Procedure-Related Access Site Pain Multimodal Management following Percutaneous Cardiac Intervention: A Randomized Control Trial.

METHODS: 137 patients who underwent PCI procedure via radial artery were randomly assigned (1 : 1) to the control (CG, n = 68) and intervention (IG, n = 65) groups. IG received MPM (paracetamol, ibuprofen, and the arm physiotherapy), CG received pain medication "as needed." Outcomes were assessed immediately after, 2, 12, 24, and 48 h, 1 week, and 1 and 3 months after PCI. The primary outcome was A-S pain prevalence and pain intensity numeric rating scale (NRS) 0-10. RESULTS: Results showed that A-S pain prevalence during the 3-month follow-up period was decreasing. Statistically significant difference between the groups (CG versus IG) was after 24 h (41.2% versus 18.5, p=0.005), 48 h (30.9% versus 1.5%, p ≤ 0.001), 1 week (25% versus 10.8%, p=0.042), 1 month (23.5% versus 7.7%, p=0.017) after the procedure. The mean of the highest pain intensity was after 2 h (IG-2.17 ± 2.07; CG-3.53 ± 2.69) and the lowest 3 months (IG-0.02 ± 0.12; CG-0.09 ± 0.45) after the procedure. A-S pain intensity mean scores were statistically significantly higher in CG during the follow-up period (Wilks' λ = 0.84 F (7,125) = 3.37, p=0.002). CONCLUSION: In conclusion, MPM approach can reduce A-S pain prevalence and pain intensity after PCI. More randomized control studies are needed.

Predictive Factors for Access-Site Pain Chronicity after Percutaneous Coronary Intervention via Radial Artery Access.

Objectives: The aim of this study is to assess the prevalence and predictive factors for developing chronic access-site (A-S) pain after percutaneous coronary intervention (PCI) via radial artery access. Methods: Data of selected patients (n = 161) who underwent elective PCI were collected prospectively and analysed in 2020. Verbal analogue scale was used to evaluate pain intensity after 12, 24, and 48 h and 3 months after PCI. The univariate logistic regression analysis was used. Results: Pain prevalence decreased from 29% straight after PCI and 54% two hours later to 3.7% following 3 months after procedure. The predictors for A-S pain chronicity are diabetes (OR = 5.77 95% CI (1.07-31.08), p = 0.041), hematoma (OR = 6.48, 95% CI (1.06-39.66), p = 0.043), A-S hand neuropathy (OR = 19.93 95% CI (1.27-312.32), p = 0.033), A-S pain immediately after PCI (OR = 14.60 95% CI (1.63-130.27), p = 0.016), after 12 h (OR = 17.2 95% CI (1.60-185.27), p = 0.019), 24 h (OR = 48 95% CI (4.87-487), p = 0.01), and 48 h (OR = 23.46 95% CI (3.81-144.17), p = 0.001), and pain intensity immediately after procedure (OR = 3.30 95% CI (1.65-6.60), p = 0.001), after 2 h (OR = 2.56 95% CI (1.15-5.73), p = 0.022), after 12 h (OR = 3.02 95% CI (1.70-5.39), p < 0.001), after 24 h (OR = 3.58 95% CI (1.90-6.74), p < 0.001), and after 48 h (OR = 2.89 95% CI (1.72-4.87), p < 0.001). Pain control was performed with Ketoprofen and Ibuprofen as most used NSAIDs. 10 mg of Morphine intravenously was the choice from strong opioids if necessary. Conclusions: The prevalence of chronic A-S pain is 3.7%. Main predictive factors for the A-S pain chronicity are diabetes, hematoma, and persistent pain and pain intensity during 48 h period after PCI.