Hong Kong Journal of Emergency Medicine

A young man with sudden unilateral blindness and hemiparesis YS Sia, YT Wong, PG Kan, W Day, YW Fan

Head and neck injuries are very common in Hong Kong, especially resulting from assaulted or traffic accidents. Delayed manifestation of post-traumatic carotid thrombo-embolism and aneurismal formation are known pitfalls that emergency physicians and neurosurgeons may encounter. We present a patient with blunt neck injury with the complication of traumatic dissection of the extracranial internal carotid artery. (Hong Kong j.emerg.med. 2001;8:212-217) Keywords: Amaurosis fugax, aneurysm, embolism,Traumatic carotid thrombosis

Case A previously healthy 40-year-old man suffered from a compound fracture with 2 cm laceration of the ramus of the right mandible after a fall from 5 feet height. No other associated injury was found. He was transferred to Queen Mary Hospital after stabilisation in the Accident & Emergency Department of Tang Shiu Kin Hospital. On admission, he complained of transient blurring of vision of the right eye. Clinical examination revealed stable vital signs and a Glasgow Coma Score (GCS) of 15/15. Visual acuity was impaired on the right (6/18) and the right pupil was non-reactive to light in a mid-dilated position. Extraocular eye movements and fundi examination

were normal and there was no other focal neurological deficit. Apart from the soft tissue swelling overlying the fractured mandible, there was no evidence of other bodily injury. The initial computerised tomography (CT) of the brain was normal and shown fracture of right side of mandible. (Figure 1)

Correspondence to: Sia Yin Shan, MBBS Ta n g Sh i u K i n Ho s p i t a l, A c c i d e n t a n d Em e r g e n c y Department, Hong Kong. Email: [email protected]

Magnetic resonance (MR) imaging, however, demonstrated early signs of infarction over the right MCA territory on diffusion-weighted image (DWI) sequence. (Figure 3)

Ruttonjee Hospital & Tang Shiu Kin Hospital, Accident and Emergency Department, Hong Kong. Wong Yau Tak, MBBS, FRCS(Edin), FHKAM(Surgery) Kan Pui Gay, MRCP(UK), FRCSEd, FHKAM(Emergency Medicine)

Occlusion of the right internal carotid artery (ICA) and right MCA was clearly shown on magnetic resonance (MR) angiography. (Figure 4) The diagnosis was traumatic dissection of the right ICA.

Queen Mary Hospital, Neurosurgical Unit, 102 Pokfulam Road, Pokfulam, Hong Kong. Weida Day, MBBS(HK) Fan Yiu Wah, MBBS(HK), FRACS, FRCSEd(NS)

While awaiting opthalmological assessment for suspected right ocular injury, the patient suddenly developed severe left hemiplegia (grade 0/5) 4 hours after admission. A second CT brain scan revealed hyper-dense signal along the right middle cerebral artery (MCA) territory but no obvious cerebral infarction or intracranial haemorrhage. (Figure 2)

The patient remained fully conscious and was managed conservatively for the next 72 hours. His

Sia et al./A young man with sudden unilateral blindness & hemiparesis

conscious level later deteriorated to GCS 10/15. A repeat CT scan showed severe brain swelling over the right MCA infarcted territory, causing significant midline shift and brain stem compression. (Figure 5) Emergency decompressive craniectomy and duroplasty was performed on the same day. Intra-operatively, the initial intracranial pressure (ICP) was found to be greater than 30 mmHg. A large right fronto-temporoparietal craniectomy was performed and augmentation of the dural compar tment over the infarcted hemisphere was achieved using temporalis fascia free graft. (Figure 6)

Figure 1. Initial CT scan of the brain.

Figure 3. Magnetic resonance (MR) imaging of the brain.

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Post-operative recovery was uneventful. The patient regained full consciousness and later underwent intensive rehabilitation and replacement of his craniectomy bone flap. When last seen, he was fully independent although his right eye remained totally blind and there was residual left hemiparesis.

Discussion Our patient suffered from traumatic dissection of the right extracranial internal carotid artery (ICAD)

Figure 2. CT scan of the brain 4 hours later.

Figure 4. Magnetic resonance (MR) angiography of the brain.

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Figure 5. Third CT scan of the brain.

secondary to a blunt neck injury. The condition is uncommon and two mechanisms have been proposed by Zelenock, et al, in 1982. 1 Firstly, hyperextension and rotation may result in stretch injury of the cervical segment of ICA against the transverse processes of the second and third cervical vertebrae. Secondly, neck flexion may result in compression injury of the ICA between the mandibular angle and cervical vertebrae. The mechanism by which ICA dissection produces neurological deficit is controversial but it is generally agreed that thrombosis and embolic events, rather than direct occlusion of the vascular lumen, play a significant role. 2-4 It is highly likely that the initial visual loss experienced by our patient was the result of embolic events causing amaurosis fugax. Subsequent occlusion of the right opthalmic artery and middle cerebral artery then produced complete blindness and extensive cerebral infarction. Amaurosis fugax is an uncommon presentation. Mokri et al reported only one out of eighteen patient who developed amaurosis fungax.5 In Zelenock's series, two out of six patients suffered from amaurosis fungax as late presentation from two to three months after the initial traumatic injury. 1 Another case was reported in a young man presented with sudden visual loss eleven weeks after trauma. The neuro-ophthalmologic examination was suggestive of central retinal artery

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Figure 6. Post-operative CT scan of the brain.

occlusion. The intra-arterial angiography revealed a traumatic pseudo-aneurysm of the ipsilateral high extracranial portion of the internal carotid artery. It was also suggested that embolisation should be considered as the most probable mechanism, which was rarely described as the aetiopathogenesis before.6 Extensive studies had been performed by Kraus et al. to study the diagnosis and treatment of post-traumatic carotid artery thrombosis. They found that this rare injury should be suspected in the presence of head and/or neck, chest injuries, basilar skull fracture or coma. Dissection is the most common cause (80%). Most of the patients eventually developed neurological deficit.7 However, Carrillo et al noticed that there was no indicator to predict who would be the victim. Worse still, most of the neurological finding initially did not correlate with the computed tomography scan.8 Post-traumatic carotid artery complication can be divided into thrombosis, emboli and even aneurismal formation. It presents with different clinical manifestation depending on the site of lesion and can happen even after various routine daily activities. 1,5,9 Jean had reported a 36-year-old woman presenting with sudden right-sided neck pain immediately after 32-minute telephone conversation. During the

Sia et al./A young man with sudden unilateral blindness & hemiparesis

conversation, she flexed her head to the side while doing her housework simultaneously. 10 The cervical pain was followed by an ipsilateral pulsatile tinnitus. Neurological finding was normal. No history of hypertension, migraine or smoking was noted. Extracranial right internal-carotid-artery dissection was diagnosed after computed tomography, doppler sonography and magnetic resonance angiography. The lumen was also occluded by intramural haematoma. Laboratory tests including coagulation studies, digital intravenous angiography of the abdominal aorta and renal arteries, did not suggest any predisposing arterial disease. Finally she was treated with warfarin for 3 months and recovered 6 months later. Post-traumatic carotid thrombosis could also result from low-energy insult with rare clinical sign. Horner's syndrome and phrenic nerve palsy were present in a 37-year-old man who sustained an accidental compression of the neck. Ultrasonography demonstrated the presence of posttraumatic carotid thrombosis and he was given an anticoagulant and discharged on the 10th day of hospitalisation, with persisting Horner's syndrome and phrenic nerve palsy. 11 Horner's syndrome, whether painless or painful, is one of the differential diagnosis of post-traumatic carotid aneurysm. Ameline-Audelan reported a case of post-traumatic carotid artery dissection presenting as a painless Horner's syndrome. This is a neurological emergency when it appears rapidly, spontaneously or after a trauma. Each painful Horner's syndrome must be considered to be due to a homonymous carotid artery dissection until proven otherwise, especially because the pain may be an inconstant finding and the Horner's syndrome incomplete. 12 In addition, Schievink et al reported one young sportsmen developing painful Horner's syndrome after direct impact of a softball to the antero-lateral neck region.13 Transient ischaemic stroke in young patient is a potential complication of internal carotid artery dissection due to trivial daily events. 14 Kumar et al. reported a young patient who suffered from bilateral internal carotid artery dissection from severe vomiting.15 Heather et al even reported a 27-year-old man who suffered from spontaneous rupture of the common carotid artery with pseudo-aneurysm formation after a Valsalva manoeuver during sexual intercourse.16

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Paediatric patient is not exempted from post-traumatic carotid complication. Localising sign of cerebrovascular accident was noted 18 hours later in a 2-yearold child who fell on a toothbrush, sustaining pharyngeal injury. Magnetic resonance angiography showed the occlusion of internal carotid artery and a cerebral infarction. Fortunately she was able to make a complete recovery after anticoagulation. 17 An extensive review of the National Pediatric Trauma Registry was performed by Lew in 1999. It was noted that the incidence of blunt carotid injury, either internal or common carotid, was about 0.03% (15 of 57,659 blunt trauma patients). Post-traumatic carotid complications is associated with various injuries including chest trauma; intracranial haemorrhage and even clavicular fractures. Thirty-three percent of the patients developed neurological deficit directly attributable to their carotid injuries. 18

Diagnosis High index of suspicion, good histor y, careful examination and appropriate specialist referral are the main essential in the emergency management of these injuries. Complication may occur even after trivial daily event or low-energy impact and it is important to be aware of its delayed clinical manifestation. Good documentation including neurovascular status is necessary. The various clinical presentations are summarised in Table 1. Generally, some authors proposed that patient with history of trauma and recurrent epistaxis, visual loss, progressive cranial nerve palsy or any neurological deficit should be admitted and evaluated with angiography or magnetic resonance angiography. 19 Several studies recommend routine angiography 2 weeks after the injury to rule out the delayed formation of aneurysm.19,20 Magnetic resonance angiography remains the investigation of choice. It is a prompt, non-invasive and it provides a clearer picture of the length, site of the lesion as well as showing residual signal that demonstrate the persistence or arrest of blood flow. 21

Treatment Oral anticoagulant is the treatment of choice for posttraumatic carotid artery thrombosis.7,8,10,17 Platelet GP IIb/IIIa blockade with an orally active antagonist was shown to be safe and effective in the prevention of

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Table 1. Clinical presentation of post-traumatic carotid complication. • Impair or loss of consciousness. Transient ischemia attack. • Transient global amnesia. • Headache. Tinnitus. Pulsatile neck mass. • Seizure. • Focal Neurological (motor or sensory) deficit. • Cranial nerve deficit, painless or painful Horner's syndrome. • Unilateral blindness. Amaurosis fugax. • Proptosis. • Chemosis. • Retro-orbital pain. • Massive or recurrent epistaxis. • Diabetes insipidus. • Palpable growing skull fracture.

1.

2.

3. 4.

6.

Lesson to learn To summarise, there are only few cases found in Hong Kong. We think that this condition may be underrecognised. Assaulted patients are very common in every Accident and Emergency department and hopefully, this short case report can alert our emergency colleague that post-traumatic thromboembolism and aneurismal formation must be considered as one of the complications associated with head and neck injuries despite its rarity. Early detection is the key to timely intervention and prevention of this devastating outcome.

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References

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carotid ar ter y occlusive thrombosis. 22 A large r a n d o m i s e d c o n t ro l l e d t r i a l o f i n t r a - a r t e r i a l thrombolysis, the Prolyse in Acute Cerebral thromboembolism (PROACT I) was published in 1998 and it showed the clinical efficacy of intraarterial thrombolysis in patient with acute ischaemic stroke from middle cerebral artery occlusion of less than 6 hours duration. This may also be useful in situation in which intravenous thrombolysis carries an excessive risk of bleeding, such as associated open fracture.23 Surgical repair, using saphenous vein patch or grafting is useful for cases of post-traumatic aneurismal formation. It is safe and effective only in patients whose prograde flow continues and only mild neurological deficits are present. In contrast, it is not helpful if severe neurological deficits and complete occlusion had already been noted. 24

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7. 8. 9.

10. 11. 12. 13.

14. 15. 16. 17.

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