Perioperative Coagulation
From the coagulation cascade to VET-guided therapy — a progressive guide for perioperative clinicians.
VET Pattern Reference
Low Fibrinogen
Why this pattern matters
Fibrinogen is the most rapidly depleted coagulation factor in major hemorrhage. It forms the fibrin backbone of the clot. Without adequate fibrinogen, clot strength is severely compromised even when platelet counts and factor levels appear acceptable.
| Device | Parameter | Treat threshold | Borderline zone |
|---|---|---|---|
| ROTEM | FIBTEM A5 | ≤ 6.9 mm | 7.0–12.0 mm |
| TEG 6s | CFF-MA | < 15 mm | — |
| Quantra | FCS | < 1.0 hPa | 1.0–1.5 hPa |
How to read the result
FIBTEM A5 (ROTEM) and CFF-MA (TEG) measure the fibrinogen contribution to clot stiffness. FCS (Quantra) measures fibrinogen contribution to clot stiffness in pressure units (hPa). These are not direct equivalents of plasma fibrinogen concentration in g/L — correlate with laboratory fibrinogen levels when available.
Clinical action
- Administer cryoprecipitate or fibrinogen concentrate
- Target FIBTEM A5 > 12 mm (or laboratory fibrinogen > 1.5–2 g/L depending on clinical context)
- Re-run VET after administration to confirm response
- In obstetric hemorrhage, target fibrinogen > 2 g/L
Example scenario
Major trauma: FIBTEM A5 = 4 mm, EXTEM CT normal, EXTEM A5 borderline. This isolated FIBTEM reduction indicates fibrinogen depletion as the primary coagulopathy — fibrinogen replacement before FFP.
Factor Deficiency / Delayed Clot Initiation
Why this pattern matters
Prolonged clotting time on VET indicates delayed thrombin generation, reflecting reduced activity of the coagulation factor pathway. Common causes include dilutional coagulopathy (from large-volume resuscitation or CPB), factor consumption in DIC, or impaired synthetic function in liver disease.
| Device | Parameter | Treat threshold | Borderline zone |
|---|---|---|---|
| ROTEM | EXTEM CT | ≥ 79 s | 71–78 s |
| TEG 6s | CK-R + CKH-R prolonged | Both > upper limit | — |
| Quantra | CT | > 200 s | 167–200 s |
ROTEM: EXTEM CT vs heparin
When EXTEM CT is prolonged, always check the INTEM/HEPTEM ratio before attributing the delay to factor deficiency. A ratio ≥ 1.25 suggests residual heparin effect — treat with protamine, not FFP. On TEG 6s, compare CK-R with CKH-R for the same differential.
Clinical action
- Borderline zone ('consider'): begin thawing FFP now — preparation takes 30–60 minutes
- Treat threshold: administer FFP (10–15 mL/kg) or PCC if FFP is contraindicated or unavailable
- Reassess VET after factor replacement
- Address the underlying cause (ongoing dilution, liver failure, DIC)
Example scenario
Post-CPB: EXTEM CT = 84 s, INTEM/HEPTEM ratio = 1.02 (heparin excluded), FIBTEM A5 = 14 mm. Isolated factor deficiency after protamine reversal — FFP is the appropriate response.
Platelet Dysfunction / Thrombocytopenia
Why this pattern matters
VET differentiates between fibrinogen-driven and platelet-driven clot weakness. When total clot strength (EXTEM A5 / CRT-MA / CS) is reduced but the fibrinogen component (FIBTEM A5 / CFF-MA / FCS) is normal, the deficit is in the platelet contribution — indicating thrombocytopenia or platelet dysfunction.
| Device | Parameter | What it reflects | Treat threshold |
|---|---|---|---|
| ROTEM | EXTEM A5 (with FIBTEM A5 normal) | Platelet contribution to clot strength | EXTEM A5 ≤ 29 mm |
| TEG 6s | CRT-MA (with CFF-MA normal) | Overall clot strength minus fibrinogen | CRT-MA < 52 mm |
| Quantra | PCS | Platelet contribution to clot stiffness | PCS < 11.9 hPa |
Platelet count vs platelet function
PCS (Quantra) and EXTEM-FIBTEM differential (ROTEM) reflect both platelet count and platelet function — they are not equivalent to a platelet count alone. Platelet dysfunction (e.g., from aspirin, CPB-induced damage, or hypothermia) can produce this pattern even with a normal or near-normal count.
Clinical action
- Platelet transfusion: target count > 50 × 10⁹/L (surgical context), > 100 × 10⁹/L (neurosurgery or active major bleeding)
- If platelet count is adequate but VET shows platelet contribution reduced: consider desmopressin (DDAVP) for platelet dysfunction
- Address reversible causes: hypothermia correction, acidosis correction, stopping antiplatelet agents
Example scenario
Post-CPB: EXTEM A5 = 25 mm, FIBTEM A5 = 12 mm (borderline). The large EXTEM-FIBTEM differential indicates predominantly platelet-related weakness. Platelet transfusion is the appropriate next step.
Hyperfibrinolysis
This is the most time-critical VET finding
Hyperfibrinolysis means plasmin is actively dissolving clots faster than they can form. Every clot that forms is immediately broken down. Standard blood product transfusion will not control bleeding until fibrinolysis is inhibited. Tranexamic acid (TXA) must be given urgently.
| Device | Parameter | Urgent threshold | Warning zone |
|---|---|---|---|
| ROTEM | EXTEM ML% | ≥ 15% | 13.5–14.9% |
| TEG 6s | LY30 | > 2.6% | — |
| Quantra | (not measured) | QPlus has no lysis parameter | — |
Quantra limitation
QPlus does not include a fibrinolysis parameter. Hyperfibrinolysis cannot be detected by Quantra. In high-risk contexts (major trauma, obstetric hemorrhage, liver transplantation), empirical TXA may be appropriate regardless of Quantra findings.
Clinical action
- Administer tranexamic acid (TXA) immediately — do not delay for other blood products
- Standard dose: 1 g IV over 10 minutes; second 1 g dose may follow
- In trauma: TXA within 3 hours of injury is most effective (CRASH-2 trial)
- Continue resuscitation and blood product replacement in parallel
- Re-run ROTEM/TEG after TXA to confirm fibrinolysis is controlled
Example scenario
Major trauma: EXTEM ML = 28% at 30 minutes, EXTEM A5 low, CT prolonged. Hyperfibrinolysis is the dominant pattern. TXA is given urgently before or alongside FFP and platelets.
Level 1 — Quick Learn
Residents and students
Why the classical coagulation cascade is incomplete
The classical coagulation cascade describes two pathways — intrinsic and extrinsic — that converge into a final common pathway producing fibrin. This model explains laboratory clotting reactions well, which is why it is widely used in textbooks. However, it does not fully explain how haemostasis actually occurs inside the body. Many patients can have normal PT and aPTT values and still bleed.
Cell-Based Model of Coagulation
Modern haemostasis is better described by the cell-based coagulation model. This model divides coagulation into three overlapping phases:
- Initiation — Tissue-factor–bearing cells generate a small amount of thrombin.
- Amplification — Activated platelets recruit coagulation factors and amplify the signal.
- Propagation — Factor Xa and Va form the prothrombinase complex on the platelet surface, producing a large thrombin burst.
Key insight: the thrombin burst
The propagation phase produces approximately 95% of the thrombin generated during clot formation. PT and aPTT measure only the very early phase of thrombin generation — the small amount required to start clotting in a test tube. They do not capture the thrombin burst, which is essential for strong clot formation and platelet activation.
Why VET is different
Viscoelastic tests (ROTEM, TEG, Quantra) measure clot formation in whole blood and follow the entire process in real time. They capture:
- clot initiation
- clot propagation
- clot strength
- fibrinolysis
This provides a dynamic picture of haemostasis rather than a single laboratory time point.
Understanding the VET tracing
Each part of the trace corresponds to a phase of coagulation.
| Parameter | What it reflects |
|---|---|
| CT / R | clot initiation |
| α angle | speed of clot propagation |
| MA / MCF / CS | maximum clot strength |
| Fibrinolysis parameters | clot breakdown |
This is why viscoelastic testing can guide targeted haemostatic therapy during surgery and trauma.