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. Author manuscript; available in PMC: 2021 Dec 1.
Published in final edited form as: Anesth Analg. 2020 Dec;131(6):1730–1750. doi: 10.1213/ANE.0000000000005191

Figure 2: Simplified overview of the cellular sources and time-course of biomarker release after surgery.

Figure 2:

Surgery (‘Trigger’) causes localized organ injury and triggers the release of danger signals, thereby activating the coagulation and complement system, and the immune response including stimulation of inflammatory and tissue cells (‘Activation’). During and after the operation, cellular damage and immunological activity lead to the release of various mediators in a timely coordinated manner, which relate to the course of the response to the surgical insult (‘Mediators and Biomarker’). These molecules are considered as biomarkers and have been suggested to have predictive values before tissue injury for specific organs becomes irreversible. The normalization of biomarker levels over time indicates recovery from tissue damage, whereas biomarker persistence points toward a significant and potentially permanent impact on organ function (‘Outcome’).

(Ang, Angiopoetin, C3 and C5, complement component 3 and 5; CRP, C-reactive protein; ICAM, Intercellular adhesion molecule 1; IL, Interleukin; MIP, Macrophage inflammatory protein; PCT, Procalcitonin; PAI-1, Plasminogen activator inhibitor 1; SAA, Serum Amyloid; TF, Tissue Factor; TNFα, Tumor-necrosis factor α; TNF-R, Tumor necrosis factor receptor; VCAM, vascular cell adhesion molecule-1)