Learning Objectives
After completing this chapter, the anesthesia resident should be able to:
Explain the three-phase cell-based model of coagulation and contrast it with the classical cascade model.
Describe the role of cellular surfaces (platelets, endothelium, tissue factor-bearing cells) in thrombin generation.
Interpret perioperative viscoelastic tests (TEG/ROTEM) based on CBM principles.
Apply CBM concepts to clinical scenarios such as massive transfusion, liver disease, trauma, and anticoagulation.
Identify pharmacologic and anesthetic influences on cellular hemostasis.
Integrate CBM understanding into perioperative transfusion algorithms and bleeding management protocols.
For decades, the classical coagulation cascade dominated our understanding of hemostasis, neatly dividing the process into intrinsic, extrinsic, and common pathways. While pedagogically convenient, this framework was biochemically accurate only in vitro — based on isolated plasma reactions. In the clinical reality of surgery and anesthesia, where blood interacts dynamically with damaged endothelium and circulating cells, this model fails to represent the true physiology of clot formation.
Modern research led by Monroe and Hoffman (2001) reframed coagulation as a cell-based, spatially organized process. The cell-based model (CBM) emphasizes the indispensable roles of cell membranes — particularly those of platelets, endothelium, and tissue factor-bearing cells — as platforms for enzyme complex assembly. It is the interaction between these cells and soluble factors that determines when, where, and how strongly clotting occurs.
In this framework, coagulation unfolds in three overlapping yet distinct stages:
Initiation on tissue factor-bearing cells
Amplification on activated platelet surfaces
Propagation producing the “thrombin burst” that stabilizes the clot
This cellular orchestration better explains clinical phenomena that puzzled the older model — such as why patients with hemophilia bleed severely despite a functioning extrinsic pathway, or why viscoelastic tests more accurately reflect bleeding risk than conventional PT/aPTT.
For the anesthesiologist, coagulation is not an abstract biochemical pathway — it’s a real-time physiologic processoccurring under our watch during surgery. Understanding the CBM offers:
Rational interpretation of viscoelastic testing (TEG, ROTEM, ClotPro)
Targeted transfusion therapy — choosing between FFP, platelets, PCC, or antifibrinolytics
Insight into coagulopathy of trauma, sepsis, and liver disease
Understanding drug mechanisms — e.g., warfarin, heparin, DOACs, TXA — within cellular contexts
Guidance for balanced massive transfusion protocols emphasizing cellular components
Ultimately, CBM transforms coagulation from a linear cascade into a dynamic, multicellular “conversation” — where endothelium, platelets, and coagulation factors act like coordinated responders in a microscopic operating room.
Think of hemostasis not as a...
