Many rat/mouse pressure ulcer (PU) models have been developed to test different hypotheses to gain deeper understanding of various causative risk factors, the progress of PUs, and assessing effectiveness of potential treatment modalities. The recently emphasized deep tissue injury (DTI) mechanisms for PU formation has received increased attention and several studies reported findings on newly developed DTI animal models. However, concerns exist for the clinical relevance and validity of these models, especially when the majority of the reported rat PU/DTI models were not built upon SCI animals and many of the DTI research did not simulate well the clinical observation. In this study, we propose a rat PU and DTI model which is more clinically relevant by including chronic SCI condition into the rat PU model and to simulate the role of bony prominence in DTI formation by using an implant on the bone-tissue interface. Histological data and imaging findings confirmed that the condition of chronic SCI had significant effect on pressure-induced tissue injury in a rat PU model and the including a simulated bony prominence in rat DTI model resulted in significantly greater injury in deep muscle tissue. Further integration of the SCI condition and the simulated bony prominence would result a rat PU/DTI model which can simulate even more accurately the clinical phenomenon and yield research more clinically relevant findings.

Primary tuberculous pyomyositis is a rare manifestation of musculoskeletal tuberculosis especially in immunocompetent individuals without a focus of tuberculosis in the body and the underlying bone disease. It can cause a diagnostic dilemma for a physician and surgeon because of its similar presentation to soft tissue sarcomas, hematomas, and myopathies. We present a case of a 45-year-old immunocompetant gentleman with a thigh swelling with sepsis due to pyomyositis of the quadriceps requiring a multimodal management of drainage of abscess, debridement of devitalized muscle, antitubercular drugs, and physiotherapy. In a tubercular endemic country, a high index of suspicion is required to diagnose this disease which can be cured completely.

Current animal models examining deep tissue injury (DTI) development as a mechanism for pressure ulcer (PU) formation are limited, as the created animal wounds do not usually reflect clinically observed tissue necrosis. This study aimed to establish a more clinically relevant rat PU model by including a SCI condition in the model and by examining the role of a simulated bony prominence in DTI formation. Tissue injury percentage of compressed tibialis anterior (TA) muscle from eight SCI (T9) rats was compared against eight neurologically intact control rats to examine PU development over the flat surface of the tibia. To examine DTI formation, five other rats were implanted with a hemispheric polypropylene bone mimic beneath the TA muscle and were allowed to heal prior to compression. The rats in the DTI model were then separated into three groups and were administered different levels of compression to determine the best experimental conditions for the model. Both MRI and light microscopy were used to analyze tissue necrosis due to compression, and histological data was processed and quantified using a custom Matlab code. Postoperative ultrasound images of the implant two weeks after surgery showed the implant was correctly oriented on the surface of the bone. Results from this experiment and subsequent histological analysis and MRI observation confirmed these models are successful in simulating a clinically relevant pressure‐induced deep tissue injury.

Deep tissue injury (DTI) is a serious pressure ulcer (PU) which initiates in deep tissue, mainly muscle, and progresses rapidly to a full-thickness wound [1, 2]. Therefore, an early indication should help in increasing awareness and providing prompt intervention to prevent it from progressing to an open wound, which is susceptible to infection and typically needs prolonged and aggressive care. However, the diagnosis of DTI is currently still vague at best[2] with only subjective tools. This situation calls for tools for objectively sensing the tissue changes while the skin is still intact, to allow development of evidence-based protocols for early diagnosis and treatment. Since DTI initiates from deep muscle layer around a bony prominence, a tool that sensitive to muscle damage may have the potential to objectively sense the onset of a DTI in clinical application. A number of molecular biomarkers have been reported in the literature as suitable for indicating muscle damage. Some of the most promising biomarkers are myoglobin and heart-type fatty acid binding protein (H-FABP). Myoglobin and H-FABP are two relatively small muscle proteins that show a very fast release time after skeletal muscle damage/necrosis when no myocardial infarction or damage is present; therefore, they may be used to identify skeletal muscle injury in DTI formation. The objective of this study was to initially test whether myoglobin and H-FABP in serum and urine respond quickly to pressure induced deep tissue injury on a rat model. It is expected that knowledge gained from this study may lead to a promising new methodology to sense the visually invisible DTI.

Deep tissue injury (DTI), as a recently emphasized mechanism for PU formation [1], has received increased attention lately and several studies reported findings on newly developed DTI animal models [2]. The clinical view of DTI emphasizes the severity of clinically identified DTI as that a true DTI progresses rapidly even with the most aggressive treatment and its massive tissue necrosis is in a similar nature of a Stage-IV full-thickness wound [3]. Many animal PU models have been developed to test different hypotheses related to deep tissue injury (DTI) [3]. However, none of DTI studies reported that the experimentally induced DTI eventually progressed to be an open wound which affected superficial skin, and the reported histological or imaging data of the induced DTI did not suggest massive tissue necrosis. Although it might be that most studies did not keep their DTI animals long enough to observe the formation of an open wound from the DTI, the results from our own observation and Kwan, et al [4], in which no skin lesion was formed after 7 days of DTI, do not support this speculation. It may be that, in these DTI studies, the injured deep layer had healed. By examination of the existing PU rat models, especially those for DTI research, we came to our assumption that the missing bony prominence may possibly be a flaw that prevents those models from yielding more clinically relevant data. It has long been the understanding that PUs often occur at tissue pressure points around a bony prominence. We believe that, to more accurately simulate the clinical scenario of DTI formation, a bony prominence is necessary for a rat DTI model.