Macular hole following electrical shock injury

Macular hole following electrical shock injury

Correspondence 2. Glusker P, Recht L, Lane B. Reversible posterior leukoencephalopathy syndrome and bevacizumab. N Engl J Med 2006; 354:980–2. 3. Levy...

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Correspondence 2. Glusker P, Recht L, Lane B. Reversible posterior leukoencephalopathy syndrome and bevacizumab. N Engl J Med 2006; 354:980–2. 3. Levy CF, Oo KZ, Fireman F, et al. Reversible posterior leukoencephalopathy syndrome in a child treated with bevacizumab. Pediatr Blood Cancer 2009;52:669–71. 4. Peter S, Hausmann N, Schuster A, Boehm HF. Reversible posterior leukoencephalopathy syndrome and intravenous bevacizumab. Clin Experiment Ophthalmol 2008;36:94–6. 5. Stott VL, Hurrell MA, Anderson TJ. Reversible posterior leukoencephalopathy syndrome: a misnomer reviewed. Intern Med J 2005;35:83–90.

Macular hole following electrical shock injury

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lectrical injuries can present with a variety of ocular manifestations but the occurrence of macular hole is uncommon.1 We report a rare case of unilateral fullthickness macular hole due to electrical shock injury. A 10-year-old boy sustained burns over his left arm and torso (20% body surface area) following accidental contact with a high-tension electrical wire (440 V). During his recovery, he noticed defective vision OS. His bestcorrected visual acuity was 6/6 OD and 6/60 OS. The anterior segment and fundus OD were unremarkable. Punctate posterior subcapsular lens opacities and Weiss ring were noted OS. The detached vitreous was translucent, with an appearance similar to coagulated egg white (Fig. 1). There was a full-thickness macular hole with a cuff of subretinal fluid (Fig. 2). The midperipheral retina showed cystic changes superiorly and temporally (Figs. 2 and 3). The patient underwent pars plana vitrectomy. Intraoperatively, the presence of posterior vitreous detachment (PVD) was confirmed and no other retinal break was noted. Dye-assisted peeling of the internal limiting membrane and injection of perfluoropropane gas was done. The patient was advised to maintain a prone position.

6. Bakri SJ, Snyder MR, Reid JM, Pulido JS, Singh RJ. Pharmacokinetics of intravitreal bevacizumab (Avastin). Ophthalmology 2007;114:855–9.

Davin Johnson, Hussein Hollands, Anya Brox, Sanjay Sharma Hotel Dieu Hospital, Kingston, Ont. Correspondence to Sanjay Sharma, MD: [email protected] Can J Ophthalmol 2010;45:186–7 doi:10.3129/i09-247

In the immediate postoperative period, the macular hole appeared closed and the retina was attached. One week later, the child noticed deterioration of vision in the left eye and visual acuity was reduced to perception of light. There was extensive pigment dispersion over the lens and in the vitreous cavity. Through the gas bubble, a large area of bare choroid with localized retinal detachment was seen nasally. The parents declined a revision vitrectomy. At follow-up 2 weeks later, a total retinal detachment with scrolled up edges and fixed folds was seen (Fig. 4). Retinal manifestations after electrical shock injury include macular cyst,2 macular hole, macular edema, vascular occlusions, retinal pigment epithelial changes, retinal detachment,

Fig. 2—Fundus photograph showing full-thickness macular hole with a cuff of subretinal fluid, with cystic changes in the midperipheral superior and temporal retina.

Fig. 1—Fundus photograph showing detached coagulated vitreous.

Fig. 3—OCT scan showing full-thickness macular hole and intraretinal cysts. CAN J OPHTHALMOL—VOL. 45, NO. 2, 2010

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Correspondence abnormal electrophysiological tests,3 and coagulative necrosis of the choroidal and retinal vessels.4 Occurrence of macular hole is uncommon and there are only 2 reports of its occurrence following high-voltage electrical injuries.1,5 Proposed pathogenic mechanisms for macular hole formation include localized elevation of temperature of the retinal pigment epithelium, focal choroidal ischemia secondary to the vascular changes that result in thinning and concussive forces of the electrical shock leading to incomplete vitreous detachment, and residual vitreomacular traction.1 In our patient, the macular hole was noticed in the immediate postinjury period and complete PVD was noted clinically and confirmed intraoperatively. A coagulated appearance of the vitreous, a finding not previously described, was also seen. Hence, it is likely that thermal shrinkage of the vitreous body caused the PVD and macular hole. In our patient, there were no intraoperative complications and the macular hole appeared closed in the immediate

postoperative period. Subsequently, retinal necrosis and detachment developed, possibly because of ischemic and coagulative changes weakening the retina. In summary, we report a rare occurrence of macular hole after electrical injury, with a new proposed pathogenic mechanism. Although an isolated occurrence is inconclusive, our experience suggests that the prognosis following surgery for such macular holes is likely to be poor. REFERENCES 1. Boozalis GT, Purdue GF, Hunt JL, McCulley JP. Ocular changes from electrical burn injuries. A literature review and report of cases. J Burn Care Rehabil 1991;12:458–62. 2. Sony P, Venkatesh P, Tewari HK, Garg SP. Bilateral macular cysts following electric burn. Clin Experiment Ophthalmol 2005;33:78–80. 3. Miller BK, Goldstein MH, Monshizadeh R, Tabandeh H, Bhatti MT. Ocular manifestations of electrical injury: a case report and review of the literature. CLAO J 2002;28:224–7. 4. Archer DB. Dermot Pierse lecture. Injuries of the posterior segment of the eye. Trans Ophthalmol Soc UK 1985;104: 597–615. 5. Wainwright DJ, Fuchshuber P. Delayed spinal cord damage and a unilateral macular hole following electrical trauma. Injury 1994;25:275–6.

Jyothsna Rajagopal,* Satyendranath B. Shetty,{ Anuradha Girish Kamath,* Girish Gurpur Kamath*

*Mahaveer Eye Hospital, and {M.S. Ramaiah Medical College, Bangalore, India Correspondence to Jyothsna Rajagopal, MS: [email protected]

Fig. 4—Fundus photograph showing a total retinal detachment with scrolled up edges and fixed folds.

Orbital mass as a presenting sign of acute leukemia

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n 11-month-old girl presented with a 2-week history of acute onset of ptosis and proptosis in the right eye. The patient had no previous illness. On examination, a firm nontender orbital mass located in the superonasal quadrant of the right eye was palpated (Fig. 1A); there was a bluish

Fig. 1—Front view of the patient. Upon presentation, the right eye was ptotic and proptotic (A); 5 days after presentation, the proptosis increased and conjunctival chemosis developed in the upper nasal quadrant of the globe (B).

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discoloration on the upper eyelid. Anterior segment and fundus examination of the right eye was otherwise normal. The left eye was normal. Protrusion of the right eye progressed, and severe conjunctival chemosis developed within 5 days of the patient’s attending the clinic (Fig. 1B). Orbital MRI showed a well-defined orbital mass in the upper nasal quadrant of the right eye with no bone destruction (Fig. 2). Complete blood count revealed a leukocytosis of 366109/L with atypical lymphocytes and blast cells on the peripheral smear. Bone marrow aspiration confirmed the diagnosis of acute myeloid leukemia (AML-M4), and cerebrospinal fluid examination disclosed malignant cells. The patient received AML-BFM 98 chemotherapy protocol, and the mass showed a rapid regression. Following the first-line treatment severe neutropenia developed, and the patient died 2 weeks later. Leukemia is a malignant neoplasm of the hematopoietic stem cells, characterized by neoplastic cell infiltration of