Saudi Journal of Kidney Diseases and Transplantation

: 2012  |  Volume : 23  |  Issue : 5  |  Page : 1028--1031

Severe upper extremity polyneuropathy due to inferior brachial plexus compression as a result of left subclavian artery pseudoaneurism

George Kosmadakis1, Paris Pappas2, Athina Gobou1, Despoina Smirloglou1, Spiridon Michail1,  
1 Department of Nephrology, "Gregorios Vosnides", Laiko General Hospital, Athens, Greece
2 Department of Radiology, "Gregorios Vosnides", Laiko General Hospital, Athens, Greece

Correspondence Address:
George Kosmadakis
Department of Nephrology, «DQ»Gregorios Vosnides, Laiko General Hospital, Athens


In the present report, we describe the case of a 76-year-old hemodialysis patient who was admitted with clinical features of neurological thoracic exit syndrome due to subclavian artery pseudoaneurism following the insertion of a dual lumen vascular internal jugular catheter (vascath) with excellent outcome after endo-arterial stent placement.

How to cite this article:
Kosmadakis G, Pappas P, Gobou A, Smirloglou D, Michail S. Severe upper extremity polyneuropathy due to inferior brachial plexus compression as a result of left subclavian artery pseudoaneurism.Saudi J Kidney Dis Transpl 2012;23:1028-1031

How to cite this URL:
Kosmadakis G, Pappas P, Gobou A, Smirloglou D, Michail S. Severe upper extremity polyneuropathy due to inferior brachial plexus compression as a result of left subclavian artery pseudoaneurism. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2020 Nov 26 ];23:1028-1031
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Full Text


Thoracic exit syndrome (TES) is clinically attributed to the compression of neurovascular structures passing through the thoracic exit. Pathophysiologically, there are three types of TES depending on the compressed anatomical structure: the neurological, arterial and venous. Ninety-five percent of TES episodes are neu­rological, and they are attributed to the com­pression of the brachial plexus or the adjacent nerves, mainly due to bone and soft tissues' abnormalities located between the scalenus anterior and the scalenus medius muscles. [1],[2] TES is relatively uncommon after an internal jugular catheter insertion, and it occurs due to hematoma or injury. We describe in this report a case of TES due to subclavian artery pseudoaneurism following the insertion of a dual­lumen vascular internal jugular catheter with excellent outcome after endo-arterial stent place­ment.

 Case Report

A 76-year-old caucasian male with end-stage renal disease on hemodialysis was admitted in the nephrology department for the investiga­tion of severe and persistent pain on the left upper extremity and functional inability of the left arm for 45 days prior to admission. The patient reported that the current progressively aggravating symptoms were associated with the insertion of a central vascular catheter for hemodialysis. Clinical examination detected a significant muscular weakness of the left upper extremity with reduced mobility, reduction of superficial and deep sensitivity and loss of ten­don reflexes unilaterally. Results of the pa­tient's laboratory tests on admission included the following:

Hematocrit: 29.7%, hemoglobin: 9.9 g/dL, white blood count: 10100/μL, platelets: 198,000/μL, prothrombin time: 16/11 s, activated partial thromboplastin time: 38/32 s, fibrinogen: 514 mg/dL, serum urea: 155 mg/dL, serum creatinine: 7.7 mg/dL, serum uric acid: 5.1 mg/dL, serum sodium: 145 mmol/L, serum potassium 3.8 mmol/L, serum calcium: 2.25 mmol/L. Chest X-ray and X-rays of the ribs, clavicles and cervical spine were unremarkable. The patient was treated consecutively with non-narcotic and narcotic analgesics, gabapentin and complex vitamin B tablets without any significant response. On the electromyogram of the left upper extremity, a reduced kinetic activation in all muscle groups was detected, especially in the area of the forearm and the hand. These findings are compatible with da­mage at the level of the left lower brachial plexus. Evoked potentials revealed a reduction in sensomotor neuronal speed and reduced pro­voked potential in the examined nerves of bra­chial plexus. In the cervical and thoracic spine computed tomography (CT) scan, a vascular "tumor-like structure" in the area of the sub-clavian artery was detected without any signs of communication with adjacent vessels. In view of this finding, the patient underwent a percu­taneous angiography of the left upper extre­mity. During the angiography, a sizable pseudoaneurism of the left subclavian artery [Figure 1]A with obvious "jet" was detected [Figure 1]B and a stent was placed intraoperatively, re­sulting in the occlusion of the pseudoaneurism orifice [Figure 2]. In the following days, a significant reduction of pain was noted and the sensomotor functions were significantly im­proved. The patient was discharged 15 days after admission without analgesia. Six months after the intervention, the patient was pain-free and the sensomotor activity of his left arm recovered completely. A signi­ficant improvement of neuromuscular conduc­tivity was seen in a new electromyogram and the evoked potentials showed improved speed of sensomotor conductivity.{Figure 1}{Figure 2}


Clinical characteristics of the TES may vary and include pain localized at the shoulder and the neck and radiates to the arm, paresis or paralysis of muscles innervated by the brachial plexus, paresthesia, sensory loss, reduction of arterial pulses at the affected extremity, ische­mia and edema. The venous TES is the most common vascu­lar type (30-40% of patients with TES). Primary venous TES is also called Paget-Schrotter syn­drome, and may be multifactorial, e.g. com­pression in a congenital narrow thoracic exit. Compression may be aggravated with certain movements of the upper extremities and the trunk. Chronic retraction or contraction may predispose to hypercoagulability, venous stasis and endothelial injury; the classic Virchow's triad that may predispose to the formation of intravascular clots. The most common etiological factors of secondary venous thrombosis are: the venous endothelial injury from foreign bodies, i.e. central venous catheters (the most common causes) and tubing of the pacemakers, [3] traumas, inflammatory causes (thrombophle­bitis), inflammations and radiotherapy as well as systemic diseases (nephrotic syndrome, de­hydration, heart failure and Pancoast tumor). Edema and cyanosis of the epsilateral upper extremity as well as dilatation of collateral venous network are the most common clinical features of subclavian vein thrombosis.

The arterial type of TES is less common than venous TES (10-20% of the cases). This type is associated with serious complications, i.e. ischemia of the extremity leading and occa­sionally amputations. The basic mechanism of damage for the subclavian artery is the chronic compression that leads to endothelial damage, fibrosis and, finally, stenosis of the blood vessel. A post-stenotic aneurism may be formed due to the turbulence of blood in the stenotic area. This predisposes to the formation of clots and thromboembolic episodes in smaller arte­rial vessels of the epsilateral extremity. Sub-clavian artery may be compressed by a cervi­cal rib (the most common etiological factor found in over 50% of the cases), a deformed first rib or a poorly treated clavicular fracture. The prevalence of traumatic and iatrogenic factors (subclavian catheters and pacemakers) is increasing with time. [4],[5],[6]

The symptoms of arterial TES are related to microembolisation into upper extremity arte­rial vessels and subclavian artery stenosis. This late condition can lead to ischemia of the extremity, ranging from Reynaud syndrome to the loss of the extremity.

For the diagnostic approach of TES, clinical examination is usually not informative. Conge­nital or acquired bone deformities can be seen in the X-rays. CT and magnetic resonance angiography scans as well as subtractive digi­tal angiography may be informative in detec­ting lesions of bone structures, blood vessels and soft tissues of the area. The diagnostic method of reference is the digital arteriography. Other supplementary methods are the electromyogram and evoked potentials.

Specific therapy of TES includes surgical correction of the congenital/acquired bone or soft tissue deformities. [7],[8] In the vascular le­sions, heparinization and infusion of thrombolytic agents are essential. During the last two decades, interventional radiology (angioplasty, intraluminal stents, etc.) has offered valuable solutions for the arterial and venous TES. [9],[10] Supportive measures that may offer sympto­matic relief can be introduced. Physiotherapy and treatment with analgesics (opioids and non-opioids, non-steroidal anti-inflammatory substances), antidepressants (tricyclic, selec­tive serotonin reuptake inhibitors) as well as anticonvulsants (gabapentin) in combination with complex vitamin Β tablets are considered the most common supportive measures for this group of patients.

In the literature, the perforation of subclavian artery during the placement of a jugular central catheter for dialysis has been reported, [11],[12] but, to our knowledge of the accessible literature, there is only one reported case of TES due to subclavian artery pseudoaneurism post-inser­tion of an internal jugular catheter. [13]

Because of the ever increasing number of hemodialysis patients receiving dialysis treat­ment through central catheters and taking into consideration the safer profile of jugular cathe­ters compared with subclavian catheters, we must bear in mind the possibility of compli­cations such as the one that was described in this report. Delays in diagnosis and treatment of vascular TES may lead to severe conse­quences, and alertness for this kind of compli­cation is essential.


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