作者：Khalil Hamzedust, Mohammad Taher Rajabi, Mohammad Solaimani, Mehdi Alizadeh 作者单位：伊朗德黑兰，德黑兰大学医学院眼科，眼科研究中心
【摘要】 本文报告1例钝器眼伤后出现的视网膜中央动脉阻塞，这种病症比较稀少，文献报告中也不多见。视网膜中央动脉阻塞尽管少见但对视力影响非常大，在对急性创伤性视力减退进行鉴别诊断时应考虑到这种情况。
【关键词】 视网膜中央动脉阻塞；外伤性的；鉴别诊断
Traumatic central retinal artery occlusion: a case report
Khalil Hamzedust, Mohammad Taher Rajabi, Mohammad Solaimani, Mehdi Alizadeh
Department of Ophthalmology, School of Medicine, Medical Sciences/Tehran University, Tehran, Iran
Abstract
We present here a case of central retinal artery occlusion (CRAO) occurring after blunt ocular trauma. This is a rare occurrence and has not been frequently reported in literature. It is important to consider this uncommon but visually catastrophic condition in the differential diagnosis of acute posttraumatic visual deterioration.
KEYWORDS: central retinal artery occlusion; traumatic; differential diagnosis
INTRODUCTION
The central retina artery occlusion (CRAO) is a wellknown cause of eye sight loss which always has a negative prognosis. Most cases of CRAO occur in elderly patients, and the main causes are atheromatous disease of the internal carotid artery with embolization of the ocular vessels [1]. In younger people, this condition is rare and is estimated at about 8% of all cases of CRAO[2]. As a cause of CRAO, trauma has been reported as a sole factor or in association with other systemic pathology such as hemoglobinopathies and coagulation abnormalities [38]. Trauma can be directed to the eyeball or the head.
We report a case of a young man who suffered a central retinal arterial occlusion following blunt trauma to one eye. To our knowledge this is a rare occurrence and has not been frequently reported in literature.
CASE REPORT
A 14yearold man was hit in the right eye by a football. He experienced immediate and total loss of the vision of this eye. He was in good health and had no past history of ocular disease.
One hour after the injury the patient attended the Farabi Eye Hospital, where his right visual acuity (VA) was found to be hand movements, and the left was 6/6 unaided. No abnormality of the left eye was detected. The right eyelids were mildly bruised. There was a mild conjunctival injection. No perforation of the cornea or sclera was found. The ocular media were clear. The right pupil was round and reacted consensually but was sluggish directly to light. There was marked relative afferent pupillary defect (RAPD). The intraocular pressure (IOP) of each eye was 12mmHg. There was no proptosis of the right eye.
Posterior segment examination showed an oval area of pallor with swelling of the nerve fibre layer along the superior and inferior vascular arcade and macula; and there was a typical cherryred spot (Figure 1).
Initial treatment consisted of intravenous acetazolamide 500 mg, oral aspirin 325mg, and carbon dioxide rebreathing, on the assumption that the blunt injury might have induced central retinal arterial spasm.
Subsequent examination after 1 week showed his vision to be FC at 3m in the affected eye. Marked RAPD was noted. Posterior segment examination showed pale right optic disc with obvious attenuation of retinal arterioles. A diagnosis of traumatic CRAO was made. Coagulative tests were normal. An orbital computer tomography (CT) scan showed no evidence of bony injury. Brain magnetic resonance imaging (MRI) scan was normal.
The patient subsequently failed to regain any vision in the left eye.
DISCUSSION
CRAO generally occurs in patients with cardiovascular risk factors and usually produces a severe impairment of central vision. The presence of macular edema and cherryred spots are the main ophthalmological signs in the diagnosis of this pathology [1]. Reported causes of CRAO in children and young adults are migraine, coagulation abnormalities, cardiac disorders, contraceptives and trauma [2].
Traumatic occlusions have been seen in patients suffering from head injury and in those with eyeball contusions. In most cases, the CRAOoccurred several hours after the trauma [9].
In cases with traumatic CRAO, the possibility of malignancy with metastatic spread causing CRAO should be considered, particularly in relatively young patients with no other evidences of systemic disease [10]. Direct compression after surgical repair of orbital blowout fracture with a Teflon plate has been reported [11]. Common to these conditions is damage to the endothelial cells of the artery with exposure of the underlying collagen, which stimulates platelet aggregation and thrombus formation [2,12]. If CT/MRI scans show a significant haematoma, the patient requires an urgent neurosurgical referral for decompression. As there was no evidence of severe ecchymosis or proptosis, we can only postulate that this was the possible mechanism in the patient. Hemorrhage within the optic nerve sheath can compress the nerve sufficiently to impair axonal transport. Jonasson and Cullen [13]reported such a case caused by diving, in which the intrasheath hematoma also produced proptosis of the globe, and it reduced vision mildly.
Figure 1Left eye showing an oval area of pallor with swelling of the nerve fibre layer along the superior and inferior vascular arcade and macula with a typical cherryred spot（略）
Severe reflex vasospasm initiated as a direct response to concussion injury to the arterial wall smooth muscle is another mechanism. Blunt ocular trauma can lead to commotioretinae, a relatively benign and selflimiting condition, which does not require any specific treatment. Trauma can also produce CRAO. Rarely, the two can coexist with commotioretinae masking the clinical appearance of CRAO. A patient with such a history but with profound visual loss and RAPD should raise suspicion of CRAO. If optic nerve contusion and compression are ruled out, spasm of the retinal artery is likely the mechanism of CRAO.
If seen within 4 hours of injury, aggressive measures may be undertaken to alleviate spasm [13].
【参考文献】
1 Rumelt S, Dorenboim Y, Rehany U. Aggressive systematic treatment for central retinal artery occlusion. Am J Ophthalmol1999;128:733738
2 Brown GC, Magargal LE, Shields JA, Goldberg RE, Walsh PN. Retinal artery obstruction in children and young adults. Ophthalmology1981;88:1825
3 Umeed S, Shafquat S. Commotioretinae and central retinal artery occlusion after blunt ocular trauma. Eye2004;18:333334
4 Cohen HL, Eidelman EM, Kaufman I. Traumatic central retinal artery occlusion: diagnosis by color Doppler imaging. J Ultrasound Med1993;12(7):411413
5 DalmaWeiszhausz J, Mezade Regil A, MartínezJardón S, OliverFernández K. Retinal vascular occlusion following ocular contusion. Graefes Arch Clin Exp Ophthalmol2005;243(5):406409
6 Noble MJ, Alvarez EV. Combined occlusion of the central retinal artery and central retinal vein following blunt ocular trauma: a case report. Br J Ophthalmol1987;71(11):834836
7 Sorr EM, Goldberg RE. Traumatic retinal artery occlusion with sickle cell trait. Am J Ophthalmol1975;80:648652
8 Michaelson PE, Phaffenbach D. Retinal artery occlusion following ocular trauma in youths with sickletrait haemoglobinopathy. Am J Ophthalmol1972;74:494497
9 Chawala JC. Traumatic central retinal artery occlusion. Trans Ophthalmol Soc UK1972;92:777784
10 Friedland S, Bukelman A, Pollack A. Central retinal artery occlusion in a young man. Harefuah1991;121:9092
11 Emery JM, Huff JD, Justice JJ. Central retinal artery occlusion after blowout fracture repair. Am J Ophthalmol1974;78:583540
12 Moake JL, Levine JD. Thrombotic disorders. Clin Symp1985;37:332
13 Jonasson F, Cullen JF. Axonal transport injury caused by diving. Am J Ophthalmol1982;94:813815
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