Perioperative Coagulation
From coagulation cascade to ROTEM, TEG, and Quantra-guided therapy — a structured guide to viscoelastic testing for perioperative clinicians.
Try the tool first
Interpret viscoelastic results in the clinical situation — read FIBTEM/CFF/FCS, clotting time, MA/MCF, and lysis as a pattern, then plan targeted replacement and reassess. Pattern recognition, not an automatic transfusion order.
Open the ROTEM trigger guideHow to use this page
- 1.Start with the bleeding pattern — Decide whether bleeding is surgical or coagulopathic before reaching for a product.
- 2.Interpret the signal in context — Low clot firmness, prolonged clotting time, low MA, and lysis each mean different things, and CPB timing changes the reading.
- 3.Give targeted treatment, then reassess — Correct the specific deficit, confirm the change after treatment, and re-check the surgical field if bleeding persists.
Tools to use alongside this page
Start with the bleeding pattern
Surgical bleeding or coagulopathy?
Before giving products, decide whether the bleeding pattern fits a surgical source, coagulopathy, or both.
Quick ReadA VET result is not a transfusion order
TEG, ROTEM, and Quantra help organize bleeding physiology, but their results must be translated through the clinical situation, surgical field, physiology, local protocol, and reassessment.
What is limiting clot strength?
Low fibrin contribution to clot strength
Low fibrin-based clot firmness suggests inadequate fibrinogen contribution to clot strength, but the result must be read with the bleeding pattern.
Quick ReadPlatelet signal: count, function, and clot strength
Platelet count and platelet contribution to clot strength are related but not identical. Interpret platelet-related signals with fibrin-based measures.
Quick ReadQuantra clot stiffness pattern
Use CS, FCS, and PCS to separate fibrin contribution, platelet contribution, and mixed clot failure before choosing a correction strategy.
Timing, heparin, lysis, and physiology
Heparin effect or factor deficiency after CPB
After CPB, prolonged clotting time may reflect heparin effect, factor deficiency, dilution, protamine effect, physiology, or timing.
Quick ReadFibrinolysis: clot breaks down after it forms
A lysis signal matters when clot forms and then breaks down, but fibrinolysis is not the explanation for every bleeding pattern.
Quick ReadTemperature, pH, calcium, and dilution
Hypothermia, acidosis, low calcium, and dilution can prevent product therapy from improving clot formation. Correct physiology and reassess.
GuideROTEM interpretation guide
Use the ROTEM guide to understand what CT, FIBTEM MCF, EXTEM clot firmness, and lysis signals answer in bleeding patients.
Case-based learning
Post-CPB diffuse bleeding
Low fibrin-based clot firmness after CPB raises the question of fibrinogen contribution, platelet contribution, physiology, and surgical source control.
CaseProlonged clotting time after CPB
A post-CPB clotting time signal may reflect heparin effect, factor deficiency, dilution, protamine effect, physiology, or timing.
CaseBleeding persists after corrected ROTEM
When the viscoelastic pattern improves but bleeding continues, source control and surgical-field reassessment move back to the center.
CaseLow clot strength after massive bleeding
Massive bleeding can produce mixed fibrinogen, platelet, dilutional, and physiologic problems. Separate the components before choosing treatment.
Bedside tools
ROTEM trigger guide
Use ROTEM patterns to organize fibrinogen, clotting time, platelet contribution, and lysis — then reassess after treatment.
ToolTEG 6s trigger guide
Use TEG 6s patterns as clinical signals, not transfusion commands. Read R-time, MA, fibrinogen contribution, and lysis together.
ToolQuantra trigger guide
Use Quantra clot stiffness patterns to separate fibrinogen and platelet contribution while keeping the surgical field in view.
CalculatorFibrinogen replacement calculator
Estimate a fibrinogen replacement strategy, then reassess clot firmness and clinical bleeding after treatment.
Anticoagulation before surgery
DOAC management answers a different question from VET-guided bleeding management: last dose, renal function, procedural bleeding risk, spinal/epidural anesthesia or regional blocks, and whether to delay or reverse.
DOAC perioperative management
Plan DOAC interruption and restart around surgical bleeding risk, renal function, spinal/epidural anesthesia or regional blocks, urgency, and reversal decisions.
CaseSpinal anesthesia and apixaban — does the timing work?
Spinal/epidural anesthesia sets the strict timing requirement. This case asks whether tomorrow's spinal anesthesia is safe after apixaban was taken this morning.
CaseDabigatran and renal function — when 72 hours is not enough
Dabigatran is renally cleared. Reduced creatinine clearance changes the spinal/epidural timing window and should not be treated like a Xa inhibitor.
CaseHigh-bleeding-risk surgery on a DOAC — does the washout change?
Surgical bleeding risk and anesthetic technique answer different questions. This case separates high surgical bleeding risk from the DOAC withhold window.
Foundational overview
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.