# Experimental evaluation of timing and preference of surgical ıntervention for crush syndrome in disaster scenarios: fasciotomy or amputation? A rat model study

**Authors:** Şehmuz Kaya, Yunus Can Ünal, Necip Güven, Abdulrahim Dündar, Ömer Faruk Keleş, Yıldıray Başbuğan

PMC · DOI: 10.1186/s13018-025-05927-5 · Journal of Orthopaedic Surgery and Research · 2025-05-22

## TL;DR

This study uses a rat model to show that early surgical intervention for crush syndrome reduces muscle and kidney damage, offering guidance for disaster scenarios.

## Contribution

The study introduces the first experimental rat model to evaluate the timing of fasciotomy and amputation for crush syndrome.

## Key findings

- Early surgical intervention (0h) reduced muscle inflammation, necrosis, and preserved renal function.
- Late interventions (12 and 24h) caused severe muscle and kidney damage due to increased inflammation and toxic metabolite accumulation.
- Immediate amputation showed superior renal protection compared to late interventions.

## Abstract

Crush syndrome is a severe condition caused by the systemic effects of rhabdomyolysis due to prolonged muscle compression. Common in disasters like earthquakes, it poses life-threatening risks, including acute renal failure, hyperkalemia, and metabolic acidosis. Although surgical interventions such as fasciotomy and amputation are critical in its management, the optimal timing and criteria remain unclear. This study investigates the impact of surgical intervention timing on crush syndrome outcomes, providing guidance through the first experimental rat model evaluating fasciotomy and amputation post-injury.

Forty-eight Wistar albino rats were divided into six groups. Rhabdomyolysis was induced experimentally, followed by amputation or fasciotomy at 0, 12, or 24 h. The control group underwent rhabdomyolysis induction without surgery. Weekly urine samples were collected during the study, and blood, muscle, and kidney tissues were examined biochemically and histopathologically at the experiment's end. Data analysis focused on the systemic and tissue-specific effects of intervention timing.

Early intervention groups (0 h) demonstrated minimal muscle inflammation and necrosis, preserved muscle fiber arrangement, and more pronounced regeneration. Late interventions (12 and 24 h) were associated with intense inflammation, necrosis, edema, and hemorrhage in muscle tissue. Immediate amputation (0 h) limited toxic metabolite effects, reducing kidney inflammation and damage. Late interventions showed increased interstitial nephritis and inflammatory cell infiltration in kidney tissue. Biochemical analyses revealed that urinary myoglobin levels decreased and renal function was preserved in the early intervention groups.

The timing of surgical intervention is critical in managing crush syndrome. Early amputation and fasciotomy minimized necrosis and inflammation in muscle tissue, supported tissue regeneration, and reduced systemic complications by preventing toxic metabolite accumulation in the kidneys. Early amputation particularly showed superior renal protection and lower systemic complication risks compared to late interventions. These findings highlight the importance of timely surgical action and provide valuable insights for developing effective treatment strategies in disaster settings. However, the descriptive nature of the study and the fact that the data obtained from the experimental model cannot be directly applied to clinical practice should be taken into account. Therefore, the findings should be supported by future clinical trials.

The online version contains supplementary material available at 10.1186/s13018-025-05927-5.

## Linked entities

- **Diseases:** crush syndrome (MONDO:0043549), acute renal failure (MONDO:0002492), metabolic acidosis (MONDO:0000440), interstitial nephritis (MONDO:0001085)

## Full-text entities

- **Genes:** Mb (myoglobin) [NCBI Gene 59108] {aka Glng}
- **Diseases:** muscle compression (MESH:D009408), inflammation (MESH:D007249), Crush syndrome (MESH:D003444), hyperkalemia (MESH:D006947), necrosis (MESH:D009336), interstitial nephritis (MESH:D009395), Rhabdomyolysis (MESH:D012206), metabolic acidosis (MESH:D000138), acute renal failure (MESH:D058186)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

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Source: https://tomesphere.com/paper/PMC12100787