LETTERS

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Blast injury-associated optic disc pit maculopathy. Congenital pits of the optic nerve head are anomalies of embryogenesis due to neuroecto- dermal fold.
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Br J Ophthalmol 2007;91:558–561

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egress of vitreous fluid into the subretinal and intraretinal space. However, an alternative hypothesis may be that the patient’s closed head trauma causing the transmission of CSF into the subretinal space.

LETTERS Blast injury-associated optic disc pit maculopathy Congenital pits of the optic nerve head are anomalies of embryogenesis due to neuroectodermal fold remnants or aplasia of Bergmeister’s papilla.1 The defect allows the vitreous to pass spontaneously into the subretinal and inner nuclear layers of the retina, resulting in serous retinal detachment with macular cyst formation.2 Alternatively, a direct communication between the optic pit and subarachnoid space may exist, leading to cerebrospinal fluid (CSF) accumulation in the subretinal space as well as passage of intraocular contents into the CSF.3 A recent case report noted a symptomatic optic pit 3 months after a blunt ocular injury,4 and another case report noted an association between optic pit maculopathy and subsequent traumatic macular hole after minor trauma.5 We report optic pit maculopathy immediately after closed head injury during a military engagement.

Case report A 32-year-old man, previously healthy, was injured during combat operations in Iraq. After a large blast, the soldier lost consciousness and was thrown several feet. He sustained no external injuries, but noted loss of vision in his left eye. Assessment immediately after the injury showed no evidence of ocular trauma and a visual acuity of 20/150 in the left eye, with ophthalmoscopy disclosing serous macular detachment of the left eye with a temporal optic pit (fig 1). There was no evidence of contusion maculopathy or traumatic macular hole formation. On arrival in the USA, visual acuity remained 20/150 and optical coherence tomography showed subretinal and intraretinal cystic hyper-reflectivity consistent with neurosensory detachment and macular schisis (fig 2). Brain magnetic resonance imaging was normal. Visual acuity varied between 20/80 and 20/400 over the ensuing 2 months. However, 81 days after injury, the patient’s neurosensory detachment resolved (fig 3A), with evidence of posterior vitreous detachment by optical

Marcus H Colyer, Eric D Weichel, Thomas P Ward Ophthalmology Service, Department of Surgery, Walter Reed Army Medical Center, Washington, DC, USA

Figure 2 Ocular coherence tomography after the blast showing subretinal fluid with intraretinal cysts. coherence tomography (fig 3B). Visual acuity has stabilised at 20/100.

Comment Two facts support the temporal relationship between injury and vision loss. Firstly, an eye examination performed 2 months before the injury documented 20/20 vision and normalappearing macula. Secondly, the soldier’s occupation requires intact central and peripheral vision and stereopsis. Admittedly, his nondominant eye was affected, but numerous military-specific tasks require monocular use of the non-dominant eye. The soldier reported no visual deficits in either eye. Few authors have noted an association between ocular trauma and the ‘‘opening’’ of an optic pit resulting in serous macular detachment. A review of injuries from the current conflict and past wars fails to note any association of optic pit maculopathy with warrelated trauma. However, the blast endured by this soldier produced enough energy to cause him to be thrown into the air and sustain closed head injury. Although speculative, we believe that this extrinsic energy caused anterior–posterior vitreous traction, allowing an

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Correspondence to: Dr M H Colyer, Ophthalmology Clinic-1F, Walter Reed Army Medical Center, Washington, DC 20307, USA; [email protected] The opinions expressed in this article are solely those of the authors and do not represent the views or official policies of the United States Army or Department of Defense.

doi: 10.1136/bjo.2006.103457 Accepted 1 September 2006 Funding: None. Competing interests: None.

References 1 Gass JD. Serous detachment of the macula. Secondary to congenital pit of the optic nervehead. Am J Ophthalmol 1969;67:821–41. 2 Brown GC, Shields JA, Goldberg RE. Congenital pits of the optic nerve head. II. Clinical studies in humans. Ophthalmology 1980;87:51–65. 3 Kuhn F, Kover F, Szabo I, et al. Intracranial migration of silicone oil from an eye with optic pit. Graefes Arch Clin Exp Ophthalmol 2006;244:1360–2. 4 Meyer CH, Rodrigues EB. Optic disc pit maculopathy after blunt ocular trauma. Eur J Ophthalmol 2004;14:71–3. 5 Billi B, Lesnoni G, Giuliano M, et al. Post-traumatic macular break associated to congenital optic disc pit and pre-existing sensory macular detachment. Int Ophthalmol 1996;20:269–72.

Histopathological findings after retinal endovascular lysis in central retinal vein occlusion Although visual results after use of the new surgical method of retinal endovascular lysis (REVL) seem encouraging,1 2 its effectiveness has not been proved in a controlled, prospective clinical trial. From a histological postmortem study of eyes with central retinal vein occlusion (CRVO), it is still questionable whether an older thrombus can be dissolved using recombinant tissue plasminogen activator (rt-PA).3 We report on the histopathological findings in a human eye 9 months after REVL.

Case report

Figure 1 Fundus photograph taken after the blast. Neurosensory detachment (solid arrows) is associated with an optic pit (hollow arrow).

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Figure 3 Clinical photograph (A) and ocular coherence tomography image (B) 81 days after the blast injury, showing resolution of subretinal fluid with interval development of posterior vitreous detachment (arrows).

We report the case of a 62-year-old woman having a 7-week-old, highly ischaemic CRVO in her left eye with hand movement vision. Although we were concerned about treating an older thrombus with rt-PA, we were interested in seeing whether thrombolysis has the potential to prevent neovascular glaucoma, for example, by minimising capillary nonperfusion. We attempted an REVL to improve retinal blood flow. The procedure was approved by our local ethics committee.

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and confirm that the vein had been successfully punctured. In this case, REVL did not prevent neovascular glaucoma despite successful rt-PA injection in a venous branch close to the papilla. Clinical, histological and angiographic findings suggest that the occlusion was not influenced by the injection and we conclude that rt-PA injection after 7 weeks of CRVO is too late. Nicolas Feltgen, Hansjuergen Agostini, Claudia Auw-Haedrich, Lutz L Hansen Figure 1 Intraoperative picture. Injection towards optic nerve head. Branch of the occluded central retinal vein just penetrated by the cannula. After a standard vitrectomy with detachment of the posterior hyaloid, the vessel wall was pierced with a glass cannula (Micron Ophthalmic, Margate, Florida, USA) as described by Weiss et al,2 and 1 ml (200 mg/ ml) rt-PA was injected successfully (fig 1). Formation of an epiretinal membrane at the injection site could be detected 3 weeks postoperatively. Angiographic examination 3 days postoperatively did not show improved arteriovenous passage time. In addition, the patient’s postoperative vision did not change, and despite intensive photocoagulation and cryotherapy in the early postoperative period, the globe had to be removed 9 months later because of painful phthisis. The entire specimen was immersed for light microscopy. Gross findings included numerous haemorrhages scattered throughout the retina. Histological examination confirmed the diagnosis of a CRVO with subretinal fluid, preretinal haemorrhage, optic atrophy and loss of ganglion cells. Unfortunately, we could not detect the thrombus histologically. In the surgically treated area of the retina, we found a thickened venous wall due to the longstanding occlusion. The internal limiting membrane was interrupted and the vessel wall was in contact with an epiretinal membrane (fig 2).

Comment

Department of Ophthalmology, University of Freiburg, Freiburg, Germany Correspondence to: Dr Nicolas Feltgen, Department of Ophthalmology, University of Freiburg, Killianstrasse 5, 79106 Freiburg, Germany; [email protected] The necessary ethics committee approval was secured for this study from the ethics committee of the University of Freiburg, Elsaesser Strasse 2m, Haus 1A, D-79110 Freiburg, Germany.

doi: 10.1136/bjo.2006.099176 Accepted 1 August 2006 Competing interests: None.

References 1 Bynoe LA, Hutchins RK, Lazarus HS, et al. Retinal endovascular surgery for central retinal vein occlusion: initial experience of four surgeons. Retina 2005;25:625–32. 2 Weiss JN, Bynoe LA. Injection of tissue plasminogen activator into a branch retinal vein in eyes with central retinal vein occlusion. Ophthalmology 2001;108:2249–57. 3 Green WR, Chan CC, Hutchins GM, et al. Central retinal vein occlusion: a prospective histopathologic study of 29 eyes in 28 cases. Retina 1981;1:27–55.

Detection of a congenital cystic eyeball by prenatal ultrasound in a newborn with turner’s syndrome Congenital cystic eyeball was first described in 1939 as a rare ocular malformation caused by

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This is the first case to show the histological changes after surgical REVL in a human eye. In other patients, we could not be certain whether the intravenous injection had succeeded using this sophisticated surgical method. Beyond the expected histological findings after CRVO without a thrombus but typical fluorescein angiography in this case, we could identify the injection site histologically

partial or complete failure of the optic vesicle to invaginate during fetal development.1 Only 35 cases have been reported. We present the clinical and histopathological findings in a newborn with Turner’s syndrome and a congenital cystic eye.

Case report A healthy 19-year-old woman underwent amniocentesis revealing a 45XO fetal karyotype, consistent with Turner’s syndrome. She had good prenatal care, no significant illness or exposures during pregnancy, and family history was noncontributory. At 33 weeks gestation, prenatal ultrasound revealed a severely hypoplastic heart, a duplicated left kidney, and a large cystic orbital mass (fig 1A). The infant was born at 38 weeks with characteristic stigmata of Turner’s syndrome including webbed neck, broad chest, widely spaced nipples, and pedal lymphedema. The cystic right orbital mass showed partial transillumination (fig 1B). The differential diagnosis included epithelial cyst, orbital cystic teratoma, microphthalmos with cyst, encephalocele, and congenital cystic eye. The left eye was normal. Ultrasonography and MRI revealed a predominantly cystic but partially solid orbital mass, with no discernable globe (fig 1C). MRI also demonstrated dysplasia of the pons and midbrain. After counseling regarding the infant’s poor prognosis, the family withdrew life support and the patient expired. Histopathology confirmed the diagnosis of cystic eyeball. A cavity lined by mixed fibroglial tissue was observed (fig 2A) with primitive muscle tissue inserting into the cyst wall (fig 2B). A segmental differentiation of sclera, choroid, retinal pigment epithelium, and retina were noted occupying 5% of the posterior wall (fig 2C). Fibroglial tissue with opening to the subarachnoid space was found posteriorly with tissue resembling brain. Primitive optic nerve with surrounding channels was identified (fig 2D). No cornea, iris, ciliary body, or lens was distinctly identified. Immunostaining with

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Figure 2 Histological findings at the site of puncture: epiretinal membrane (asterisk), interrupted ILM (arrow) and thickened venous wall (haematoxylin and eosin; 2006).

Figure 1 (A) Prenatal fetal ultrasound at 33 weeks’ gestation revealed a cystic mass in the right orbit. (B) External photograph of the patient shows the large right cystic orbital mass with partial transillumination. (C) Both cystic and solid (asterisk) components to the mass are appreciated on T2 weighted MRI studies. No globe is discernable on the right side. Parental/guardian informed consent was obtained for publication of this figure.

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