Sitting Biomechanics Laboratory

Part of the
Sensory Motor Performance Program
Room 1340, Rehabilitation Institute of Chicago

Spinal Cord Injury (SCI) Animal Model for Pressure Ulcers (PU) in Denervated Tissues

The prevalence of Pressure Ulcers (PU) is reported as 40% or higher among individuals with spinal cord injury (SCI) in the United States. Pressure injury on muscle tissues has been considered the single most important etiologic factor for Pressure Ulcers. It has been noticed that muscle stiffness changes after pressure load and accompanied by necrotic damage of muscle tissue. Denervation and atrophy of muscle post SCI may magnify such reaction by significantly decrease muscle volume and lower their pressure endurance threshold. It is hypothesized that chronic SCI may affect material properties of soft tissue below the injury level. This property alteration may contribute to soft tissue breakdown in wheelchair users with chronic SCI. Due to the difficulties in conducting such an assessment on humans, it is necessary to validate the ability of the probe to detect and measure differences in tissue stiffness near wounds in a more controlled subject. Initial testing is therefore done on rats to construct a model of expected tissue response to the wound.

 

 

Objectives:

  • Establish animal model for research on Pressure Ulcers post Spinal Cord Injury (SCI)
  • To examine the changes of tibialis anterior (TA) muscle stiffness induced by compressive load applied on skin surface over the muscle on a rat model at 3 time points post-compression. Muscle stiffness estimated in vivo will be correlated with quantitative histological observations on the distribution of fiber size, the segmental necrosis of the fibers, the percentage of necrotic muscle fibers, and the quantified extent of the inflammatory reactions.
  • To examine the changes of tibialis anterior muscle histology and stiffness induced by compressive load applied on skin surface over the muscle in a chronic SCI rat model and compare the findings with those obtained from the neurologically intact rats.

Tissue stiffness was measured under 3 conditions:

  • Rat with SCI and Pressure Ulcers
  • Rat with SCI and no Pressure Ulcers
  • Healthy control

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Rats were anesthetized and were paralyzed through a complete Spinal Cord Transection at the level of T10 (A) and (B). The rats were then given 6 weeks to heal from their surgery, and to allow muscle atrophy to set in.

 

 

 

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Controlled compressive load is applied to the skin surface over the TA muscle of one of the hind limbs of the rats with a custom-designed apparatus (A) and (B). the tissue is tested for passive stiffness in vivo by MTS machine

 

At the same time, a comparative value= of the tissue stiffness is then obtained in vivo non-invasively with TUPS to validate the non-invasive method for future clinical applications

 

Stiffness measurements of the TA muscle is collected using a Materials testing platform (A). The TA muscle is exposed, and its stiffness measured. The animals are then euthanized and TA muscles removed for histological testing.

 

 

 



 

 

 

Findings:

  • Soft tissue stiffness decreased significantly at 1 week post SCI, and continued to decrease over time.
  • Soft tissue stiffness was largely decreased post compression injury.

 

 

 

 

 

Histological methods were used to quantify the extent of the injury by the percentage of the necrotic fibers (less stained with Gomori’s trichrome) on transverse sections and the distribution of the segmental necrosis on longitudinal sections. Also by histology, the signs of muscle fiber injury will be identified by the distribution of ruptured membrane and swollen or squeezed fibers, the distortion of striation, and the quantitative distribution of the inflammatory reactions. Below is a comparison between the healthy leg muscle (A) and the leg with a wound (B).

 

Last updated May 25, 2008 by Makhsous.
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