Case Report Posttraumatic Axillary False Aneurysm after Luxatio Erecta of the Shoulder: Case Report and Literature Review Maxime Iakovlev,1 Jean-Baptiste Marchand,2 Philippe Poirier,3 Kevin Bargoin,2 and Yann Gou€effic,1 Nantes and La Roche sur Yon, France
Vascular complications after dislocation of the shoulder are rare. We report a case of glenohumeral inferior dislocation (luxatio erecta) responsible for an acute ischemia of the upper limb. Endovascular treatment with a covered stent associated with the evacuation of the compressive hematoma was privileged. In the second stage, an axillary bypass was carried out because of an intrastent thrombosis responsible for an acute ischemia of the right upper limb. The stabilization of the glenohumeral articulation was obtained later with an anterior coracoid bone block. The conventional surgical treatment remains the standard treatment. Hybrid techniques with endovascular clamping can be useful in the presence of proximal arterial lesions. Endovascular treatment is an interesting therapeutic alternative in the urgency and in selected cases but its mid- and long-term results should still be evaluated.
Erecta shoulder dislocations are rare. They account for 0.5% of dislocations of the shoulder versus 95% for anterointernal dislocations which are the most frequent.1,2 The clinical presentation of luxatio erecta is characterized by an upper limb in hyperabduction, hand raised to the top of the head, and an impossibility to bring back the elbow close to the body.1 The treatment of dislocation consists of a reduction by external maneuvers under analgesia. In >50% of the cases, one does not observe reccurence of the dislocation.3 The incidence of luxatio
1 Service de Chirurgie Vasculaire, Institut du thorax, CHU de Nantes, Nantes, France. 2 Clinique chirurgicale orthopedique et traumatologique, P^ole osteoarticulaire, CHU de Nantes, Nantes, France. 3 Service de chirurgie vasculaire et thyroı¨dienne, Centre Hospitalier Departemental de La Roche sur Yon, La Roche sur Yon, France.
Correspondence to: Yann Gou€effic, MD, PhD, Service de Chirurgie Vasculaire, Institut du thorax, CHU de Nantes, Nantes, 44000 France; E-mail: [email protected] Ann Vasc Surg 2014; -: 1–6 http://dx.doi.org/10.1016/j.avsg.2014.01.006 Ó 2014 Elsevier Inc. All rights reserved. Manuscript received: June 12, 2013; manuscript accepted: January 3, 2014; published online: ---.
erecta is low, and it is difficult to determine the rate of complications. We report the case of a 69year-old patient presenting an arterial complication of an inferior glenohumeral dislocation treated using endovascular technique, then in a second stage of an acute ischemia of the ipsilateral upper limb after stent thrombosis.
CASE REPORT We report the case of a 69-year-old man presenting a right luxatio erecta. He previously presented 5 noncomplicated episodes of anterior dislocation of the right shoulder. A surgery of stabilization of the shoulder had been evoked before, even if it is seldom carried out in patients older than 65. However, the patient had refused a repair intervention of the shoulder. The single cardiovascular risk factor of the patient was noneinsulin-dependant diabetes mellitus. The dislocation had occurred spontaneously, during the patient’s sleep. Before reduction, the neurovascular examination was regarded as normal. The distal pulses were perceived. Radiography showed a luxatio erecta of the right shoulder without associated fracture (Fig. 1). The reduction was carried out by an external maneuver of traction-adduction of the member under general anesthesia. Postoperative X-rays found a reduction 1
2 Case Report
Fig. 1. X rays (face and profile) of the right shoulder before reduction. of the dislocation without associated fracture (Fig. 2). In spite of the reduction, the patient was hyperalgic with the constitution in a few minutes of a bulky hematoma of the axilla, the deltopectoral groove, and the right anterior thoracic wall. On clinical examination, the patient presented an acute ischemia of the right upper limb associating palor and abolition of the ulnar and radial pulses. In addition, one observed a complete sensory-motor deficit of the forearm and the hand. The sensitivity of the shoulder stump was preserved. The angio-computed tomography (angio-CT)carried out in emergency showed an arterial false aneurysm developed at the junction between the axillary artery and the brachial artery, with a bulky hematoma compressing the brachial plexus (Fig. 3). The downstream flow was strongly decreased but the arteries were patent. An arteriography was carried out through the right brachial artery after a short surgical approach at the elbow groove. The arteriography showed an extravasation of contrast on the lateral side of the axillobrachial junction. The circumflex humeral artery was not visualized, which meant that the false aneurysm was most probably related to the traumatic avulsion of this artery. No stenosis was visualized (Fig. 4). Because of the bulky hematoma complicating the access to the subclavian artery and increasing the risk of peripheral neurologic lesions, endovascular treatment was decided. After general heparinization (50 IU/kg), a covered stainless steel AdvantaÒ V12 stent (Atrium Interventional, Hudson, NH) was implanted to cover the neck of the false aneurysm (Fig. 5). Arteriographic control showed a complete exclusion of the false aneurysm and a patent arterial axis. After ablation of the introducer, because of a poor backward flow, a downstream thrombectomy was carried out making it possible to extract a fresh thrombus and to recover a backward flow of good quality. The axillary hematoma was evacuated by a short incision in the deltopectoral groove to decompress the brachial plexus. The distal pulses were perceived at the end of the intervention. The postoperative course was uneventful. Antiplatelet treatment was begun with acetyl salicylic acid (160 mg/ day). The upper limb was immobilized with the elbow to the body for 3 weeks. The patient was discharged at the
Annals of Vascular Surgery
Fig. 2. X Rays (face and profile) of the right shoulder after reduction. third postoperative day in the absence of motor deficit. After 29 days, 2 days after beginning a passive rehabilitation, the patient presented an acute ischemia of the right upper limb. Ultrasounds showed a thrombosis of the covered axillary stent. The patient was revascularized in emergency with an axillobrachial reversed saphenous vein bypass in anatomic position. The implanted stent during the first intervention was crushed. At the sixth postoperative month, the patient had a stabilization of his shoulder by an anterior coracoid bone block. At 1 year, the patient presented a complete recovery of mobilities of the shoulder, with a coracoid block in place and consolidated, a patent venous bypass on duplex ultrasound, and without any sensory-motor deficit.
DISCUSSION Glenohumeral dislocations are commonly observed in the young man 90% of the cases with nerve damage.4e6 Vascular complications occur in 1e2% of the cases after shoulder dislocation. The occurrence of vascular complications is related to the intensity of the traumatism, the difficulties of shoulder dislocation reduction, the age of the patient, and the presence of atheroma.7,8 More than 80% of the cases of arterial lesions described in the literature were described in patients aged >50 years.8 Recurrent shoulder dislocation is in favor of the occurrence of an arterial lesion in the mid- and long-term.8 Several physiopathological hypotheses were proposed to explain the vascular complications of shoulder dislocations. The circumflex humeral artery and the subscapular artery are limiting elements of the mobility of the axillary artery. In the thoracobrachial outlet, the artery is subjected to 5 types of static or dynamic
Vol.
-,
No.
-, -
2014
Case Report 3
Fig. 3. Angio-CT: right axillary false aneurysm with a bulky hematoma.
extrinsic compressions. The pectoralis minor tendon may be a traumatic element for the artery.9 Finally, some reports of perioperative dissections also describe adherent fibrous elements between the glenohumeral capsula and the axillary artery. These cicatricial lesions of previous dislocations are constraining elements for the artery.8,10,11 The arterial lesions can be diagnosed several days, weeks, or even years after the episode of dislocation.6,11,12 Three types of arterial lesions were described. The false aneurysms may be related to direct wounds, but they are mostly due to the avulsion of collateral arteries.6 The circumflex humeral artery and the subscapular artery are involved.13 The false aneurysm presents as a painful and extensive hematoma of the axilla, associated, according to the anatomic situation of the arterial rupture, with an hematoma of the arm or the thorax. Several cases of vascular complications were reported with perceived distal pulses.6 It is necessary to differentiate primitive nervous damage associated with an arterial lesion,12 from a secondary nervous lesion due to plexic or troncular compression by the axillar hematoma.7,12,14 Contained rupture with an extensive axillary hematoma was also described in several cases, and this up to 6 months after the traumatism.15,16 An old false aneurysm can create an ischemia of the upper limb by embolization of the downstream arterial bed.11 Few cases of dissections were also reported. They preferentially affect a young population and can be complicated by a thrombosis, symptomatic or not.17 The prevalence of the dissections is probably underestimated because of the initial absence of symptoms of the
immobilization of the upper limb and an excellent collaterality. Dissections can also occur for minor traumatisms without a dislocation or an associated fracture.18 In 7e68% of the cases, the vascular complications are an arterial rupture, often associated with a major nerve damage with a poor prognosis.8,19 In our case, 2 causes could be evoked concerning the physiopathology of the false aneurysm. Dislocation could be the initial cause of the arterial lesion. The hemorrhage would then have been contained by the pressure exerted by the dislocated humeral head. The hematoma would thus have appeared after the reduction of dislocation. In addition, the reduction of dislocation could be also at the origin of the arterial trauma. The occurrence of the dislocation during the sleep and the normality of the neurovascular examination before reduction make it the most probable cause of hemorrhage. Until now, the treatment of reference of posttraumatic vascular lesions remained open surgery with a venous autologous bypass or of an arterial resection with end-to-end anastomosis if the resection of the pathologic zone could be limited to
Vascular complications after dislocation of the shoulder are rare. We report a case of glenohumeral inferior dislocation (luxatio erecta) responsible for an acute ischemia of the upper limb. Endovascular treatment with a covered stent associated with the evacuation of the compressive hematoma was privileged. In the second stage, an axillary bypass was carried out because of an intrastent thrombosis responsible for an acute ischemia of the right upper limb. The stabilization of the glenohumeral articulation was obtained later with an anterior coracoid bone block. The conventional surgical treatment remains the standard treatment. Hybrid techniques with endovascular clamping can be useful in the presence of proximal arterial lesions. Endovascular treatment is an interesting therapeutic alternative in the urgency and in selected cases but its mid- and long-term results should still be evaluated.
Erecta shoulder dislocations are rare. They account for 0.5% of dislocations of the shoulder versus 95% for anterointernal dislocations which are the most frequent.1,2 The clinical presentation of luxatio erecta is characterized by an upper limb in hyperabduction, hand raised to the top of the head, and an impossibility to bring back the elbow close to the body.1 The treatment of dislocation consists of a reduction by external maneuvers under analgesia. In >50% of the cases, one does not observe reccurence of the dislocation.3 The incidence of luxatio
1 Service de Chirurgie Vasculaire, Institut du thorax, CHU de Nantes, Nantes, France. 2 Clinique chirurgicale orthopedique et traumatologique, P^ole osteoarticulaire, CHU de Nantes, Nantes, France. 3 Service de chirurgie vasculaire et thyroı¨dienne, Centre Hospitalier Departemental de La Roche sur Yon, La Roche sur Yon, France.
Correspondence to: Yann Gou€effic, MD, PhD, Service de Chirurgie Vasculaire, Institut du thorax, CHU de Nantes, Nantes, 44000 France; E-mail: [email protected] Ann Vasc Surg 2014; -: 1–6 http://dx.doi.org/10.1016/j.avsg.2014.01.006 Ó 2014 Elsevier Inc. All rights reserved. Manuscript received: June 12, 2013; manuscript accepted: January 3, 2014; published online: ---.
erecta is low, and it is difficult to determine the rate of complications. We report the case of a 69year-old patient presenting an arterial complication of an inferior glenohumeral dislocation treated using endovascular technique, then in a second stage of an acute ischemia of the ipsilateral upper limb after stent thrombosis.
CASE REPORT We report the case of a 69-year-old man presenting a right luxatio erecta. He previously presented 5 noncomplicated episodes of anterior dislocation of the right shoulder. A surgery of stabilization of the shoulder had been evoked before, even if it is seldom carried out in patients older than 65. However, the patient had refused a repair intervention of the shoulder. The single cardiovascular risk factor of the patient was noneinsulin-dependant diabetes mellitus. The dislocation had occurred spontaneously, during the patient’s sleep. Before reduction, the neurovascular examination was regarded as normal. The distal pulses were perceived. Radiography showed a luxatio erecta of the right shoulder without associated fracture (Fig. 1). The reduction was carried out by an external maneuver of traction-adduction of the member under general anesthesia. Postoperative X-rays found a reduction 1
2 Case Report
Fig. 1. X rays (face and profile) of the right shoulder before reduction. of the dislocation without associated fracture (Fig. 2). In spite of the reduction, the patient was hyperalgic with the constitution in a few minutes of a bulky hematoma of the axilla, the deltopectoral groove, and the right anterior thoracic wall. On clinical examination, the patient presented an acute ischemia of the right upper limb associating palor and abolition of the ulnar and radial pulses. In addition, one observed a complete sensory-motor deficit of the forearm and the hand. The sensitivity of the shoulder stump was preserved. The angio-computed tomography (angio-CT)carried out in emergency showed an arterial false aneurysm developed at the junction between the axillary artery and the brachial artery, with a bulky hematoma compressing the brachial plexus (Fig. 3). The downstream flow was strongly decreased but the arteries were patent. An arteriography was carried out through the right brachial artery after a short surgical approach at the elbow groove. The arteriography showed an extravasation of contrast on the lateral side of the axillobrachial junction. The circumflex humeral artery was not visualized, which meant that the false aneurysm was most probably related to the traumatic avulsion of this artery. No stenosis was visualized (Fig. 4). Because of the bulky hematoma complicating the access to the subclavian artery and increasing the risk of peripheral neurologic lesions, endovascular treatment was decided. After general heparinization (50 IU/kg), a covered stainless steel AdvantaÒ V12 stent (Atrium Interventional, Hudson, NH) was implanted to cover the neck of the false aneurysm (Fig. 5). Arteriographic control showed a complete exclusion of the false aneurysm and a patent arterial axis. After ablation of the introducer, because of a poor backward flow, a downstream thrombectomy was carried out making it possible to extract a fresh thrombus and to recover a backward flow of good quality. The axillary hematoma was evacuated by a short incision in the deltopectoral groove to decompress the brachial plexus. The distal pulses were perceived at the end of the intervention. The postoperative course was uneventful. Antiplatelet treatment was begun with acetyl salicylic acid (160 mg/ day). The upper limb was immobilized with the elbow to the body for 3 weeks. The patient was discharged at the
Annals of Vascular Surgery
Fig. 2. X Rays (face and profile) of the right shoulder after reduction. third postoperative day in the absence of motor deficit. After 29 days, 2 days after beginning a passive rehabilitation, the patient presented an acute ischemia of the right upper limb. Ultrasounds showed a thrombosis of the covered axillary stent. The patient was revascularized in emergency with an axillobrachial reversed saphenous vein bypass in anatomic position. The implanted stent during the first intervention was crushed. At the sixth postoperative month, the patient had a stabilization of his shoulder by an anterior coracoid bone block. At 1 year, the patient presented a complete recovery of mobilities of the shoulder, with a coracoid block in place and consolidated, a patent venous bypass on duplex ultrasound, and without any sensory-motor deficit.
DISCUSSION Glenohumeral dislocations are commonly observed in the young man 90% of the cases with nerve damage.4e6 Vascular complications occur in 1e2% of the cases after shoulder dislocation. The occurrence of vascular complications is related to the intensity of the traumatism, the difficulties of shoulder dislocation reduction, the age of the patient, and the presence of atheroma.7,8 More than 80% of the cases of arterial lesions described in the literature were described in patients aged >50 years.8 Recurrent shoulder dislocation is in favor of the occurrence of an arterial lesion in the mid- and long-term.8 Several physiopathological hypotheses were proposed to explain the vascular complications of shoulder dislocations. The circumflex humeral artery and the subscapular artery are limiting elements of the mobility of the axillary artery. In the thoracobrachial outlet, the artery is subjected to 5 types of static or dynamic
Vol.
-,
No.
-, -
2014
Case Report 3
Fig. 3. Angio-CT: right axillary false aneurysm with a bulky hematoma.
extrinsic compressions. The pectoralis minor tendon may be a traumatic element for the artery.9 Finally, some reports of perioperative dissections also describe adherent fibrous elements between the glenohumeral capsula and the axillary artery. These cicatricial lesions of previous dislocations are constraining elements for the artery.8,10,11 The arterial lesions can be diagnosed several days, weeks, or even years after the episode of dislocation.6,11,12 Three types of arterial lesions were described. The false aneurysms may be related to direct wounds, but they are mostly due to the avulsion of collateral arteries.6 The circumflex humeral artery and the subscapular artery are involved.13 The false aneurysm presents as a painful and extensive hematoma of the axilla, associated, according to the anatomic situation of the arterial rupture, with an hematoma of the arm or the thorax. Several cases of vascular complications were reported with perceived distal pulses.6 It is necessary to differentiate primitive nervous damage associated with an arterial lesion,12 from a secondary nervous lesion due to plexic or troncular compression by the axillar hematoma.7,12,14 Contained rupture with an extensive axillary hematoma was also described in several cases, and this up to 6 months after the traumatism.15,16 An old false aneurysm can create an ischemia of the upper limb by embolization of the downstream arterial bed.11 Few cases of dissections were also reported. They preferentially affect a young population and can be complicated by a thrombosis, symptomatic or not.17 The prevalence of the dissections is probably underestimated because of the initial absence of symptoms of the
immobilization of the upper limb and an excellent collaterality. Dissections can also occur for minor traumatisms without a dislocation or an associated fracture.18 In 7e68% of the cases, the vascular complications are an arterial rupture, often associated with a major nerve damage with a poor prognosis.8,19 In our case, 2 causes could be evoked concerning the physiopathology of the false aneurysm. Dislocation could be the initial cause of the arterial lesion. The hemorrhage would then have been contained by the pressure exerted by the dislocated humeral head. The hematoma would thus have appeared after the reduction of dislocation. In addition, the reduction of dislocation could be also at the origin of the arterial trauma. The occurrence of the dislocation during the sleep and the normality of the neurovascular examination before reduction make it the most probable cause of hemorrhage. Until now, the treatment of reference of posttraumatic vascular lesions remained open surgery with a venous autologous bypass or of an arterial resection with end-to-end anastomosis if the resection of the pathologic zone could be limited to
