Search

Trigger finger is a common condition affecting the hand. Therapeutic variability surrounds the management of trigger finger, especially in the mild cases. The aim of this study was to survey secondary care surgeons to describe the current management of trigger fingers. The steering group developed a survey for hand surgeons. Following piloting, the survey was distributed to hand surgeons in the United Kingdom and The Netherlands. A total of 713 plastic surgeons and orthopaedic surgeons were invited to participate in the online survey and 440 (62%) surgeons completed the survey. In both mild and moderate cases of trigger finger, steroid injection was the preferred treatment option. Open surgery was the treatment of choice for severe cases. However, there was variation in delivery of care, including type and dosage of steroid, site of injection, interval between injections, maximum number of injections, type of incision and treatment of patients with diabetes or rheumatoid arthritis. This highlights the need for a better evidence base for the treatment of trigger fingers.

Ulnar artery revascularization in hypothenar hammer syndrome has repeatedly been shown to reduce ischaemic symptoms, however with varying graft patency percentages. This study prospectively assesses the effect of revascularization surgery with a vein graft using validated questionnaires in seven patients. The Disabilities of the Arm, Shoulder and Hand (DASH) and the Cold Intolerance Symptom Severity (CISS) questionnaires have been used to compare the preoperative and postoperative functionality and cold intolerance. All patients showed improvement in either functionality, or cold intolerance, or both from disabled to nearly normalized levels and resumed their occupation at final follow-up (mean of 28 months). Strikingly this was also the case in a patient with graft stenosis. Patients with the highest preoperative questionnaire scores showed most postoperative improvement. In conclusion, revascularization surgery seems to improve the symptomatology irrespective of graft patency. Questionnaires can be a valuable contribution to quantify and to follow the symptomatology in hypothenar hammer syndrome.

Purpose Cold-induced vasodilatation (CIVD) is a cyclic regulation of blood flow during prolonged cooling of protruding body parts. It is generally considered to be a protective mechanism against local cold injuries and cold intolerance after peripheral nerve injury. The aim of this study was to determine the role of the sympathetic system in initiating a CIVD response. Methods Eight rats were operated according to the spared nerve injury (SNI) model, eight underwent a complete sciatic lesion (CSL) and six underwent a sham operation. Prior to operation, 3, 6 and 9 weeks postoperatively, both hind limbs were cooled and the skin temperature was recorded to evaluate the presence of CIVD reactions. Cold intolerance was determined using the cold plate test and mechanical hypersensitivity measured using the Von Frey test. Results No significant difference in CIVD was found comparing the lateral operated hind limb for time (preoperatively and 3, 6 and 9 weeks postoperatively; p = 0.397) and for group (SNI, CSL and Sham; p = 0.695). SNI and CSL rats developed cold intolerance and mechanical hypersensitivity. Conclusion Our data show that the underlying mechanisms that initiate a CIVD reaction are not affected by damage to a peripheral nerve that includes the sympathetic fibres. We conclude that the sympathetic system does not play a major role in the initiation of CIVD in the hind limb of a rat. Clinical relevance No substantial changes in the CIVD reaction after peripheral nerve injury imply that the origin of cold intolerance after a traumatic nerve injury is initiated by local factors and has a more neurological cause. This is an important finding for future developing treatments for this common problem, as treatment focussing on vaso-regulation may not help diminish symptoms of cold-intolerant patients. © 2013 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.

Purpose: Cold intolerance is defined as pain after exposure to non-painful cold. It is suggested that cold intolerance may be related to dysfunctional thermoregulation in upper extremity nerve injury patients. The purpose of this study was to examine if the re-warming of a rat hind paw is altered in different peripheral nerve injury models and if these patterns are related to severity of cold intolerance. Methods: In the spared nerve injury (SNI) and complete sciatic lesion (CSL) model, the re-warming patterns after cold stress exposure were investigated preoperatively and at 3, 6 and 9 weeks postoperatively with a device to induce cooling of the hind paws. Thermocouples were attached on the dorsal side of the hind paw to monitor re-warming patterns. Results: The Von Frey test and cold plate test indicated a significantly lower paw-withdrawal threshold and latency in the SNI compared to the Sham model. The CSL group, however, had only significantly lower paw-withdrawal latency on the cold plate test compared to the Sham group. While we found no significantly different re-warming patterns in the SNI and CSL group compared to Sham group, we did find a tendency in temperature increase in the CSL group 3 weeks postoperatively. Conclusion: Overall, our findings indicate that re-warming patterns are not altered after peripheral nerve injury in these rat models despite the fact that these animals did develop cold intolerance. This suggests that disturbed thermoregulation may not be the prime mechanism for cold intolerance and that, other, most likely, neurological mechanisms may play a more important role. Clinical relevance: There is no direct correlation between cold intolerance and re-warming patterns in different peripheral nerve injury rat models. This is an important finding for future developing treatments for this common problem, since treatment focussing on vaso-regulation may not help diminish symptoms of cold-intolerant patients. (C) 2011 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.

Background: Conditioned pain modulation (CPM) is a phenomenon of 'pain inhibiting pain' that is important for understanding idiopathic pain syndromes. Because the pathophysiology of posttraumatic cold intolerance is still unknown but it could involve similar mechanisms as idiopathic pain syndromes, we evaluated the functioning of the CPM system in patients with posttraumatic cold intolerance compared to healthy controls. Methods: Fourteen healthy controls and 24 patients diagnosed with cold intolerance using the Cold Intolerance Symptom Severity questionnaire were included in the study. Of the 24 patients with cold intolerance, 11 had a nerve lesion and 13 an amputation of one or more digits. To quantify the CPM, pain threshold for mechanical pressure was measured at the affected region as a baseline measure. Then, the contralateral hand received a cold stimulus of ice water to evoke the noxious conditioning. Af Results: The absolute and relative changes in algometer pressure (CPM effect) between pre- and post-conditioning were significantly smaller in the cold intolerance group compared to the control group (absolute p = 0.019, relative p = 0.004). The CPM effect was significantly different between the control group and the subgroups of nerve lesion (p = 0.003) and amputation patients (p = 0.011). Conclusions: In this study, we found a CPM effect after a cold stimulus in both controls and patients. A significant weaker CPM effect compared to the controls was found, as in other chronic pain conditions. The CPM system within patients with cold intolerance is altered. Crown Copyright (C) 2013 Published by Elsevier Ltd on behalf of British Association of Plastic, Reconstructive and Aesthetic Surgeons. All rights reserved.

Purpose It is often assumed that cold intolerance is associated with abnormalities in the skin temperature due to changes in the blood flow of the hands. In this study, we determined whether patients with and without cold intolerance after a hand fracture or healthy controls have a diminished rewarming after a cold stimulus. Methods The severity of cold intolerance was evaluated using the Cold Intolerance Symptom Severity (CISS) questionnaire. To determine whether abnormal rewarming plays a major role in the underlying pathophysiology of cold intolerance, a cold-stress test was applied at a mean of 30 months (with a range of 11 mo) after the patients recovered from a hand fracture. A control group also underwent identical cold-stress testing for comparison. Temperature during the rewarming phase was measured using videothermography. Results Thirteen control subjects and 18 patients participated. Control subjects did not report any symptoms of cold intolerance (CISS score, 0) and no loss of sensibility was measured. The mean CISS score of all patients was 27.8; 9 patients scored above the cut-off value for normal cold intolerance. No significant differences were found in the rewarming patterns between (1) the affected and non-affected hand of the postfracture patients, (2) the dominant and non-dominant hand of the control subjects, and (3) the patients and controls. Conclusions The results of this study revealed no relation between the severity of cold intolerance and rewarming patterns after cold stress testing. This might suggest that temperature regulation of the hands in post-fracture patients might not be responsible for the symptoms of cold intolerance, based on cold-stress test response. (J Hand Surg 2011;36A:670-676. Copyright (c) 2011 by the American Society for Surgery of the Hand. All rights reserved.) Type of study/level of evidence Prognostic II.

con-tributed to the debate on the influence of nerve injuryand nerve repair on the CIVD reaction. The studyreported a significant decrease in the CIVD reaction ofthe hind paw following a nerve transection of the sciaticnerve as compared to a sham-treated group (same opera-tion procedure, without nerve manipulation). In addition,they measured the CIVD reaction after an autograft repairof the sciatic nerve and found no significant differenceswith the sham-treated group. Therefore, the authors con-cluded that the CIVD reaction is controlled by the nerv-ous system, more specifically, by the autonomic nervoussystem. In this reply, we question if Hu et al. use thedefinition of a CIVD in an accurate manner. It is possiblethat the CIVD reaction defined and measured by Huet al. was not a CIVD reaction but an active rewarmingpattern.A CIVD is currently defined as a cyclic oscillation inblood flow that occurs in extremities on cold exposure.