Background: In acute compartment syndrome (ACS), clinicians have difficulty diagnosing muscle ischemia provoked by increased intra-compartmental pressure in a timely and non-invasive manner. Phonomyography records the acoustic signal produced by muscle contraction. We hypothesize that alterations in muscle contraction caused by muscle ischemia can be detected with phonomyography, serving as a potential non-invasive technique in the detection of ACS.
Methods: The left hind limb of 15 Sprague-Dawley rats was submitted to a reversible ischemic model of limb injury for 30min and 1, 2, 4, 6h (3 rats in each group). The right limb served as control. Phonomyography microphones were placed over the posterior calf of both limbs and the sciatic nerve was stimulated percutaneously at 10-min intervals to evaluate muscle contraction. Histopathological analysis of muscles and nerves biopsies was performed and correlation was made between duration of injury, phonomyography output and degree of muscle and nerve necrosis.
Results: There was a statistically significant decrease in the phonomyography signal output in the ischemic limb that correlated with the duration of ischemia and histological findings of muscle and nerve necrosis. The phonomyography signal decrease and histological findings were respectively: 55.5% (n=15;p=0.005) with rare muscle and nerve necrosis at 30min, 65.6% (n=12;p=0.005) with 5-10% muscle necrosis at 1h, 68.4% (n=9;p=0.015) with 100% muscle necrosis and little nerve damage at 2h, 72.4% (n=6;p=0.028) with 100% muscle necrosis and severe nerve damage at 4h, and 92.8% (n=3;p=0.109) with 100% muscle necrosis and severe nerve degeneration at 6h.
Conclusion: Changes in phonomyography signal are observed in early ischemic injury prior to the onset of nerve or muscle necrosis. Therefore, phonomyography could serve as a non-invasive technique to detect early ischemic muscle changes in acute compartment syndrome.
Clinical Relevance: The detection of abnormal muscle contraction in a timely fashion and non-invasive manner is of interest in clinical settings where the presence of ischemia is not easy to diagnose.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.injury.2017.08.051 | DOI Listing |
Front Biosci (Landmark Ed)
December 2024
Department of Cardiovascular Medicine, The Affiliated Changsha Hospital of Xiangya School of Medicine, Central South University, 410008 Changsha, Hunan, China.
Background: Chronic heart failure (CHF) is a serious cardiovascular condition. Vascular peroxidase 1 (VPO1) is associated with various cardiovascular diseases, yet its role in CHF remains unclear. This research aims to explore the involvement of VPO1 in CHF.
View Article and Find Full Text PDFFront Microbiol
December 2024
Department of Laboratory Medicine, Shengjing Hospital of China Medical University, Shenyang, China.
Aim: The current study aims to delineate subcutaneous adipose tissue (SAT), visceral adipose tissue (VAT), the sacrospinalis muscle, and all abdominal musculature at the L3-L5 vertebral level from non-contrast computed tomography (CT) imagery using deep learning algorithms. Subsequently, radiomic features are collected from these segmented images and subjected to medical interpretation.
Materials And Methods: This retrospective analysis includes a cohort of 315 patients diagnosed with acute necrotizing pancreatitis (ANP) who had undergone comprehensive whole-abdomen CT scans.
Cureus
November 2024
Orthopaedics and Traumatology, Istanbul University Cerrahpasa - Cerrahpasa Faculty of Medicine, Istanbul, TUR.
Shoulder septic arthritis is a severe infection of the shoulder joint, commonly caused by bacteria such as . It leads to inflammation, severe pain, swelling, and reduced mobility in the affected shoulder. The condition is typically diagnosed through clinical evaluation, blood tests, imaging studies, and joint aspiration.
View Article and Find Full Text PDFJpn J Radiol
December 2024
Department of Radiology, Gifu University, 1-1 Yanagido, Gifu, 501-1194, Japan.
Objective: The purpose of this study was to evaluate MRI findings of ovarian endometrioid carcinoma (OEC) as a predictor of histological grade.
Materials And Methods: This study included 60 patients with histopathologically confirmed OEC (20, 30, and 10 with grades 1, 2, and 3, respectively). Clinical and MRI results were retrospectively reviewed.
Sci Rep
December 2024
Clinical Laboratory, Hebei General Hospital, Shijiazhuang, Hebei, China.
Objective: To explore the influence of SALL4 in cardiac fibroblasts on the progression of myocardial infarction.
Methods: Analysis of genes specifically expressed in myocardial infarction by bioinformatics methods; The impact of SALL4 on myocardial infarction was assessed using mouse ultrasound experiments and Masson staining; The effect of SALL4 on the expression levels of collagen-I and collagen-III in myocardial tissue was examined by immunohistochemical staining; The migration ability of cardiac fibroblasts was evaluated using a Transwell assay; The proliferative ability of cardiac fibroblasts was tested using a CCK-8 assay; The relative fluorescence intensity of α-SMA and CTGF in cardiac fibroblasts were checked through immunofluorescence staining experiment; The expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, α-SMA, CTGF, and PAI-1 in myocardial tissues or cardiac fibroblasts was detected using western blot analysis.
Results: SALL4-specific high expression in myocardial infarction; SALL4 intensified the alterations in the heart structure of mice with myocardial infarction and worsened the fibrosis of myocardial infarction; SALL4 also promoted the expression of SALL4, DOT1L, H3K79me2, P53, SHP2, YAP, nucleus-YAP, collagen-I, collagen-III, α-SMA, CTGF, and PAI-1 in myocardial infarction tissues and cardiac fibroblasts; Subsequently, SALL4 could enhance the immunofluorescence intensity of α-SMA and CTGF; Moreover, SALL4 could promote the proliferation and migration of cardiac fibroblasts.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!