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Jiang Xiaoqiong,Xu Jie,Ling Xiangwei,et al.Role and mechanism of infrared thermography in early identification of necrosis risk in random-pattern flaps[J].Chin J Burns Wounds,2026,42(8):1-11.DOI: 10.3760/cma.j.cn501225-20241118-00453.
Citation: Jiang Xiaoqiong,Xu Jie,Ling Xiangwei,et al.Role and mechanism of infrared thermography in early identification of necrosis risk in random-pattern flaps[J].Chin J Burns Wounds,2026,42(8):1-11.DOI: 10.3760/cma.j.cn501225-20241118-00453.

Role and mechanism of infrared thermography in early identification of necrosis risk in random-pattern flaps

doi: 10.3760/cma.j.cn501225-20241118-00453
Funds:

Zhejiang Basic Public Welfare Research Program Project LGF22H110002

Wenzhou Applied Basic Research Project GK20250162

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  • Corresponding author: Xiao Jian, Email: xfxj2000@126.com
  • Received Date: 2024-11-18
  •   Objective  To investigate the role and mechanism of infrared thermography (IRT) in early identification of necrosis risk in random-pattern flaps (RPFs).  Methods  This study was designed as a group-comparison experimental study. A RPF model was established on the dorsum of 92 male C57BL/6 mice aged 6-8 weeks. The flap was divided into three equal zones (zones Ⅰ, Ⅱ, and Ⅲ) from the caudal to the cephalic end. The relative temperatures (RTs) of the three zones were measured using an infrared thermal imager at postoperative day (PPD) 0 (immediately), 3, and 7. At PPD 3 and 7, receiver operating characteristic (ROC) curves were used to evaluate the predictive efficacy of the RT of zone Ⅱ for flap necrosis, and the optimal cutoff values were determined. Based on the RT of flap zone Ⅱ at PPD 3, mice were divided into >-0.1 ℃ group and ≤-0.1 ℃ group; based on the RT of flap zone Ⅱ at PPD 7, mice were divided into >0.1 ℃ group and ≤0.1 ℃ group, with 4 mice in each group. The percentage of surviving area of flap zone Ⅱ was calculated for the first two groups of mice at PPD 3 and for the latter two groups of mice at PPD 7. Laser Doppler perfusion imaging was used to measure blood perfusion volume in flap zone Ⅱ of the above groups at the corresponding time points. At PPD 3, the tissue from flap zone Ⅱ of >-0.1 ℃ and ≤-0.1 ℃ groups of mice was collected for transcriptomic sequencing to identify differentially expressed genes (DEGs), for immunofluorescence staining to calculate the ratios of inducible nitric oxide synthase (iNOS)/CD68 and arginase 1 (ARG1)/CD68, for immunohistochemical staining to detect the expression of chemokine ligand 2 (CCL2), for dihydroethidium (DHE) staining to detect the expression of DHE, for real-time fluorescence quantitative reverse transcription polymerase chain reaction to measure mRNA expressions of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and IL-10, and for Western blotting to detect protein expressions of CD68, iNOS, ARG1, heme oxygenase-1 (HO-1), and superoxide dismutase 1 (SOD1).  Results  From PPD 0 to 7, RTs in flap zones Ⅰ and Ⅱ showed an increasing trend, while RTs in flap zone Ⅲ showed a trend of initial increase followed by decrease. At PPD 3 and 7, the areas under the ROC curves of the RT of flap zone Ⅱ for predicting flap necrosis were 0.82 and 0.85 (with 95% CIs of 0.72-0.93 and 0.78-0.93, respectively), with optimal cutoff values of -0.1 and 0.1 ℃, respectively. At PPD 3, there were no statistically significant differences in the percentage of surviving area or blood perfusion volume in flap zone Ⅱ between ≤-0.1 ℃ group and >-0.1 ℃ group of mice (P>0.05). At PPD 7, the percentage of surviving area (t=4.19, P<0.05) and blood perfusion volume (t=5.58, P<0.05) in flap zone Ⅱ were significantly decreased in ≤0.1 ℃ group of mice compared with those in >0.1 ℃ group. At PPD 3, compared with that in >-0.1 ℃ group, there were 2 849 DEGs in tissue of flap zone Ⅱ in ≤-0.1 ℃ group of mice, including 1 509 upregulated DEGs and 1 340 downregulated DEGs. At PPD 3, there were significantly lower iNOS/CD68 ratio (t=4.97, P<0.05) and significantly higher ARG1/CD68 ratio (t=3.42, P<0.05), significantly lower expressions of CCL2 and DHE, mRNA expressions of TNF-α and IL-1β, as well as protein expressions of CD68 and iNOS (with t values of 4.82, 4.51, 4.43, 5.47, -3.69, and -6.14, respectively, P<0.05), and significantly higher mRNA expression of IL-10 and protein expressions of ARG1, SOD1, and HO-1 (with t values of 8.58, 8.61, 6.24, and 11.03, respectively, P<0.05) in tissue of flap zone Ⅱ in >-0.1 ℃ group of mice compared with those in ≤-0.1 ℃ group.  Conclusions  IRT enables early and objective prediction of necrosis risk of RPFs in mice through monitoring flap temperature. The RT ≤-0.1 ℃ in flap zone Ⅱ at PPD 3 is associated with marked inflammatory response, immune cell infiltration, and oxidative stress in the tissue. CCL2 may serve as a key chemokine inducing macrophage polarization.

     

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