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Pain after surgery is usually temporary and improves as healing occurs, but for some, it persists and develops into chronic postsurgical pain (CPSP). CPSP affects recovery, quality of life and contributes to opioid overuse. With increasing surgical demand in the aging population, understanding how pain after surgery becomes chronic is vital.

This thesis investigates how short-term postsurgical pain turns into long-lasting CPSP, focusing on early detection and the sensory and immunological mechanisms involved. Two prediction models were developed to identify vulnerability to CPSP. Patients at risk for CPSP could best be identified two weeks after surgery by a high pain intensity, painful cold sensations, use of opioids before surgery, and surgery involving bones. The link between painful cold sensations and CPSP suggests changes in nervous system pain processing, possibly triggered by the body’s immune response to tissue injury.

The SCIP-Pain study examines these mechanisms in leg surgery patients by assessing pain intensity through questionnaires, pain sensitivity with Quantitative Sensory Testing (QST), and immune changes via blood analysis. 
Early results reveal that thermal sensitivity during QST does not match patient’s reports of painful cold sensations and that QST procedures can be simplified. Preliminary immune data indicate that patients who develop CPSP have fewer white blood cells that are linked to help control inflammation and promote tissue healing in their blood two to four weeks after surgery.

Overall, this thesis points to a critical two-to four-week period after surgery when chronic pain mechanisms emerge, offering an important window for early detection and timely intervention to prevent the onset or progression of CPSP.