Dynamic muscle damage monitoring in pig crush injury: T2-weighted Dixon and 2D ultrasound applications.

Abstract

BACKGROUND: Crush injury (CI) involves compressive trauma causing muscle swelling, compartment syndrome, and neurological damage. We examined T2-Dixon and ultrasound for CI evaluation in pigs, integrating imaging with lab and tissue findings. METHODS: Twelve 15-16-month-old Bama miniature pigs were randomly divided into three extrusion groups: Group A (4&#x202f;h), Group B (8&#x202f;h), and Group C (16&#x202f;h), using custom equipment. Blood samples were collected at baseline (T0), decompression (T1), and 12&#x202f;h (T2), 24&#x202f;h (T3), and 72&#x202f;h (T4) post-decompression. MRI and ultrasound were performed at each time point. At T4, pigs were euthanized, and compressed muscles underwent HE staining for pathological assessment. RESULTS: Following decompression, Creatine Kinase (CK), Lactate dehydrogenase (LDH), and Klevels initially rose, then declined across all groups. CK peaked at T2 or T3 (&#x202f;<&#x202f;0.05), with Group B&#x202f;>&#x202f;Group A at T3/T4, and Group C&#x202f;>&#x202f;Group A at T1-T3 (&#x202f;<&#x202f;0.05). LDH peaked at T2/T3, with Groups B and C&#x202f;>&#x202f;Group A (&#x202f;<&#x202f;0.05). Kpeaked at T1/T2, with Group C showing a significant increase (&#x202f;<&#x202f;0.05) but no difference between Groups A and B. T2-weighted signal values rose then fell in Groups A/B but increased continuously in Group C, peaking at T2/T3 (&#x202f;<&#x202f;0.05). Group B&#x202f;>&#x202f;Group A at T2/T3; Group C&#x202f;>&#x202f;Group A at T1-T3 and > Group B at T3 (&#x202f;<&#x202f;0.05). CK and LDH correlated positively with T2 signal values (strongest in Group C), while Kshowed no correlation. Ultrasound revealed mildly enhanced echogenicity and structural disorganization in Group A. Groups B and C showed more severe damage, featuring a homogeneous, featureless appearance with complete loss of normal muscle architecture and heterogeneous echogenicity with sieve-like hypoechogenicity and fat layer edema, respectively. HE staining at T4 demonstrated progressively worse muscle damage with longer extrusion times. CONCLUSION: This study confirmed the viability of the CI model through biochemical verification and demonstrated that T2-Dixon and ultrasound synergistically assessed muscle damage, providing a more thorough evaluation that surpasses the constraints of biochemical markers alone.