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Vol. 61 No. 10

Table 1: Demographics, type of injury with duration, time of surgery with 20G silicone as stent and outcome in 12 patients with canalicular laceration Age/ gender

Type of injury

Outcome

Complication

Syringing Epiphora

Follow up (months)

Lower

1 day

10

Patent

Absent

Nil

17

Indirect (bucket handle) Upper

7 days

2

Partially patent

Absent

Spontaneous extrusion

17

Absent

Punctal granuloma, corneal abrasion

5

19 yrs/M Indirect (iron rod) 28 yrs/F

Canaliculus Lag time Stent removal involved before repair (weeks)

29 yrs/M Indirect (cow horn)

Lower [Fig. 1d-e]

6 days

8

Patent

41 yrs/M Indirect (cow horn)

Lower

3 days

6

Not patent Present

Partial extrusion

9

60 yrs/M Indirect (bull horn)

Lower

3 days

7

Not patent Present

Canalicular obstruction

8

28 yrs/M Indirect (bear paw)

Upper and lower

3 days

7

Both patent

Absent

Nil

2

34 yrs/M Indirect (cracker injury)

Lower

2 days

8

Patent

Absent

Nil

9

5 yrs/M

Lower

4 days

8

Patent

Absent

Nil

6

32 yrs/M Indirect (bicycle handle) Lower [Fig. 1a,b]

3 days

6

Patent

Absent

Nil

5

44 yrs/M Indirect (road traffic accident)

Lower

9 days

2

Not patent Present

Spontaneous extrusion, canalicular obstruction

2

15 yrs/M Direct (bamboo)

Upper

3 days

15

Patent

Nil

15

5 days

4 5

Patent Absent Not patent Absent

Tube migration

5

Indirect (iron rod)

32 yrs/M Indirect (road traffic accident)

Lower Lower

Absent

yrs: Years, M: Male, F: Female

patency. Finally the 20G silicone rod offers a significant cost advantage compared to standard mono‑canalicular stents. This may be relevant to developing countries with large underprivileged sections in the society and poor access to affordable health care. In our experience the 20G silicone rod was an effective and economical alternative in canalicular lacerations with reasonable success.

References 1. Kennedy RH, May J, Dailey J, Flanagan JC. Canalicular laceration, an 11 year epidemiologic and clinical study. Ophthal Plast Reconstr Surg 1990;6:46‑53. 2. Jordan  DR, Ziai  S, Gilberg  SM, Mawn  LA. Pathogenesis of canalicular lacerations. Ophthal Plast Reconstr Surg 2008;24:394‑8. 3. Leibovitch  I, Kakizaki  H, Prabhakaran  V, Selva  D. Canalicular

Pigmented paravenous chorioretinal atrophy with Coat’s like response Manish Tandon, Dhananjay Shukla, Rubina Huda, Kim Ramasamy

lacerations: Repair with the Mini‑Monoka R monocanalicular intubation stent. Ophthalmic Surg Lasers Imaging 2010;41:472‑7. 4. Naik  MN, Kelapure A, Rath  S, Honavar  SG. Management of canalicular lacerations: Epidemiological aspects and experience with Mini‑Monoka monocanalicular stent. Am J Ophthalmol 2008;145:375‑80. 5. Reifler  DM. Management of canalicular laceration. Surv Ophthalmol 1991;36:113‑32. 6. Tint NL, Alexander P, Cook AE, Leatherbarrow B. Eyelid avulsion repair with bi‑canalicular silicone stenting without medial canthal tendon reconstruction. Br J Ophthalmol 2011;95:1389‑92. Cite this article as: Chatterjee S, Rath S, Roy A, Shrestha E. 20G silicone rod as monocanalicular stent in repair of canalicular lacerations: Experience from a tertiary eye care centre. Indian J Ophthalmol 2013;61:585-6. Source of Support: Nil. Conflict of Interest: None declared.

Pigmented paravenous chorioretinal atrophy  (PPCRA) is an uncommon retinal disorder of unknown etiology that is neither well understood nor classified. We report an atypical case of PPCRA, associated with Coat’s like response (CLR) in a 64‑year‑old man of Asian origin. Both the eyes were involved, though asymmetrically. Access this article online Quick Response Code:

Department of Retina‑Vitreous, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai, Tamil Nadu, India Correspondence to: Dr. Manish Tandon, Retina and Vitreous Services, Aravind Eye Hospital and Postgraduate Institute of Ophthalmology, Madurai - 625 020, Tamil Nadu, India. E‑mail: [email protected] Manuscript received: 13.10.12; Revision accepted: 09.09.13

Website: www.ijo.in DOI: 10.4103/0301-4738.121083 PMID: ***

587

Brief Communications October 2013

Key words: Coat’s like response, pigmented paravenous chorioretinal atrophy, Retinochoroiditis radiata

aneurysms with capillary nonperfusion areas OS akin to Coat’s disease (CD) [Fig. 1c‑e].

PPCRA is an uncommon, asymptomatic, slowly progressive disease of unknown etiology, although some authors have attributed it to be the sequela of ocular inflammation. It has been described as pigmentary retinopathy, and is characterized by the presence of bilateral and symmetrical chorioretinal atrophy and corpuscular pigmentation along the retinal veins, extending nearly half to one disc diameter on either side of the vein and its branches.[1]

Discussion The first case of this disorder was described as Retinochoroiditis radiata,[2] and since then there have been several reports of varied presentations. The characteristic presentation of PPCRA is bilateral, restricted to the paravenous area, and slowly progressive disorder with macular sparing. Hence, it is believed not to be sight threatening degenerative condition of the eye. Visual field evaluation has been reported to be variable ranging from normal fields to significant field defects. Electrophysiological tests are usually normal but diminution of b‑wave and prolongation of a‑wave and b wave implicit time have also been described.[3] Although most reports have been of sporadic presentation but there have been reports on hereditary pattern as well.[4]

CLR is characterized by clinical features like telangiectasia, exudation and sometimes exudative retinal detachment. We report an unusual association of PPCRA with CLR.

Case Report

CLR has been described often in relation to retinitis pigmentosa (RP), and it differs from the classical CD as there is no age and gender predisposition in CLR as opposed to CD where young boys are affected in early childhood. CLR tends to involve inferior and/or temporal quadrants of both retinae in most cases in contrast to CD where the most common involvement is unilateral and in superotemporal quadrant.[5]

A 64‑year‑old man of Asian origin presented to us with complains of slowly progressive defective vision left eye (OS) for five years. There was no history of suggestive of previous inflammation, trauma or nyctalopia, or family history of retinal disorder. He was a known hypertensive on regular treatment. His best corrected visual acuity  (BCVA) was 20/20 right eye (OD) and 20/32 OS. Anterior segment was unremarkable both eyes (OU). Central fields were normal. Fundus evaluation showed pigment clumps along the retinal veins with variable chorioretinal atrophy extending from the disc up to equator OU [Fig. 1a and b] and intraretinal and subretinal exudation with telangiectasia along the superotemporal vein OU w(more evident clinically in OS). A clinical diagnosis of PPCRA with CLR, OU was made.

Our case is unusual because a bilateral CLR has not been described before with PPCRA, however there has been an earlier report of asymmetric predominantly unilateral PPCRA with microangiopathy, along with field defect in the involved eye, and ERG changes.[6] Our case had no field defects and the ERG was normal OU. Systemic diseases that may mimic the vasculopathy of this disorder such as diabetes mellitus, retinal vein occlusion, Eales’ disease and sickle cell retinopathy were excluded by history, clinical examination and laboratory investigations.

Electroretinography  (ERG) was normal OU. Fluorescein angiography showed areas of hyperfluorescence in atrophic areas in the peripapillary area and hypofluorescence corresponding to the pigment clumps along the retinal veins along with its branches with telangiectasia and exudation along superotemporal vein OU and multiple macro

a

The cause for vasculopathy cannot be fixed with certainty but an array of clinicopathological explanations for exudative vasculopathy that have been described are an existence

c

b

d

e

Figure 1: (a and b) Fundus pictures OD and OS respectively showing pigment clumps along the retinal veins and chorioretinal atrophy extending from the disc, with intraretinal and subretinal exudation and telangiectasia along the superotemporal vein OU (OS is more obvious clinically). (c-e) Fluorescein angiogram OS (c,d) and OD (e) depicting areas of hyperfluorescence in atrophic areas and hypoflourescence corresponding to the pigment clumps with telangiectasia and exudation along superotemporal vein OU and multiple macro aneurysms with capillary nonperfusion areas OS

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Indian Journal of Ophthalmology

of congenital vascular anomalies akin to CD which get stimulated to progress by concurrent degeneration of the retina, choroidal origin for vascular exudative lesions, and acquired degeneration of the Bruch’s membrane leading to venous anastomosis between retinal and choroidal vasculature. This exudative vasculopathy leads to a break in the blood retinal barrier resulting in macular edema; and sometimes shallow inferior retinal detachments and subsequent telangiectasia.[7,8]

Vol. 61 No. 10

pigmented paravenous retinochoroidal atrophy. Br J Ophthalmol 1989;73:463‑7. 2. Brown  TH. Retino‑choroiditis radiata. Br J Ophthalmol 1937;21:645‑8. 3. Pearlman  JT, Kamin  DF, Kopelow  SM. Pigmented paravenous retinochoroidal atrophy. Am J Ophthalmol 1975;80:630‑5. 4. Skalka  HW. Hereditary pigmented paravenous chorioretinal atrophy. Am J Ophthalmol 1979;87:286‑91.

In our case chronic progressive atrophic changes of retinal pigment epithelium and photoreceptors along the retinal veins probably caused a chronic decompensation of the microvasculature leading to telangiectasia, leakage and exudation.

5. Khan JA, Ide CH, Strickland MP. Coats’‑type retinitis pigmentosa. Surv Ophthalmol 1988;32:317‑32.

The chronicity of vasculopathy lead to the development of minimal macular edema in OS and the patient had blurring of vision but as the BCVA was too good, no active intervention was contemplated. The cause for subnormal vision OS could not be determined with certainty. Our case expands the clinical spectrum of PPCRA and adds this disease into the list of RP syndromes associated with CLR.

7. Fogle JA. Welch RB, Green WR. Retinitis pigmentosa and exudative vasculopathy. Arch Ophthalmol 1978;96:696‑702.

References 1. Yamaguchi  K, Hara  S, Tanifuji  Y, Tamai  M. Inflammatory

6. Limaye  SR, Mahmood  MA. retinal microangiopathy in pigmented paravenous chorioretinal atrophy. Br J Ophthalmol 1987;71:757‑61.

8. Pruett  RC. Retinitis pigmentosa: Clinical observations and correlations. Trans Am Ophthalmol Soc 1983;81:693‑73.

Cite this article as: Tandon M, Shukla D, Huda R, Ramasamy K. Pigmented paravenous chorioretinal atrophy with Coat's like response. Indian J Ophthalmol 2013;61:586-8. Source of Support: Nil. Conflict of Interest: None declared.

Infestation of the lacrimal sac by Rhinosporidium seeberi: A clinicopathological case report

features of idiopathic orbital inflammatory disease in a young male patient. Clinical features, pathophysiology, and management of lacrimal sac rhinosporidiosis have been discussed.

Bipasha Mukherjee, Ashwin Mohan, Sumathi V1, Jyotirmay Biswas2

Oculosporidiosis is caused by Rhinosporidium seeberi, a parasite endemic in southern parts of India. It usually presents with swelling of the lacrimal sac with bloody tears. Management is by complete surgical removal followed by hispathological confirmation as the organism is always found in the lesions.

Rhinosporidium seeberi, till recently known as a fungus, has been reclassified as a protistan parasite. It infects humans and many animal species. The authors describe a rare case of oculosporidiosis with involvement of the lacrimal sac exhibiting Access this article online Quick Response Code:

Website: www.ijo.in DOI: 10.4103/0301-4738.121084 PMID: ***

Departments of Orbit, Oculoplasty, Reconstructive and Aesthetic Services, 2Ocular Pathology, Medical Research Foundation, Sankara Nethralaya, Chennai, 1Department of Otolaryngology, Sundaram Medical Foundation, Chennai, Tamil Nadu, India Correspondence to: Dr.  Bipasha Mukherjee, Department of Orbit, Oculoplasty, Reconstructive and Aesthetic Services, Medical Research Foundation, Sankara Nethralaya, 18, College Road, Chennai ‑ 600 006, Tamil Nadu, India. E‑mail: [email protected] Manuscript received: 14.04.12; Revision accepted: 20.05.13

Key words: Dacryocystectomy, oculosporidiosis, Rhinosporidium

Case Report A 25‑year‑old North‑Indian male presented to our center with history of recurrent painful swelling below the right lower lid for the past 1 year with associated watering. He also gave history of chronic sinusitis for the past 10  years. There was no history of purulent or serosanguineous discharge. He was diagnosed elsewhere as a case of chronic dacryocystitis of the right lacrimal sac and treated with systemic antibiotics with no resolution in symptoms. A computerized tomography (CT) scan was done 1 year back which reported a small oval swelling in the right medial canthal region with deviated nasal septum, bilateral small maxillary sinus polyps, and concha bullosa. On examination, vision was 6/6 N6 in both eyes. Anterior and posterior segment examinations of both eyes revealed normal findings. There was fullness of the right lower lid with erythema, induration, and tenderness. Regurgitation on pressure on the lacrimal sac  (ROPLAS) was negative and syringing showed the lacrimal drainage system to be bilaterally patent. A  clinical diagnosis of right partial nasolacrimal duct obstruction with preseptal cellulitis was made. An otolaryngology opinion was sought. Nasal endoscopic evaluation revealed a deviated nasal septum

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