Journal of Pediatric Ophthalmology and Strabismus

Short Subjects 

Traumatic Vitreous Hemorrhage From a Persistent Hyaloid Artery

Osman Çkiç, MD; Yuksel Totan, MD; Cosar Batman, MD

Abstract

INTRODUCTION

The central hyaloid artery is seen in fetuses of approximately 20 weeks' gestational age and undergoes involution in the third trimester. Regression usually is completed at birth. Although partial persistence of the central hyaloid artery is fairly common, persistence of the entire hyaloid artery is rare. Vitreous hemorrhage,1'6 intralenticular hemorrhage,7 and vitreoretinal traction8'9 from a persistent hyaloid artery have been reported only rarely.

This article reports a case of traumatic vitreous hemorrhage from a persistent hyaloid artery.

CASE REPORT

A 14-year-old boy presented with a 3-day history of blurred vision and floating spots in his left eye. His symptoms began after being hit in the face with a soccer ball. There was no significant past history of ocular or systemic disease including premature birdi or family history of eye disease.

On examination, visual acuity in die left eye was 20/32. A mobile persistent hyaloid artery filled with blood, extending from die posterior lens capsule to the back, was detected by slit-lamp examination (Figure 1). Ultrasonographic examination revealed mild intravitreal hemorrhage and a persistent hyaloid artery (Figure 2). The right eye was normal.

On follow-up examinations, the vitreous hemorrhage gradually cleared, and the persistent hyaloid artery could be followed from die posterior lens capsule to the optic disc. Fluorescein angiograms (Figure 3) also confirmed die persistent hyaloid artery originating from the optic disc. No peripheral retinal abnormalities, posterior vitreoretinal traction, or posterior vitreous or retinal detachment were detected by fundus examination.

Fluorescein angiographic evaluation of persistent hyaloid artery has rarely been reported.4,6 Among previously reported cases,1'6 only one had faint fluorescein staining of a persistent hyaloid artery root, suggesting the vitreous hemorrhage was from arterial circulation.4 In our case, no obvious fluorescein staining in die hyaloid artery root and no fluorescein leakage were observed. No blood flow, the usual circumstance for a persistent hyaloid artery, could be detected in the hyaloid artery by Doppler ultrasonography. The lack of obvious fluorescein staining, leakage, and blood flow indicates the lumen may have been totally occluded at that time. These findings also make it uncertain to ascertain whether the hemorrhage occurred from die hyaloid artery. However, die location of preretinal intravitreal hemorrhage observed in fluorescein angiogram was consistent with mobility of the hyaloid artery, and a complete retinal examination including fluorescein angiography revealed no orher possible etiology of the vitreous hemorrhage. The distribution of the hemorrhage also suggested the bleeding site might be the posterior portion of the artery.

Aldiough we have no direct proof the hemorrhage occurred from die patient's hyaloid artery, and vitreous hemorrhage in traumatized eyes without a persistent hyaloid artery is not an infrequent finding, die persistent hyaloid artery in this patient was presumably die origin of the hemorrhage based on the patient's history, clinical course, and complete ophdialmic examination, which included fundus fluorescein angiography and ultrasonography.

This mild intravitreal hemorrhage resolved without any sequelae, and die patient's visual acuity returned to normal. Due to the clinical course of vitreous hemorrhage from a persistent hyaloid artery, normally no treatment is required,6 as in die patient described here. However, when persistent intravitreal hemorrhage or fractional retinal detachment exist, vitrectomy may be necessary.6,9

Persistent hyaloid artery should be considered in die differential diagnosis for traumatic vitreous hemorrhage and confirmed with fluorescein angiogram. Such patients should be informed about die possibility of recurrent vitreous hemorrhage and warned against even minor trauma.

1. Vangsted P. Galactosemia with cataract and persistent hyaloid artery. Acta Ophthalmol Scand. 1980;58:812-818.

2. Delaney WV Jr. Prepapillary hemorrhage and persistent hyaloid artery. Am J Ophthalmol 1980;90:419-421.

3. Yap EY. Buettner H. Traumatic rupture of a persistent hyaloid artery. Am…

INTRODUCTION

The central hyaloid artery is seen in fetuses of approximately 20 weeks' gestational age and undergoes involution in the third trimester. Regression usually is completed at birth. Although partial persistence of the central hyaloid artery is fairly common, persistence of the entire hyaloid artery is rare. Vitreous hemorrhage,1'6 intralenticular hemorrhage,7 and vitreoretinal traction8'9 from a persistent hyaloid artery have been reported only rarely.

This article reports a case of traumatic vitreous hemorrhage from a persistent hyaloid artery.

CASE REPORT

A 14-year-old boy presented with a 3-day history of blurred vision and floating spots in his left eye. His symptoms began after being hit in the face with a soccer ball. There was no significant past history of ocular or systemic disease including premature birdi or family history of eye disease.

On examination, visual acuity in die left eye was 20/32. A mobile persistent hyaloid artery filled with blood, extending from die posterior lens capsule to the back, was detected by slit-lamp examination (Figure 1). Ultrasonographic examination revealed mild intravitreal hemorrhage and a persistent hyaloid artery (Figure 2). The right eye was normal.

On follow-up examinations, the vitreous hemorrhage gradually cleared, and the persistent hyaloid artery could be followed from die posterior lens capsule to the optic disc. Fluorescein angiograms (Figure 3) also confirmed die persistent hyaloid artery originating from the optic disc. No peripheral retinal abnormalities, posterior vitreoretinal traction, or posterior vitreous or retinal detachment were detected by fundus examination.

Figure 1 : The anterior part of the persistent hyaloid artery attached to the posterior pole of the lens.

Figure 1 : The anterior part of the persistent hyaloid artery attached to the posterior pole of the lens.

Figure 2: B-mode ultrasonogram shows vitreous hemorrhage (arrows) near the posterior part of the persistent hyaloid artery.

Figure 2: B-mode ultrasonogram shows vitreous hemorrhage (arrows) near the posterior part of the persistent hyaloid artery.

Vitreous hemorrhage cleared and vision returned to 20/20 after 6 weeks. The persistent hyaloid artery did not undergo regression, but no additional intravitreal hemorrhage and visual deterioration were observed during the follow-up period.

DISCUSSION

Hemorrhage from the hyaloid artery has been reported only rarely and has been attributed to various mechanisms such as rapid eye movements during sleep4 or posterior vitreous detachment6 due to external trauma to the eye,3 or to occur spontaneously.2 In our case, external trauma on die globe was the cause of vitreous hemorrhage, probably from the hyaloid artery.

Figure 3: Fundus fluorescein angiogram showing the posterior part of the persistent hyaloid artery arising from the optic disc (upper arrow) and an area of preretinal intravitreal hemorrhage (lower arrow) without any leakage of venous circulation.

Figure 3: Fundus fluorescein angiogram showing the posterior part of the persistent hyaloid artery arising from the optic disc (upper arrow) and an area of preretinal intravitreal hemorrhage (lower arrow) without any leakage of venous circulation.

Fluorescein angiographic evaluation of persistent hyaloid artery has rarely been reported.4,6 Among previously reported cases,1'6 only one had faint fluorescein staining of a persistent hyaloid artery root, suggesting the vitreous hemorrhage was from arterial circulation.4 In our case, no obvious fluorescein staining in die hyaloid artery root and no fluorescein leakage were observed. No blood flow, the usual circumstance for a persistent hyaloid artery, could be detected in the hyaloid artery by Doppler ultrasonography. The lack of obvious fluorescein staining, leakage, and blood flow indicates the lumen may have been totally occluded at that time. These findings also make it uncertain to ascertain whether the hemorrhage occurred from die hyaloid artery. However, die location of preretinal intravitreal hemorrhage observed in fluorescein angiogram was consistent with mobility of the hyaloid artery, and a complete retinal examination including fluorescein angiography revealed no orher possible etiology of the vitreous hemorrhage. The distribution of the hemorrhage also suggested the bleeding site might be the posterior portion of the artery.

Aldiough we have no direct proof the hemorrhage occurred from die patient's hyaloid artery, and vitreous hemorrhage in traumatized eyes without a persistent hyaloid artery is not an infrequent finding, die persistent hyaloid artery in this patient was presumably die origin of the hemorrhage based on the patient's history, clinical course, and complete ophdialmic examination, which included fundus fluorescein angiography and ultrasonography.

This mild intravitreal hemorrhage resolved without any sequelae, and die patient's visual acuity returned to normal. Due to the clinical course of vitreous hemorrhage from a persistent hyaloid artery, normally no treatment is required,6 as in die patient described here. However, when persistent intravitreal hemorrhage or fractional retinal detachment exist, vitrectomy may be necessary.6,9

Persistent hyaloid artery should be considered in die differential diagnosis for traumatic vitreous hemorrhage and confirmed with fluorescein angiogram. Such patients should be informed about die possibility of recurrent vitreous hemorrhage and warned against even minor trauma.

REFERENCES

1. Vangsted P. Galactosemia with cataract and persistent hyaloid artery. Acta Ophthalmol Scand. 1980;58:812-818.

2. Delaney WV Jr. Prepapillary hemorrhage and persistent hyaloid artery. Am J Ophthalmol 1980;90:419-421.

3. Yap EY. Buettner H. Traumatic rupture of a persistent hyaloid artery. Am J Ophthalmol 1992;114:225-227.

4. Chen TL, Yamg SS. Vitreous hemorrhage from a persistent hyaloid artery. Retina. 1993;13:148-151.

5. Williamson W, Barac'h D, Poirier L, et al. Vitreous hemorrhage associated with persistent hyaloid artery. Apropos of a case. J Fr Ophtalmol 1994;17:361-364.

6. Goncalves A, Cruysberg JRM, Draaijer RW, et al. Vitreous haemorrhage and other complications of a persistent hyaloid artery. Doc Ophthalmol 1996;92:55-59.

7. Utwki IC, Nakao K, Ohba N. Haemorrhage in die lens: spontaneous occurrence in congenital cataract. Br J Ophthalmol 1986:70:593-595.

8. Cockburn DM, Dwyer PS. Posterior persistent hyperplastic vitreous. AmJ Optom Physiol Opt. 1988;65:316-317.

9. Thumann G, Bara-Schmidt KU. Kirchhof B, Heimann K Branch retinal artery occlusion by diathermy of a persistent hyaloid artery. AmJ OphthalmoL 1997;124:415-416.

10.3928/0191-3913-20000301-13

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