British journal of Oral surgery (1973), II, 25-29 TRAUMATIC INTERNAL CAROTID ARTERY OCCLUSION FOLLOWING FRACTURE OF THE MANDIBLE ROBER TREGGIDEN~ B.D.S., F.D.S., R.C.S., GEOFFREY D. WOOD, B.D.S. and E. G. BASHA M.B., B.Ch. The Departments of Oral Surgery and Neurosurgery, Manchester, 8 Crumpsall Hospital, OCCLUSION of the internal carotid artery following closed injury to the neck is a rare occurrence, which leads to a variable hemiparesis, and dysphasia if the dominant hemisphere is affected. There is a latent period of up to 24 hours before the symptoms appear (Murray, 1957). The neurological deficit is maximal soon after onset and death may occur. In those patients who survive there is usually a gradual improvement in the condition but complete recovery is very rare. CASE REPORT The patient, a man of 28 years of age, was referred to Crumpsall Hospital Oral Surgery Unit from the Casualty Department of a nearby hospital. He had been assaulted 12 hours previously, being rendered unconscious for a short, undetermined period. On arrival at the unit he was fully conscious, co-operative, well orientated in time and space and he gave a clear history. His gait was stable. He had neither sensory nor motor dysplasia, but his speech was a little slurred due to his facial injury. There were no symptoms related to damage of cranial nerves, motor, sensory or co-ordinating systems. The patient had bilateral facial swelling (this being more pronounced over the left body and angle of the mandible), and soft tissue contusions localised to the left temporal and Sterno-mastoid areas. There was marked tenderness on palpation of both angles of the mandible. Palpation of the left angle gave a crepitant sensation, and the lower border of the mandible was felt to be impaired. There was left mental nerve anaesthesia. Intraoral examination revealed a mobile displaced lower left second molar and bone projecting into the mouth in this region. No other intra-oral soft tissue injury was detected. Neck movements were within normal limits and no tenderness was detected over the cervical spines. All cranial nerves were intact except for sensory loss in the distribution of the left mental nerve. No weakness was detected in the limbs, reflexes were bilaterally symmetrical and plantars were flexor. The various sensory modalities and his co-ordination were intact. Carotid pulsation was bilaterally symmetrical. No bruit was heard over the head and neck. Vital signs were within normal limits. Radiographs of the skull and facial bones (Figs. I, and 2) showed a fracture of both angles of the mandible. There was minimal displacement on the right side, but marked comminution and displacement on the left side with separation of a large triangular fragment. No fracture of the base or vault of the skull was seen. X-rays of the cervical spine in flexion and extension showed no abnormality. The patient was admitted for further management and observation. After a period of 12 hours the patient was noticed to be dysphasic and not moving his right limbs fully. A repeated neurological examination was undertaken immediately and l Present address: University Dental Hospital of Manchester, Manchester, IS. 25
26 BRITISH JOURNAL OF ORAL SURGERY FIG. I P.A. radiograph of mandible showing bilateral fracture. FIG. 2 Oblique lateral radiograph of left mandible.
TRAUMATIC INTERNAL CAROTID ARTERY OCCLUSION 27 showed that the patient now suffered from a gross sensory as well as motor dysphasia, although he looked alert. His pupils were equal and reacting well to light, but he had a right hemianopia. The right cornea1 reflex was impaired as well as sensation on the right side of the face. He had a right lower facial weakness. All other cranial nerves were intact. A gross right hemiparesis was noted involving the upper more than the lower limb, with exaggerated reflexes and a positive Babinski sign. He also had a right hyposthenia. Bilateral carotid pulsations were still normal and a carotid bruit was not detected. The lucid interval was rather long and the patient too conscious to have been suffering from an intracranial compressing haemorrhage. The possibility of an un- FIG. 3 FIG. 4 Fig. 3.-Left carotid angiogram showing occlusion of the left internal carotid artery. Fig. 4.-Right carotid angiogram showing degree of cross-circulation. observed Jacksonian fit and his present condition being attributable to Todd s paresis were considered. Vascular occlusion was thought to be the most probable diagnosis. However, to exclude the possiblity of a fit, an E.E.G. was performed and this showed low activity in the left hemisphere, which was more marked in the temporal and frontal regions. Angiography of the carotid system revealed complete occlusion of the left internal carotid artery about one inch above its origin (Fig. 3). The right carotid filled well and there was good cross circulation through the anterior communicating artery to the anterior cerebral artery (Fig. 4). A streak of contrast medium passed into the left middle cerebral artery, In view of this cross-circulation, it was decided to treat the patient conservatively and Decadron (8 mg. q.d.s) and papaverine (60 mg. q.d.s) were prescribed. The next day there was some recovery of his sensory and motor dysphasia, and he
28 BRITISH JOURNAL OF ORAL SURGERY could move his right leg more positively. One week later the patient was fit enough for reduction and fixation of his mandibular fracture. This was achieved by a lower border wire on the left side, cast metal splints and intermaxillary fixation. Within a month following injury marked progress had been made. He was able to walk with the aid of a stick; there was considerable improvement in the tone and action of his facial muscles and his speech was fully understandable though a little halting. However, his right arm remained in a state of complete flaccid paralysis. DISCUSSION A fractured mandible is a fairly common result of facial trauma. Of 188 cases of fracture of the facial skeleton (excluding nasal and dento-alveolar fractures) treated at Crumpsall Hospital in 1972, 64 per cent had mandibular fractures. Rowe and Killey s 1952 survey gave this figure as 76.4 per cent and their later (x966) survey of IOOO cases recorded it as 61.7 per cent (Rowe & Killey, 1969). Fractures of the jaws should not be considered in isolation. Full examination of all parts and systems of the body should always be undertaken to exclude any otherwise unsuspected injury or impairment. Traumatic neurological deficits have a wide range of causes: contusion and laceration of the brain, extradural, subdural and intracerebral haematomas, direct compression by a depressed fracture of the skull, occlusion and thrombosis of blood vessels either in the neck or intracranially, etc. In cases of occlusion and thrombosis the main causative factors may be direct trauma to the vessel wall, sudden torsion of the vessels, overstretching of the vessels, e.g. by a bony ridge or the edge of the tentorium, or hyperextension of the vertebral artery at the cervicocranial junction (Simeone & Goldberg, 1968). Besides, occlusion and thrombosis of the vessels, dissecting aneurysms, delayed ruptures of vessels and false and true aneurysm may similarly occur (Shaw 8z Alvord, 1972). The principal strength of an artery depends on one of its three layers i.e. interna, media or adventitia. The sequelae of the pathological processes will depend on the type of vessel involved, as well as the extent of the damage to these three layers, as shown by experiments in dogs by Wintermitz et al. (1938). In the intracranial arteries, the strength of the arterial walls lies principally with the intimal internal elastic lamina. In the cervical portion of the carotid artery the principal strength depends on the adventitial elastic tissue. It is known that stretching and blunt contusion of the artery tends to lacerate the intima and media with preservation of the adventitia (Shaw & Alvord 1972). Blunt trauma to the intracranial arteries will therefore damage their intimal and medial layers, on which their strength depends. The outcome is usually a delayed rupture or saccular aneurysm formation as their remaining adventitial coat is poor in elastic tissue. In the cervical carotid artery, trauma to the intima and medial layer will usually lead to occlusion of the artery after thrombosis formation or a dissecting aneurysm. Aneurysm formation is rare in the neck due to the strongly developed adventitial layer. Schneider and Lemmen (1952) were among the first to review the literature and report two cases of internal carotid artery thrombosis following closed head and neck injury. They also stressed the importance of including this entity in the differential diagnosis of closed head injury.
TRAUMATIC INTERNAL CAROTID ARTERY OCCLUSION 29 The traumatic process can either involve a singlevessel or more than one vessel. Heilburn and Ratcheson (1972) reported a case in which both vertebral arteries were occluded; the right internal carotid artery showed traumatic aneurysm formation and there was occlusion of many of the branches of the middle cerebral artery with multiple embolisation of the right posterior and anterior cerebral arteries. Their patient was blind in the left eye with bilateral fifth and seventh nerve involvement; loss of gag reflex; paralysis of tongue; a flaccid left arm and weakness of all the other limbs. After 14 months this patient had almost completely recovered. In all cases of neck injury showing signs suggestive of intracranial pressure the possibility of internal carotid artery occlusion should be considered. Also, it should be remembered that pulsation can often be palpated over the thrombosed vessel by transmission from nearby patent vessels (Schneider & Lemmen 1952). The most important investigation in these cases is angiography. Authorities differ with regard to the number of vessels requiring investigation. Heilburn and Ratcheson (rgp) state that bilateral internal and external carotid angiography by catheterisation of the femoral artery is advisable. This will not only show the extent and level of the occlusion but also the number of arteries involved, the cause, whether thrombosis or embolisation and the degree of cross-circulation. It is also essential in the planning of thromboendarterectomy. SUMMARY A case of occlusion of the internal carotid artery following facial trauma is presented. This case underlines the need for careful neurological monitoring of all cases of facial trauma. ACKNOWLEDGEMENTS We would like to thank Mr H. Maslowski, neurosurgeon and Mr B. N. White, oral surgeon, for allowing us to publish details of their patient. We also extend our thanks to Miss J. Perry for her assistance with the clinical photographs. REFERENCES HEILBURN, M. P. & RATCHESON, R. A. (1972). Journal of Neurosurgery, 37, 219. MURRAY, D. S. (1957). British Journal of Surgery, 44, 556. ROWE, N. L. & KILLEY, H. C. (1969). Fractures of the Facial Skeleton. Edinburgh: E. & S. Livingstone. SCHNEIDER, R. C. & LEMMEN, L. J. (1952). Journal of Neurosurgery, 9,495. SHAW, C. M. & ALVORD, F. C. (1972). 3 ournal of Neurology, Neurosurgery and Psychology, 35 247. SIMEONE, F. A. & GOLDBERG, H. I. (1968). Journal of Neurosurgery, 29, 540. WINTERMITZ, M. C., THOMAS, R. M. & LE COMPTE, P. M. (1938). sclerosis. Springfield: Thomas. The Biology of Arterio-