Traumaticthrombosis artery in the neck - BMJJ. TrevorHughesandBettyBrownell:....4 i.:C. FIG. 1. Case...

J. Neurol. Neurosurg. Psychiat., 1968, 31, 307-314

Traumatic thrombosis of the internal carotidartery in the neck

J. TREVOR HUGHES AND BETTY BROWNELL

From the Department of Neuropathology, Radcliffe Infirmary, Oxford

Hugh Cairns (1942), in describing the vascularaspects of head injuries, referred to damage to theinternal carotid artery, which might be injuredeither in the neck or within the skull in connexionwith fractures of the base. Trauma to the internalcarotid artery in the neck can produce thrombosisor embolism, and this may result in ischaemia orinfarction affecting the corresponding cerebralhemisphere. Cases of this nature may be caused by adirect penetrating wound involving the artery in theneck, but also may be associated with an injurywhich has not breached the skin of the neck. Theclinical importance of this syndrome is that the effectsof the carotid artery obstruction may be falselyattributed to direct injury to the brain or spinalcord. We present here three cases of this type inwhich the nature of the injury and the subsequentcerebral infarction were studied clinically and atnecropsy. In case 1 there was a penetrating neckwound, while in cases 2 and 3 the carotid arteryhad been injured without a skin laceration.

CASE 1

This pensioner (E.F., A. 1728), at the age of 21 inSeptember 1914, enlisted in the British Army and joinedthe Rifle Brigade. On 3 June 1916 he was wounded atYpres in Belgium, receiving a wound in the left sideof the neck from a bullet which caused a left facial palsy,deafness in the left ear, and paralysis of the right armand leg. The bullet was removed at a field hospital inFrance, and he was evacuated to England on 15 June1916, by which time the left-sided deafness and facialweakness had recovered. He had also regained themovement of the right leg, but the right arm remainedcompletely paralysed and anaesthetic. The neck woundhealed and he was discharged from the Army on16 October 1916. He was awarded a disability pensionin 1918, when he was found to have a 3 in. scar on theleft side of the neck, slight weakness of the left side ofthe face, and weakness of the left stemomastoid andtrapezius. There was wasting of the muscles of the rightarm with some loss of co-ordination. He was consideredat this time to have had a contusion affecting the leftside of the medulla and the spinal cord. A radiograph

showed no evidence of a bony injury or of a foreignbody in the region of the old wound in the left side of theneck. Subsequently he obtained employment and heremained at work until 1945. In December 1951 he wasfound to have diabetes mellitus of a mild type whichwas controlled with regular insulin therapy. He was thenunable to work because of general disability and theparalysis of his right hand, some weakness of the rightleg having also appeared at this time. Forsometimehehadcomplained of angina, and this further limited his exertioncapacity. On 5 March 1953, a medical report indicatedthat he had an upper motor neurone weakness of boththe right arm and the right leg, with an increase in tendonreflexes on the right side, and a right extensor plantarresponse. There was also some impairment of positionsense on the right side. He had some arthritis of hisleft shoulder causing him pain, and electrocardiographicevidence of an anterior myocardial infarction. His bloodpressure was 130/100. His final medical examination bythe Ministry of Pensions took place on 24 August 1965when he complained of forgetfulness, lack of concentra-tion, irritability, and occasional headaches. His limbparesis now prevented him from walking more than afew yards. His neurological state was unchanged, exceptthat he had slight bilateral deafness of the conductiontype. His last admission was to a hospital in Carshaltonwhere he died on 25 November 1965. A necropsy was per-formed and the fixed brain was sent to us by theDepartment of Pathology, St. Helier Group of Hospitals,Carshalton, Surrey.

NECROPSY FINDINGS

Fixed Brain The external examination showed an oldsoftening in the left cerebral hemisphere and a recenthaemorrhagic infarct on the right side. At the base of thebrain, the vessels of the circle of Willis were of normalpattern, but showed moderately severe atheroma,particularly affecting the internal carotid arteries.The brain in coronal slices showed two vascular lesions,

one in each hemisphere (Fig. 1). On the left side, therewas a very old vascular softening, involving most of theterritory of the left middle cerebral artery. What remainedwas a cavity in the central part of the hemisphere,communicating with the body of the lateral ventricle,and lined by a mixture of ependyma, meninges, and somefibrous tissue. Branches of the left middle cerebral arterycould be seen cut across, but no occluded vessels were

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FIG. 1. Case 1. Posterior aspect of a coronal slice of thecerebrum at the level of the third ventricle. On the left sidethere is a cavity from an old vascular softening in theterritory of the middle cerebral artery. There is acuteinfarction on the right side. x 04.

visible. This old vascular lesion probably dated from theinjury in the first world war, but was clearly an oldinfarction and there was no evidence of a cerebraltraumatic lesion. The thalamus on the left side wasconsiderably smaller than that on the right, due tosecondary degeneration. The corpus callosum had alsosuffered atrophic degeneration and was very thin. Thelesion in the right hemisphere was a recent haemorrhagicinfarct, involving the territory supplied by the distalbranches of the right middle cerebral artery. The onlyabnormality in the brain-stem was that the left pyramidwas shrunken and grey. The cerebellum was normal.

In histological sections, the old infarct on the leftside was seen as a large astrocytic glial scar, involvingcortex and white matter by total destruction of neuronecell bodies, axons, and myelin tubes (Fig. 2). On the rightside there was recent haemorrhagic infarction involvingthe cerebral cortex and white matter. Both these infarctswere in the territories of the middle cerebral arteries, butno occlusions were visible in the branches of thesevessels. Sections of the midbrain, pons, and medullashowed Wallerian degeneration in the left pyramidaltract.

CASE 2

This 40-year-old motor cyclist (A.K., N.8508) wasadmitted to hospital 45 minutes after a road accident.He was alert and orientated, and showed no abnormalneurological signs. There were cuts over the left side ofthe face, a fracture of the right malar bone, and tender-ness over the angles of the jaw, and over the stemum.Twelve hours after the accident he was found to have ahemiplegia which had probably developed during sleep.On examination, he was drowsy and had a left hemiplegiaand hemianaesthesia, complete in the face and arm,

ir .

FIG. 2. Celloidin-embedded section, stainedfor myelin, ofleft cerebral hemisphere ofcase 1. Kultschitzky-Pal, x 1.

but incomplete in the lower limb. There was also a lefthomonymous hemianopia with defective conjugatemovement of the eyes to the left. His blood pressurewas 115/70, his pulse 66, and his retinal artery pressureon the left was 90/50 whereas on the right it was 20/10.Carotid pulsation appeared equal on both sides. Thediagnosis of right carotid thrombosis was suspected fromthe time of his readmission, because of the profoundhemisphere signs and the relative preservation of hisconscious level. The retinal artery pressure readingssupported this diagnosis, which was confirmed bybilateral carotid angiography. On the right side therewas a complete obstruction of the intemal carotidartery halfway along its course, and the left cerebralarteriogram showed a minimal displacement of themidline vessels to the left with only a very slight amountof filling of the right anterior cerebral artery. There wasa little filling of the branches of the right pericallosalartery. Twenty-four hours after the accident the rightcarotid arteries were explored. A small opening was madeat the bifurcation and there was virtually no backbleeding from the right internal carotid artery, andpulsation could be felt foronly 1 I in. upwards.Acorkscrewreamer was then passed up the internal carotid artery andthe clot was removed, after which there was a suddenpowerful jet of back bleeding. The operation was doneunder heparin therapy and this was continued for a

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Traumatic thrombosis of the internal carotid artery in the neck

further 24 hours while oral Dindevan was started. Fourhours after the operation he had recovered from theanaesthetic and was again alert and fully orientated,but with unchanged neurological signs. His generalcondition was maintained up to 17 hours after theoperation when he became drowsy, restless, and unableto speak more than a few words. His respiration appearedobstructed and a tracheostomy was performed, butwithout improvement. He continued to deteriorate and48 hours after his accident his right pupil became fixedand dilated. In spite of treatment with intravenous ureaand cooling to 90°F he became decerebrate and remainedso, developing a profound metabolic disturbance whichended in his death six days after the accident.

NECROPSY FINDINGS In addition to the lacerations andfractures described in the clinical report, a transversefracture across the middle of the sternum was found, withunderlying haemorrhage into the anterior mediastinum.The skull was intact apart from the fracture of theright malar bone. Other abnormalities were confinedto the cardiovascular and nervous systems. The heartappeared normal. The aorta and major arteries were mildlyaffected by atheroma in the form of small plaqueswithout ulceration or calcification. Linear deposits ofthis nature were present in both common carotidarteries, but not in their internal or external branches.Both common carotid arteries had been entered byangiogram needles which had not caused any untowardlocal effect, and the left internal carotid artery containedmerely post-mortem thrombus.

Right internal carotid artery The right internalcarotid artery was embedded in an operative haematoma,4 cm in diameter and 10 cm in length, which had spreadbetween the muscles of the neck and around the rightlobe of the thyroid. A sutured incision extended for1-5 cm upwards from the carotid bifurcation. Situated2-5 cm above the bifurcation, on the anterior wall ofthe vessel, was a transverse intimal tear 0 4 x 0 4 cm inarea, with attached blood clot extending into the vesselwall (Fig. 3). Apart from this clot, there was no thrombusremaining in the lumen of thevessel. Histological sectionsof the artery in the region of the intimal tear showedthat this extended into the tunica media, where therewas a haematoma of moderate size (Fig. 4).Fixed brain The brain weighed 1,800 g and there was

swelling of the right hemisphere causing subtentorialherniation of the right uncus. The vessels of the circleof Willis were normal. Coronal slices of the brain showedrecent softening in the territory of the right middlecerebral artery, with sparing of the anterior and posteriorcerebral territories on that side, and no signs of infarctionin the left hemisphere (Fig. 5). The infarction was mostintense in the centre of the cerebral hemisphere, and thiswas attributed to the complete blockage of the rightlateral striate arteries at their origin. The brain-stemshowed considerable lateral compression, with midlinebruising, due to herniation of the right uncus. A histo-logical section of the region of the right insula showedchanges of acute infarction, and in the same section, abranch of the middle cerebral artery was seen to bepartially blocked by organizing blood clot. This clot

X L ALMM 1 ::

FIG. 3. Case 2. Right carotid arteries opened and viewedfrom the posterior aspect. There is an intimal tear in theinternal carotid artery 2 5 cm above the bifurcation.x 3.

was irregular in shape and was not attached to the vesselwall, and for these reasons it was considered to be anembolus.

CASE 3

A 29-year-old man (D.R., N. 8981) was admitted tohospital 30 minutes after a car accident. He was fullyconscious and orientated, with no abnormal neurologicalsigns, and complained only of pain in the chest onbreathing. There was a small cut at the angle of the leftmandible, but radiographs revealed no fracture of jawor skull. Thirty-two hours after the injury he was foundto have a right hemiplegia and hemianaesthesia, righthomonymous hemianopia, and an expressive aphasia.A left carotid angiogram, performed 37 hours after theaccident, showed a marked irregular narrowing of theinternal carotid artery in the neck with no contrastmedium reaching the cerebral circulation. The rightcarotid angiogram showed a moderate shift of the

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FIG. 5. Case 2. Posterior aspect of a coronal slice of thecerebrum at the level of the optic chiasm. There is recentsoftening in the whole territory of the right middle cerebralartery. Half life size.

FIG. 4. Case 2. Longitudinal section of the internalcarotid artery through the intimal tear. There is a largehaematoma in the tunica media beneath the intimal breach.Van Gieson and elastic, x 10.

midline vessels to the right with very little spontaneouscross circulation. He held his own for another five hoursbut then deteriorated, becoming decerebrate 42 hoursafter his accident. In spite of a tracheostomy, intravenousurea, and cooling to 900F, his pupils became fixed anddilated and he died 72 hours after the accident.

NECROPSY FINDINGS A necropsy was carried out 48 hoursafter death. Lacerations and bruising were seen asdescribed in the clinical report, and fractures werepresent through the right third and fourth costochondraljunctions, and transversely through the middle of thesternum. There was haemorrhage into the anteriormediastinum, with retropharyngeal haemorrhage andoedema of the pharynx and glottis. There was contusionof the right lung near the hilum, and both lungs showedbasal collapse and scattered subpleural haemorrhages.The heart, aorta, and major arteries, with the exceptionof the internal carotid arteries, were normal, withnegligible atheroma.

Left internal carotid artery The left internal carotidartery contained grey thrombus commencing at a point4 cm above the origin of the vessel, and extendingupwards for about 2 cm. Sections through the lower endof the thrombus showed fresh haemorrhage surroundingthe artery, intimal damage with a polymorph reaction,and haemorrhage in the tunica media which encircledhalf of the lumen. The thrombus showed earlyorganization.

Fixed brain The brain weighed 1,460 g, and wasswollen, with tentorial grooving of both unci andprominence of the cerebellar tonsils. The circle of Williswas abnormal in that the left posterior cerebral arterywas mainly fed from the internal carotid artery througha large posterior communicating artery. The terminalportion of the left internal carotid artery containedgrey ante-mortem thrombus which, from its position,was considered to be an embolus lodging at the bifurca-tion of the artery.Coronal slices showed the cause of the cerebral swelling

to be recent infarction of the whole of the territories ofthe left middle and posterior cerebral arteries (Fig. 6).The anterior cerebral territory was spared, this regionbeing fed from the right side via the anterior com-municating artery. In the centre of the left hemispherewas a region of haemorrhagic extravasation situated inthe territory of the left lateral striate arteries, whichwere directly obstructed by the embolus at their origin.The brain-stem showed lateral compression due to thesubtentorial herniation. In histological sections of theleft cerebral hemisphere, changes of infarction wereseen in the middle and posterior cerebral territories,with more severe infarction centrally in the regionsupplied by the lateral striate arteries. Ante-mortemthrombus (Fig. 7) was found in a main branch of theleft middle cerebral artery in the Sylvian fissure.

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of a middle cerebral artery and this, in Case 1, tookthe form of an old healed cavity. In Cases 2 and 3the arterial obstruction was due to the lodgementof an embolus in the terminal part of the internalcarotid and the origin in the middle cerebral artery,and this had produced the picture of softening inthe middle cerebral territory with intense infarctionin the territory of the lateral striate arteries.

REVIEW OF LITERATURE

Thrombosis of the carotid artery due to a penetratingwound of the neck is a complication which is seenmost frequently when large numbers of battlecasualties are dealt with. In the first world war,Makins (1919) was familiar with this type of caseand Caldwell and Hadden (1948) saw eight similarcases in the second world war. The latter, who weretreating casualties in Europe at the 5th EvacuationHospital, found these eight cases among over25,000 battle casualties treated during a period of15 months. Of these eight cases, five were confirmedby necropsy examination of the carotid arteries,which contained ante-mortem thrombus. In severalcases, the thrombosis extended throughout thecarotid artery as far as its termination. The localdamage to the carotid artery in the neck was usuallyextensive and intimal tears were found whichsometimes showed separation of the intima andcurling up of the free edge into the more distalpart of the damaged artery. Ecker (1945), in report-ing his experience with second world war casu-alties, makes the point that penetrating woundsin which a high-velocity missile does not actuallystrike the internal carotid artery may yet inducethrombosis from the indirect trauma of the missilepassing the artery. These cases of the type describedby Ecker (1945) form a connecting link with thesecond group that we shall now review.

This group, in which the carotid artery is injuredindirectly, and where there is no penetrating woundin the neck, is less well recognized. The first caseof this nature in the literature is probably that ofVerneuil (1872). In this case, after a railway accidentwith multiple injuries, left cerebral infarction wascaused by thrombosis of the left internal carotidartery. There was no laceration or bruising of theneck but the outline of the left sternomastoid musclewas obscured by swelling. At necropsy, thrombuswas found in the left internal carotid artery 2 cmdistal to the carotid bifurcation. The external wallof the vessel was intact but the intima and the mediawere torn. Verneuil suggested that a suddenwrenching of the neck might have caused this tear.A similar case was reported by Greco (1935) whosepatient, a 23-year-old butcher, was knocked from

his bicycle, receiving cuts to his chin and lower lipwith tenderness of his left mandible. He remountedand rode home where, 16 hours after his accident,he developed a right hemiplegia which led to hisdeath. Necropsy showed a transverse laceration ofthe tunica intima and media of the left internalcarotid artery, which contained ante-mortemthrombus. Subsequently, further cases in whichnecropsy was performed have been added to thesetwo early cases and the literature was reviewed byMurray (1957), who added one case to a review ofeight cases with recorded necropsy findings. Murraydid not mention a case by Egas Moniz (1941), andsubsequently a further case was added by Toakleyand McCaffrey (1965).

In all these cases, there has been some type ofviolent accident involving the head or the neck andsometimes the clavicle or upper thoracic cage. Therehas usually been an interval of several hours beforethe development of the neurological syndrome.In the more recent reports angiography, whenperformed, has shown a blocked internal carotidartery. The necropsy findings have been, in themajority of reports, very similar. The affectedcerebral hemisphere has contained a very largeinfarct in the appropriate arterial territory. Thecarotid artery concerned has usually shown atear affecting the tunica intima and tunica mediabut not involving the adventitial coat of the artery.Ante-mortem thrombus has always been demon-strated within the injured vessel, and has usuallybeen confined to the injured internal carotid artery.

COMMENT

Three points of interest merit further discussion.

CLINICAL RECOGNITION OF THE SYNDROME Theclinical features of this syndrome are important indistinguishing it from the more common case ofhead injury with direct cerebral damage. As we havementioned earlier, the external injuries have beenremarkably similar in many of the cases. It hasalso been possible to recognize the syndrome fromthe spectrum of the neurological signs and theirmode of onset. The diagnostic features are the rapidonset of a hemiplegia with the relative preservationof the level of consciousness, and the absence, atleast initially, of signs of cerebral compression.Confirming signs are the absence of carotid pulsationand the findings on ophthalmodynamometry.Bilateral angiography will demonstrate the originalintravascular thrombosis in the internal carotidartery in the neck. This procedure may also help inshowing a subsequent embolus in the middle cerebral

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artery and the amount of cross-filling from the otherside.

MECHANISM OF INJURY In cases such as Case 1,in which there is a direct penetrating wound injuringthe carotid artery, the mechanism of the injury isrelatively simple, and no elaborate theories arerequired to explain why there is thrombosis in theinjured artery. The sequel of thrombosis followingtrauma is similar to that seen in other arteries.In this type of injury the trauma of the close passageof a high velocity missile may cause thrombosis in avessel which is not directly struck.

Cases 2 and 3 belong to the second group, inwhich the carotid artery is injured indirectly withouta penetrating wound in the neck. In both casesthere are clues in the clinical and the pathologicalexaminations to the mechanism of the injury.There was evidence of trauma to the chin and angleof the jaw, and of injury to the sternum, which wasfound to be transversely fractured in both cases.These cases may be compared with others in whichfractures of the thoracic cage were found. If onevisualizes an injury in which there is a blow to theangle of the jaw with the head being thrown back-wards, anda simultaneous injury totheanterior thoraxwith a fracture of the sternum, it seems clear thatthere is a mechanism involved in which the carotidarteries on one side could be forcibly stretched.The necropsy findings in the affected carotid arterywere consistent with a stretching injury, since inboth these cases there was a tear of the intima andmedia, but no damage to the adventitia. We havediscussed in the review of the literature howfrequently such findings have been noted in casesof indirect trauma to the carotid artery. We haveconducted experiments on cadavers and these showthat when the head is thrust forcibly backwards andto one side, the carotid arteries on the oppositeside are stretched. The effect is magnified if the stern-um is sawn through transversely-simulating fracture-when pressure on the lower part of the sternumtethers the innominate artery.The way in which this tear of the tunica intima

and media will cause thrombosis requires someconsideration. It is not certain whether an intimaltear is necessarily important, and Poole, Sanders,and Florey (1958) in their experiments to removethe tunica intima of the aorta of rabbits, found thatif damage to the other coats of the vessel wasavoided thrombosis rarely occurred. Honour andMitchell (1963) found that damage to the tunicamedia was the more important feature, and sug-gested that a chemical stimulus was exerted bysome component of damaged smooth muscle. Itmay be that this is so, and that the intimal tear is

of some importance in allowing this substanceeasy access to the arterial lumen where it will causethe formation of a thrombus.

THE CAUSE OF THE CEREBRAL INFARCTION Someexplanation is required as to why the obstructionof one internal carotid artery results in cerebralinfarction. Experience relevant to this problem hasbeen gained from the treatment, by surgical ligationof a carotid artery, of subarachnoid haemorrhagedue to intracranial aneurysm. It is relatively un-common for patients with healthy arteries to developa cerebral infarction following ligation of theinternal carotid artery in the neck, provided thereis an adequate anastomotic circulation around thecircle of Willis. In these circumstances the cerebralhemisphere on the side of the ligation will usuallyreceive an adequate blood supply from the otherinternal carotid artery or the vertebral arteries.

In both Cases 2 and 3 the evidence at necropsyshowed that the most significant obstruction to thecerebral circulation was situated in the middlecerebral artery-distal to the anastomosis of thecircle of Willis-and was caused by an embolus(Fig. 8). Obstruction at this particular point willalmost always cause infarction of the correspondingmiddle cerebral artery territory. The additionalfeature seen in cases of embolus at this particularpoint is severe haemorrhagic infarction in theterritory of the lateral striate arteries, which arisefrom the middle cerebral artery at this point. A

A B

Li P ANT. CMID C.

MBOLUS

POST. C

THROMBUS

INT.CAR.

FIG. 8. Diagram ofmajor arteries supplying the brain. InFig. 8A, the proximal obstruction of the internal carotidartery does not usually cause cerebral infarction, becauseof the anastomosis provided by the circle of Willis. InFig. 8B, the obstruction is more distal and there will beinfarction in the territory of the middle cerebral artery.

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feature of both cases 2 and 3 was that, superimposedon the rather pale infarction in the middle cerebralterritory, was an intense haemorrhagic infarction ofthe central territory of the lateral striate arteries.

SUMMARY

Three cases of cerebral infarction due to traumaticinternal carotid thrombosis in the neck aredescribed. In the first case, the mechanism of theinjury was a direct penetrating wound, while in thesubsequent two cases, indirect trauma was respon-sible. The mechanism of the injury to the internalcarotid artery in these two last-mentioned cases isdiscussed, and evidence is presented that thecerebral infarction occurred as a result of embolismfrom the proximal into the distal carotid circulation.The recognition of this clinical syndrome isdiscussed.

Dr. Brownell is receiving a grant from the National Fundfor Research into Poliomyelitis and other CripplingDiseases.The authors thank the Department of Pathology,St. Helier Group of Hospitals, Carshalton for Case 1,

and the consultants of the United Oxford Hospitals forthe use of their clinical records of Cases 2 and 3.

REFERENCES

Cairns, H. (1942). The vascular aspects of head injuries. Lisboa med.,19, 375-410.

Caldwell, H. W., and Hadden, F. C. (1948). Carotid artery thrombosis:report of eight cases due to trauma. Ann. inter. Med., 28,1132-1142.

Ecker, A. D. (1945). Spasm of the internal carotid artery. J. Neurosurg.,2, 479-484.

Egas Moniz, A. (1941). Trombosis y Otras Obstrucciones de lasCarotidas. Salvat Editores, Barcelona.

Greco, T. (1935). Le trombesi post-traumatiche della carotide. Arch.ital. Chir., 39, 757-784.

Honour, A. J., and Mitchell, J. R. A. (1963). Platelet clumping invivo. Nature (Lond.), 197, 1019-1020.

Makins, G. H. (1919). On Gunshot Injuries to the Blood Vessels.John Wright, Bristol.

Murray, D. S. (1957). Post-traumatic thrombosis of the internalcarotid and vertebral arteries after non-penetrating injuries ofthe neck. Brit. J. Surg., 44, 556-561.

Poole, J. C. F., Sanders, A. G., and Florey, H. W. (1958). Theregeneration of aortic endothelium. J. Path. Bact., 75, 133-143.

Toakley, G., and McCaffrey, J. (1965). Traumatic thrombosis of theinternal carotid artery. Aust. N.Z. J. Surg., 34, 261-264.

Verneuil, A. A. S. (1872). Contusions multiples, d6fire violent,h6miplegie a droite, signes de compression c6r6brale. Mort lecinquieme jour. Rupture complete des tuniques profondesde la carotide interne gauche au cou. Oblit6ration des vaisseauxau point l6se par un caillot qui remonte jusqu'aux dernieresbranches de l'arttre sylvienne: ramollissement c6r6bral6tendu a la presque totalit6 du lobe moyen, Bull. Acad. Med.(Paris) (2nd ser.), 1, 46-56.

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