Rectus muscle cysticercosis- A rare case study in Western Rajasthan By Arvind Chouhan, MS; Taruna Lakhotia MBBS; Prabhu Prakash, MD

ROS TIMES	ROS	RJO Content  Page	Contact Us	About Us
Editor                                   Dr Sudhir Singh   Advisors Prof. P.K Mathur Dr  Pavan Shorey   Editorial Board Dr Anshoo Choudhary Dr Arun Kshetrapal Dr L S Jhala Dr Mayank Agrawal Dr Mukesh Sharma Dr Sandeep Arora Dr Sonu Goel Dr Subodh Saraf Dr Sukesh Tandon Dr Sunil Gupta Dr Suresh Kumar Pandey Dr Swati Tomar Dr Virendra Agrawal   Rectus muscle cysticercosis- A rare case study in Western Rajasthan   Arvind Chouhan, MS; Taruna Lakhotia MBBS; Prabhu Prakash, MD Corresponding Author Dr.Arvind Chouhan Dr.S. N. Medical College, Jodhpur Article Code RJO20110111 INTRODUCTION Orbital cysticercosis is well documented disease entity but isolated involvement of extra ocular muscle by Cysticercus cellulosae is uncommon. Cysticercosis is serious health problem in developing countries, commonly seen in Latin American, Eastern Europe, India, Pakistan, Indonesia and China. It is caused by Cysticercosis cellulose, which is a larval form of pork tapeworm Taenia solium.  Rarely it is caused by the larvae of beef tapeworm T. saginata. Humans are infected by eating contaminated raw pork or beef or by drinking contaminated water. We hereby present two cases of cysticercosis affecting the EOM discussing their presenting features, investigations done, treatment prescribed and their follow-up. CASE REPORT 1 -    A 35 years old non-diabetic and non-hypertensive man presented with history of  pain in   left eye since 2 months with  drooping  of  upper eye   Figure 1: Showing proptosis of left eye lid since one month duration along with protrusion of globe and lacrimation. There was no fever, nausea, vomiting, visual disability and double vision. No redness was noted in the affected eye. The left eye’s  movements were restricted in horizontal gaze. Corneal sensations were normal. Examination of right eye did not reveal any abnormality.  Investigations     All routine investigation including Hb, ESR, CBC, TDLC, blood urea, serum creatinine, random blood sugar, SGOT, SGPT, ELISA for HIV, T3, T4, TSH level and X-ray chest were in normal limits. On ophthalmic examination his vision was 20/20 OU. S/L examination and fundus (on direct ophthalmoscopy) were normal. IOP was 17.0 mmHg (by applanation tonometer) in both eyes. CNS examination was normal. On imaging:- B. Scan- left eye disclosed a cystic lesion measuring 6x5mm with hyperechoic speck (Scolex) within it,  causing compression over posterior aspect of eyeball with  bulky lateral rectus muscle.   Figure: 2 B Scan of left eye showing cystic lesion  with  scolex. CT scan orbit was done which suggested mild proptosis of left eyeball with enhancing lesion measuring 6x6 mm seen in lateral rectus with thickening of lateral rectus muscle in its anterior 2/3rd. Figure 3: CT Scan Eccentric module sign of scolex was seen within the lesion. Remaining findings were normal in CT appearance. So a diagnosis of proptosis left eye with ptosis left eye as a manifestation of cysticercosis of lateral rectus was made.  CASE REPORT 2 A young girl of age 7 yrs. came to our O.P.D. with complaints of a mass in the inner portion of her right eye of duration since one month, noticed by her parents that increased gradually in size. She also complained of watering. The patient was vegetarian and from low profile family. On examination of right eye a fleshy, red, protuberant mass of size 1.0cm x 0.5cm was seen at the medial part of palpebral aperture. Eyes were orthophoric but the growth was restricting the movements of right eye towards the medial side. Rest of the extraocular movements were normal. Vision of the patient was normal in both eyes and the IOP with applanation tonometer was within normal limits. Both eyes fundi were also normal.                          Figure 4-Showing a mass in the nasal side of palpebral aperture.      Investigations 1.Complete urine profile – No abnormality detected 2.Stool examination: No abnormality detected 3.Hematology: Hb:12.7gm% TLC: Within normal range DLC: Within normal range ESR – 25mm in first hour 5. USG right eye- Showed a well defined cystic anechoic lesion of size 9.8 x 4.5mm in medial rectus muscle with a small 1.2 x 1.7mm echogenic speck noted in mid portion of anechoic area.    Figure 5-showing enlargement of medial rectus muscle  6. NCCT & CECT of head and orbit- stated a well defined cystic lesion   with enhancing walls and tiny intralesional hyperdense speck involving anterior portion of medial rectus muscle. Medial rectus muscle was bulky and edematous.   Figure 6  Both USG & CT findings suggested the diagnosis of cysticercosis of medial rectus muscle. Discussion Cysticercosis is a serious health problem in developing countries like Latin America. Asia and Africa specially in areas of poverty and poor hygiene(1,2). As per the Indian literature, ocular involvement occurs in 1.8-4.5% cases only(3). Despite the high  incidence of brain and ocular involvement  in cypticercosis, extraocular muscle cycticercosis is rare(5).  It has been reported primarily in pediatric and young adult population(4). In a series of 9 patients of cysticercosis, extra ocular muscle involvement was as following- MR in 5, IR in 5, SR in 2 & LR in 2 cases. 4 patients had moderate to severe inflammation around the cyst. In one of our case, the cyst was located in LR muscle of left orbit which is a less common site but the other case showed the involvement of MR. However the cyst may lodge in any of extra ocular muscle. The prominent symptoms are protusion of eyeball, pain, diplopia, ptosis and diminution of vision. Imaging modalities like orbital USG, CT scan, or MRI brain with orbital cuts are essential for diagnosis. Brain parenchymal involvement was not seen in our patients as seen in most of the studies on ocular cysticercosis(6). Literature on the treatment for orbital cysticercosis is quite conflicting. Resolution of the lesion can occur spontaneously or after therapy. The parasite if left untreated eventually dies after 2 to 4 years. Cysticidal therapies can provoke the inflammatory response around residual dying cysticerci due to release of toxin. So the therapy must be individualized according to location of parasite and activity of the disease. Combination of oral albendazole (15 mg/kg b.w.) and steroid ( 1 mg/kg b.w.) may be efficacious in selected cases provided there is no threat to vision  as a consequence of therapy(7). In our case the patient was given minimum dose steroid which was followed by combined steroid and albendazole therapy. In conclusion involvement of extra ocular muscles by cysticercus cellulose is very rare. Rarer still is the involvement of LR muscle presenting clinically as unilateral ptosis, mild proptosis and pain. B scan is best investigation module and conservative treatment with albendazole and steroid after ruling out CNS involvement show early regression.  REFERENCES 1.Coker-Vann MR,Subianto DB,Brown P et al.ELISA antibodies of Cysticerci Of Taenia Solium In human population in New Guinea, Oceania and South-East Asia.Southeast Asian J Trop Med Public Health 1981;12:499-505. 2.Sekhar GC ,Honavar SG.Myo-cysticercosis:Experience with imaging and therapy.Ophthalmology 1999;106:2336-40. 3.NHWadia.Neurocysticercosis. Neurological practice  in Indian prospective 2005;215-51. 4 Puri P,Grover AK.Medical management of orbital myo-cysticercosis:a pilot study.Eye 1998;12:795-9. 5.Yanoff  Duker 3rd edition;835-36. 6.Pushker N,Bajaj MS,Chandra M,Neena.Ocular and orbital cysticercosis.Acta Ophthalmol Scand 2001;79:408-13. 7.Sihota R,Honaver SG.Oral albenazole in the management of extraocular cysticercosis.Br J Ophthalmol 1994;78:621-3.               Disclaimer Rajasthan Journal Of Ophthalmology An Official Publication Of The Rajasthan Ophthalmological Society
Chief Web Editor Dr Sudhir Singh All Rights Are Reserved To Rajasthan Ophthalmological Society

A rare orbital foreign body penetrating into maxillary sinus: A brake lever By Subodh Saraf ,MS;Ravindra Singh,MS; Vijay Gupta, MS; Kamal Arora, MS

ROS TIMES	ROS	RJO 2011 Contents	Contact Us	About Us
Editor                                   Dr Sudhir Singh   Advisors Prof. P.K Mathur Dr  Pavan Shorey   Editorial Board Dr Anshoo Choudhary Dr Arun Kshetrapal Dr L S Jhala Dr Mayank Agrawal Dr Mukesh Sharma Dr Sandeep Arora Dr Sonu Goel Dr Subodh Saraf Dr Sukesh Tandon Dr Sunil Gupta Dr Suresh Kumar Pandey Dr Swati Tomar Dr Virendra Agrawal   A rare orbital foreign body penetrating into maxillary sinus: A brake lever   Subodh Saraf ,MS;Ravindra Singh,MS; Vijay Gupta, MS; Kamal Arora, MS Corresponding Author: Dr. Subodh Saraf, MS Registrar Global Hospital Institute of Ophthalmology Abu Road 307510 Article Code RJO20110108 Abstract In this report, we introduce a case with unusual large foreign body (part of a brake lever around 7cm in length) which entered in the orbit after a motorcycle accident. The brake lever made a laceration in the left lower lid and then displacing the eyeball upward, its bigger rounded end fractured the floor of orbit and entered in maxillary sinus. Rest of the part was protruding outside from the eyelid. There was no ocular laceration, extra ocular muscle and optic nerve injury. Management strategy is discussed in the report. Patient had final post operative vision of 20/200. Ocular movements were normal. There was no enophthalmos or hypoglobus post operatively. Introduction Large orbital foreign bodies (FBs) usually associated with ocular laceration and occur after a high-velocity injuries such as a gunshot or industrial accident. [1, 2] Only few cases have been reported with motorcycle brake lever acting as foreign body. Large size of foreign body, simultaneous involvement of orbit and maxillary sinus & excellent post operative results make this case unique. Case Report A 40-year-old man presented to our outdoor who had a motorcycle accident. Part of brake lever (7 cm in length) had lacerated the left lower lid and had entered the orbit displacing the eyeball upward. [Fig. 1]. No ocular laceration or hypotony was seen. Pupil was semidilated non reactive. Since the patient was not cooperative, owing to discomfort following trauma, slit-lamp examination and visual acuity assessment could not be done. X-ray of the orbit A.P and lateral view was performed which revealed that the foreign body was not only involving orbit, but also maxillary sinus. Rounded bigger end of the brake liver had fractured floor of the orbit was lying in the maxillary sinus. Rest of the part of foreign body was protruding outside the skin. To know about further extent of injury and to plan the approach for the operation, 3 Dimensional Computerized tomography (CT) was done. To our surprise, none of the extra ocular muscles were damaged. The optic nerve and optic nerve canal were also not injured. Orbital margins were secure. Fracture was less than 50% of total floor area and it was located more towards the temporal side. Nasal bone was fractured. [Fig. 2]. The patient was taken for operation under general anesthesia. Surgical area was cleaned of sand particles and broken lashes. Securing the globe using optic nerve guide, we tried to simply pull out the foreign body but were unable to mobilize it.  So we decided to explore the fracture site. Taking care of bleeders, we displaced orbital fat and fascial tissue and again tried to remove the brake lever. This time we could slightly mobilize it. Looking into the 3D CT scan we slightly enlarged the fracture opening temporally with the help of artery forcep. Ultimately, the foreign body was removed by pulling it out in the same direction through which it entered. The operation was done in presence of maxillofacial surgeon. Then we assessed the fracture size clinically. The findings correlated with CT findings. There was no entrapment of muscles. No significant prolapsed of orbital tissue was seen. So it was decided to follow up the patient for 6 weeks to look for development of any enophthalmos or diplopia.  Entry wound was sutured 2 layers using 5-0 catgut for internal and 4-0 silk for external sutures. Next post operative day, patient’s vision was 20/200. On slit lamp examination anterior chamber was found to be shallow and the lens was subluxated. No enophthalmos was seen and ocular movements were normal Figure 1 Penetrating orbital injury with brake lever Figure 2   3 D computerized tomography shows foreign body: rounded end s has fractured the floor of orbit and lying in maxillary sinus. Figure 3 Computerized tomography shows foreign body: rounded end s has fractured the floor of orbit and lying in maxillary sinus. Figure 5 Eyeball guarded by optic nerve guide. Figure 6 The brake lever after surgical removal Figure 7 Finally repaired wound Figure 8 1st postoperative day   Discussion Intraorbital FBs can be associated with severe injuries leading to loss of vision or may lead to sight-threatening complications.[1,2] A retained metallic intraorbital FB may cause a variety of signs, symptoms, and clinical findings, based on its size, location, and composition.[5] Loss of vision is usually due to the initial trauma and is generally not influenced by surgical intervention.[1] The best management of retained metallic intraorbital FBs remains a controversial subject.[5,6] The decision regarding surgical removal depends mainly on the location and type of intraorbital FBs.[5] However, the removal of foreign body from the orbit, which is crowded with delicate structures, is not safe.[6] Retained metallic intraorbital FBs are well tolerated and should be managed conservatively in the absence of specific indications for removal.[1,2] When the foreign body is impinging on neurological structures or causing mechanical restriction to ocular movements or is composed primarily of copper, one should consider removal of the FB after detailed and precise localization to minimize damage to the adjacent ocular structures.[1,2,5,6] Our experience shows that some orbital FBs especially those with round and smooth surfaces can simply be removed from their tract through which they entered, obviating the need for more sophisticated surgery. This approach may especially be useful in large orbital FBs in which the tract is easily visible radiologically and removal of foreign body with other approaches may cause significant trauma to orbital structures. References 1. Finkelstein M, Legmann A, Rubin PA. Projectile metallic foreign bodies in the orbit; A retrospective study of epidemiologic factors, management, and outcomes. Ophthalmology. 1997; 104:96–103. [PubMed] 2. Michon J, Liu D. Intraorbital foreign bodies. Semin Ophthalmol. 1994;9:193–9. [PubMed] 3. Sukhija J, Bandyopadhyay S, Ram J, Bansal S, Das P, Brar GS. Unusual intraorbital foreign body: A case report. Ann Ophthalmol (Skokie) 2006;38:145–7. [PubMed] 4. Cartwright MJ, Kurumety UR, Frueh BR. Intraorbital wood foreign body. Ophthal Plast Reconstr Surg. 1995;11:44–8. 5. Cooper W, Haik BG, Brazzo BG. In: Smith's Ophthalmic Plastic and Reconstructive Surgery. Nesi FA, Levine MR, Lisman RD, editors. Mosby: St. Louis; 1998. pp. 260–9. 6. Fulcher TP, McNab AA, Sullivan TJ. Clinical features and management of intraorbital foreign bodies. Ophthalmology. 2002;109:494–500. [PubMed] Disclaimer   The Rajasthan Journal Of Ophthalmology an Official Publication Of TheRajasthan Ophthalmological Society
Chief Web Editor Dr Sudhir Singh All Rights Are Reserved To Rajasthan Ophthalmological Society

Combined inner limiting membrane peeling and intravitreal triamcinolone acetonide in diffuse diabetic macular oedema By Pankaj Dhaka,MD ; Atul Kumar,MD; R V Azad,MD; Y R Sharma,MD.

ROS TIMES	ROS	RJO Content  Page	Contact Us	About Us
Editor                                   Dr Sudhir Singh   Advisors Prof. P.K Mathur Dr  Pavan Shorey   Editorial Board Dr Anshoo Choudhary Dr Arun Kshetrapal Dr L S Jhala Dr Mayank Agrawal Dr Mukesh Sharma Dr Sandeep Arora Dr Sonu Goel Dr Subodh Saraf Dr Sukesh Tandon Dr Sunil Gupta Dr Suresh Kumar Pandey Dr Swati Tomar Dr Virendra Agrawal   Combined inner limiting membrane peeling and intravitreal triamcinolone acetonide in diffuse diabetic macular oedema   Pankaj Dhaka,MD ; Atul Kumar,MD;  R V Azad,MD; Y R Sharma,MD. Corresponding Author Dr.Pankaj Dhaka                                                                                  M.N Hospital and Research Centre,Bikaner                                                                                 Pin-334001, Phone no. 0151 -2230347, 9314806609                                                                                  E- mail ID- pankajdhaka79@gmail. Article Code RJO20110114 Purpose: To evaluate the comparative effect on regression of diabetic diffuse macular edema using combination of surgical ILM peeling and intravitreal triamcinolone acetonide versus intravitreal triamcinolone acetonide (4 mg/0.1 ml) alone versus frequency double Nd:YAG focal/grid photocoagulation (532 nm). Design: Prospective, comparative case series. Participants:  Thirty eyes of diabetic patients with diffuse diabetic macular oedema were studied dividing into three groups on the basis of randomization. The study was conducted at Dr. R. P. Centre for Ophthalmic Sciences, AIIMS, New Delhi . Methods: Three groups were made. In group one,Parsplana vitrectomy with trypan blue (0.2%) assisted ILM peeling was done along with intravitreal triamcinolone acetonide (2 mg/0.1 ml) injection at the end of surgery. In group two, Intravitreal triamcinolone acetonide (4 mg/0.1 ml) is injected in patients with diffuse diabetic macular oedema under topical anaesthesia, and in group three, Focal/grid laser photocoagulation with double frequency Nd: YAG-532 nm was done in patients with diffuse diabetic macular oedema. Results:  The results showed that in patients who had undergone ILM peeling + IVTA has statistically significant improvement in vision and in patients who had undergone IVTA injection has improvement in vision but it is not statistically significant. But in patients who had undergone focal/grid laser photocoagulation had shown a statistically significant drop in visual acuity. The maximum reduction in central macular thickness after 3 months follow up is patients who had undergone ILM peeling + IVTA followed by patients who had undergone IVTA injection. In patients who were treated with laser photocoagulation the decrease in central macular thickness is less as compared to other groups. Mean contrast sensitivity before laser was 0.825 which was reduced to 0.825 at 6 weeks follow up and remained same (0.825) after 3 months. These results suggest that in group II patients who were treated by IVTA injection, there is no change in contrast sensitivity but in patients treated with ILM peeling + IVTA and laser photocoagulation, there is decrease in contrast sensitivity and more decrease was in patients treated with laser photocoagulation. Conclusions: In patients treated with inner limiting membrane peeling + intravitreal triamcinolone acetonide, there is a statistically significant decrease in central macular thickness with statistically significant improvement in visual acuity. In patients treated with intravitreal triamcinolone acetonide, there is a statistically significant decrease in central macular thickness with a statistically non significant improvement in visual acuity. In patients treated with focal/grid laser photocoagulation, there is a statistically significant decrease in central macular thickness with a statistically significant decrease in visual acuity and statistically significant decrease in contrast sensitivity. There is a decrease in contrast sensitivity in patients treated with inner limiting membrane peeling + intravitreal triamcinolone acetonide which is statistically not significant. INTRODUCTION Diabetic macular oedema is an important cause of visual impairment in patients with diabetic retinopathy. According to a recent WHO report, India has 31.7 million diabetic subjects and the number is expected to increase to a staggering 79.4 million by the year 2030.1The Wisconsin epidemiologic study of diabetic retinopathy estimated that after 15 years of known diabetes, the prevalence of diabetic macular oedema is ~ 20% in patients with type 1 diabetes, 25% in patients with type 2 diabetes who are taking insulin and 14% in patients with type 2 diabetes who do not take insulin.2Diabetic macular oedema because of the frequency with which it is seen, is a condition that has considerable public health importance. Currently the only demonstrated means to reduce the risk of vision loss from diabetic macular oedema are intensive glycaemic control, as demonstrated by diabetes control and complications trial (DCCT)3 and the U.K. prospective diabetes study4 and laser photocoagulation as demonstrated by early treatment diabetic retinopathy study.5 In the ETDRS, laser photocoagulation of eyes with diabetic macular oedema   reduced the risk of moderate visual loss by ~ 50% (from 24 to 12%, 3 years after initiation of treatment).5 These results show that for some patients, laser photocoagulation is effective but that 12% of treated eyes developed moderate visual loss in spite of treatment furthermore, ~ 40% of treated eyes that had retinal oedema involving the center of macula at baseline still had oedema involving the center at 12 months, as did 25% of treated eyes at 36 months. Diabetic macular oedema is of two types:           a)Focal – Focal macular oedema derives from individual or small clusters of micro aneurysms that histopathologically leak in more limited extent. b)Diffuse – Diffuse macular oedema derives from extensively damaged capillaries, micro aneurysms and arterioles in a generally dilated capillary bed. Diffuse diabetic macular oedema is defined as retinal thickening of two or more disc areas and involving some portion of the foveal avascular zone (FAZ) with or without cystoid macular oedema.. ETDRS defines diabetic macular oedema as -(a)Clinically significant macular oedema (CSME) and (b)Non clinically significant macular oedema. CSME is defined as -          Thickening of retina at or within 500 micron of the center of macula,hard exudates at or within 500 micron of the center of macula, if associated with thickening of adjacent retina and a zone or zones of retinal thickening at least one disc area or larger, any part of which is within one disc diameter of center of macula. Diffuse diabetic macular oedema does not response to grid laser photocoagulation in nearly 25% of cases.6The frequency of an unsatisfactory outcome following laser photocoagulation in some eyes with diabetic macular oedema has prompted interest in other treatments. One treatment is intravitreal steroids injection.Triamcinolone acetonide has traditionally been used as a periocular injection of the treatment of macular oedema secondary to inflammation or following intraocular surgery.7,8 To achieve a higher intraocular concentration of corticosteroid to treat retinal disease, the intravitreal injection of triamcinolone acetonide was first proposed in 1970, in an animal model, as a pharmacological adjunct to prevent the formation of proliferative vitreoretinopathy in order to improve outcomes following retinal detachment surgery.9 Intravitreal triamcinolone acetonide was first proposed in 1999 as a treatment for diabetic macular oedema because of the safety profile demonstrated in animal models, prior clinical experience with other retinal diseases and the rationale of attenuating the VEGF-mediated retinal capillary permeability that is presumed to contribute to diabetic macular oedema. The use of intravitreal triamcinolone acetonide is now widespread. Martidis et al10 reported results using intravitreal triamcinolone acetonide injection in 16 eyes with macular oedema due to diabetic retinopathy. They conclude that the intravitreal injection of triamcinolone effectively reduces macular thickening due to diffuse diabetic macular oedema. Jonas et al11 described results of intravitreal triamcinolone acetonide injection in 26 eyes with diabetic macular oedema. The study concluded that intravitreal triamcinolone injection is beneficial for improving visual acuity in patients of diffuse diabetic macular oedema.Pascale Massin et al12 in these study has also shown reduction of macular oedema in patients of diabetic retinopathy. The commonly used dose of 4 mg / 0.1 mg of triamcinolone is principally being used because of convenience. At a short dose of 40 mg/ml, triamcinolone is easily aliquoted to a 4 mg/0.1 ml dose. A volume of 0.1 ml is readily tolerated when injected into vitreous cavity, other than the convenience of this dose, there are no data that support the use of 4 mg over any other alternative dose. Role of parsplana vitrectomy and internal limiting membrane peeling in diffuse diabetic macular oedema. Previous studies have reported favorable anatomic and functional results after vitrectomy and removal of the posterior hyaloid and tractional forces associated with a thickened and taut premacular hyaloid in patients with diabetic macular oedema.13,14,15The surgical procedure consisted of removal of the posterior hyaloid, including peeling of epiretinal fibrocellular proliferations. The inner limiting membrane (ILM) was not approached. In macular hole surgery, the role of removal of the ILM is controversial. A number of vitreoretinal surgeons have reported better success rates with peeling of the ILM.16,17 Although this theory is unproven tangential traction also play a role in the formation and progression of diffuse diabetic macular oedema associated with advanced vitreoretinal interface disease. Grandorfer et al18 investigated impact of parsplana vitrectomy with ILM peeling in eyes with otherwise refractory diffuse diabetic macular oedema and concluded that, vitrectomy including removal of the ILM leads to expedited resolution of diffuse diabetic macular oedema and improvement of visual acuity.Kumagai et al19 also concluded that the period required for absorption of macular oedema in eyes with ILM peeling was shorter in type II DM. ILM peeling accelerates the absorption of oedema in more severe diabetic macular oedema, but they could not find any improvement of visual acuity. Mateo C, et al20 from Spain also reported that PPV with ILM peeling could be an effective procedure in the management of non tractional diabetic macular oedema, which is reflected in a reduction of macular thickness and an improvement or stabilization in visual acuity. OCT versus biomicroscopy in the detection of CSME The sensitivity of biomicroscopy and OCT in the diagnosis of macular thickening and CSME has been compared by Hee MR, et al.21 The two methods are equally effective in the detection of advanced cases with definite thickening or wide cystic changes. However, shallow changes in retinal thickening of less than 100 microns are invisible at slit lamp and easily observed at OCT.21 OCT therefore seems to be more sensitive in the early diagnosis of DME and in the detection of small changes in retinal thickness after treatment. Moreover, the presence of shallow retinal detachments or fine epiretinal membranes or a partially detached posterior hyaloid are only observed by OCT.22 For our study we used optical coherence tomographer, model-3000 by Carl Zeiss ophthalmic systems, including which have 18 acquisition protocols and 18 analysis protocols. In this study we used fast macular scan as acquisition protocol and retinal thickness single eye (line scan) for analysis purpose. MATERIALS AND METHODS  Patient selection The study was conducted at Dr. R. P. Centre for Ophthalmic Sciences, AIIMS, New Delhi .Thirty eyes of diabetic patients with diffuse diabetic macular oedema were studied dividing into three groups on the basis of randomization. Group I: Study group (10 eyes) Parsplana vitrectomy with trypan blue (0.2%) assisted ILM peeling was done along with intravitreal triamcinolone acetonide (2 mg/0.1 ml) injection at the end of surgery. The surgical technique will include a standard three port parsplana vitrectomy, complete posterior cortical vitrectomy, followed by careful identification, engagement and removal of posterior cortical vitreous layer. Sterile trypan blue dye (0.2%) is then squirted over macula and kept for 5 minutes. Excess of dye is aspirated from vitreous cavity with a vitrector. The ILM is pinched with pic forceps and flap grasped with the forceps and a shexis is created by slowly tearing the ILM in a circular motion, concentric with the fovea. ILM peeling is combined with injecting triamcinolone acetonide (2 mg/0.1 ml) intravitreal at the end of surgery. Group II: Study group (10 eyes) Intravitreal triamcinolone acetonide (4 mg/0.1 ml) is injected in patients with diffuse diabetic macular oedema under topical anaesthesia. Group III: Control group (10 eyes) Focal/grid laser photocoagulation with double frequency Nd: YAG-532 nm was done in patients with diffuse diabetic macular oedema.   PATIENTS ELIGIBILITY CRITERIA Inclusion criteria -Patients having persisting diffuse diabetic macular oedema (with cystoid changes on OCT line scan) inspite of previous focal/grid laser photocoagulation at least 3 months back,patients having type-2 diabetic mellitus,patients having nonproliferative diabetic retinopathy (NPDR) with diffuse diabetic macular oedema ,patients having best corrected visual acuity: Snellen’s < 6/60,media clarity, papillary dilatation and patients cooperation sufficient for adequate fundus photography.Informed consent was taken. Exclusion criteria- patients having age related macular degeneration (ARMD),patients having vascular occlusive disease affecting macula, patients having optic disc disease like open angle glaucoma, patients with macular oedema due to other cause e.g. pseudophakic macular oedema, patients having any major intraocular surgery done within 3 months, patients having any focal/grid laser photocoagulation done or intravitreal triamcinolone injected within 3 months, patients having uncontrolled DM, patients having chronic renal failure, presence of macular traction (on OCT). WORKUP AND STUDY PARAMETERS After the patients were selected based on the inclusion/exclusion criteria, work up was done as follows: General examination -Demographic data, presenting complaints, history of presenting complaints, detailed blood chemistry study done which includes Hb1AC levels, serum urea, serum creatinine, fasting blood sugar levels, postprandial blood sugar levels, systemic examination.   Ocular examination- Snellen’s best corrected visual acuity (BCVA), ETDRS best corrected visual acuity ,Contrast sensitivity (Pelli Robson chart), + 90D slit lamp biomicroscopy, Fundus fluorescein angiography (FFA), Colour fundus photography, Macular thickness measured by OCT. FOLLOW UP Follow up of patient was done at 1 week, 6 week and 3 months postoperatively. At each follow up, the above study parameters were recorded and repeated. Also, fluorescein angiography and OCT was done at 6 weeks and 3 months.   STATISTICAL ANALYSIS Data were recorded on a predesigned Performa and managed on an excel spread sheet. All the entries were checked for any possible keyboard error. Data obtained was statistically analyzed by student t test. Friedman’s test was used for intra group comparison. For inter group comparison chi-square test was used. In this study, p value of < 0.05 has been taken as statistically significant. OBSERVATIONS AND RESULTS For the purpose of study, total 30 patients were taken, 10 each in three groups. 1.         DEMOGRAPHIC PROFILE -In our study the mean age in group I in 59.1 years and standard deviation 6.790 and out of 10 patients, 5 patients were females (50%).In group II patients the mean age is 59.6 years and standard deviation in 8.003 and 3 out of 10 patients were females (30%). In group III patients the mean age is 58.4 years and standard deviation is 7.351 and 2 out of 10 patients were females (20%).In all 30 patients in our study, 33% were females and 67% males with p value of 0.01. 2.         VISUAL ACUITY- (a)Group I: 3 patients showed significant visual improvement (Snellen’s BCVA) by 1 line, p value – 0.049, and the remaining 7 patients showed no improvement.(b)Group II: 2 patients showed visual improvement (Snellen’s BCVA) by 1 line, p value – 0.1353, not significant. The remaining 8 patients showed no improvement in vision.(c)Group III: 2 patients showed a decrease in vision (Snellen’s BCVA) by 2 lines and 1 patient showed a decrease in vision by 1 line (Snellen’s BCVA), p value – 0.049, statistically it is a significant decrease in vision. 3.         CENTRAL MACULAR THICKNESS (a)          Group I: All 10 patients showed as statistically significant decrease in central macular thickness (p value – 0.0003). (b)          Group II: All 10 patients showed a statistically significant decrease in central macular thickness (p value – 0.0001). (c)          Group III: All 10 patients showed a significant decrease in central macular thickness (p value – 0.0003). Comparison of mean CMT values of all the 3 groups.  4.CONTRAST SENSITIVITY (a)          Group I: 3 patients showed a decrease in contrast sensitivity and the remaining 7 patients did not show any change in contrast sensitivity. The decrease is not statistically significant (P value – 0.061). (b)          Group II: Patients in this group did not show any change in contrast sensitivity (p value – 1.0) (c)          Group III: 3 patients showed a decrease in contrast sensitivity which is statistically significant decrease (p value – 0.049). Comparison of mean of contrast sensitivity values of all the three groups.   DISCUSSION The results of our study has shown that there is statistically significant visual improvement in patients who had undergone ILM peeling + intravitreal triamcinolone but in patients in which intravitreal triamcinolone was injected (Group II patients), the visual recovery is not statistically significant. In 3 months follow up the central macular thickness was reduced maximally in group I patients followed by group II patients.It seems that ILM peeling has additive role in decreasing central macular thickness over intravitreal triamcinolone. Studies have shown the close relationship between the vitreous, especially the posterior hyaloid and diabetic macular oedema. Hikichi et al23demonstrated that vitreomacular separation may promote the spontaneous resolution of diabetic macular oedema. Nasarallah et al24 showed that diabetic eyes with macular oedema have a lower rate of PVD than those without macular oedema, and speculated on a possible role of the vitreous in the pathogenesis of diabetic macular oedema. Lewis et al13 found that vitrectomy with removal of the thickened, taut premacular posterior hyaloid resulted in reduced macular oedema and improved visual acuity. Tachi and Nobuchika further noted that removal of loose posterior hyaloid also had a significant effect on the reduction of macular oedema. The vitreous may behave as a reservoir of inflammatory substances and its cortex may be a source of tangential traction on the retinal vessels. Structural changes of the vitreous gel, such as liquification and posterior vitreous detachment are associated with aging and the development of diabetic retinopathy. Stitt et al25 recently reported significantly increased evels of advanced glycation end products in the vitreous of patients with diabetes, forming increased irreversible cross linking of vitreous collagen. Moreover, the ILM thickens with age, and an increase in the bilaminated pattern of fibronectin deposits has been observed. Little is known about the molecular structure of the vitreoretinal interface in the eyes of patients with diabetes, but it seems unlikely that changes of the vitreous in these eyes would be limited exclusively to the vitreous gel. More likely, these changes may affect the vitreoretinal interface including the ILM. The ILM is known to play an important role as a scaffold for proliferating astrocytes. Its removal not only may result in an almost complete release of tractiona forces, but also may inhibit. The reproliferation of fibrous astrocytes on the retinal surface. Moreover, the removal of the basal lamina of muller cells theoretically may lead to changes in the protoplasmic skeleton of the retina and thereby enable more rapid resolution of diffuse macular oedema. The rationale for the use of triamcinolone acetonide to treat diabetic macular oedema follows from the observation that the increase in retinal capillary permeability that results in a macular oedema may be caused by a breakdown of the blood retinal barrier mediated in part by VEGF, a 45-kD a glycoprotein. Antonetti et al26 demonstrated that VEGF may regulate vessel what could be the reason of such decrease in contrast sensitivity after ILM peeling? The structural boundary between the retina and the vitreous consists of the ILM, which is adherent to the collagenous cortex of the vitreous on its one side, and to the muller (glial) cells end feet on the other. This latter adhesion is strong enough to cause tearing between the end feet and the rest of muller cells if the ILM is peeled.28 Removal of the end feet may cause changes in physiological features of muller cells even if membranes eventually seal and the cells survive.28 Because the muller cells are known to be sites of an intense exchange of waste products of active retinal neurons with the vitreous body acting as a buffering sink, any loss of muller cell end feet or even of their normal interaction with the vitreous, should interfere with retinal function.29 Unfortunately, it is difficult to assess whether ILM peeling causes impairment of the human retina. Permeability by increasing the phosphorylation of tight junction proteins such as occluding and zonula occluding.1 This model provides, at the molecular level, a potential mechanism for VEGF-mediated vascular permeability in the eye. With anti-inflammatory properties, triamcinolone acetonide have been demonstrated to inhibit the expression of the VEGF gene.27 In a study by Nauck et al,27 the platelet-derived growth factor induced expression of the VEGF gene was inhibited by corticosteroids in a dose dependent manner. Nauck et al27 also demonstrated that corticosteroids down regulate the induction of VEGF by the proinflammatory mediator platelet-derived growth factor and platelet-activating factor, in a time and dose dependent manner. Increased diffusion by modulation of calcium channels could also account for the efficacy of the corticosteroids in reducing macular oedema. In our study, the results are showing that these in statistically nonsignificant decrease in contrast sensitivity in group I patients and no change in contrast sensitivity in group II patients in 3 months follow up. Electron microscopic studies of excised membranes showed a varying degree of adherent cellular structures of presumed glial origin. The damage to muller cells during surgery and obvious surgical trauma may be the cause of reduction in contrast sensitivity as seen in our study in group I patients. Our study clearly indicates the beneficial role of ILM peeling + IVTA in reduction of macular oedema in improvement of visual acuity as compared to conventional focal/grid laser photocoagulation.   CONCLUSION In patients treated with inner limiting membrane peeling + intravitreal triamcinolone acetonide, there is a statistically significant decrease in central macular thickness with statistically significant improvement in visual acuity. In patients treated with intravitreal triamcinolone acetonide, there is a statistically significant decrease in central macular thickness with a statistically non significant improvement in visual acuity. In patients treated with focal/grid laser photocoagulation, there is a statistically significant decrease in central macular thickness with a statistically significant decrease in visual acuity and statistically significant decrease in contrast sensitivity.There is a decrease in contrast sensitivity in patients treated with inner limiting membrane peeling + intravitreal triamcinolone acetonide which is statistically not significant. REFERENCES 1.            Diabetes Care. 2004; 27: 1047-1053. 2.            The Wisconsin epidemiologic study of diabetic retinopathy: Ronald Klein, Barbara E.K. Klein, Scot E. Moss, Mathew D. Davis, David L. Demets. Ophthalmology: December 1984; 91(12). 3.            Diabetes control and complication trial research group: The effect of intensive treatment of diabetes on the development and progression of long term complications in insulin dependent diabetes mellitus. N Engl J Med 1993; 329: 977-986. 4.            United Kingdom prospective diabetes study group: Intenive blood-glucose control with sulphonyl weas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes. UKPDS 33 Lancet. 1998; 352: 837-853. 5.            Early treatment diabetic retinopathy study research group: Photocoagulation for diabetic macular oedema: ETDRS report number 1. Arch Ophthalmol 1985; 103: 1796-1806. 6.            Lee CM, Olk RJ. Ophthalmology 1991l 98: 1594-1602. 7.            Yeoshikawa K, Kotake S, Ichiishi A, Sasamoto Y, Kosaka S, Matsuda H. Posterior subtenon’s corticosteroid therapy for cystoid macular oedema refractory to typical medications, ophthalmology 1997; 104: 2003-2008. 8.            Thach A, Dugel P, Flindall R, Sipperley J, Sneed S. A comparison of retrobulbar versus subtenon’s corticosteroid therapy for cystoid macular oedema refractory to typical medications. Ophthalmology 1997; 104: 2003-2008. 9.            Machomer R, Sugita G, Tano Y. Treatment of intraocular proliferations with intravitreal steroids. Tr Am Ophthal Soc. 1979; 77: 177-178. 10.         Martidis A, dukes JS, Greenberg PB, Rogers AH, Puliafita CA, Reichel E, Baumal C. Intravitreal tramicinolone for refractory diabetic macular oedema. Ophthalmology. 2002; 109: 920-927. 11.         Jonas J, kreissig J, Sofker A, Degenring R. Intravitreal injection of triancinolone for diffuse diabetic macular oedema. Arch Ophthalmol 2003; 121: 57-61. 12.         Pascale Massin et al. Intravitreal triancinolone acetonide in diffuse diabetic macular oedema. Ophthalmology 2004; 111: 218-225. 13.         Lewis H, et al. Role of vitrectomy in treatment of diabetic macular oedema. Am J Ophthalmol 2001; 13: 123-125. 14.         Harbour J, Smiddy W, Flynn HJ, Rubsamen P. Vitrectomy for diabetic macular oedema associated with a thickened and taut posterior hyaloid membrane. Am J Ophthalmol 1996; 125: 405-413. 15.         Tachi N, Ogina N. Vitrectomy for diffuse diabetic macular oedema in cases of diabetic retinopathy. Am J Ophthalmol 1996; 122: 258-260. 16.         Messmer FM, et al. Vitrectomy including removal of ILM in diffuse diabetic macular oedema. Retina 2000; 20: 126-133. 17.         Rice TA, et al. Macular hole: Pathogenesis, diagnosis and treatment. Boston: Buttorworth Meinemann. 1998; 125-146. 18.         Grandorfer, et al. Surgical resolution of diabetic macular oedema: Retina 2000; 20: 126-133. 19.         Kumagai K, Nippon Ganka Gakkai Zasshi. 2002; 106(9): 590-594. 20.         Mateo C, et al. Institute de micro urciga, ocular de Barcelona-spain. 21.         Hee MR, et al. Arch Ophthalmol 1995; 113: 1019-1029. 22.         Kausir PK, Riemann CD, Scars JE, Lewis H. Macular traction detachment and diabetic maculr oedema. Am J Ophthalmol 2001; 131: 44-49. 23.         Hikichi T, Fujio N, Akiba Y, Takahashi M, Yoshida A. Association between the short term natural history of iabetic macular oedema and the vitreo-macular relationship in type-2 diabetes mellitus. Ophthalmology 1997; 104: 473-478. 24.         Narrallah FP, Alen E. Jalkh, Francis Van, Coppenolle, Masanorikado, Clement L. Prempe, J Wallace Mcmeel, Charles L. Schepens. The role of vitreous in diabetic macular oedema. Ophthalmology 1998; 95(10): 1335-1339. 25.         Stitt AW, Moore JE, Sharkey JA, et al. Advanced glycation end products in vitreous: structural and functional implications for dabetic vitreopathy. Invest Ophthalmol Vis Sci 1998; 39: 2517-2523. 26.         Antonetti D, Barber A, Hollingea L, Wolpert E, Gardner T. Vascular endothelial growth factor induces rapid phosphorylation of tight junction proteins occluding and zonula occluden. J Bio Chem 1999; 274: 23463-23467. 27.         Nauck M, Roth M, Tamm H, Eickelberg O, Wieland H, Stulz P, Perruchoud AP. Induction of vascular endothelial growth factor by platelet activating factor and platelet derived growth factor is down regulated by corticosteroids. Am J Resp Cell Mob Bio 1997; 16: 398-406. 28.         Newman EA. Nature 1984; 309: 155-157. 29.         Sebastian Wolf, et al. Ophthalmology 2004. 30.         Pendergast SD. Vitrectomy for diabetic macular edema sssociated with a taut premacular posterior hyaloid. Curr Opin Ophthalmol 1998; 9: 71-75. 31.         Kampik A, Green WR, Michels RG, Nase PK. Ultrastructrual features of progressive idiopathic epiretinal membrane removed by vitreous surgery. Am J Ophthalmol 1980; 90: 797-809. 32.         Kampik A, Kenyon KR, Michels RG, et al. Epiretinal and vitreous membranes: comparative study of 56 cases. Arch Ophthalmol 1981; 99: 1445-1454. 33.         Nussenblatt RB, Kaufman SC, Palestina AG, et al. Macular thickening and visual acuity. Measurement in patients with cystoid macular edema. Ophthalmology. 1987; 94: 1134-1139. 34.         Hee MR, Izatt JA, Swanson EA, et al. Optical coherence tomography of the human retina. Arch Ophthalmol. 1995; 113: 325-332. 35.         Hee MR, Puliafito CA, Wong C, et al. Quantitative assessment of macular edema with optical coherence tomography. Arch Ophthalmol 1995; 113: 1019-1029. 36.         Hee MR, Puliafito CA, Duker JS, et al. Topography of diabetic macular edema with optical coherence tomography. Ophthalmology 1998; 105: 360-370. 37.         Puliafito CA, Hee MR, Lin CP, et al. Imaging of macular diseases with optical coherence tomography. Ophthalmology 1995; 102: 217-229. 38.         Wilkins JR, Puliafito CA, Hee MR, et al. Characterization of epiretinal membranes using optical coherence tomography. Ophthalmology 1996; 103: 2142-2151. 39.         Van Efferente G, Guot-Argenton C, Guiberteau B, Hany I, Lacotte JL. Macular edema caused by contraction of the posterior hyaloid in diabetic retinopathy. Surgical treatment of a series of 22 cases. J Fr Ophthalmol. 1993; 16: 602-610. 40.         Otani T, Kishi S. Tomographic assessment of vitreous surgery for diabetic macular edema. Am J Ophthalmol. 2000; 129(4): 487-494.   Disclaimer The Rajasthan Journal Of Ophthalmology An Official Publication Of TheRajasthan Ophthalmological Society
Chief Web Editor Dr Sudhir Singh All Rights Are Reserved To Rajasthan Ophthalmological Society