace.

Types of VH Assay:

All are VHA’s are useful tests and there is little difference between ROTEM and TEG. They are based on the same technology both are viscoelastic methods that provides graph of clotting process.

  • Thromboelastography (TEG) – Whole blood into cup with activator. Cup moves around pin that is static and resistance recorded using torsion wire.
  • Thromboelastometry (ROTEM) – Like TEG uses whole blood in cup but this time pin moves and cup is static. Change in optical density detected.
  • SONOCLOT – Plastic probe on electromagnetic transducer vibrates vertically resistance as blood clot forms is measured.

Each system has its own nomenclature and interpretation system. Our hospital in the case had TEG so we will focus on this for the interpretation. There is a good summary in BSH guidance if your hospital uses other systems.

INTERPRETING TEG:

  • CK TEG OVERVIEW:

R time – Time taken for the pin to start to detect resistance and is when fibrin starts to form. Long R suggests prolongation in PT/APTT. FFP is the agent of choice to address this.

K time- Time for clot to form and fibrin to polymerise.

MA – Maximum clot strength. Depends on PLT and FFP. Referring to CFF trace will help assess if platelet dysfunction or fibrinogen issue mainly to blame for reduced MA.

Ly30 – Defines the amount of fibrinolysis. If prolonged Tranexamic acid will help here. If MA increased alongside increased LY 30 this is functional fibrinolysis and doesn’t need TXA.

Types of trace on TEG:

  • Citrated Kaolin (CK) – Kaolin only the “standard” TEG
  • Heparinise (CKH) – Kaolin and Heparinase. Useful to detect if heparin affecting results.
  • Functional fibrinogen (CFF) – Tissue factor and platelet inhibitor. Shows the function of fibrinogen. Results should show 20-30% contribution by fibrinogen. 
  • Rapid TEG (CRT) – Kaolin and tissue factor. Result in 10-15 mins so useful in MHP. Tells the MA but no R time as uses Kaolin and tissue factor to activate coagulation. 
  • Platelet mapping – ADP and Arachidonic acid.

REFERENCE TABLE FOR ACTIONS WITH VARIOUS RESULTS ON TEG: (Reference ranges vary according to local standards hence not used in table)

Profile/TestTEG Measure ResultActions
CKRProlonged**check CKHeparinase R time?Heparin contamination
Otherwise consider FFP
CK or CRTMADecreased**Check CFF MA if normal give PLT. If abnormal CFF Cryo or consider both Plt/Cryo
CKLY30Increased*Consider TXA 
*If MA on CK is increased then TXA not indicated as likely reactive Hyperfibrinolysis
CFFMADecreasedCryo 
CKHeparinaseRIf R time shorter than CK R timeSuggests Heparin in sample

Evidence for VHA use in trauma:

Interestingly as mentioned earlier although the use of VHA is fairly widespread in the context of trauma the evidence base for VHA driven Major Haemorrhage protocols is actually fairly weak. There has been a recent large RCT of 390 patients (ITACTIC study) with major bleeding comparing conventional coagulation test driven MHP to VHA driven MHP. This failed to show improved patient mortality or reduced massive transfusion in first 24 hours for the VHA group. This study perhaps shows that although tempting to adopt novel therapies on the basis they seem superior the evidence for VHA driven MHPs is still lacking. Enthusiasts for the role VHA has would suggest this is due to poor interpretation of the VHAs. In the centres that used VHA in ITACTIC study were not familiar in applying the technique in a pressurised situation that may have affected outcomes.

In reality VHA may have a role to play but certainly this doesn’t replace the use of conventional haemostatic tests at present. VHA is advocated in American college of surgeons advanced trauma life support recommendations. It has a 1C recommendation in European guidelines of major bleeding and coagulopathy following trauma 4th edition. The same European guidelines give conventional coagulation driven MHP protocols a rating of 1A. Therefore VHA are adjuncts to usual care and do not replace laboratory tests in major haemorrhage at this stage.

There are some other things we do know about VHA in trauma and these are outlined below:

  • There is evidence to suggests a Normal VHA is useful to rule out need for transfusion. (2B recommendation from BSH guideline on VHA).
  • Low clot strength (MA) and Ly30 >3% can be used as increased risk factor for transfusion. (2C recommendation BSH guideline on VHA).
  • Use of VHA seems to reduce transfusions used in terms of Red cells and FFP. (Gonzalez et al).
  • There is no basis to withhold TXA based on VHA results in trauma. (1B BSH guideline on VHA)
  • BSH guidelines state there may be a reduction in mortality when using VHA driven MHP based on Gonzalez et al study. This however as discussed above has not been found in more recent large multi-centre study ITACTIC.

I hope this case has been helpful and thank you for your contributions to the case. Please feel free to post any comments.

References:

NICE DG13 – detecting, managing and monitoring haemostasis: vistoelastometric point of care testing. (ROTEM, TEG and Sonoclot systems. 20/8/14.

Curry et al. The use of viscoelastic haemostatic assays in the management of major bleeding. British Journal of Haematology (2018) 182; 789-806.

The use of viscoelastic haemostatic assays in goal-directing treatment with allogeneic blood products – A systematic review and Meta-analysis. Scandinavian journal of trauma, resuscitation and emergency medicine. (2017) 25:39.

Gonzalez E et al. Goal directed haemostatic resuscitation of trauma -induced coagulopathy: a pragmatic randomised clinical trial comparing a viscoelastic assay to conventional coagulation assays. Ann Surg 2016;263:1051-9.

Casper et al. Clinical validation of precision medicine protocols: the last mile is the longest. intensive care med (2021) 47;80-82.

Baksaas-Arsenal K et al. Viscoelastic haemostatic assay augmented protocols for major trauma haemorrhage (ITACTIC): a randomised controlled trial. Intensive care med (2020)

Rossaint R et al. The European guideline on management of major bleeding and coagulopathy post trauma: fourth edition. 2016. Crit care 20:100.

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