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Thromboelastography (TEG) - MD Anaesthesia PG Examination Answer

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Introduction

Miller's Anesthesia, 10e | Barash Clinical Anesthesia, 9e

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Principle and Mechanism

How TEG Works

• Before clotting begins: the cuvette rotates freely; no motion is transferred to the pin.
• As clot forms: fibrin strands bridge the cuvette wall and the pin; the pin begins to move with the cuvette.
• As clot strengthens: increasing resistance is transferred through the torsion wire to the recorder, generating a characteristic waveform.
• As fibrinolysis occurs: the clot breaks down, the pin slips, and the waveform amplitude decreases.

Barash Clinical Anesthesia, 9e, p. 1278

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TEG Tracing and Parameters

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TEG Parameters (Normal Values - Kaolin-Activated)

Miller's Anesthesia, 10e, p. 6747 | Barash Clinical Anesthesia, 9e, p. 1278

Interpretation of Parameters by Phase

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ROTEM vs TEG: Comparison

ROTEM-Specific Test Channels

Barash Clinical Anesthesia, 9e, p. 1278

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Newer Devices

Miller's Anesthesia, 10e, p. 6748

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TEG Tracings in Various Pathological States

Common Patterns

1. Normal trace: Symmetric spindle shape, normal R, K, alpha, MA, minimal LY30
2. Factor deficiency (e.g., hemophilia, warfarin): Prolonged R value (wide "gap" at start), prolonged K → FFP or PCC
3. Thrombocytopenia / platelet dysfunction: Low MA, reduced alpha angle → Platelet transfusion
4. Hypofibrinogenemia: Prolonged K, reduced alpha angle, low MA → Cryoprecipitate or fibrinogen concentrate; FIBTEM MCF reduced
5. Hyperfibrinolysis (e.g., liver failure, trauma, abruption): LY30 >7.5%, clot "falls apart" - narrow trace that diminishes rapidly → Tranexamic acid, epsilon-aminocaproic acid
6. Hypercoagulability: Short R and K, high MA, wide trace → Anticoagulation
7. Heparin effect: Prolonged R/K (corrected in HEPTEM channel or with heparinase addition)
8. DIC: Initially hypercoagulable then progresses to hypocoagulable with hyperfibrinolysis - evolving trace

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Treatment Thresholds (TEG-Guided Transfusion Protocol)

PMC review (PMID not directly cited) | Barash 9e

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Clinical Applications of TEG in Anaesthesia

1. Cardiac Surgery (Most Established)

• Detects heparin effect and residual heparin after protamine reversal
• Identifies platelet dysfunction from CPB
• Distinguishes surgical bleeding from coagulopathic bleeding
• Guides rational blood product use, reducing transfusion requirements
• Detects protamine excess

2. Liver Transplantation

• Detects hyperfibrinolysis (which is common and dramatic during the anhepatic phase)
• Guides fibrinogen and antifibrinolytic therapy
• Identifies the "rebound hypercoagulability" after reperfusion
• TEG-guided protocols significantly reduce blood product usage compared to INR/platelet-guided approaches (RCT evidence)

3. Trauma - Trauma-Induced Coagulopathy (TIC)

• Identifies early TIC: prolonged R, low MA, elevated LY30
• Rapid TEG (rTEG) provides actionable results within 5-10 minutes
• Guides massive transfusion protocols and damage control resuscitation
• Detects hyperfibrinolysis - a major contributor to traumatic coagulopathy
• Guides antifibrinolytic therapy (TXA) timing

4. Obstetric Haemorrhage

• Detects coagulopathy in postpartum haemorrhage (PPH)
• Guides management of placental abruption, HELLP syndrome, amniotic fluid embolism
• Some evidence for modest reduction in blood loss vs. conventional tests

5. Neuraxial Anaesthesia Decision-Making

• Assesses adequacy of reversal before neuraxial blocks in patients on anticoagulants
• Useful when timing of anticoagulant dosing is uncertain

6. Paediatric Cardiac Surgery and ECMO

• Guides anticoagulation monitoring on ECMO circuits
• Detects coagulopathy in complex paediatric cardiac repairs

7. Monitoring Anticoagulation

• Detects effect of unfractionated heparin (prolonged R, corrected with heparinase)
• Can detect effect of direct oral anticoagulants (DOACs) - though nonspecific
• Monitors reversal of anticoagulation

8. Other Applications

• Sepsis-associated coagulopathy
• Hepatic disease assessment
• Pre-operative risk stratification
• Monitoring fibrinolytic therapy

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Advantages of TEG Over Conventional Coagulation Tests

Barash Clinical Anesthesia, 9e, Table 53-3

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Limitations of TEG

1. Does not assess primary hemostasis: Cannot detect von Willebrand disease, platelet adhesion defects, or vascular endothelial function
2. Sample heated to 37°C: Masks effects of hypothermia and hypocalcemia on coagulation
3. Re-calcification of citrated blood: Does not reflect in vivo ionized calcium levels
4. Cannot reliably detect Warfarin (INR-based assays remain superior)
5. Nonspecific for DOACs: Cannot differentiate DOAC effect from TIC
6. Vibration sensitivity: First-generation devices (TEG 5000) prone to vibration artifact
7. Operator variability: High intra- and inter-operator variability with older devices; improved with cartridge-based TEG 6s
8. Learning curve: Steep learning curve for both performance and interpretation
9. Cost: More expensive than conventional coagulation tests
10. Limited sensitivity for mild factor deficiencies: Some patients with mild hemophilia may have normal TEG
11. Limited evidence in non-surgical patients: Most robust data in cardiac surgery; limited data in general ward patients

Barash Clinical Anesthesia, 9e, p. 4525-4526 | Miller's Anesthesia, 10e, p. 6748-6749

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TEG vs Conventional Tests: Evidence Summary

• Cardiac surgery with CPB: Strongest evidence - TEG/ROTEM-guided algorithms reduce blood product transfusion (Level I evidence, multiple RCTs)
• Liver transplantation: RCT evidence shows significantly lower blood component use vs INR/platelet-guided transfusion (Maiwall et al., Hepatology 2020)
• Trauma: Two large RCTs showed adding viscoelastography to routine coagulation studies did not improve overall outcomes after major trauma; however rTEG is still useful in massive transfusion protocols
• PPH: TEG-guided management led to only small reduction in blood loss vs conventional tests (RCT)

Goldman-Cecil Medicine, 2024 | Miller's Anesthesia, 10e

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Comparison with Sonoclot

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Summary Table: TEG Parameters at a Glance

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Key Points for Examination

1. TEG was first described by Hartert (1948) - a viscoelastic hemostatic assay, not just a coagulation test.
2. It measures global hemostasis - primary + secondary hemostasis + fibrinolysis in whole blood.
3. The key difference: TEG uses a rotating cuvette; ROTEM uses a rotating pin - both measure clot viscoelasticity.
4. R value (reaction time) - reflects coagulation factors/thrombin; prolonged by heparin, factor deficiency.
5. MA (maximum amplitude) - reflects clot strength; primarily reflects platelet function and number (80%) + fibrinogen (20%).
6. LY30 - detects fibrinolysis; most important in liver transplantation and trauma.
7. FIBTEM channel (ROTEM) - isolates fibrinogen contribution from platelet contribution to clot strength.
8. HEPTEM channel (ROTEM) - distinguishes heparin effect from intrinsic factor deficiency.
9. Most robust clinical evidence for TEG use is in cardiac surgery (reduces blood product use).
10. TEG cannot detect primary hemostasis defects (VWD, platelet adhesion), warfarin reliably, or the effect of hypothermia (sample is heated).

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• Miller's Anesthesia, 10th Edition - Viscoelastic Measures of Coagulation, p. 6747-6749
• Barash, Cullen and Stoelting's Clinical Anesthesia, 9th Edition - Viscoelastic Testing, p. 1278; Table 53-3, Figures 53-1, 53-2
• Goldman-Cecil Medicine, International Edition - Thromboelastography section
• de Oliveira et al. [Systematic Review & Meta-Analysis, 2025] - Viscoelastic tests and blood products in liver transplantation [PMID: 40288081]