Aims: Pharmacological modulation of skeletal muscle reperfusion injury after trauma associated ischaemia may improve limb salvage rates and prevent the associated systemic sequelae. Resuscitation with hypertonic saline restores the circulating volume and has favourable effects on tissue perfusion and blood pressure. The purpose of our study was to evaluate the effects of hypertonic saline on skeletal muscle ischaemia reperfusion (I/R) injury and the associated endorgan injury. Methods: Adult male Sprague Dawley rats (n=24) were randomised into three groups: control group, I/R group treated with normal saline and I/R group treated with hypertonic saline. Bilateral hind-limb ischaemia was induced by rubber band application proximal to the level of the greater trochanters for 2.5 hours. Treatment groups received either normal saline or hypertonic saline prior to tourniquet release. Following twelve hours reperfusion, the tibialis anterior muscle was dissected and muscle function assessed electrophysiologically by electrical field stimulation. The animals were then sacrificed and skeletal muscle harvested for evaluation. Lung tissue was also harvested for measurement of wet-to-dry ratio, myeloperoxidase content and histological analysis. Results: Hypertonic saline significantly attenuated skeletal muscle reperfusion injury as shown by reduced twitch and tetanic contractions of the skeletal muscle (Table). There was also a significant reduction in lung injury as demonstrated by differences in wet-to-dry ratio, myeloperoxidase content and histological analysis. Conclusion: Resuscitation with hypertonic saline may have a protective role in attenuating skeletal muscle ischaemia reperfusion injury and its associated systemic sequelae

Background

Open fracture wounds are well known to be associated with infection & prolonged healing. Activity in scientific research to improve wound healing has often provided variable results. This study was done to question the de facto nature of Normal Saline as best irrigant in management of such wounds and to find out a better irrigant, if so, that does exist with due consideration to the mechanism by which saline dressings act.

Aims. To achieve expert clinical consensus in the delivery of hydrodilatation for the treatment of primary frozen shoulder to inform clinical practice and the design of an intervention for evaluation. Methods. We conducted a two-stage, electronic questionnaire-based, modified Delphi survey of shoulder experts in the UK NHS. Round one required positive, negative, or neutral ratings about hydrodilatation. In round two, each participant was reminded of their round one responses and the modal (or ‘group’) response from all participants. This allowed participants to modify their responses in round two. We proposed respectively mandating or encouraging elements of hydrodilatation with 100% and 90% positive consensus, and respectively disallowing or discouraging with 90% and 80% negative consensus. Other elements would be optional. Results. Between 4 August 2020 and 4 August 2021, shoulder experts from 47 hospitals in the UK completed the study. There were 106 participants (consultant upper limb orthopaedic surgeons, n = 50; consultant radiologists, n = 52; consultant physiotherapist, n = 1; extended scope physiotherapists, n = 3) who completed round one, of whom 97 (92%) completed round two. No elements of hydrodilatation were “mandated” (100% positive rating). Elements that were “encouraged” (≥ 80% positive rating) were the use of image guidance, local anaesthetic, normal saline, and steroids to deliver the injection. Injecting according to patient tolerance, physiotherapy, and home exercises were also “encouraged”. No elements were “discouraged” (≥ 80% negative rating) although using hypertonic saline was rated as being “disallowed” (≥ 90% negative rating). Conclusion. In the absence of rigorous evidence, our Delphi study allowed us to achieve expert consensus about positive, negative, and neutral ratings of hydrodilatation in the management of frozen shoulder in a hospital setting. This should inform clinical practice and the design of an intervention for evaluation. Cite this article: Bone Jt Open 2022;3(9):701–709

Introduction: Recent data report increased trunk stiffness in semi-sitting in people with recurrent low back pain (LBP) during remission. This is likely to be due to increased trunk muscles activity. Although this adaptation may provide a short term strategy to protect the spine from further pain/injury it may increase the potential for pain recurrence due to increased trunk loading and compromised performance of the spine in dynamic functions. An interesting observation was that trunk damping (i.e. decay in trunk velocity) was reduced. Damping is likely to be largely related to reflex control of trunk muscles. It is possible that trunk stiffness increased in this population because reflex control was inadequate. This study aimed to determine whether stiffness and damping adapt in a similar manner in healthy individuals, with presumably normal reflex function, when challenged by pain. Methods: Fourteen males with no history of LBP were semi-seated with their pelvis fixated and a harness placed over their shoulders. Weights (~15% of body mass) were attached via an electromagnet and force transducer to a pulley system that attached to the front and rear of the trunk harness at T9. Subjects sat upright in a relaxed, neutral posture. At an unpredictable time either the front or back weight was dropped 10 times (each) in random order. Trials were repeated in three conditions; pre-pain, pain and post-pain. During the pain condition subjects were injected with a single bolus of hypertonic saline (5% NaCl, 1.5 ml) into the right erector spinae at L4. Trunk mass (M), damping (B) and stiffness (K) were estimated when the trunk was perturbed either backwards (BW) or forwards (FW) in an identical manner to our earlier study. Parameters were described by a second order linear model and the standard least squares procedure was used to solve the estimation using the equation: F(t)=M.x(acc)(t)+B. x(vel)(t)+K.x(disp)(t). Damping and stiffness were normalized to the peak. Perturbation displacement and duration were calculated from the onset to perturbation maximum. Data were compared with repeated measures ANOVA and Duncan’s multiple range test. Results: During experimental pain, trunk stiffness decreased in both perturbation directions (both: p< 0.02). Damping increased with FW perturbations (p=0.01). Both the displacement (p=0.03) and duration (p=0.01) of the trunk perturbation were increased during experimental pain with BW perturbation. There was no change in either parameter in the FW direction. Estimated trunk mass was lower during pain and post-pain compared to pre pain (p=0.01) with BW perturbations. Discussion: In contrast to increased stiffness and decreased damping in people with recurrent LBP, healthy individuals respond to pain by decreasing stiffness and increasing damping of the trunk. However, this was only true for the FW perturbation. In the BW direction, damping was not increased and there was a resultant increase in the displacement and duration of the perturbation. Taken together these data suggest that damping of the trunk is adaptable and is increased to protect the spine in healthy individuals. As trunk damping is associated with reflex control of the trunk muscles these data suggest although healthy individuals may be able to tune this control during pain, this is compromised in spinal pain

Aims

We retrospectively report our experience of managing 30 patients with a primary malignant tumour of the distal tibia; 25 were treated by limb salvage surgery and five by amputation. We compared the clinical outcomes of following the use of different methods of reconstruction.

To clarify the pathomechanisms of discogenic low back pain, the sympathetic afferent discharge originating from the L5-L6 disc via the L2 root were investigated neurophysiologically in 31 Lewis rats. Sympathetic afferent units were recorded from the L2 root connected to the lumbar sympathetic trunk by rami communicantes. The L5-L6 discs were mechanically probed, stimulated electrically to evoke action potentials and, finally, treated with chemicals to produce an inflammatory reaction. We could not obtain a response from any units in the L5-L6 discs using mechanical stimulation, but with electrical stimulation we identified 42 units consisting mostly of A-delta fibres. In some experiments a response to mechanical probing of the L5-L6 disc was recognised after producing an inflammatory reaction. This study suggests that mechanical stimulation of the lumbar discs may not always produce pain, whereas inflammatory changes may cause the disc to become sensitive to mechanical stimuli, resulting in nociceptive information being transmitted as discogenic low back pain to the spinal cord through the lumbar sympathetic trunk. This may partly explain the variation in human symptoms of degenerate discs.