Thoracic outlet syndrome has been reported as a complication following nonoperative midshaft clavicular fractures resulting from nonunion, malunion, and/or excessive callus formation7-12. There is little evidence describing iatrogenic thoracic outlet syndrome following clavicular osteosynthesis for nonunion6,13-15. Most reports describe thoracic outlet syndrome as a late complication. We describe a patient with acute dynamic thoracic outlet syndrome following atrophic clavicular nonunion revision osteosynthesis. Based on this experience, we now recommend a passive intraoperative arm abduction test for all surgically treated midshaft clavicular fractures, particularly nonunions and malunions.
The potential effects of neurovascular compromise within the thoracic outlet have been documented13,15,16. Arterial thoracic outlet syndrome has been reported (as a late complication) to cause potential limb-threatening complications, including a partially thrombosed aneurysm and upper-extremity emboli13,15. Our patient’s symptoms were evident in the immediate postoperative period when he, against our prescribed protocol, performed active shoulder abduction of the operative upper extremity. It is unknown if the symptoms would have progressed to thoracic outlet syndrome with the arm in the resting position, would have resolved with time, or perhaps would have advanced acutely to limb-threatening ischemia had he adhered to the postoperative protocol of no shoulder range of motion.
The acuity of the thoracic outlet syndrome we report is rare when compared with other reports of osteosynthesis following clavicular nonunion. Papagelopoulos et al.14 reported a case of an acute thoracic outlet syndrome after internal fixation for atrophic nonunion. The patient reported paresthesias, had visible superficial swelling and congestion of the operative extremity, and had an absent radial pulse in the upright position, although these symptoms were not evident in the supine position. The patient underwent immediate revision without imaging because of the indisputable clinical presentation of acute thoracic outlet syndrome, and the symptoms completely resolved after surgery. In contrast, our patient was asymptomatic in both the supine and upright positions. He had a dramatic change in the examination when the arm was in the abducted position (over 80°), with paresthesias and an absent radial pulse, which completely resolved when the arm was returned to his side. Similar to the aforementioned case14, our patient remained asymptomatic at the time of follow-up.
Our patient’s postoperative arteriogram showed an enlargement of the collateral vessels, suggestive of some degree of chronic compression of the subclavian artery. The chronic scarring and displacement of the index fracture of the clavicle thirteen years ago may have contributed to the compromise of the thoracic outlet. We concluded that the compression was subclinical because the patient reported no symptoms and the baseline preoperative neurovascular examination was normal. In reviewing the intraoperative imaging during the initial revision surgery, both fracture fragments demonstrated slight inferior displacement. It is also likely that the debridement of bone ends and attrition of these surfaces over the years resulted in considerable shortening of the length of the clavicle. This displacement and shortening, in conjunction with some degree of chronic thoracic outlet obstruction, likely contributed to the postoperative clinical presentation. The final surgical procedure might have been avoided had we performed the passive arm abduction test intraoperatively.
Fracture callus following revision osteosynthesis after multiple subacute fixation failures has been reported as a cause of thoracic outlet syndrome. Skedros et al.6 described a patient with progressive neurovascular symptoms. In this case, a stenosed subclavian vein that had been noted intraoperatively had not been detectable on standard radiographs. In our case, there was no evidence of callus at the time of revision surgery, and the bone graft did not appear to compromise the thoracic outlet.
At our institution, the use of an intramedullary device and corticocancellous allograft chips for acute midshaft clavicular nonunion has yielded excellent results. In retrospect, our initial intervention should have utilized plate fixation for our patient’s chronic nonunion9,10. To achieve osteoinductive and osteoconductive properties, the corticocancellous allograft chips could have been supplemented with bone morphogenetic protein, or we could have used an autogenous bone graft. The use of an autogenous iliac crest bone graft to assist with restoration of length and offset surgical shortening in chronic nonunion has been previously described10.
To our knowledge, this is the first case report of an acute dynamic thoracic outlet syndrome after midshaft clavicular osteosynthesis for nonunion. Although this is a solitary case with relatively short follow-up, our experience with this patient has taught us to use the intraoperative passive arm abduction test to detect the presence of this infrequent yet potentially limb-threatening complication. The importance of a baseline preoperative neurovascular assessment (static and dynamic) cannot be overemphasized. In addition, surgeons must be vigilant in obtaining an anatomic reduction to avoid compromising the thoracic outlet. During osteosynthesis, we suggest that surgeons avoid overshortening or angulating the free ends of the clavicle and use safe drilling angles and depths, which have previously been described7. We also advise assessing the fracture callus intraoperatively because this may be a potential source of thoracic outlet syndrome. Surgeons should have a low threshold for diagnostic testing if symptoms of thoracic outlet syndrome develop after clavicular osteosynthesis.
Note: The authors acknowledge Donald T. Kirkendall, ELS, for his assistance in the preparation of this case report.
Disclosure: None of the authors received payments or services, either directly or indirectly (i.e., via his or her institution), from a third party in support of any aspect of this work. One or more of the authors, or his or her institution, has had a financial relationship, in the thirty-six months prior to submission of this work, with an entity in the biomedical arena that could be perceived to influence or have the potential to influence what is written in this work. No author has had any other relationships, or has engaged in any other activities, that could be perceived to influence or have the potential to influence what is written in this work. The complete Disclosures of Potential Conflicts of Interest submitted by authors are always provided with the online version of the article.