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Thromboelastogram (TEG) - 10 Marks Answer for AIIMS MD Anaesthesia
(Sourced exclusively from Miller's Anesthesia 10e, Barash's Clinical Anesthesia 9e, and Morgan & Mikhail's Clinical Anaesthesiology 7e)
1. Introduction and Historical Background
The thromboelastograph (TEG) was developed by Hartert in 1948 and has undergone a resurgence in popularity due to its unique ability to measure the entire spectrum of clot formation in whole blood - from early fibrin strand generation through clot retraction and fibrinolysis.
"The early thromboelastograph (TEG) developed by Hartert in 1948 has evolved into two independent viscoelastic monitors: the modern TEG (TEG 5000 Hemostasis Analyzer System, Haemnetics) and rotational thromboelastometry (ROTEM, TEM Systems)." - Miller's Anesthesia 10e, Ch. 46
"These tests measure the rate of clot initiation, maximum clot strength, and time to lysis using citrated whole blood samples with the potential for point-of-care testing. As opposed to standard coagulation assays such as PT, aPTT, and INR studies, viscoelasticography provides a more complete assessment of coagulation in vivo, as it assesses the primary and secondary hemostatic pathways in a cell-based format." - Barash's Clinical Anesthesia 9e, Ch. 17
2. Principle and Mechanism
TEG 5000 (Traditional):
- A small 0.35 mL sample of whole blood is placed into a disposable cuvette maintained at 37°C
- The cuvette continuously rotates around an axis of approximately 5 degrees
- A sensor "piston" attached by a torsion wire to an electronic recorder is lowered into the blood
- An activator (most often kaolin or celite) initiates clot formation
- As the fibrin-platelet plug evolves, the piston becomes enmeshed within the clot, transferring rotation of the cuvette to the piston, torsion wire, and electronic recorder
- The mechanical resistance is translated into an electronic waveform subject to quantitative analysis
TEG 6s (Newer generation):
- Measures movement of a meniscus formed by whole blood in a microfluidics chamber
- Using frequencies from 20-500 Hz, the meniscus is vibrated; as a clot forms, clot-strength-specific resonance frequencies are detected by a photodetector and converted into TEG-equivalent units
(Miller's Anesthesia 10e, Ch. 46, p. 6747)
3. The TEG Tracing and Parameters
Diagram 1: Standard TEG Parameters (from Sabiston/Barash framework)
Standard TEG trace showing the four key phases: clot formation (R), clot propagation (α angle), clot strength (MA), and clot lysis (LY30). Source: Sabiston Textbook of Surgery, 10e, Fig. 46.1
Diagram 2: TEG vs ROTEM Parameters Side-by-Side (Barash Fig. 17-5)
Figure 17-5 from Barash's Clinical Anesthesia 9e: TEG (blue) parameters - R, K, α, MA, LY30%. ROTEM (green) parameters - CT, CFT, α, MCF, LI30%. Note that the ROTEM trace runs as a mirror image below the axis.
TEG Parameters - Normal Values and Meaning
| Parameter | Full Name | Normal Value | What it Measures | Abnormality → Treatment |
|---|
| R | Reaction time | 5-10 min | Time to initial clot formation; coagulation factor activity; thrombin generation | R prolonged → FFP / Factor concentrates |
| K | Kinetical time (BiKoatugulierung) | 1-3 min | Time until clot reaches specific viscosity; fibrin cross-linking; fibrinogen level | K prolonged → Cryoprecipitate |
| α angle | Alpha angle | 53-72° | Slope / rate of fibrin polymerization during K time | α decreased → Cryoprecipitate / Fibrinogen concentrate |
| MA | Maximum amplitude | 50-70 mm | Peak clot strength; platelet-fibrin interaction (platelets = 70-80% of MA) | MA decreased → Platelet transfusion / DDAVP |
| LY30 | Lysis at 30 min | 0-8% | % clot breakdown 30 min after MA; fibrinolysis rate | LY30 elevated → Tranexamic acid |
| EPL | Estimated % lysis | 0-15% | Predicted lysis before 30 min | EPL elevated → TXA |
| G | Clot strength (shear elastic modulus) | 4.5K-11.0K d/sc | Mathematical derivation of clot strength from MA | - |
"R value (reaction time) measures time to initial clot formation. Maximum amplitude provides a measure of clot strength and may be decreased by either qualitative or quantitative platelet dysfunction or decreased fibrinogen concentration. The α angle and K values measure rate of clot formation..." - Miller's Anesthesia 10e, Ch. 46
"VHA tracings typically represent four phases of clot kinetics: initiation, propagation, clot strength, and fibrinolysis. Platelets account for 70-80% of the peak resistance curve." - Barash's Clinical Anesthesia 9e, Ch. 53
4. Actual TEG Tracings from Miller's (Fig. 46.5)
Figure 46.5 from Miller's Anesthesia 10e: Kaolin-activated TEG 5000 tracings. (A) Normal - R=5.8, K=1.9, α=65.2°, MA=55.9mm, LY30=0%. (B) Hypocoagulable - R=9.2, K=9.1, α=31.1°, MA=30.9mm. (C) Fibrinolysis - MA=7.7mm, EPL=89.4%, LY30=89.4%.
5. Typical TEG Patterns in Common Conditions (Morgan & Mikhail Fig. 33-7)
Figure 33-7 from Morgan & Mikhail's Clinical Anaesthesiology 7e: Examples of typical TEG tracings. A: Normal (symmetrical rounded shape). B: Hypercoagulation (wide, flat-ended shape with large MA). C: Hypocoagulation / thrombocytopenia (narrow, pointed shape with small MA). D: Fibrinolysis (small closed loop - clot forms briefly then dissolves).
6. TEG vs ROTEM - Key Differences
| Feature | TEG (Haemonetics) | ROTEM (Werfen) |
|---|
| Mechanism | Cup oscillates; piston pin is fixed | Cup is fixed; pin oscillates |
| Activator | Kaolin (standard); Tissue factor (Rapid TEG) | EXTEM (TF+PL), INTEM (ellagic acid), FIBTEM, HEPTEM |
| R time equivalent | R time | CT (Clotting Time) |
| K time equivalent | K time | CFT (Clot Formation Time) |
| MA equivalent | MA (Maximum Amplitude) | MCF (Maximum Clot Firmness) |
| LY30 equivalent | LY30 | CLI30 / LI30 |
| Key advantage | Platelet mapping assay | Specific pathway testing via multiple reagent channels |
| Interchangeable? | NO - values are NOT interchangeable between platforms | |
"TEG provides results in terms of R = reaction time and K = clot formation kinetics, α-angle = tangential angle to midline, MA = maximum amplitude indicating clot strength, and LY30 = percent lysis at 30 minutes. ROTEM measures similar metrics with different labels including CT = clot time, CFT = clot formation time, MCF = maximum clot formation, and CLI30 = clot lysis index at 30 minutes." - Barash's Clinical Anesthesia 9e, Ch. 17, Fig. 17-5
7. TEG-Guided Transfusion Algorithm - Flowchart
BLEEDING PATIENT WITH SUSPECTED COAGULOPATHY
│
Obtain TEG (citrated whole blood)
Add kaolin activator → run at 37°C
Actionable results in 5-10 minutes
│
┌───────────────┼──────────────────┐
│ │ │
R > 10 min K↑ / α < 53° MA < 50 mm
(prolonged) (fibrinogen (low platelet
│ deficiency) function)
│ │ │
Give FFP Give Cryoprecipitate Platelet
10-15 mL/kg or Fibrinogen transfusion
or PCC concentrate or DDAVP
│
LY30 > 8% OR EPL > 15%?
│
YES ────┴──── NO
│ │
Tranexamic acid Observe
(TXA) 15 mg/kg Monitor
Aminocaproic acid
│
Reassess TEG after each intervention
(Based on Barash Table 53-3 and Morgan & Mikhail Ch. 33, 39)
8. CCT vs VHA - Comparison Table (Barash Table 53-3)
| Feature | Conventional Coagulation Tests (CCT) | Viscoelastic Hemostatic Assays (VHA / TEG/ROTEM) |
|---|
| Turnaround time | 15-60 min | 20-40 min (actionable in 5-10 min) |
| Cost | Less | More |
| Sample | Citrated plasma | Whole blood |
| Detect hyperfibrinolysis | No | Yes |
| Detect hypercoagulation | No | Yes |
| Detect Warfarin | Yes | Unreliable |
| Detect DOAC | No | Nonspecific |
| Detect primary hemostasis | No | No |
(Barash's Clinical Anesthesia 9e, Ch. 53, Table 53-3)
9. Clinical Applications in Anaesthesia
Cardiac Surgery
"Many TEG-guided and ROTEM-guided algorithms have been studied and shown to reduce blood product use effectively in cardiac surgery-related hemorrhage." - Miller's Anesthesia 10e, Ch. 46
- Identifies residual heparin effect post-CPB
- Differentiates surgical bleeding from coagulopathic bleeding
- Detects excess fibrinolysis during bypass
- Some centers routinely use TEG to identify causes of bleeding after CPB (Morgan & Mikhail 7e)
Trauma / Massive Hemorrhage
"TEG and ROTEM identify the specific deficiencies, freeing the practitioner from reliance solely on the 1:1:1 transfusion ratio DCR approach. Both TEG and ROTEM assess the rate of clot formation and clot stability, reflecting the interactions between the coagulation cascades, platelets, and the fibrinolytic system." - Morgan & Mikhail 7e, Ch. 39
- Detects trauma-induced coagulopathy (TIC) early
- VHA can identify both hyperfibrinolysis (early TIC) and fibrinolytic shutdown (late TIC)
- CCT cannot reliably identify hyperfibrinolysis; VHA can
- Clot amplitude <35mm at 5 min on ROTEM predicts need for massive transfusion (detection rate 77%)
Liver Disease / Transplantation
"TEG, ROTEM, and Sonoclot are the optimal methods of demonstrating the global state of the coagulation system at a specific moment in time in any patient with liver disease. A patient with an INR of 3, for example, may also have anticoagulant factors so reduced that the patient is in a hypercoagulable state." - Morgan & Mikhail 7e, Ch. 33
- INR only examines the procoagulant side; VHA reveals the full picture
- Detects real-time fibrinolysis during reperfusion
- Prevents over-transfusion in patients with apparent but balanced coagulopathy
Obstetric Anaesthesia
"At term gestation, TEG analysis reflects a hypercoagulable state with decreased time to start of clot formation (R), decreased time to specified clot strength (K), increased rate of clot formation (α), and increased clot strength (MA)." - Miller's Anesthesia 10e, Ch. 58, Table 58.4
- Guides management of PPH
- Physiological pregnancy TEG: ↓R, ↓K, ↑α, ↑MA (changes begin in 1st trimester)
10. Limitations of TEG
- Does not assess primary hemostasis (platelet adhesion, vWF-vessel wall interaction)
- Unreliable for patients on anticoagulants (Warfarin, DOACs) or antiplatelet therapy
- Susceptible to vibration artifacts (addressed in newer cartridge-based devices)
- Requires frequent calibration (1st generation devices)
- Lack of specificity with abnormal findings; qualitative interpretation challenges
- Results not interchangeable between TEG and ROTEM platforms
- ITACTIC trial (cited in Barash 9e): most recent multicenter RCT - no difference in mortality compared to CCT-guided resuscitation (though criticised for low TIC prevalence in study population)
Key Points Summary (Memory Aid: R-K-Alpha-MA-LY)
| Parameter | Abnormality | Defect | Treatment |
|---|
| R ↑ | Prolonged R | Coagulation factors ↓ | FFP / PCC |
| K ↑ / α ↓ | Slow fibrin polymerisation | Fibrinogen ↓ | Cryoprecipitate |
| MA ↓ | Weak clot | Platelet dysfunction/count ↓ | Platelets / DDAVP |
| LY30 ↑ | Early lysis | Hyperfibrinolysis | TXA / Aminocaproic acid |
References:
- Miller's Anesthesia, 10e - Ch. 46 (Viscoelastic Measures of Coagulation, p. 6747-6751), Ch. 58 (Table 58.4), Ch. 66 (Trauma)
- Barash, Cullen & Stoelting's Clinical Anesthesia, 9e - Ch. 17 (Viscoelastic Testing, p. 1278), Ch. 53 (VHA in Trauma, p. 4522-4524, Table 53-3)
- Morgan & Mikhail's Clinical Anaesthesiology, 7e - Ch. 33 (Point-of-Care Viscoelastic Coagulation Monitoring, Fig. 33-7), Ch. 39 (TEG in Trauma, Fig. 39-5)