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

TL;DR

This study uses MRI and ultrasound to monitor muscle damage in pigs after crush injuries, showing that these imaging techniques provide a more complete assessment than blood tests alone.

Contribution

The study introduces a synergistic use of T2-Dixon MRI and ultrasound for dynamic evaluation of muscle damage in a pig crush injury model.

Findings

T2-weighted signal values increased continuously in pigs with longer extrusion times, showing more severe muscle damage.

Ultrasound revealed structural disorganization and severe damage in pigs with 8 and 16-hour extrusion times.

Biochemical markers like CK and LDH correlated with T2 signal values, but K+ did not.

Abstract

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.

Twelve 15–16-month-old Bama miniature pigs were randomly divided into three extrusion groups: Group A (4 h), Group B (8 h), and Group C (16 h), using custom equipment. Blood samples were collected at baseline (T0), decompression (T1), and 12 h (T2), 24 h (T3), and 72 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.

Following decompression, Creatine Kinase (CK), Lactate dehydrogenase (LDH), and K+ levels initially rose, then declined across all groups. CK peaked at T2 or T3 (p < 0.05), with Group B > Group A at T3/T4, and Group C > Group A at T1–T3 (p < 0.05). LDH peaked at T2/T3, with Groups B and C > Group A (p < 0.05). K+ peaked at T1/T2, with Group C showing a significant increase (p < 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 (p < 0.05). Group B > Group A at T2/T3; Group C > Group A at T1–T3 and > Group B at T3 (p < 0.05). CK and LDH correlated positively with T2 signal values (strongest in Group C), while K+ showed 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.

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.

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