In order to evaluate the possibility of compression of axillar artery by medial and lateral fascicle of brachial plexus, authors performed 26 axillar dissections on cadavers. Second part included analysis of 24 selective angiograms of axillar artery of patients with diagnosis of TOS. Third part included the use of modified hyperabduction test for determination of vascular bruit as safe test for diagnosis of axillar compression. Macroscopic changes of axillar artery by compression of medial and lateral fascicle of brachial plexus were present in 11.5%. Specific angiographic horizontal spike-shaped stop of contrast behind the surgical neck of humerus was present in 12.5%. Use of modified hyperabduction test revealed vascular bruit 29.5%. Specific relation of axillar artery and medial and lateral fascicle of brachial plexus revealed another possible etiologic factor in hyperabduction syndrome as a part of TOS. Use of modified hyperabduction test revealed subclinical phase of possible syndrome

Goran Augustin

Mate Majerović

Željko Jelinčić

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Coll. Antropol. 28 (2004) 2: 809–815UDC 611.97:616-001.35Original scientific paperAxillar Compression Syndrome:Anatomical and Clinical StudyMate Majerovi}, @eljko Jelin~i} and Goran AugustinDepartment of Surgery, Division of Abdominal Surgery, University Hospital Center, Zagreb,CroatiaA B S T R A C TIn order to evaluate the possibility of compression of axillar artery by medial and lat-eral fascicle of brachial plexus, authors performed 26 axillar dissections on cadavers.Second part included analysis of 24 selective angiograms of axillar artery of patientswith diagnosis of TOS. Third part included the use of modified hyperabduction test fordetermination of vascular bruit as safe test for diagnosis of axillar compression. Macro-scopic changes of axillar artery by compression of medial and lateral fascicle of brachialplexus were present in 11.5%. Specific angiographic horizontal spike-shaped stop of con-trast behind the surgical neck of humerus was present in 12.5%. Use of modified hype-rabduction test revealed vascular bruit 29.5%. Specific relation of axillar artery andmedial and lateral fascicle of brachial plexus revealed another possible etiologic factorin hyperabduction syndrome as a part of TOS. Use of modified hyperabduction test re-vealed subclinical phase of possible syndrome.Key words: Thoracic outlet syndrome (TOS), axillar compression syndrome, arte-rial compression, brachial plexus, hyperabduction test, scalenotomyIntroductionThoracic outlet syndrome (TOS) is thepreferred term for those syndromes thatresult from compression of the neurovas-cular structures to the upper extremities.The syndrome is caused by compressionof the brachial plexus or sublavian-axilla-ry artery and/or vein in the region be-tween the thoracic outlet and the inser-tion of the pectoralis minor muscle ontothe coracoid process. Many syndromesare included in the term thoracic outletsyndrome, such as the cervical rib syn-drome1, scalenus anterior syndrome, hy-perabduction syndrome, costoclavicularsyndrome and the first thoracic rib syn-drome. Syndromes that cause similar cli-nical manifestations include scapulocos-tal syndrome, suprascapular nerve syn-drome and syndrome of lateral axillarhiatus2,3.809Received for publication December 10, 2003Clinical evaluation is started with pro-vocative tests of arterial compression4.Symptoms may arise from neural, vas-cular, or combined neural and vascularcompression, with neural compressioncausing 90% to 95% of these symptoms5.The reason for investigating furthercause of TOS was guided by the results ofoperative therapy of TOS. Using all possi-ble operative modalities and techniques,there was significant percentage of pa-tients with persisting symptoms rangingfrom 8% to 66%6,7,8. There are two possi-ble answers: one is that current operativeprocedures are not perfected yet, and an-other that unknown causes of TOS arepresent that have not been defined yet.Accidentaly, we found interesting rela-tionship between axillar artery and plexusbrachialis in the region where medial andlateral fascicle cross over the axillar arte-ry to form median nerve. Lord et al. in1971. described the possibility of com-pression of axillar artery by median ner-ve9, but we did not found any objectivesigns, tests, diagnostic and therapeuticmodalities for this type of compression inthe medical literature.Materials and MethodsResearch was divided into three parts.First part included anatomical dissectionof axillar regions of 26 cadavers randomlychosen, with preservation of all structu-res in axilla. All cadavers were fresh, dis-sected in the Department of PathologyKBC Zagreb 3–6 hours after death deter-mination (legaly, cadaver must be in thedepartment where death occured for 2hours and then it is transported to depar-tment of pathology). The dissected cadav-ers did not have history of vascular com-pression and other vascular diseases intheir medical files. Axillar dissections we-re unilateral (13 left and 13 right). We fo-cused on relationship between axillar ar-tery and plexus brachialis in the regionwhere medial and lateral fascicle crossover the axillar artery. We analysed neu-rovascular relationships in functional po-sitions of upper extremity. These positio-ns included: full adduction, 90° abductionand maximal elevation of 180°.Second part included clinical analysisof patients with diagnosis of TOS andanalysis of 24 selective angiograms ofaxillar artery in patients with suspectedTOS. Between 1995 and 1999 we exami-ned 109 patients with symptoms of TOS.Thirty one of them were subsequently op-erated. All 24 selective angiograms wereindicated in subsequently operated pa-tients. Nineteen of these angiograms weretaken with upper extremity in maximalelevation of 180°. All operated patientswere clinically evaluated postoperatively(Table 1).Third part included the possibility ofexistence of physical signs of compressionof axillar artery by tensed medial and lat-eral fascicle that cross axillar artery inmaximal elevation. Physical examinationwas performed on 122 pupils in NursingSchool in Zagreb and included extendedhistory taking, inspection, palpation andauscultation of axillar region. Examina-810M. Majerovi} et al.: Axillar Compression Syndrome, Coll. Antropol. 28 (2004) 2: 809–815TABLE 1RESULTS AFTER SURGICAL PROCEDURES IN 31 OPERATED PATIENTSProcedure Excellent Good PoorScalenotomy 2 5 7Resection of the first rib with scalenotomy 1 3 5Transaxillar resection of the first rib 4 3 1tion was completed with the use of provo-cative test. Provocative test was hyperab-duction test introduced byWright in 194510that was modified for detecting eventualcompression site between axillar arteryand its crossing by medial and lateral fas-cicle.Modified hyperabduction test is per-formed with patient sitting straight withhead looking straight forward and upperextremity fully adducted. In this positionauscultation is performed in supraclavi-cular and infraclavicular region. Auscul-tation is repeated with patient takingdeep breath. Now patient performes 90°abduction and auscultations in the samepositions are repeated. With this ma-noeuvre more proximal compression isexcluded if exists. Next step is patientsmaximal elevation of the upper extremityin supination. In this position, as in pre-vious, simultaneous palpation of radialartery with auscultation of anterior andupper border of axilla is performed. Thesame examination can be performedthrough whole process of hand elevationto its maximal elevation. Decrease of pal-pabile radial pulse or its absence and de-tection of localization and intensity ofvascular bruit, is reliable sign of the height(localization) and the degree of compres-sion of axillary artery (Fig. 1).ResultsDissection of axillar regions of 26 ca-davers, randomly chosen, with special at-tention on region of crossing of axillar ar-tery by medial and lateral fascicle revea-led interesting biomechanical relations.Nervous fibers of brachial plexus glideover the axillar artery in the range of fulladduction to 90° abduction of upper ex-tremity, and finally, in the maximal ele-vation, axillar artery is compressed be-tween these nervous fibers. Anatomicalrelations were similar, only differencewas level of connection of medial and lat-eral fascicle into median nerve, which dif-fered in 1–2 cm.In 3 of 26 cases (11.5%) of dissected ca-daveric axillar arteries, we found advan-ced atherosclerotic-stenotic changes oncrossing of medial and lateral fascicleover axillar artery. Another interestingmoment is that in these three cases withatherosclerotic-stenotic changes of axillarartery, signs of generalized atherosclero-sis were not present. In all three casestrophical changes of digits were present(Fig. 2), and in two of this three cases wefound poststenotic dilatation of axillar ar-tery (Fig. 3).Second part of investigation includedclinical analysis of 24 selective arteriog-rams of axillar artery. Stop of contrastwas evident in 9 cases (37.5%) in maxi-mal elevation of upper extremity. Anot-811M. Majerovi} et al.: Axillar Compression Syndrome, Coll. Antropol. 28 (2004) 2: 809–815Fig. 1. Modified hyperabduction test for detec-tion of localization of vascular bruit in axillarcompression syndrome.her crucial element is that stop of con-trast is observed on different levels ofsubclavian-axillar arterial segment (Tab-le 2). In three angiograms which showedstop of contrast behind surgical neck ofhumerus (12.5%), we found horizontalspike-shaped stop of contrast. Positionand shape correspond to anatomical siteof crossing of medial and lateral fascicleover axillar artery. On additional selecti-ve arteriograms in 90° abduction of upperextremity stop of contrast was not pres-ent. All three arteriograms of spike-sha-ped stop of contrast around surgical neckof humerus are seen on figure 4 (Fig. 4).Third part. Use of modified hyperab-duction test in 122 healthy female volun-teers showed results and distributionsummarized in table 3. Positive sign wasvascular bruit in anterior and upper bor-der of axilla where anatomical site ofcrossing of medial and lateral fascicleover axillar artery is located. The signwas positive in 36 of 122 cases (29.5%)(Table 3).DiscussionAnatomical structures in axilla cancompress either artery, vein, or nerves insome pathologic conditions because of in-terstructural incongruence11–13.The subject of this study are anatomi-cal relations between structures of axilla,namely nerves and axillar artery as acause of development of compression syn-812M. Majerovi} et al.: Axillar Compression Syndrome, Coll. Antropol. 28 (2004) 2: 809–815Fig. 2. Trophical changes of digits observed inthree cases with atherosclerotic-stenotic changesof axillar artery, without signs of generalized at-herosclerosis.Fig. 3. Poststenotic dilatation of axillar artery.Arrow points to the place where medial and la-teral fascicle unite and cross over axillar arte-ry. Poststenotic dilatation evident on the rightside of resected segment (arrowhead).TABLE 2LEVEL OF STOP OF CONTRAST ON 24SELECTIVE AXILLAR ARTERIOGRAMSLevel Number ofpatients%Did not occuredScalenus triangleCostoclavicular triangleHumeroscapular spaceSurgical neck of humerus1525*13*62.58.320.84.212.5*There was compression on two levels on sameangiogram in two patients and their resultsare in both costoclavicular triangle and behindsurgical neck of humerusTABLE 3VASCULAR BRUIT IN 122 HEALTHY FEMALEVOLUNTEERS IN ANTERIOR AND UPPERBORDER OF AXILLA DURING MODIFIEDHYPERABDUCTION TESTAxilla Positive test %Left 17 13.9Right 19 15.6Total 36 29.5drome. In normal state, when arm is infull adduction, medial and lateral fasciclesurround axillar artery and on the ante-rior surface of the artery they connect inthe shape of letter ''V'' to form mediannerve. Such anatomical relations of axil-lar artery and neural bundle predisposeto arterial compression in specific posi-tions of upper extremity.When the upper extremity is in maxi-mal elevation, neurovascular bundle be-comes tensed over the first rib, muscles ofthat region and ligamentous structures.Geometricaly, axillar artery travels lon-ger linear distance in cranial directionthan nervous fibers because of two rea-sons: first, nervous fibers are positionedabove the axillar artery, and second, ori-gin of nervous fibers of plexus brachialis(C5-Th1) is localized above the origin ofsubclavian artery. ''V'' formation of late-ral and medial fascicle above the axillarartery serve as fixation point of axillar ar-tery thus further decreasing its mobility(Fig. 5).In the process of arm abduction ner-vous fibers of brachial plexus glide overthe artery, and finally, in the maximal el-evation artery is compressed betweenthese nervous fibers, because, simply geo-metricaly, axillar artery travels longer li-near distance in cranial direction thannervous fibers. ''V'' formation of medialand lateral and fascicle serve as fixationpoint. Another element which contribute813M. Majerovi} et al.: Axillar Compression Syndrome, Coll. Antropol. 28 (2004) 2: 809–815Fig. 4. Spike-shaped stop of contrast (arrows)around surgical neck in anatomical positionwhere medial and lateral fascicle unite in 'V'shaped form to form median nerve when arm isin maximal elevation (note narrowing of con-trast in costoclaviclar space in figure 3C poin-ted with smaller arrow).Fig. 5. Anatomical relations between axillar ar-tery and medial and lateral fascicle of brachialplexus (see text for details).to this phenomenon is that arteries aresofter and more elastic that nerves. Prob-able pathophysiological processes on thesite of compression are the result of chro-nic irritation and include reparative pro-cesses: fibrous changes of arterial walland activation of sympathetic nervoussystem, with resulting atherosclerotic-ste-notic changes on crossing of medial andlateral fascicle over axillar artery. Finalchanges include hemodynamic disturban-ces with development of poststenotic dila-tation of axillar artery, mural thrombiand consecutive microembolisation of digi-tal arteries with subsequent trophicalchanges of digits. It was not possible tofind out if these cadavers had any clinicalsymptoms of upper extremity, but trophicalchanges of digits of involved upper extrem-ity made that asumption almost certain.Searching through literature thereare studies that define some structuresand conditions as a cause of compression.Wright10 described compression of axillarartery under the insertion of minor pecto-ral muscle to coracoid process, and Lord9described mutual compression of neuralbundle and axillar artery but withoutspecific localization and objective signs ofthis entity.In 36 of 122 healthy female volun-teers, presence of vascular bruit in ante-rior and upper part of axilla indicate thatthere is large number of potential candi-dates for the development of this syndromewhich may be termed fascicular compres-sion syndrome of axillar artery. Gergou-dis and Barnes14 concluded that significantarterial obstruction resulted from one ormore of provocative tests in healthy per-sons in 60% unilaterally and 33% bilater-ally. Rare symptomatology of this, rela-tivley frequent condition in ''healthy''population with predominant neurologicsimptoms is explained with the hypothe-sis that potential candidates subconsci-ously avoid movements that cause neuro-logic symptoms with painful sensations15.Modified hyperabduction test for de-termination of mutual compression of axil-lar artery and medial and lateral fasciclepoint that there is significant percentageof subclinical types of this syndrome (simp-tomless volunteers), which, with furtherprogression of the disease, may becomemanifest, or remain asymptomatic becau-se of subconscious avoidance of provocati-ve positions with subsequent ischaemia.ConclusionAfter anatomical dissections of cada-veric axilla, it was obvious that clinicalmanifestations and radiologic findingswere not the result of anatomic variati-ons, but specific functional relations ofaxillar artery and medial and lateral fas-cicle. Positive modified hyperabductiontest used for determination of mutualcompression of axillar artery and brac-hial plexus, confirms that these compo-nents, both vascular and neural are com-pressed, either mutualy, or by rigid struc-tures of the roof of axilla.Vascular bruit in the axilla in maxi-mal elevation of upper extremity withpoint of maximal loudness in the anteriorand upper part of axilla is evident sign ofaxillar artery compression by neural bun-dles of brachial plexus.Now, with possible new etiologic factorin TOS there is much more to be done. Ifangiographic diagnosis is evident there isa question of therapy of this fascicularcompression syndrome of axillar artery.Probably neurolysis or transposition ofaxillar artery will give some answers tothat question but it has to be evaluated inthe future.Abbrevations:TOS – thoracic outlet syndrome814M. Majerovi} et al.: Axillar Compression Syndrome, Coll. Antropol. 28 (2004) 2: 809–815R E F E R E N C E S1. LOVRENCIC-HUZJAN, A., V. DEMARIN, M.BOSNAR, V. VUKOVIC, S. PODOBNIK-SARKANJI,Coll. Antropol., 23 (1999) 175. — 2. KUTZ, J. E., E. B.ROWLAND JR., Hand. Clin., 9 (1993) 131. — 3. KA-RAS, S. E., Clin. Sports. Med. 9 (1990) 297. — 4. GIL-LARD, J., M. PEREZ-COUSIN, E. HACHULLA,Joint. Bone. Spine., 68 (2001) 416. — 5. HEMPEL, G.K., W. P. SHUTZE, J. F. ANDERSON, Ann. Vasc. Su-rg., 10 (1996) 456. — 6. STALLWORTH, J. M., G. J.QUINN, A. F. AIKEN, Ann. Surg., 185 (1977) 581. —7. AXELROD, D. A., M. C. PROCTOR, M. E. GEIS-SER, Vasc. Surg., 33 (2001) 1220. — 8. LANDRY, G.J., G. L. MONETA, L. M. TAYLOR JR., J. Vasc. Surg.,33 (2001) 312. — 9. LORD, J. W. JR., Ann. Surg., 173(1971) 700. — 10. WRIGHT, I. S., Am. Heart. J., 29(1945) 1. — 11. BRANNON, E. W. JR., J. WICK-STROM, Clin. Orthop., 51 (1967) 65. — 12. COCCIA,M. R., B. SATIANI. Curr. Surg., 41 (1984) 10. — 13.GILLIATT, R. W. Br. Med. J., 287 (1983) 764. — 14.GERGOUDIS, R., R. W. BARNES, Angiology, 31(1980) 538. — 15. DUNANT, J. H., H. J. HEHNE, E.F. GAUER, Thoraxchir. Vask. Chir., 23 (1975) 23.M. Majerovi}Department of Surgery, Division of Abdominal Surgery, University Hospital CenterZagreb, Ki{pati}eva 12, 10000 Zagreb, Croatiae-mail: mate.majerovic@zg.htnel.hrAKSILARNI KOMPRESIVNI SINDROM – ANATOMSKA I KLINI^KASTUDIJAS A @ E T A KAutori su proveli 26 sekcija na kadaverima da bi istra`ili mogu}nost kompresije ak-silarne arterije medijalnim i lateralnim snopom brahijalnog pleksusa. Drugi dio radasastojao se od analize 24 selektivna angiograma aksilarne arterije s dijagnosticiranimsindromom gornje aperture toraksa. Tre}i dio rada uklju~ivao je modificirani test hipe-rabdukcije s vaskularnim {umom kao siguran dijagnosti~ki test aksilarne kompresije.Makroskopske promjene aksilarne arterije zbog kompresije bile su prisutne u 11,5%.Posebno oblikovani horizontalno u{iljeni obris kontrasta iza kirur{kog vrata humeru-sa bio je prisutan u 12,5%. Kori{tenje hiperabdukcijskog testa pokazalo je {um u 29,5%.Veza izme|u aksilarne arterije i brahijalnog pleksusa otkrila je jo{ jedan mogu}i etio-lo{ki ~imbenik u hiperabdukcijskom sindromu kao dio sindroma gornje aperture torak-sa. Kori{tenje modificiranog hiperabdukcijskog testa ukazivalo je na subklini~ku fazumogu}eg sindroma.815M. Majerovi} et al.: Axillar Compression Syndrome, Coll. Antropol. 28 (2004) 2: 809–815

Axillar Compression Syndrome: Anatomical and Clinical Study

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