10.3 Point-of-Care Coagulation: TEG, ROTEM & Perioperative Coagulopathies

10.3 Point-of-Care Coagulation: TEG, ROTEM & Perioperative Coagulopathies

Standard plasma coagulation tests (Prothrombin Time [PT/INR], activated Partial Thromboplastin Time [aPTT], and platelet counts) evaluate isolated biochemical components in platelet-poor plasma at static endpoints. They fail to reflect dynamic cellular-protein interactions, platelet function, clot tensile strength, or hyperfibrinolysis, and their 45–60 minute turnaround time limits their utility during active hemorrhage. Viscoelastic point-of-care (POC) testing with Thromboelastography (TEG) and Rotational Thromboelastometry (ROTEM) provides real-time functional assessment of whole-blood clot initiation, propagation, stabilization, and lysis.

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1. Principles of Viscoelastic Coagulation Testing

Viscoelastic testing models the cell-based theory of hemostasis (Initiation, Amplification, Propagation, and Fibrinolysis) using whole blood maintained at $37^\circ\text{C}$:

• TEG Mechanics: Whole blood ($360\ \mu\text{L}$) is placed in an oscillating cylindrical cup that rotates through an angle of $4.75^\circ$ every 10 seconds. A stationary pin suspended by a torsion wire is lowered into the blood. As fibrin-platelet meshes assemble, torque from the oscillating cup is transmitted to the pin, producing electrical signals that plot amplitude (mm) over time (min).
• ROTEM Mechanics: In ROTEM, the cup is stationary while the pin oscillates through $4.75^\circ$. The optical detection system is less susceptible to external mechanical vibrations and movement artifacts.

                          THE THROMBOELASTOGRAPHY (TEG) TRACING

             <- R ->
             +-----+  <- K ->
            /       \+-------+                                     ---
           /         \        \                                     |
          /   α-angle \        \==================================  |  MA
  -------+-------------+--------+                                 | (50-70 mm)
          \            /        /=================================  |
           \          /        /                                    |
            \        /+-------+                                    ---
             +-----+                                                |
                                                        LY30 (<3%)  V
  --------------------------------------------------------------------> Time (min)

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2. TEG Parameters, Normal Values & Targeted Transfusion Algorithm

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3. ROTEM Assays & Algorithmic Hemostatic Decision-Making

ROTEM utilizes standardized chemical activators and inhibitors to isolate specific pathways within 10–15 minutes.

+-------------------------------------------------------------------------+
|                    ROTEM ASSAYS & SPECIFIC REAGENTS                     |
+---------------------+-----------------------+---------------------------+
| Assay Name          | Activator / Inhibitor | Diagnostic Target         |
+---------------------+-----------------------+---------------------------+
| INTEM               | Ellagic acid (Contact)| Intrinsic pathway (Heparin|
| EXTEM               | Tissue Factor (TF)    | Extrinsic pathway (Screen)|
| FIBTEM              | TF + Cytochalasin D   | Fibrinogen (Platelets OFF)|
| HEPTEM              | Ellagic acid + Hep'ase| Unmasks Heparin effect    |
| APTEM               | TF + Aprotinin/TXA    | Confirms Hyperfibrinolysis|
+---------------------+-----------------------+---------------------------+

ROTEM Nomenclature vs. TEG Equivalents

• Clotting Time (CT): Equivalent to TEG R-time (Normal EXTEM CT: $38 - 79\text{ sec}$). Prolonged CT $\rightarrow$ give FFP or PCC.
• Clot Formation Time (CFT): Equivalent to TEG K-time (Normal EXTEM CFT: $34 - 159\text{ sec}$). Prolonged CFT $\rightarrow$ give Cryoprecipitate.
• Alpha Angle ($\alpha$): Equivalent to TEG $\alpha$-angle (Normal EXTEM $\alpha$: $63 - 83^\circ$). Reduced $\alpha$ $\rightarrow$ give Cryoprecipitate.
• Maximum Clot Firmness (MCF): Equivalent to TEG MA (Normal EXTEM MCF: $50 - 72\text{ mm}$). Reduced MCF $\rightarrow$ evaluate FIBTEM.
• Maximum Lysis (ML): Equivalent to TEG LY30 (Normal EXTEM ML: $<15%$). Elevated ML ($>15%$) $\rightarrow$ give TXA.

The FIBTEM Differential (Critical Clinical Strategy)

In a bleeding patient with a low EXTEM clot strength ($MCF < 50\text{ mm}$):

1. Check FIBTEM MCF: FIBTEM contains cytochalasin D, a fungal alkaloid that depolymerizes platelet actin filaments, completely paralyzing platelet contraction and isolating the pure fibrinogen contribution to clot firmness.
2. If FIBTEM MCF is LOW ($<9 - 10\text{ mm}$): The coagulopathy is driven by hypofibrinogenemia $\rightarrow$ administer Cryoprecipitate (10 units) or Fibrinogen Concentrate.
3. If FIBTEM MCF is NORMAL ($>10 - 12\text{ mm}$) while EXTEM MCF is LOW ($<45\text{ mm}$): Fibrinogen is adequate; the defect is pure thrombocytopenia or platelet dysfunction $\rightarrow$ administer Platelets (1 apheresis unit).

The HEPTEM Differential (Heparin Reversal)

• INTEM CT is prolonged, but HEPTEM CT (which contains heparinase) is NORMAL: Confirms residual heparin effect $\rightarrow$ administer Protamine Sulfate.
• If both INTEM CT and HEPTEM CT are prolonged $\rightarrow$ true clotting factor deficiency $\rightarrow$ administer FFP or 4F-PCC.

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4. Disseminated Intravascular Coagulation (DIC)

Disseminated Intravascular Coagulation is an acquired, life-threatening consumptive thrombohemorrhagic syndrome characterized by systemic intravascular activation of coagulation cascades.

+-------------------------------------------------------------------------+
|                    PATHOPHYSIOLOGIC CASCADE OF DIC                      |
+-------------------------------------------------------------------------+
| Massive Tissue Factor (TF) Exposure / Endothelial Injury / Cytokines    |
|                                    │                                    |
|                                    ▼                                    |
| Uncontrolled Thrombin Generation & Microvascular Fibrin Deposition      |
| ├──────────────────────────────────┼──────────────────────────────────┤
| ▼                                  ▼                                  ▼
| Microvascular Thrombosis     Consumption of Factors &     Secondary Hyper-
| & Multiorgan Dysfunction     Platelets (Exhaustion)       fibrinolysis (tPA)
| (Ischemia, AKI, ARDS)        (Thrombocytopenia/Low Fibrin) (FDPs / D-Dimer)
|                                    │                                  │
|                                    └─────────────────┬────────────────┘
|                                                      ▼
|                                          SEVERE SYSTEMIC HEMORRHAGE
+-------------------------------------------------------------------------+

Etiologies & Triggering Mechanisms

1. Obstetric Catastrophes: Amniotic Fluid Embolism (AFE) (amniotic fluid contains abundant tissue factor and procoagulant mucin), Placental Abruption (decidual tissue factor entry into maternal circulation), retained dead fetus, and severe HELLP syndrome.
2. Severe Trauma & Burns: Massive tissue necrosis, crush injuries, fat embolism, and traumatic brain injury (brain parenchyma has the highest concentration of tissue factor in the human body).
3. Severe Sepsis & Septic Shock: Gram-negative lipopolysaccharide (LPS / endotoxin) and inflammatory cytokines (TNF-$\alpha$, IL-1, IL-6) induce monocyte tissue factor expression, downregulate thrombomodulin, and consume protein C.
4. Malignancy: Acute promyelocytic leukemia (APL) and mucin-secreting adenocarcinomas.
5. ABO Incompatible Hemolytic Transfusion Reactions

Diagnostic Laboratory Profile in Overt DIC

• Platelet Count: Severely decreased ($<50,000 - 100,000/\mu\text{L}$) due to widespread consumption.
• Fibrinogen: Markedly depressed ($<100 - 150\text{ mg/dL}$); profound depletion is a hallmark of severe decompensated DIC.
• PT / INR & aPTT: Markedly prolonged due to global clotting factor exhaustion.
• D-Dimer & Fibrin Degradation Products (FDPs): Markedly elevated (reflecting secondary plasmin degradation of cross-linked fibrin clots).
• Peripheral Blood Smear: Schistocytes (helmet cells / fragmented red blood cells) resulting from microangiopathic shearing across microvascular fibrin strands.

Anesthetic & Resuscitative Management of DIC

1. Etiologic Treatment: Definitive management requires immediate eradication of the underlying trigger (e.g., immediate emergent delivery of the fetus and placenta in abruption/AFE; surgical debridement of necrotic tissue; broad-spectrum antibiotics and source control in sepsis).
2. Goal-Directed Transfusion Support:
   • Cryoprecipitate: Transfuse 10-unit pools to maintain fibrinogen $>150 - 200\text{ mg/dL}$.
   • Platelets: Transfuse apheresis units to maintain platelets $>50,000/\mu\text{L}$ (or $>100,000/\mu\text{L}$ with severe bleeding).
   • FFP: Transfuse $10 - 15\text{ mL/kg}$ to keep INR $<1.5$ and correct global factor deficiencies.
3. Antifibrinolytic Precaution: Tranexamic acid (TXA) and aminocaproic acid are generally contraindicated in classic overt DIC because blocking fibrinolysis in the presence of ongoing systemic thrombin generation promotes uninhibited microvascular thrombosis, diffuse tissue infarction, and cortical renal necrosis (exception: documented primary hyperfibrinolytic state or severe trauma with TEG LY30 $>7.5%$).

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5. Heparin-Induced Thrombocytopenia (HIT Type II)

Heparin-Induced Thrombocytopenia is an immune-mediated, life-threatening prothrombotic disorder triggered by exposure to unfractionated heparin (UFH) or, less commonly, low-molecular-weight heparin (LMWH).

+-------------------------------------------------------------------------+
|                    HIT TYPE II IMMUNOPATHOGENESIS                       |
+-------------------------------------------------------------------------+
| Unfractionated Heparin (UFH) binds Platelet Factor 4 (PF4)              |
|                                    │                                    |
|                                    ▼                                    |
| Formation of Immunogenic Heparin-PF4 Macromolecular Complexes           |
|                                    │                                    |
|                                    ▼                                    |
| Patient synthesizes IgG Autoantibodies against Heparin-PF4              |
|                                    │                                    |
|                                    ▼                                    |
| IgG-Heparin-PF4 Complexes crosslink Platelet FcgRIIa Receptors          |
|                                    │                                    |
|                                    ▼                                    |
| Massive Platelet Activation, Procoagulant Microparticle Release         |
| ├──────────────────────────────────┴──────────────────────────────────┤
| ▼                                                                     ▼
| Consumption of Platelets (>50% drop)           PARADOXICAL THROMBOSIS
|                                                (White Clot Syndrome)
|                                                - Venous: DVT, PE
|                                                - Arterial: Stroke, MI, Limb
+-------------------------------------------------------------------------+

HIT Type I vs. HIT Type II Comparison

The 4T Clinical Scoring System

• T - Thrombocytopenia: $>50%$ drop in platelets with nadir $\ge 20,000/\mu\text{L}$ (2 pts); $30-50%$ drop (1 pt); $<30%$ drop (0 pts).
• T - Timing of Platelet Fall: Onset between Days 5–10, or $\le 1\text{ day}$ with heparin exposure in past 30 days (2 pts); onset after Day 10 or Day 1 with exposure 30–100 days ago (1 pt); onset $<4\text{ days}$ without recent exposure (0 pts).
• T - Thrombosis: Proven new thrombosis, skin necrosis at injection site, or acute systemic reaction after IV bolus (2 pts); progressive/recurrent thrombosis or silent DVT (1 pt); none (0 pts).
• T - oTher Causes Excluded: No other cause apparent (2 pts); possible alternative cause (1 pt); definite alternative cause (0 pts).
• Scoring: $6 - 8\text{ points}$ = High Probability; $4 - 5\text{ points}$ = Intermediate; $\le 3\text{ points}$ = Low Probability.

Definitive Management of HIT Type II

1. DISCONTINUE ALL HEPARIN IMMEDIATELY: Stop all therapeutic and prophylactic heparin, LMWH, heparin flushes, heparin-coated central lines, and dialysis catheters.
2. DO NOT TRANSFUSE PLATELETS: Platelet transfusions are strictly contraindicated in HIT Type II because transfused platelets provide fresh substrate and $Fc\gamma\text{RIIa}$ receptors for antibody-mediated activation, precipitating catastrophic arterial thrombosis ("fueling the fire"). Transfuse platelets only for life-threatening intracranial hemorrhage.
3. Initiate Alternative Non-Heparin Anticoagulation: Because HIT is a hypercoagulable state with a $30-50%$ risk of thrombosis, stopping heparin alone is insufficient; active alternative anticoagulation must be started immediately:
   • Argatroban (Direct Thrombin Inhibitor): Small-molecule univalent direct thrombin inhibitor. Metabolized and cleared by the LIVER (hepatic clearance). Drug of choice in patients with renal failure or renal insufficiency. Monitored using aPTT (target $1.5 - 3.0\times$ baseline).
   • Bivalirudin (Direct Thrombin Inhibitor): Synthetic bivalent direct thrombin inhibitor. Enzymatically degraded in plasma ($80%$) and renally cleared ($20%$). Drug of choice for cardiac surgery requiring cardiopulmonary bypass (CPB) and in patients with severe hepatic failure.
   • Fondaparinux (Factor Xa Inhibitor): Synthetic pentasaccharide; renally cleared.
4. Warfarin Warning: Do NOT start warfarin until the platelet count has fully recovered to baseline or $>150,000/\mu\text{L}$ and the patient is therapeutic on a direct thrombin inhibitor. Starting warfarin during acute HIT precipitates rapid depletion of Protein C (short $t_{1/2} = 6\text{ hours}$) before factor II/X are suppressed, creating an uninhibited procoagulant state that triggers warfarin-induced skin necrosis and venous limb gangrene.