Advanced interactive coagulation laboratory suite
Practise the full haemostasis bench across specialised virtual workstations, from PT/INR to complex factor assays and emergency protocols. Built for graduates through advanced practitioners.
Advanced Interactive Coagulation Laboratory Suite is available to premium subscribers and trial users.
Advanced coagulation LIMS
Next-generation laboratory information management for comprehensive coagulation testing, validation and cross-departmental result correlation.
Advanced Coagulation LIMS is available to premium subscribers and trial users.
DOAC / NOAC analysis & dosage
Anti-Xa quantification, calibrator selection and emergency reversal interpretation for direct oral anticoagulants.
Types of DOACs/NOACs
Clinical Indications
Advantages and Limitations Compared to Vitamin K Antagonists
Advantages
- Predictable pharmacokinetics
- Fixed dosing without routine monitoring
- Rapid onset of action
- Fewer food and drug interactions
Limitations
- Higher cost
- Contraindicated in severe renal impairment
- Limited options for reversal agents
- Shorter half-life requires strict adherence
Thrombophilia screen & interpretation
Comprehensive thrombophilia work-up: Protein C / S, Factor V Leiden, antithrombin and prothrombin gene mutations.
Thrombophilia Overview
Thrombophilia refers to a group of inherited or acquired disorders that increase the risk of venous or arterial thrombosis. These conditions disrupt the normal balance between pro-coagulant and anti-coagulant systems.
Key Principles:
- • Thrombophilia testing is not routinely recommended for all VTE patients
- • Results rarely alter acute management but may influence long-term decisions
- • Protein C, protein S and antithrombin should be measured only after 3 months of anticoagulation for acute thrombosis; anticoagulants interfere with some assays
- • Routine testing of first-degree relatives of people with VTE is not recommended; selective testing may be considered only where the proband has protein C, protein S or antithrombin deficiency
Indications for Testing
Testing May Be Considered For:
- • Antiphospholipid antibodies after unprovoked VTE, or VTE provoked by a minor risk factor
- • Antiphospholipid antibodies after thrombosis at an unusual site without clear provoking factors
- • Antiphospholipid antibodies in arterial thrombosis without other vascular risk factors
- • Antiphospholipid antibodies after recurrent or late pregnancy loss (not during pregnancy)
- • Selected asymptomatic first-degree relatives of a proband with protein C, protein S or antithrombin deficiency, where the result may change management
- • Neonatal purpura fulminans (suspected severe protein C or S deficiency)
- • Warfarin-induced skin necrosis (Protein C deficiency)
Testing Not Recommended For:
- • Routine heritable thrombophilia testing after VTE to guide management
- • Routine testing of first-degree relatives on family history of VTE alone
- • Heritable testing where the only indication is thrombosis at an unusual site
- • Heritable testing for arterial thrombosis or pregnancy complications
- • Protein C, protein S or antithrombin testing within 3 months of acute thrombosis
- • Routine screening before hormonal therapy
Source: Arachchillage et al. Thrombophilia testing: a British Society for Haematology guideline. Br J Haematol 2022.
Lupus anticoagulant analysis
Testing methodology, result interpretation and quality control for lupus anticoagulant: the senior-BMS competency interview panels probe most often.
Lupus Anticoagulant Testing
Clinical Significance
- Associated with increased risk of thrombosis (venous/arterial) despite prolonging clotting tests in vitro
- Key diagnostic marker for antiphospholipid syndrome (APS)
- Causes prolonged APTT that doesn't correct with normal plasma
- Present in 20-40% of SLE patients
- Associated with pregnancy morbidity: recurrent miscarriage, intrauterine growth restriction
- Rarely causes bleeding (only with concurrent thrombocytopenia or other coagulation factors)
Key Characteristics
- Heterogeneous group of autoantibodies against phospholipid-binding proteins
- Interferes with phospholipid-dependent clotting assays
- Not corrected by 1:1 normal plasma mixing studies
- Demonstrates phospholipid dependence (correction with excess phospholipid)
- Transient or persistent - requires confirmation at ≥12 weeks
- May coexist with other antiphospholipid antibodies (anticardiolipin, anti-β2 glycoprotein I)
Pathophysiology and Mechanisms
LA antibodies target phospholipid-binding proteins, primarily β2-glycoprotein I and prothrombin. These antibodies disrupt the assembly of coagulation complexes on phospholipid surfaces, paradoxically causing:
- In vitro: Prolongation of phospholipid-dependent coagulation tests
- In vivo: Hypercoagulable state through multiple mechanisms:
- Interference with natural anticoagulants (protein C pathway)
- Increased tissue factor expression
- Disruption of annexin V anticoagulant shield
- Enhanced platelet activation
- Complement activation
Coagulation quick guide
Essential knowledge areas for coagulation, from foundational concepts to specialised techniques.
Coagulation Cascade Overview
The coagulation cascade is traditionally divided into the intrinsic pathway (activated by contact with damaged vessel surfaces) and extrinsic pathway (activated by tissue factor). These pathways converge at the activation of factor X, leading to thrombin generation and fibrin formation.
Key Coagulation Factors
- Factor I (Fibrinogen) - Converted to fibrin by thrombin
- Factor II (Prothrombin) - Converted to thrombin
- Factor VII - Initiates extrinsic pathway
- Factor VIII - Cofactor in intrinsic pathway, deficient in Haemophilia A
- Factor IX - Activates Factor X in intrinsic pathway, deficient in Haemophilia B
Natural Anticoagulants
- Antithrombin - Inhibits thrombin and factors Xa, IXa, XIa, XIIa
- Protein C/Protein S system - Inactivates factors Va and VIIIa
- Tissue Factor Pathway Inhibitor (TFPI) - Inhibits factor VIIa/TF complex
Coagulation data visualisation
Interactive charts and graphs showcasing key coagulation parameters and their clinical significance.
PT/INR Warfarin Monitoring
The chart shows a typical warfarin initiation with target INR 2-3. Note how PT and INR rise together as warfarin takes effect.
Sources and guidance
This hub's content aligns with the UK's professional and regulatory references for the specialty: