Statement of purpose

To demonstrate how contemplating reconstructive options among members of Orthoplastic team can prevent accidental damage during initial wound debridement in foot and ankle injuries

Complex defects of the foot and ankle often require input from plastic and orthopaedic surgeons. There are different reconstructive options but one excellent regional option for small defects is the Extensor Digitorum Brevis muscle (EDB) flap. The anatomy of the flap and surgical technique and utility are described and demonstrated through a case series.

We present a series of 4 consecutive cases of the use of the pedicled EDB flap for soft tissue coverage of difficult defects around the foot and ankle. This regional pedicled flap can be proximally based to cover defects around the ankle or distally based for distal foot coverage. When possible, it facilitates a reconstruction with minimal donor site morbidity, shorter operating times, and fewer complications than alternative options

The flap would usually be performed by the plastic surgical member of the orthoplastic team, but an understanding of it by foot and ankle and reconstructive orthopaedic surgeons is relevant as it's vascular supply via the lateral tarsal artery can be easily damaged, preventing its use in the management of wound complications or trauma.

Aim

Case Report presentation of traumatic cartilage loss in a child.

Introduction: Enlarging cystic cavitations (syrinxes) form within the spinal cord in up to 28% of spinal cord injured patients. These post-traumatic syrinxes can cause neurological deterioration, and treatment results remain poor. Syrinxes are often found adjacent to regions of arachnoiditis.

The understanding of biological systems is increasingly dependent on modelling and simulations. Numerical simulation is not intended to replace in vivo experimental studies, but to enhance the understanding of biological systems. This study tests the hypothesis that pressure pulses in the SAS are high adjacent to areas of arachnoiditis and investigates the validity of a numerical model by comparison with in vivo experimental findings.

Methods: Experimental Model: Post-traumatic syringomyelia was induced in eight sheep by injection of kaolin into the subarachnoid space (SAS), and excitotoxic amino acid into the spinal cord of the upper thoracic spine. Cerebrospinal fluid (CSF) pressure studies were undertaken at either 3 or 6 weeks. Fibre-optic monitors were used to measure the pressure in the SAS 1 cm rostral and 1 cm caudal to the induced arachnoiditis.

Numerical Model: An axisymmetric fluid-structure interaction model was developed to represent the spinal cord and SAS under normal physiological conditions and in the presence of arachnoiditis. Arachnoiditis was modeled as a porous obstruction in the SAS.

Results: In both models the SAS pressure rostral to the arachnoiditis was found to be higher than the caudal SAS pressure. There was no statistically significant difference between the sheep at 3 and 6 weeks. Under normal conditions, both experimentally and in the numerical model, the pressure drop along the SAS was negligible. In the presence of arachnoiditis, the pressure drop across the arachnoiditis in the experimental model was 1.6 mmHg, whereas the numerical model predicted a pressure difference of 1.3 mmHg.

Discussion: The numerical model accurately predicts CSF pressures in the animal model under both normal and abnormal conditions, allowing predictions to be made to within 20% accuracy. The local increases in SAS CSF pressure demonstrated may act to increase fluid flow through perivascular spaces and be implicated in syrinx formation and enlargement.

Introduction: This study aimed to analyse immunohis-tochemically the proteolysis of Amyloid Precursor Protein (APP) using Caspase-3-mediated APP proteolytic peptide (CMAP), beta-Amyloid (Aβ) and Active Caspase-3 in post-mortem human specimens in acute and chronic compressive myelopathy.

Compressive myelopathy, occurring through traumatic fracture/dislocation of vertebrae, iatrogenic injury, cervical spondylotic myelopathy (CSM), or metastatic tumour, causes much socio-economic and emotional disability for patients as well as physical consequences. In such conditions, APP is recognised as an early and specifi c marker of axonal injury. The proteolysis of APP in both acute and chronic compressive myelopathy has not yet been described. Studies analysing axonal injury after brain trauma suggest a role for Caspase-3 in the cleavage of APP¹. In addition, Caspase-3-mediated cleavage of APP has been found to be associated with the formation of Aβ, a neurotoxic protein thought to contribute to cell death in Alzheimer’s disease². Furthermore, A? may subsequently encourage activation of Caspases −2, −3, and −6, the major effector molecules in apoptosis². The current study addressed two hypotheses; that APP provides a substrate for the Caspase-3 enzyme, and, that this event is associated with Aβ production in the compressed spinal cord.

Methods: Spinal cord material from 17 patients with documented SCI was analysed. The spatial distribution of cellular immunoreactivity was qualitatively assessed in injury due to trauma (n=5), iatrogenic event (n=1), CSM (n=6) and metastatic tumour (n=5). Morphological, immunohistochemical and immunofl uorescent techniques were used to investigate APP proteolysis.

Results: Caspase-3, APP, CMAP and Aβ were present in anterior horn cells of the grey matter and axons of the white matter. An association was found between neuronal immunoreactivity and that of axons in motor tracts. Dual-immunolabelling revealed axonal co-localisation of CMAP with Aβ and Caspase-3 with Aβ. Although CMAP was present in axons which were immunoposi-tive for APP, an inverse relationship was found as each marker was limited to its own, distinct region, consistent with the theory that CMAP actively cleaves APP. In neurons, co-localisation occurred between Caspase-3 and Aβ, and CMAP with Aβ. No neuronal co-localisation was shown between CMAP and APP in the acute and chronic state.

Discussion: Caspase-3 appears likely to contribute to the proteolytic cleavage of APP in compressive myelop-athy. CMAP was associated with the production of Aβ as demonstrated using single and dual immunolabelling. Furthermore, evidence is given for the association of Caspase-3 itself with the neurotoxic peptide, Aβ. It is possible that activation of Caspase-3 via these secondary mechanisms may trigger the advancement of the apoptotic cascade with the subsequent demise of the cell.

Introduction: Apoptosis, or secondary cell death, has been demonstrated in a number of neurological conditions, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and brain ischaemia. It is well established from studies of acute spinal cord injury that apoptosis seems an important factor in secondary cell death and irreversible neurological deficit. It is only recently that studies have emerged analysing secondary cell death in chronic injury to the cord. In this study, the spatial and temporal expression of apoptotic cells was analysed in acute traumatic spinal cord injury (SCI) (n=6) and chronic myelopathies due to metastatic tumour (n=5), degenerative spondylosis (n=6) and syringomyelia (n=4). The study aimed to demonstrate apoptosis in compressive spinal cord injury and to analyse the spatial and temporal distribution of apoptosis in acute and chronic myelopathy.

Method: Archival material from 21 spinal cords of patients with documented myelopathy during life and definitive evidence on post mortem examination were available for study. The spatial and temporal expression of apoptotic cells was analysed in acute traumatic spinal cord injury (SCI) (n=6) and chronic myelopathy due to metastatic tumour (n=5), degenerative spondylosis (n=6) and syringomyelia (n=4).

Immunohistochemical analysis of each specimen was conducted using markers of apoptosis, as well as the biochemical apoptotic marker TUNEL. A total of 1800 histopathological slides were analysed. Specimens were also analysed using confocal microscopy to identify the immunopositive cell type. A combination of morphological, immunohistochemical and in situ end-labelling techniques were used to investigate the mechanism of cell death in this experiment. The analytical techniques employed were aimed at showing firstly the presence of apoptosis and secondly the size and position of the damaged regions.

Results: Positivity for active Caspase-3, DNA-PKCS, PARP, TUNEL and active Caspase-9 was found in glia (oligodendrocytes and microglia) axons and neurons in both acute and chronic compression above, below and at the site of compression. In chronic compression, the severity of positivity for apoptotic immunological markers was positively correlated with the severity of white matter damage, as measured by APP immunostaining for axonal injury, and Wallerian degeneration. There was no correlation between the duration of chronic compression and immunopositivity for apoptotic markers. In acute SCI, axonal swellings were consistently positive for Caspases −9 and -3, suggesting mitochondrial activation of apoptotic pathways.

Conclusion: Apoptosis occurs in both acute and chronic spinal cord injury. In acute compression, axonal injury is associated with apoptotic immunopositivity of glia and neurons. In chronic compression, apoptosis of oligodendrocytes and microglia correlates with demyelination of axons within the white matter.

Introduction: It has been suggested that arachnoiditis predisposes to post-traumatic syringomyelia formation by obstructing subarachnoid cerebrospinal fluid flow and enhancing perivascular flow into the cord. In an animal model of post-traumatic syringomyelia (PTS), fluid flow in spinal cord perivascular spaces (PVS) is greater at the level of arachnoiditis and syrinx than at other levels and fluid enters the syrinx via the PVS. This study was performed to determine the effects of cerebrospinal fluid (CSF) diversion from the subarachnoid space on perivascular flow and syrinx formation in PTS.

Methods: Twenty six male Sprague-Dawley rats were investigated using the CSF tracer horseradish peroxidase (HRP), the excitotoxic and arachnoiditis model of PTS, and lumboperitoneal shunt insertion. Four experimental groups consisted of syrinx only and shunt only controls, and shunt insertion before or after syrinx formation. CSF flow studies were performed 6 weeks following the final intervention. Grading scales were used to quantify HRP staining.

Results: Syrinxes formed in all animals. Perivascular flow was greatest at the level of the syrinx. Cerebral cortex perivascular flow was significantly reduced following shunt insertion in animals with a syrinx (p< 0.05). Shunt insertion did not alter syrinx length or size, but did reduce the number of animals with evidence of sensory disturbances. There were no significant differences between shunt and syrinx first groups.

Discussion: Increasing distal subarachnoid space compliance does not affect local CSF flow into the spinal cord and syrinx. These results suggest that localised alterations in compliance, as opposed to obstruction from traumatic arachnoiditis, act as an important factor in syrinx pathogenesis.

Introduction: Modern imaging techniques have demonstrated that up to 28% of patients with spinal cord injury develop syringomyelia. Cyst formation and enlargement are thought to be related to abnormalities of cerebrospinal fluid hydrodynamics, however the exact mechanism and route of entry into the spinal cord remain incompletely understood. Previous work in rats has demonstrated that experimental post-traumatic syrinxes occur more reliably and are larger when the excitotoxic injury is combined with arachnoiditis produced by subarachnoid kaolin injection. A sheep model of post-traumatic syringomyelia (P.T.S.) has been characterised and studies of cerebrospinal fluid dynamics are currently being undertaken. The aim of this study was to assess the effect of focal subarachnoid space blockage on spinal fluid pressures and flow.

Methods: Arachnoiditis was induced in 5 sheep by injection of 1.5 mls of kaolin in the subarachnoid space (SAS) of upper thoracic spinal cord. The animals were left for 6–8 weeks before C.S.F. studies were undertaken. In another 5 sheep, a ligature was passed around the spinal cord to simulate an acute blockage of the subarachnoid space. Fluid-coupled monitors were used to measure blood pressure, central venous pressure and subarachnoid pressure (1cm rostral and 1 cm caudal to the arachnoiditis or ligature). Fiberoptic monitors were used to measure intracranial pressure. In the ligature group, subarachnoid pressures were also measured prior to tying the ligature to obliterate the SAS and served as baseline control pressures. The effects of Valsalva and Queckenstedt manoeuvres on SAS pressures were examined in both groups.

CSF flow was studied at 0 and 10 minutes after injection of the CSF tracer horseradish peroxidase (HRP). Vibratome sections of the spinal cord were processed using tetramethylbenzidine and sections examined under light microscopy.

Results: The mean SAS pressure rostral to the arachnoiditis was found to be greater than the mean caudal SAS pressure by 1.7 mmHg. In the ligature group, the difference was 0.9 mmHg, being higher in the caudal SAS. Queckenstedt manoeuvre exaggerated this difference to 3 mmHg in the Kaolin group and 4 mmHg in the ligature group. The effect of Valsalva was much less marked in both groups.

Perivascular spaces were enlarged in most cases of arachnoiditis and HRP was seen to stain these spaces and the central canal within 10 minutes.

Discussion: Post-traumatic syrinxes are usually juxtaposed to the injury site with 80% occurring rostral, 4% caudal and 15%in both directions. The finding of a higher subarachnoid pressure rostral to the injury site may help explain this phenomenon. We hypothesize that a reduction of compliance in subarachnoid space increases the pulse pressure and hence increases perivascular flow of C.S.F. contributing to the formation and enlargement of PTS. We are currently investigating this hypothesis by measuring subarachnoid space compliance directly in the sheep model of arachnoiditis described above.

INTRODUCTION: Apoptosis, or secondary cell death, has been demonstrated in a number of neurological conditions, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and brain ischaemia. It is well established from studies of acute spinal cord injury that apoptosis seems an important factor in secondary cell death and irreversible neurological deficit. It is only recently that studies have emerged analysing secondary cell death in chronic injury to the cord. In this study, the spatial and temporal expression of apoptotic cells was analysed in acute traumatic spinal cord injury (SCI) (n=6) and chronic myelopathies due to meta-static tumour (n=5), degenerative spondylosis (n=6) and syringomyelia (n=4). The study aimed to demonstrate apoptosis in compressive spinal cord injury and to analyse the spatial and temporal distribution of apoptosis in acute and chronic myelopathy.

METHOD: Archival material from 21 spinal cords of patients with documented myelopathy during life and definitive evidence on post mortem examination were available for study. The spatial and temporal expression of apoptotic cells was analysed in acute traumatic spinal cord injury (SCI) (n=6) and chronic myelopathy due to metastatic tumour (n=5), degenerative spondylosis (n=6) and syringomyelia (n=4).

Immunohistochemical analysis of each specimen was conducted using markers of apoptosis, as well as the biochemical apoptotic marker TUNEL. A total of 1800 histopathological slides were analysed. Specimens were also analysed using confocal microscopy to identify the immunopositive cell type. A combination of morphological, immunohistochemical and in situ end-labelling techniques were used to investigate the mechanism of cell death in this experiment. The analytical techniques employed were aimed at showing firstly the presence of apoptosis and secondly the size and position of the damaged regions.

RESULTS: Positivity for active Caspase-3, DNA-PKCS, PARP, TUNEL and active Caspase-9 was found in glia (oligodendrocytes and microglia) axons and neurons in both acute and chronic compression above, below and at the site of compression. In chronic compression, the severity of positivity for apoptotic immunological markers was positively correlated with the severity of white matter damage, as measured by APP immunostaining for axonal injury, and Wallerian degeneration. There was no correlation between the duration of chronic compression and immunopositivity for apoptotic markers. In acute SCI, axonal swellings were consistently positive for Caspases −9 and -3, suggesting mitochon-drial activation of apoptotic pathways.

CONCLUSION: Apoptosis occurs in both acute and chronic spinal cord injury. In acute compression, axonal injury is associated with apoptotic immunopositivity of glia and neurons. In chronic compression, apoptosis of oligodendrocytes and microglia correlates with demyelination of axons within the white matter.

INTRODUCTION: Modern imaging techniques have demonstrated that up to 28% of patients with spinal cord injury develop syringomyelia. Cyst formation and enlargement are thought to be related to abnormalities of cerebrospinal fluid hydrodynamics, however the exact mechanism and route of entry into the spinal cord remain incompletely understood. Previous work in rats has demonstrated that experimental post-traumatic syrinxes occur more reliably and are larger when the excitotoxic injury is combined with arachnoiditis produced by subarachnoid kaolin injection. A sheep model of post-traumatic syringomyelia (P.T.S.) has been characterised and studies of cerebrospinal fluid dynamics are currently being undertaken. The aim of this study was to assess the effect of focal subarachnoid space blockage on spinal fluid pressures and flow.

METHODS: Arachnoiditis was induced in five sheep by injection of 1.5 mls of kaolin in the subarachnoid space (SAS) of upper thoracic spinal cord. The animals were left for 6–8 weeks before C.S.F. studies were undertaken. In another five sheep, a ligature was passed around the spinal cord to simulate an acute blockage of the subarachnoid space. Fluid-coupled monitors were used to measure blood pressure, central venous pressure and subarachnoid pressure (1 cm rostral and 1 cm caudal to the arachnoiditis or ligature). Fiberoptic monitors were used to measure intracranial pressure. In the ligature group, subarachnoid pressures were also measured prior to tying the ligature to obliterate the SAS and served as baseline control pressures. The effects of Valsalva and Queckenstedt manoeuvres on SAS pressures were examined in both groups.

CSF flow was studied at 0 and 10 minutes after injection of the CSF tracer horseradish peroxidase (HRP). Vibratome sections of the spinal cord were processed using tetramethylbenzidine and sections examined under light microscopy.

RESULTS: The mean SAS pressure rostral to the arachnoiditis was found to be greater than the mean caudal SAS pressure by 1.7 mmHg. In the ligature group, the difference was 0.9 mmHg, being higher in the caudal SAS. Queckenstedt manoeuvre exaggerated this difference to 3 mmHg in the Kaolin group and 4 mmHg in the ligature group. The effect of Valsalva was much less marked in both groups.

Perivascular spaces were enlarged in most cases of arachnoiditis and HRP was seen to stain these spaces and the central canal within 10 minutes.

DISCUSSION: Post-traumatic syrinxes are usually juxtaposed to the injury site with 80% occurring rostral, 4% caudal and 15% in both directions. The finding of a higher subarachnoid pressure rostral to the injury site may help explain this phenomenon. We hypothesise that a reduction of compliance in subarachnoid space increases the pulse pressure and hence increases peri-vascular flow of C.S.F. contributing to the formation and enlargement of PTS. We are currently investigating this hypothesis by measuring subarachnoid space compliance directly in the sheep model of arachnoiditis described above.

INTRODUCTION: It has been suggested that arachnoiditis predisposes to post-traumatic syringomyelia formation by obstructing subarachnoid cerebrospinal fluid flow and enhancing perivascular flow into the cord. In an animal model of post-traumatic syringomyelia (PTS), fluid flow in spinal cord perivascular spaces (PVS) is greater at the level of arachnoiditis and syrinx than at other levels and fluid enters the syrinx via the PVS. This study was performed to determine the effects of cere-brospinal fluid (CSF) diversion from the subarachnoid space on perivascular flow and syrinx formation in PTS.

METHODS: Twenty six male Sprague-Dawley rats were investigated using the CSF tracer horseradish peroxidase (HRP), the excitotoxic and arachnoiditis model of PTS, and lumboperitoneal shunt insertion. Four experimental groups consisted of syrinx only and shunt only controls, and shunt insertion before or after syrinx formation. CSF flow studies were performed six weeks following the final intervention. Grading scales were used to quantify HRP staining.

RESULTS: Syrinxes formed in all animals. Perivascular flow was greatest at the level of the syrinx. Cerebral cortex perivascular flow was significantly reduced following shunt insertion in animals with a syrinx (p< 0.05). Shunt insertion did not alter syrinx length or size, but did reduce the number of animals with evidence of sensory disturbances. There were no significant differences between shunt and syrinx first groups.

DISCUSSION: Increasing distal subarachnoid space compliance does not affect local CSF flow into the spinal cord and syrinx. These results suggest that localised alterations in compliance, as opposed to obstruction from traumatic arachnoiditis, act as an important factor in syrinx pathogenesis.