158 Injury 12, 158-160 Primedin GreatBritain

Traumatic aneurysm of the internal carotid artery and rupture of the duodenum following seat belt injury

Patrick Clarke

Neurosurgical Unit, Middlesbrough General Hospital

Malcolm Whittaker

Department of Surgery, The Friarage Hospital, Northallerton

Summary

Cerebral embolism, due to a traumatic aneurysm of the internal carotid artery, and a duodenal tear occurred in a young woman who was wearing a seat belt at the time of a motor car accident. The aneurysm was treated by proximal carotid ligation.

INTRODUCTION TRAUMATIC thrombosis of the internal carotid artery due to blunt injury to the neck is a well- recognized pathological and clinical entity. Aneurysm of this vessel at the level of the atlas followed by thromboembolism is, however, rare. In the case reported here, traumatic aneurysm of the internal carotid artery and a tear in the first part of the duodenum followed abrupt deceler- ation of a motor car. The patient was wearing an inertia seat belt with diagonal and transverse straps.

CASE REPORT On 20 December I977 a woman aged 22 years was in the front passenger seat of a car that collided with a stationary vehicle in thick fog while travelling at about 40 mph. Immediately after the impact, she was observed to be unconscious and to be leaning forward with her head acutely flexed over the diagonal strap of her seat belt, which was pressing on her neck just behind the angle of the mandible. Within two minutes she had recovered consciousness, and was able to step out of the car. At that time she mentioned that she had upper abdominal pain.

She was admitted to hospital. and five hours later

was noticed to have intermittent weakness of the right arm and leg together with dysphasia. Sixteen hours after injury she had right hemiplegia and aphasia and was unconscious, although the left arm and leg were moving vigorously. At the same time she had de- veloped signs of a ruptured intra-abdominal viscus.

Immediate laparotomy was performed under general anaesthesia, and a split through the anterior wall of the duodenum at the junction of its second and third parts was found. There was no evidence of surrounding contusion. The opening in the duodenum was closed by simple suture. It was considered that cerebral infarction was the probable cause of the neurological deficit. Rather than move her at that stage a distance of 25 miles to the neurosurgical centre for further investigation, burr hole exploration was carried out in the left temporal region in case an intracranial haematoma was present. No evidence of extradural or intradural haemorrhage was found. The patient’s neurological state steadily improved, and on IO January 1978 (3 weeks after injury), she was transferred to the neurosurgical centre. She was then fully conscious and orientated, and was able to walk unaided. There was moderate weakness of the right leg, and severe weakness of the right arm. In addition she had mild dysphasia, severe dyslexia and dysgraphia, acalculia, finger agnosia, right-left dis- orientation and inability to distinguish between heat and cold on the right side of the body, including the face. A left carotid angiogram on I 7 January 1978 (4 weeks after injury) (Fin. I) showed a posterior ftllina defect in the internal carotid artery at the level of the atlas with post-stenotic dilatation for a distance of 2 cm. The distal branches of the middle cerebral artery were poorly filled with contrast medium. On 22

Clarke ana Whittaker: Seat Belt Injury 159

b

Fig. 1. Left carotid arteriograms 28 days after injury. Posterior filling defect in internal carotid artery at level of atlas, and aneurysmal dilatation. Poor filling of distal branches of middle cerebral artery.

a

February 1978 (9 weeks after injury) the neurological deficit was slightly less marked, and a second carotid angiogram (Fig, 2) showed a smaller filling defect in the internal carotid artery but a persistent aneurysmal dilatation. It was considered that, because of the dangers of further aneurysmal enlargement and thromboembolism, proximal internal carotid ligation should be performed.

On 16 March 1978 (12 weeks after injury) the left internal carotid artery was exposed at its origin under local anaesthesia. The vessel was occluded with a Crile’s clamp for 30 minutes, during which time there was no increase in the neurological signs and the intra- arterial stump pressure was 100 mmHg. The artery was ligated in continuity with a double strand of number 1 linen thread, and the Crile’s clamp was removed. Apart from a slight increase in the muscle tone of the right arm and leg for 14 days, further progress was satisfactory, and the patient went home on 5 April 1978, having been in hospital for three and a half months.

On 3 August 1979 (20 months after injury) the patient’s condition was noted to have improved considerably. There was still marked weakness of the right arm and leg, but she could walk a mile. The patient had taught herself to write with her left hand. Speech was good, apart from a little nominal dysphasia. She was able to read slowly. There was impaired appreciation of heat on the right side of the body below the level of the clavicle. Her chief disability consisted of difficulty in memorizing facts that were new to her.

DISCUSSION In this case, injury to the anterolateral aspect of

the upper part of the neck was followed by the development of an internal carotid aneurysm and cerebra1 embolism. The first neurological evidence of this was present five hours after injury in the form of contralateral hemiparesis and dysphasia. The lesion of the artery was on the left, and the patient is right-handed. A filling defect in the artery at the proximal limit of the aneurysm indicates the probability of an intimal tear here with either adherent thrombus or subintimal dissection, or both. The combination of acute compression of the internal carotid artery between the diagonal strap of the seat belt and the transverse process of the atlas, together with the abrupt angulation of the artery during sudden flexion of the neck, is considered to have been the mechanism by which the vessel was injured.

Taylor and Lumley (1977) have reported the case of a 30-year-old man who developed right hemiparesis and dysphasia four years after a contusion of the left side of the neck. Carotid angiography showed a small aneurysm of the internal carotid artery at the level of the atlas. Spontaneous recovery from the stroke took place apart from speech hesitancy and facial weakness. Proximal internal carotid ligation was performed under local anaesthesia, and the patient has remained well.

Rittenhouse et al. (1972) reported a patient with a ruptured internal carotid aneurysm at the level of the tonsil. He was treated with a bovine

160 Injury: the British Journal of Accident Surgery Vol. 1 Z/No. 2

Fig. 2. Left carotid arteriograms 36 days after first arteriogram. Filling defect in internal carotid artery less marked, but aneurysm unchanged.

a

arterial heterograft between the common and internal carotid arteries. They reviewed the records in the English literature of 42 cases of resections of carotid aneurysms with restoration of arterial continuity. The rarity of aneurysmal rupture is emphasized by these authors, who noted that 5 of the 42 patients had hemiparesis, considered to be due to thromboembolism from the aneurysm. They concluded that resection of an aneurysm near the base of the skull is not possible, and in such a case carotid ligation is the only effective treatment.

Blunt injury of the internal carotid artery is a very rare cause of aneurysm. Most traumatic carotid aneurysms follow penetrating wounds. Winslow (1926) traced 106 cases of extracranial aneurysm of the internal carotid artery. Twenty- seven of these were due to trauma and, although some of the records were inadequate, it appeared likely that the injury in 26 cases was of the penetrating variety.

If internal carotid interruption is not tolerated during a trial period of occlusion, the possibility of an anastomosis between the superficial temporal and middle cerebral arteries, followed by another trial of internal carotid occlusion, might be considered (Yasargil, 1967).

The association of blunt injury to the first part of the duodenum with the carotid artery lesion is interesting, and suggests that the intestinal lesion was due to acute compression between the

transverse strap of the seat belt and the vertebral column in a patient who is of very slender build. The absence of any sign of contusion round the split in the duodenum may mean that the compressing force was transmitted to the contents of the intestine between a closed pyloric sphincter and the duodenojejunal flexure, result- ing in a bursting effect.

Acknowledgement We wish to express our thanks to Professor G. W. Taylor for information about his case.

REFERENCES Rittenhouse E. A., Radke H. M. and Sumner D. E.

(1972) Carotid artery aneurysm: review of the literature and report of a case with rupture into the oropharynx. Arch. Surx. 105,786.

Taylor G: W. and Lumley J. S. P. (1977) In: Kravenbiihl H. (ed.) Advances and Technical Standards in Neur&&r~ Vol. 4. Berlin, Springer- Verlag, p. 30.

Winslow N. (1926) Extracranial aneurysms of the internal carotid artery: historical analysis of the cases registered up until August 1st 1925. Arch. Surg. 13,689.

Yasargil M. G. (1967) Experimental small vessel surgery in the dog, including patching and grafting of cerebral vessels-and the formation of functional extra-intracranial shunts. In: Donaghv R. M. P. and Yasargil M. G. (ed.) .tficrowsculur Sur~ycr~~ St Louis, Mosby, p. 87.

Requetr, /iv rqwlnl, thou/d hc addretsed fc, Mr Patrick Clarke. Consultant Neurosurgeon. Mlddlesbrough General Hospital. Ayresome Green Lane, Middlesbrough. Cleveland.